perspectives in high frequency ventilation: proceedings of the international symposium held at...
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PERSPECTIVES IN HIGH FREQUENCY VENTILATION
DEVELOPMENTS IN CRITICAL CARE MEDICINE AND ANESTHESIOLOGY
Other volumes in this series:
Prakash, Omar (ed.): Applied Physiology in Clinical Respiratory Care. 1982. ISBN 90-247-2662-X.
McGeown, Mary G.: Clinical Management of Electrolyte Disorders. 1983. ISBN 0-89838-559-8.
Klain, Miroslav: High Frequency Ventilation. Scheck, P.A., Sjostrand, U.H., and Smith, R.B. (eds.): Perspectives in High Fre
quency Ventilation. 1983. ISBN 0-89838-571-7. Stanley, Th.H. and Petty, W.C.(eds.): New Anesthetic Agents, Devices and Monitor
ing Techniques. 1983. ISBN 0-89838-566-0.
PERSPECTIVES IN HIGH FREQUENCY VENTILATION
Proceedings of the international symposium held at Erasmus University, Rotterdam, 17-18 September 1982
edited by
PAUL A. SCHECK
Erasmus University Academic Hospital Rotterdam, The Netherlands
ULF H. SJOSTRAND
University of Texas San Antonio, TX, USA Orebro Medical Center Hospital Orebro, Sweden
R. BRIAN SMITH
University of Texas San Antonio,TX, USA
1983 MARTINUS NIJHOFF PUBLISHERS a member of the KLUWER ACADEMIC PUBLISHERS GROUP BOSTON I THE HAGUE I DORDRECHT I LANCASTER
Distributors
for the United States and Canada: Kluwer Boston, Inc., 190 Old Derby Street, Hingham, MA 02043, USA for all other countries: Kluwer Academic Publishers Group, Distribution Center, P .O.Box 322, 3300 AH Dordrecht, The Netherlands
Library of Congress Cataloging in Publication Data
Main entry under title:
Perqpectives in high frequency ventilation.
(Developments in critical care medicine and anesthesiology; v. 4)
Proceedings of the International Symposium on High Frequency Ventilation, held Sept. 1982 at Erasmus University Medical School.
Includes index. 1. Respiratory therapy--Congresses. 2. Ventilation
--Congresses. r. Scheck, Paul A. II. Sjostrand, Ulf H. III. Smith, R. Brian. IV. International Symposium on High Frequency Ventilation (1982 : Erasmus Ul:iversity
Medical School) V. Erasmus Universiteit Rotterdam. Faculteit der Geneeskunde. VI. Series. [DNLM: 1. Respiration, Artificia1--Congresses. WO 250 p46T 1982] RCT35.15P4T 1983 616.2'40636 83-2386
ISBN-13: 978-94-009-6713-7 001: 10.1007/978-94-009-6711-3
Copyright
e-ISBN-13: 978-94-009-6711-3
© 1983 by Martinus Nijhoff Publishers, Boston. Softcover reprint of the hardcover 1 st edition 1983 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publishers, Martinus Nijhoff Publishers, 190 Old Derby Street, Hingham, MA 02043, USA.
CON TEN T S
Preface XI
List of contributors XIII
A. Experimental studies
A simple mathematical model of High Frequency Ventilation. 1
A. Versprille.
Development and clinical application of High Frequency Ventilation. 12
U.H. Sjostrand- L. Bunegin, R.B. Smith, ~i.F. Babinski.
Convective diffusion in oscillatory flow as a gas transport
mechanism during High Frequency Ventilation.
H.J. van Ouwerkerk, P. Gieles, J.M. Bogaard.
Pressure flow pattern and gas transport using various types of
High Frequency Ventilation.
M. Baum, H. Benzer, W. Goldschmied, N. Mutz.
A review of experimental and theoretical studies of High Frequency
Ventilation.
A.S. Slutsky, R.D. Kamm, J.M. Drazen.
Effects of High Frequency Jet Ventilation design and operational
variables upon arterial blood gas tensions.
J.M. Calkins, C.K. Waterson, S.F. Quan, H.W. Militzer,
Th.J. Conahan, C.W. Otto, S.R. Hameroff.
Airway pressure as a determining factor for ventilation and
haemodynamic efficiency during HFJV.
M. Jimenez Lendinez, J.A. Cambronero, J. Lopez, B. Galvan,
A. Garcia, R. Denia, A. Aguado.
B. Experimental studies and mechanics
High Frequency Ventilation: an experimental comparison of HFPPV
and HFJV.
U.H. Sjostrand, M.F. Babinski, U.R. Borg, R.B. Smith.
39
51
59
71
81
87
VI
Alveolar pressures during High Frequency Ventilation.
P.R. Fletcher.
Carbon dioxide clearance during High Frequency Jet Ventilation
(HFJV) .
J.L. Bourgain, A.J. Mortimer, M.K. Sykes.
Hemodynamic effects of High Frequency Ventilation.
F.R. Gioia, A.P. Harris, R.J. Traystman, M.C. Rogers.
Cardiovascular consequences of High Frequency Ventilation.
C.W. Otto, J.M. Calkins, S.F. Quan, Th.J. Conahan, C.K. Waterson,
S. R. Hameroff.
Pneumatic controlled circulation: PCC.
W.L. den Dunnen, T. Mostert.
C. ~1echanics and bloodgases
Microcomputer-based signal averager for analysis of pulsed gas
streams intended for use in High Frequency Jet Ventilation.
L. Deen, T. Dijkhuis.
Evaluation of a new valveless all purpose ventilator: effect of
ventilating frequency PEEP, PAC02 and PA02 on phrenic nerve
activity.
M.K. Chakrabarti, J.G. Whitwam.
Humidification of the respiratory tract in HFJV.
W. Fuchs, R. Fechner, E. Racenberg.
Efficiency of intrapulmonary gas distribution during High Frequency
92
93
105
115
122
132
140
146
Ventilation. 150
I. Eriksson.
Gas exchange in High Frequency Ventilation: an experimental study. 158
M. Klain.
Gasanalysis by masspectrometry during High Frequency Ventilation. 164
G. Rolly, L. Versichelen.
Digital ventilation. 172
M. Wendt, L. Freitag, F. Dankwart.
VII
D. Clinical use - part I
One lung High Frequency Ventilation for intrathoracic surgery.
N. EI-Baz, A. EI-Ganzouri, A. Ivankovich.
High Frequency Insufflation technique during endolaryngeal
178
microsurgery. 180
L. Versichelen, G. Rolly, H. Vermeersch.
Total intravenous anaesthesia during High Frequency Ventilation. 193
C. Mallios, P.A. Scheck.
High Frequency Ventilation for laser surgery of the larynx. 204
P.A. Scheck, C. Mallios, P. Knegt.
High Frequency Jet Ventilation via a nasotracheal tube for
surgery of the larynx and trachea.
W.K. Hirlinger, A. Deller, o. Sigg, W. Dick, H.H. Mehrkens.
E. Clinical use - part II
High Frequency positive pressure ventilation for major airway
surgery.
N. EI-Baz, A. EI-Ganzouri, A. Ivankovich.
High Frequency Jet Ventilation for pulmonary resection.
P. Moulaert, G. Rolly.
Clinical experience with High Frequency Ventilation.
M. Klain, J. Fine, A. Sladen, K. Guntupalli, J. Marquez,
H. Keszler.
Peri and postoperative application of various types of High
Frequency Ventilation (HFV).
H. Benzer, M. Baum, St. Duma, A. Geyer, N. Mutz.
High Frequency Jet Ventilation in the postoperative period.
A. Sladen, K. Guntupalli, M. Klain, C. McConaha.
212
216
227
233
240
251
VIII
F. Intensive Care
High Frequency Jet Ventilation compared to volume cycled
ventilation: a prospective randomized evaluation.
G.C. Carlon, J.S. Groeger.
Comparative studies of CPPV and HFPPV in critical care patients:
262
Clinical evaluation and studies on intrapulmonary gas distribution. 272
U.H. Sjostrand, U.R. Borg, I.A. Eriksson, R.B. Smith, L.M. Wattwil.
Alternatives to conventional ventilation. 284
T.J. Gallagher.
Combined High Frequency Ventilation for treatment of severe
respiratory failure. 292
N. El-Baz, A. El-Ganzouri, A. Ivankovich.
High Frequency Jet and intermittent positive pressure ventilation,
with PEEP: A comparison of peak and mean airway pressures.
A. Sladen, K. Guntupalli, f.l. Klain and R. Romano.
High Frequency Jet Ventilation and conventional ventilation: A
comparison of cardiorespiratory parameters.
A. Sladen, K. Guntupalli, M. Klain, R. Romano.
Early clinical experience with High Frequency in our UCI.
M. Jimenez Lendinez, J. Lopez Diez, J.A. Cambronero Galache,
M.A. Palma Gamiz, J.A. Lapuerta, A. Aguado ~latorras.
What is the role of transtracheal ventilation in emergency and
long-term respiratory support ?
M. Klain, H. Keszler.
High Frequency Ventilation and IPPV in the presence of a
bronchopleural fistula.
R.B. Smith, B.H. Hoff, E.V. Bennett, E.A. Wilson, F.L. Grover,
M.F. Babinski, U.H. Sjostrand.
302
305
309
314
316
IX
High Frequency Ventilation with topical anaesthesia as an aid
to physiotherapy.
C.J.J. Westerman, C.D. Laros, J.M. Dolk.
Index
319
325
PREFACE
In the last fifteen years, there has been increasing
interest in the experimental and clinical use of ventilation
at high respiratory frequencies. The International Symposium
on "High Frequency Ventilation" held at Erasmus University
Medical School in September 1982, was designed to bring
together researchers and individuals interested in this
field. They presented experimental and clinical data, and
exchange of information was encouraged. Individuals attended
from several European countries and from the United States.
The Symposium lasted two days and presentations were
assigned to various groups including experimental,
mechanical and clinical studies. On the final day, there was
a panel discussion on "HFV - Present and Future". Additional
features of the Symposium were film presentations and posters.
These proceedings contain the almost complete Symposium
presentations. As the format was an "Open Forum" it should
be emphasized that these proceedings have not undergone peer
review or major editorial changes. Thus, they are expressly
the opinions of the individual authors and not those of the
Symposium Committee, the Editors of the Proceedings, or the
Institutions of these individuals.
The Editors.
LIST OF CONTRIBUTORS
Agudo Matorras, A., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compos tela 62, Madrid 34, Spain
Anderson, J.B., MD, Department of Anaesthesia, University of Copenhagen, Herlev Hospital, Herlev Ringvej, DK-2730 Herlev, Denmark
Babinski, M.F., MD, Department of Anesthesiology, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
Baum, M., Ing., Allgemeines Krankenhaus der Stadt Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, A-I090 Vienna, Austria
Bennett, E.V., MD, Department of Anesthesiology, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
Benzer, H., MD, Allgemeines Krankenhaus der Stadt Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, A-I090 Vienna, Austria
Boogaard, J.M., Department of Pulmonary Diseases, Erasmus University, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Borg, U.R., MD, Department of Anesthesiology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
Bourgain, J.L., MD, (Universite de Paris) University of Oxford, Nuffield Department of Anaesthetics, Oxford OX2 6HE, United Kingdom
Calkins, J.M., MD, Ph D, Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell, Room 5304, Tucson AZ 85724, USA
Cambronero, J.A., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compostela 62, Madrid 34, Spain
Carlon, G.C., MD, Department of Critical Care, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York NY 10021, USA
Chakrabarti, M.K., BSc, MPhil, University of London, Department of Anaestehics, Royal Postgraduate Medical School, Hammersmith Hospital, Ducane Road, London W12 OHS, United Kingdom
Conahan, Th.J., MD, Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell, Room 5304, Tucson AZ 85724, USA
Dankwart, F., MD, Department of Anesthesiology, Klinik fur Anasthesiologie, Universitat Munster, Jungeblodtplatz 1, D 44 Munster, BRD
Deen, L., MD, Ph D, Department of Anesthesiology, Academisch Ziekenhuis Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Deller, A., MD, Department of Anesthesiology, Steinhoevelstrasse, 0-7900 Ulm, BRD
Denia, R., MD, C. Intensivos, CSSS "La paz", c/Santiago de Compostela 62, Madrid 34, Spain
Dick, W., MD, Department of Anesthesiology, Steinhoevelstrasse, 0-7900 Ulm, BRD
Dolk, J.M., St. Antonius Ziekenhuis, J. van Scorelstraat 2, 3583 CP Utrecht, The Netherlands
Drazen, J.M., MD, West Roxbury V.A. Hospital, 1400 VFW Parkway, West Roxbury MA 02132, USA
Duma, St., Allgemeines Krankenhaus der Stadt Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, 1-1090, Vienna, Austria
Dunnen, W.L., den, MD, Erasmus University, P.O. Box 1728, 3000 DR Rotterdam, The Netherlands
Dijkhuis, Th., MD, Department of Anesthesiology, Academisch Ziekenhuis Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
EI-Baz, N., MD, Rush-Presbyterian-St. Luke's Medical Center, 1753 W Congress Parkway Chicago, IL 60612, USA
EI-Ganzouri, A., MD, Rush-Presbyterian-St. Luke's Medical Center, 1753 W Congres Parkway, Chicago IL 60612, USA
Eriksson, J., MD, Department of Anesthesiology, Orebro Medical Center Hospital, S-70185 Orebro, Sweden
Fechner, R., MD, Institut fur Anaesthesie der Universitat des Saarlandes, 6650 Homburg/Saar, BRD
Fletcher, P.R., MD, University of Connecticut, Health Center, Farmington CT 06032, USA
Fine, J., MD, Department of Anesthesiology, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Freitag, L., MD, Klinik fur Anaesthesiologie, Universitat Munster, Jungeblodtplatz 1, 0-44 Munster, BRD
Fuchs, W., MD, Institut fur Anaesthesie der Universitat des Saarlandes, 6650 Homburg/Saar, BRD
Gallagher, T.J., MD, University of Florida College of Medicine, Box J-254, JHMHC, Gainesville FL 34610, USA
Geyer, A., MD, Allgemeines Krankenhaus der Stadt Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, A-I090, Wien, Austria
Gieles, P., Department of Physics, Technical University Eindhoven, Eindhoven, The Netherlands
Gioia, F.R., MD, Pediatric Intensive Care Unit, Department of Anesthesiology/ Critical Care Medicine, The Johns Hopkins University, Baltimore MD 21205, USA
Goldschmied, W., MD, Allgemeines Krankenhaus der Stadt Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, A-I090 Wien, Austria
Groeger, J., MD, Department of Critical Care, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York NY 10021, USA
Guntupalli, K., MD, Department of Anesthesiology, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Hameroff, S.R., MD, Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell, Tucson AZ 85724, USA
Harris, A.P., MD, Pediatric Intensive Care Unit, Department of Anesthesiology/ Critical Care Medicine, The Johns Hopkins University, Baltimore MD 21205, USA
Hirlinger, W.K., MD, Department of Anesthesiology, Steinhoevelstrasse, D-7900 Ulm, BRD
Hoff, B.H., MD, Department of Anesthesiology, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
Ivankovich, A.D., MD, Department of Anesthesiology, Rush-Presbyterian-St. Luke's Medical Center, 1753 West Congress Parkway, Chicago IL 60612, USA
Jimenez-Lendinez, J., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compostelc 62, ~adrid 34, Spain
Kamm, R.D., MD, Harvard Medical School, West Roxbury V.A. Hospital, 1400 VFW Parkway, West Roxbury MA 02132, USA
Keszler, H., MD, Department of Anesthesiology, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Klain, M., MD, Ph 0, Research Divison, Department of Anesthesiology, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Knegt, P., MD, Department of Anesthesiology, Erasmus University/Academic Hospital Rotterdam, Dr. Molewaterplein 40, 3015 GO Rotterdam, The Netherlands
xv
Lapuerta, J.A., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compostela 62, Madrid 34, Spain
Laros, C.D., MD, St. Antonius Ziekenhuis, J. van Scorelstraat 2, 3583 CP Utrecht, The Netherlands
Lopez-Diez, J., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compostela 62, Madrid 34, Spain
Mallios, C., MD, Department of Anesthesiology, Erasmus University/Academic Hospital Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands
Marquez, J., MD, Department of Anesthesiology, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
McConaha, C., MD, Department of Anesthesiology, Montefiore Hospital, University of Pittsburgh, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Mehrkens, H.H., MD, Department of Anesthesiology, Steinhoevelstrasse, D-7900 Ulm, BRD
Militzer, H.W., MD, Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell, Tucson AZ 85724, USA
Mortimer, A.J., MD, University of Oxford, Nuffield Department of Anaesthetics, Oxford OX2 6HE, United Kingdom
Mostert, T., MD, Erasmus University, Thorax Center, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Moulaert, P., MD, Academic Hospital-University Gent, De Pintelaan 185, B-9000 Gent, Belgium
Muts, N., MD, Allgemeines Krankenhaus der Stad Wien, Klinik fur Anaesthesie und Allgemeine Intensivmedizin der Universitat Wien, Spitalgasse 23, A-l090 Vienna, Austria
Otto, C.W., MD, Department of Anesthesiology and Internal Medicine, University of Arizona, Health Sciences Center, 1501 N Campbell Avenue, Tucson AZ 85724, USA
Ouwerkerk, H.J., van (Tl Department of Physics, Technical University Eindhoven, The Netherlands
Palma-Gamiz, M.A., MD, C. Intensivos, CSSS "La Paz", c/Santiago de Compostela 62, Madrid 34, Spain
Quan, S.F., MD, Department of Anesthesiology, Arizona Health Sciences Center 1501 N Campbell, Tucson AZ 85274, USA
Racenberg, E., MD, Institut fur Anaesthesie der Universitat des Saarlandes, 6650 Homburg/Saar, BRD
Rogers, M.C., MD, Pediatric Intensive Care unit, Department of Anesthesiology/ Critical Care Medicine, The Johns Hopkins University, Baltimore MD 21205, USA
Rolly, G., MD, Department of Anesthesiology, Academic Hospital, University of Gent, De Pintelaan 185, B-9000 Gent, Belgium
Romano, R., MD, Department of Anesthesiology, Montefiore Hospital, University of Pittsburgh, School of Medicine, 3459 Fifth Avenue, Pittsburgh PA 15213, USA
Rouby, J.J., MD, Department of Anesthesiology, 83 Boulevard de l'Hopital, 75651 Cedex 13 Paris, France
Scheck, P.A., MD, Department of Anesthesiology, Erasmus University/Academic Hospital Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam. The Netherlands
Sigg, 0., MD,. Department of Anesthesiology, Steinhoevelstrasse, D-7900 Ulm, BRD
Sjostrand, U.H., MD, Ph D, Department of Anesthesiology, The University of Texas Health Science Center at San Antonio, San Antonio TX 79284, USA & Department of Anesthesiology and Intensive Care, Orebro Medical Center Hospital, Orebro, S-70l85, Sweden
Sladen, A., MD, Department of Anesthesiology and Surgery, Montefiore Hospital, University of Pittsburgh School of Medicine, Pittsburgh PA 15213, USA
Slutsky, A.S., MD, Harvard Medical School, West Roxbury V.A. Hospital, 1400 VFW Parkway, West Roxbury, MA 02132, USA
Smith, R.B., MD, Department of Anesthesiology, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
Sykes, M.K., MD, University of Oxford, Nuffield Department of Anaesthetics Oxford, OX2 6HE, United Kingdom
Traystman, R.J., Pediatric Intensive Care Unit, Department of Anesthesiology/ Critical Care Medicine, The Johns Hopkins University, Baltimore MD 21205, USA
Vermeersch, H., MD, Academic Hospital, University of Gent, Department of Anesthesiology, De Pintelaan 135, B-9000 Gent, Belgium
Versichelen, L., MD, Academic Hospital, University of Gent, Department of Anesthesiology, De Pintelaan 135, B-9000 Gent, Belgium
Versprille, A., Ph D, Laboratory of Pathophysiology of Ventilation, Erasmus University Medical School, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Waterson, Ch.K., MD, Department of Anesthesiology and Internal Medicine, University of Arizona, Health Sciences Center, 1501 N Campbell Avenue, TUcson AZ 85724, USA
Wattwil, L.M., MD, Department of Anesthesioiogy and Intensive Care, Orebro Medical Center Hospital, Orebro, S-70l85, Sweden
Wendt, M., MD, Abteilung fur Anaesthesiologie, Klinik fur Anaesthesiologie, Universitat Munster, Jungeblodtplatz 1, D-44 Munster, BRD
Westermann, C.J.J., MD, St. Antonius Ziekenhuis, J. van Scorelstraat 2, 3583 CP Utrecht, The Netherlands
Whitwam, J.G., ME, Ph D, University of London, Department of Anaesthetics, Royal Postgraduate Medical School, Hammersmith Hospital, Duncane Road, London W12 ORS, United Kingdom
Wilson, E.A., MD, Department of Anesthesiology, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio TX 78248, USA
A. EXPERIMENTAL STIJDIES
A SHIPLE MA'.FHBMAT-IC1H .. MODEL OF HIGH FREQUENCY VENTILATION
A, VERSPRILLE Pathophysiological laboratory, Department of Pulmonary Diseases, Erasmus University, Rotterdam, The Netherlands
It took the human being 420 years from the first scienti
fic studies on flying and aircrafts by Leonardo da Vinci
(4) to the first flight by the Wright brothers in 1903,
whereas sailing was practised from the very beginning of
known history.
When positive end expiratory pressure (PEEP) was reintroduced
by Ashbaugh in 1967 (1), it was soon accepted as one of the
beneficial modes of ventilatory support. High frequency venti
lation (HFV) was introduced at almost the same moment (5),
but has not yet been generally accepted as a superior therapy
above conventional ventilation as demonstrated by "The Experts
Opine" in 1981 (2).
Undoubtedly the very complex physical problems of gas exchange
achieved by jet and oscillatory ventilation in comparison with
the simple logic of PEEP will be jOintly responsible for this
tardy progress. We badly need experimental and theoretical
physicists to solve the complicated processes of gas exchange
under conditions of HFV.
Taylor diffusion.
In 1980 Slutsky et al. (6) introduced Taylor diffusion (7) as
one of the main mechanisms for gas transport under circum
stances of high frequency oscillatory ventilation (HFO). For
this hypothesis Chatwin's studies (3) on longitudinal disper
sion of a substance in an oscillatory fluid flow served as a
model. High frequency jet ventilation (HFJV) has not yet
received such a fundamental attention. The more complicated
physical characteristics of jet flows cDmpared with the sinu
soidal fluctuations as used in HFO might be one of the reasons.
2
For understanding of Taylor diffusion we consider one alveolar
compartment and its airway tube (fig. l.a). We assume the
oscillation sinusoidal. In fig. I.e the expiratory period of
the cycle is between the 90° and 270° phase of the cycle and
the inspiration between 270° and 90° of the following cycle.
a
b
c
d
~i+L e p=o EXp:°;E°O
270 0
Insp . . .; rJr P---- FIGURE I:
CO 2 transport from alveolar compartments (left) through airway tubes (right) by oscillatory ventilation based on Taylor diffusion. CO 2-concentration is simulated by the density of the shading. a: 90°; b. during the phase between 90° and 2700; c: 270°; d: during 270°-90° of the next cycle; e: HFO delivery system: a bias flow from P+ to P- across two resistances RI and R2 , causing a P = 0 at the outlet on which an oscillation is performed. The sinus gives the position of the piston as a function of the phase of the cycle.
In fig. I oscillation is started without CO 2 in the airway
tube at the 90° phase of the cycle, i.e. the piston of the
pump or the membrane of the speaker is in full inspiratory
position and at the beginning of the expiratory movement (fig.
l.a). Under laminar flow conditions alveolar air extends into
the airway tube according to a three dimensional parabolic
curve (fig. l.b). During this convective transport CO2 dif
fuses in radial direction. When the diffusion coefficient for
CO 2 (DC02 ) is sufficient, a concentration gradient will exist
only in longitudinal direction at the end of the first half
of the oscillation (fig. l.c). Thus, a combination of convec
tive transport (airflow) and radial diffusion establishes the
longitudinal dispersion of the CO 2 in the tube.
During the next inspiratory period of the cycle air moves
backward into the alveoli (fig. l.d) leaving a part of the
3
CO2 in the tube, which diffuses in axial direction.
Once more a longitudinal gradient will develop, but at a
lower concentration gradient. It will be obvious that for
gases with a low diffusion coefficient a small radial disper
sion occurs. Then, the concentration remains high in the
axial part of the tube during the expiratory period of the
oscillation. In consequence more gas is moved backward
during the following reversed part of the oscillation. This
results in a smaller transport of gas from the alveoli to the
outlet of the oscillatory system.
A model of convective and diffusive transport.
For clinical practice it will be necessary to find simple
mathematical relationships between the imposed parameters of
ventilation and the dependent variables of gas exchange.
Otherwise HFV will not gain a much greater clinical signifi
cance than its empirically proven usefulness for bronchoscopy
and laryngeal and tracheal surgery.
Reduction of complex processes to simple models might help us
to understand and to predict what happens. To support this
development a simple model of gas transport will be presented.
In this model ventilation is performed with tidal volumes
smaller than that of the anatomical dead space. The airways
are lumped to one tube of constant cross section, which commu
nicates with one alveolar compartment (fig. 3.a). In conse
quence the progressive increase in volume from the upper to
the peripheral airways is represented in the tube as a cor-
responding progression in length (fig. 2).
FIGURE 2
Projection of airway volume (A) on the tube length of the model (B).
A Vertically the volume is given, horizontally the length, both in arbitrary units. The airways are subdivided in parts of equal length. The corresponding volume between each pair of projection lines (-.-.-) are the same in airways and model.
B
4
The parabolic flow pattern is simplified to a displacement of
a cylinder of air, representing the forward transport in this
pattern (fig. 3.b). While the cylinder moves forward, CO2 diffuses radially and a compartment with a lower CO2 concen
tration than in the alveoli results (fig. 3.c). Next a
cylinder of this lower concentration is moved backward (fig.
3.d) and the airway compartment remains with a still lower
concentration (fig. 3.e). The next half cycle is again in
expiratory direction (fig. 3.f) and the whole process reiter
ates leading to a further displacement of CO2 in the direction
of the outlet.
a -d
b e
=
c -f
FIGURE 3: Model of oscillatory gas transport. (8)
C 1
I I I J I FIGURE 4: Concentration cascade, representing the concentra
tion gradient from the alveolar compartment, C4 , over the airways C3-C 1 before the next expiratory phase of the cycle.
5
After a series of oscillations a stationary state will be
reached and a cascade of concentrations results (fig. 4).
In nature a continuous fall from alveoli to outlet will be
present.
During oscillatory ventilation under stationary circumstances,
first a cylinder of all concentrations moves up one step in
expiratory direction followed by a back flow of the cylinder
with the new equilibrium concentrations. At the outlet a
cylinder with the lowest concentration is eliminated which
is replaced by a cylinder with concentration zero.
Calculations.
Suppose there are (n) compartments, including the alveolar
compartment. The airway tube compartments are numbered 1, 2
(n-1) from the outlet to the alveoli. The ratio (a)
between the volume of the cylinder, which is moved up, and
the total volume of its corresponding airway compartment is
assumed to be constant over the total length of the airways.
This allows us to calculate the forward and backward trans
port of the gas for each compartment, as well as the net
forward transport, i.e. the difference between the two
(Table 1). Forward transport occurs during the expiratory
phase and backward transport during the inspiratory phase of
the oscillation.
TABLE 1
NET TRANSPORT FROM ONE COMPARTMENT TO THE NEXT IN TERMS OF COMPARTMENT CONCENTRATIONS (C) OF A GAS
Compartmen t Forward Backward Net forward transport
1 aC1 0 aC1 2 aC2 a{aC 2+(1-a)C 1 } a{ (l-a)C2-(1-a)C 1 }
3 aC3 a{aC3+(1-a)C 2 } a{ (l-a) C3- (l-a) C2 }
n aCn a{aCn+(1-a)Cn_ 1 } a{(1-a)Cn-(1-a)Cn_1}
C1 ,C 2 , C3 .... C : concentrations of gas in compartments 1, n 2, 3 and .. . n .
Net forward transport = forward - backward transport.
6
Under stationary circumstances the net forward flow is the same
in all compartments and equal to aC 1 , which is the amount of
gas expelled at the outlet. C2 , C3 ... Cn can be solved in terms
of C1 , according to a{(1-a)C 2-(1-a)c 1 }=ac1 , which gives
C2 =C 1 (2-a)/(1-a). Substitution of this value in the equation
a{(l-a)C 3-(l-a)C 2 }=aC1 , gives C3 =C 1 (3-a)/(1-a). The general
formula for the concentration Cn in the compartment n is:
(1)
In a numerical example (Table 2) we assumed n = 4, a = 0.5 and
PAC02 = 42 rrunHg (C 4 in Table 2). Then, during the oscillations
each expiratory stroke eliminates a volume VT with a PC02 = 6
rrunHg (C 1 in Table 2) at the outlet. During the inspiratory
stroke of the cycle the same volume returns without CO 2 ,
TABLE 2
CONCENTRATION CASCADE AND ELIMINATION OF GAS PER CYCLE
n = 4, number of compartments; a = 0 .5, the ratio between the volume of the displaced cylinder and that of each total compartment I, 2 and 3. Compartment 4 is the alveolar compartment where we assume the PAC02 to be constant at 42 rrunHg.
a. equilibrium before the forward movement
C4 C3 C2 C1
30 18 6 42 outlet
30 18 6 -----------------------------
b. forward
42
movement
30
42
18
30
6
18 6
c. equilibrium before the backward movement
42 36
36
d. backward movement
42 36
24
24
24
24
12
12
12
12
o
e. equilibrium before forward movement see a.
7
In the lower line of a-e the gas concentration of the cylinder
are printed, which move forward and backward; in the
upper line the concentrations of the non-movable gas of the
airway compartments are given.
Efficiency of ventilation and CO 2 elimination.
The Bohr equation for dead space (Vo) is
(Cn-C I ) VO=VT Cn
where Cn is the alveolar CO2 concentration, CI the concentra
tion of CO 2 near the outlet, which is expelled during each
oscillation, and VT the oscillatory volume. If we use the data
from Table 2 VO =VT (42-6)!42= (6!7)VT .
The concept of dead space for an oscillatory volume is confus
ing because the total oscillatory volume participates in eli
mination of CO2 albeit at a lower concentration than the
alveolar value, which is due to the CO2 gradient over the air
ways as simulated by the cascade. The term effective ventila
tory volume (VT,eff) seems preferable, being the product of
oscillatory volume and the ratio between expelled (C I ) and
alveolar (Cn ) concentration or tension (PI and Pn resp.). Thus,
VT,eff = VT.CI!Cn (2)
In our example of Table 2 VT,eff = (1!7)VT .
The efficiency of ventilation could be expressed as VT,eff/VT
or CI!Cn. In fig. S.A the efficiency of ventilation is plot
ted as a function of (a) with (n) as a parameter. According
to equation (1) CI/Cn = (I-a) I (n-a) .
At all values of (n) we see a decrease of the efficiency when
(a) inc+eases. At each level of (a) the efficiency is higher
when (n) is smaller (fig. S.B). Thus, a thin cylinder of air
eliminates a higher CO2-concentration than a wide one, and
the effectiveness is the highest when the thin cylinder runs
the total length of the airways from outlet to alveoli (n = 2) .
When the airways are subdivided in many compartments (n-l) the
efficiency decreases drastically.
8
CI A
Cn B
.50 2
.50 .1
.40
.30 3
4 .20 5
6
.10
2 3 5 6 a n
FIGURE 5: Efficiency of the ventilatory volume (CI/C ) depending on (a) in A and (n) in B with parameters (n) and Ya) respectively given in values left from each relation.
The efficiency counts for the oscillatory volume, VT , but does
not apply to the elimination of CO 2 per oscillatory cycle,
because that also depends on the value of VT .
VC02 per cycle = VT . P 1 .c, where c is a correction for tempera
ture and ambient air pressure Pair; c = To/(Tbody.Pair).
VT = aVDI (n-l), where VDI (n-l) is the volume of an "airway com
partment and (a) the part of that volume displaced during an
oscillation. PI = (l-a)Pn/(n-a) , see eqn. (1). Thus,
a (I-a) VC02, cycle = (n-l) (n-a) . PAC02 · VD·c (3)
where PAC02 = P n.
trhe first ratio in this equation, depending on (a)
and (n), reflects the amount of CO 2 elimination in arbitrary
units, when PAC02 ' VD and c are assumed to be constant. In
fig. 6 this ratio is plotted as a function of (a) with (n) as
a parameter.
This figure demonstrates that CO2-elimination has an optimum
value for (a) between 0.5 and 0.6. An increase of airway com
partments (n-l) causes a deep fall in CO2-elimination.
The model also predicts the oscillatory frequency (f) for all
values of (n) and (a) and a certain CO 2-production, VC02 .
9
.15 FIGURE 6:
c: o -:;; .10 c:
CO 2 elimination per oscillatory cycle in arbitrary units {a(1-a)/(n-1) (n-a)} as a function of (a) with (n) as a parameter in values left of each relation.
E a;
'" o C).05
.1 .2 .3 .4 .5 .6 .7 .8 .9 a
Calculation of f in Herz.
Assumptions: . . -1
VD =150 ml, n=2 and a=0.5, VC02 =240 mlmln , PAC02=42
Torr, Pair = 760 Torr, TO = 273 K and Tbody = 310 K.
From " C0 2 = f. VC02 , cycle and equation (3) follows: . a(l-a) Vco2/60 = f. (n-l) (n-a) PAC02· VD .TO/Tbody·P air
f=3.3 Hz
V T = 0 .5 V D/ 1 = 75 ml
When we change n = 4 and a = 0 .5
f = 23 Hz
VT =0.5 VD/3=25 ml
Washout technique.
The model demonstrates that a washout technique for estimation
of alveolar volume fails under circumstances of oscillation
with smaller volumes than anatomical dead space. In Table 3
this is illustrated in a model with n = 2 and a = 0.5. The CN2
in i-age, which is washed out, falls profoundly during the
first oscillations with pure oxygen. This steep fall is
exclusively the result of a washout of the airways.
IO
TABLE 3
WASHOUT OF N2
Equilibrium states Forward movement --+
Alveoli Airways Backward movement~
I 80
I 80
al 80 a2 80 -+ 80 80 80
I 80
I 80
bl 80 b2 80 +--80 0
I 40
I 40
cl 80 c2 80 --+ 40 40 80
I 60
I 60
d 1 80 d2 80 +--60 0
I 30
I 30
el 79.5 e2 79.5 79.5 ---+ 30 30
Conditions: n= 2; a= 0.5; alveolar CN = 80%. Alveolar CN2 = 79.5 (el)was estimated ~rom: V~ = 150 ml and VA =2925 mI, then CN2= (2.975 Lx 80%+0.07 Lx 60%)/3L
Closing remarks.
The model visualizes Taylor diffusion in the branched tree of
airways lumped to one tube. This implies that due to airways of
different resistance and diameter, in series as well as in
parallel, regional differences might be expected in (a) and
(n). We have to realize that (a) and (n) are virtual values,
not only depending on geometric features of the airways, but
also on the molecular diffusion coefficient (Dmol) of the gas,
the oscillatory volume (VT), and the volume flow (V), and
therefore presumably also f. When in normal lungs (a) and (n)
could be related to Dmol ' VT ' f and V in relatively simple
equations it could be possible to predict alveolar gas concen-
11
tration. Cn from Cl ' f, VT and V.
In view of the complicated physical problems of gas exchange
during HFV this simplified model merits future consideration.
References.
1. Ashbaugh DG, Petty TL, Bigelow DB, Harris TM. 1969. Continuous positive-pressure breathing (CPPB) in adult respiratory distress syndrome. J. Thorac. Cardiovasc. Surg. 57, 31-41.
2. Bishop MJ, and respectively Froese AB, Mathewson HS, Otto CW, and Watson CB, Bowen EA, Klein EF, Jr. 1981 The experts opine. Survey of Anesthesiology 25, 125-129.
3. Chatwin PC. 1975. On the longitudinal dispersion of passive contaminant in oscillatory flows in tubes. J. Fluid Mech. 71, 513-527.
4. Cutry F. 1975. "Der Vogelflug" in "Leonardo da Vinci. Das Lebensbild eines Genies", Emil Vollmer Verlag, WiesbadenBerlin, 7th edition, pp. 337-347.
5. Sjostrand U. 1977. Review of the physiological rationale for and development of high-frequency positive pressure ventilation, HFPPV. Acta Anaesthesiol. Scand. (Suppl.) 64, 7-27.
6. Slutsky AS, Drazen JM, Ingram RH, Karnrn RD, Shapiro AH, Fredberg JJ, Loring SH, Lehr J. 1980. Effective pulmonary ventilation with small-volume oscillations at high frequency. Science 209, 609-611.
7. Taylor GI. 1953. Dispersion of soluble matter in solvent flowing slowly through a tube. Proc. Soc. A. 219, 186-203.
8. This "cake walk" model is an idea of H.J. van Ouwerkerk, who died on July 4th, 1982, and whose work promised a lot. See chapter in this book by him, Gieles and Bogaard.
DEVELOPMENT AND CLINICAL APPLICATION OF HIGH FREQUENCY VENTILATION
U.H. SJOSTRAND, L. BUNEGIN, R.B. SMITH, M.F. BABINSKI
Department of Anesthesiology, The University of Texas Health Science Center, San Antonio, TX 78284, USA
The literature on the development of artificial r~spiration
includes Genesis 4: 7, and some other importants steps which
may be listed briefly.
1543 - Vesalius ventilated a dog's lungs with bellows connected to the trachea by a hollow reed.
1667 - Hooke ventilated a dog with bellows through a slit in the trachea.
1887 - Fell and 0' Dwyer (36) introduced a foot bellows ventilator for postoperative ventilatory support (Fig. 1).
1896 - Tuffier and Hallion (56) were the first to apply intraoperative artificial respiration by insufflation in an "intubated patient".
1904 - Sauerbruch (38) introduced the "differential-pressure method" for ventilation.
1909 - Meltzer and Auer (37) described intratracheal insufflation for "continuous respiration without respiratory movements".
1916 - Giertz (27) recommended rhythmic inflation rates of 12-16 breaths/min for better ventilation.
1938 - Andersson, Frenckner and Crafoord (1) developed the first commercially available ventilator "Spiropulsator".
1951 - Engstrom (22) introduced the first volume-cycled ventilator (Fig. 2).
1955 - Bjork and Engstrom (8) introduced artifical ventilation for postoperative ventilatory insufficiency.
1963 - Bendixen, Hedley-White and Laver (6) introduced the concept of large tidal volume ventilation (hyperinflation) •
FIGURE 1. The Fell-O'Dwyer (1887) foot bellows ventilator (36).
To Patient
13
~~.~- Gas Exhaust
:'=:::!~=::::;::r== - Gas Inlet
FIGURE 2. Engstrom volume-cycled ventilator system 1951 (22).
In intermittent (IPPV) and continuous (CPPV) positive-
pressure ventilation, today's conventional types of controlled
mechanical ventilation, the lungs are rhythmically inflated
as described by Bjork and EngstrCim in 1955 (44,54). Since
then, the functional characteristics of "conventional" venti-
lator (respirator) systems have been basically the same. They
generally have a large compressible volume and usually operate
at frequencies up to 3D/min.
High frequency po~itive pressure ventilation (HFPPV)
In 1915, Henderson et ale (29) stated that " ••• there may
easily be gaseous exchange sufficient to support life even
when tidal volume is considerably less than dead space".
14
Several decades later, Comroe et al. (19) and Briscoe et al.
(13) further evaluated alveolar ventilation with low tidal
volumes.
Since the late 1930's, it has been known that ventilatory
patterns with high mean airway pressure may hamper adequate
central and peripheral circulation and may increase the inci
dence of barotrauma (43). To overcome this, in 1967, 5berg
and Sj8strand reasoned that endotracheal insufflation with
high ventilatory frequency and small tidal volumes would pro
vide adequate ventilation (40,41). An insufflation catheter
created a ventilator system whose compressible volume and
internal compliance were negligible (Fig. 3). This should
compensate for the increased VO/VT with positive pressure ven
tilation of high frequency (41,43). Lower maximal and mean
airway pressures (ITP) were expected during HFPPV, reducing
the depressing effects on the cardiovascular system.
Technical development and research
Much of the research in high frequency ventilation (HFV)
is centered around ventilator development. These instruments
are based on three general principles: HFPPV, proposed by
5berg and Sjostrand, 1967 (31,41); high frequency oscillation
(HFO), by Lunkenheimer et al., 1972 (34); and high frequency
jet ventilation (HFJV), by Klain and Smith, 1977 (33).
HFPPV initially utilized endotracheal insufflation via an
insufflation catheter positioned within the endotracheal tube,
with expiration through an expiratory valve connected to the
outer orifice (Fig. 3). Later, a pneumatic valve (Fig. 4),
based on the Coanda or wall effect, was developed in which
FIGURE 3. HFPPV insufflation and expiratory systems 1967-1972 (31,41).
FIGURE 5. pneumatic valve approach to HFPPV 1973 (41).
I NSUFFLA TlON EXPIRATION
Expiratory gas
~t
It To patient From patient
FIGURE 4. Pneumatic valve connector 1973 (41).
15
INSuFFLATION EXPIRATION
To patient From patient
FIGURE 6. System H (1974) for volume-controlled ventilation (42,43).
a conditioned gas mixture was intermittently delivered via a
large diameter side-arm branching off the main channel of the
pneumatic valve connector (41). This main channel remained
open and could be utilized for insertion of broncho- or laryn-
goscopic equipment (F ig. 5). Even though both techniques
16
utilize "open systems", gas entrainment does not occur. Later,
an expiratory valve was added to the outlet of the main chan
nel of the pneumatic valve (42,43). During insufflation, the
main channel was closed, opening at end-inspiration for the
expiration phase (Figs. 6 and 7). This system (Sjostrand,
system H) permits low-compressive volume-controlled ventila
tion (35,47). Ventilatory rates (f) ranged from 60 to 110
per min with inspiratory:expiratory (I:E) time ratios less
than 1:2.
FIGURE 7. System H for volume-controlled ventilation (35,48).
In 1981, a double-lumen endotracheal tube with an inspira
tion:expiration lumen (IL:EL) ratio of 1:10 was introduced
(4), with similar functional and dimensional characteristics
of the original HFPPV insufflation technique (31,41). As
recently described (47), this makes it suitable as an integral
part of a low-compressive patient circuit (3) for volume-con
trolled ventilation (Sjostrand, system J). With an expiratory
valve, attached to the expiratory port (EL) of the double
lumen tube (Fig. 8), closed during inspiration through the
17
FIGURE 8. System J for volume-controlled ventilation (47).
insufflation line (IL), pressure/flow-generated volume-con-
trolled ventilation (42,43) can be provided (47). Due to the
small functional dead space of system J, also at a ventilatory
frequency of 60/min (47,54), normocarbia is produced more
efficiently (Figs. 9 and 23) in comparison to system H or con
ventional ventilator systems and ventilatory rates (47,48).
In fact, with system J both with and without PEEP, inspiratory
work with HFPPV (f 60/min) is only 4-5% of that with IPPV (47).
HFO, as described by Lunkenheimer and coworkers (34), uti-
lized a large electromagnet which oscillated a membrane
Experimental Comparison of IPPV and HFPPV -~---.~---.--
Normocarbia IPPV HFPPV HFPPVlPEEP
(PaC02 40 mmHg) (f/t% - 20/33) (f/t% - 60/22) (f /t% - 60/22)
VT (ml) 369±31 9S±28 148±30
'if VENT (ml/mln) 7380±620 S700±1680 8800±1800
Paw (mmHg) 5.7±0.7 0.8±0.02 11.3±0.S
Inspiratory Work 447 22 19 (cm H20 xl/sec)
Ventilatory frequency (f; breaths/min). inspiratory time (t%) in percent of the ventilatory cycle. tidal volumes (VT). ventilator gas outputs (VVENT) and mean airway pressures (Paw) producing normocarbia (PaC02 40 mmHg). Mean values ± SD in 8 anesthetized dogs are given.IPPV: ER-312; HFPPV: System J; HFPPV/PEEP: System J with PEEP of 10 cm H20.
FIGURE 9. Comparative studies of IPPV and HFPPV in dogs (47).
18
attached to a rigid chamber (Fig. 10). This, in turn, was
connected to the animal airway. A fresh gas supply was deli-
vered via a side-arm to the chamber with a second sidearm for
ga"s exhaust. Frequencies up to 40 Hz were investigated. Ven-
tilatory patterns were more or less oscillatory (often sinu-
soidal). Volume-control with this system is difficult despite
no gas entrainment during the ventilatory cycle. Gas exchange
during HFO is thought to occur by enhanced molecular diffusion
(9,16,26).
HFJV (17,33) introduces a high velocity jet stream into the
airway via a narrow cannula (Fig. 11). The cannula may be
placed in a tracheal tube (17) or percutaneously (33) in the
trachea (Fig. 12). The high velocity jet causes gas from the
surrounding environment to be entrained making it difficult to
control volume and gas composition. Gas exchange probably
results partially from jet mixing and partially from enhanced
molecular diffusion (52). Adequate gas exchange with tidal
volumes at or below dead space has been achieved using fre-
quencies up to 400/min (52). The inspiratory phase was about
33% of the ventilatory cycle.
Airway
Frequency Generator
FIGURE 10. Oscillating membrane 1972 (34).
FIGURE 11. Jet injector 1978 (17).
19
FIGURE 12. Transtracheal approach to HFJV 1977 (33).
High frequency ventilation (HFV)
At the present time, the definitions and terms used .for
positive pressure ventilation at high rates are confusing
(46). One approach (Fig. 13), though not entirely satisfac
tory, is to use a range of rate (46). In the frequency
domain, ADO refers to apneic diffusion oxygenation, IPPV
refers to "conventional rates", HFPPV refers to ventilatory
rates of 60-l10/min, HFJV refers to rates of 110-400/min and
HFO refers to rates above 400 and up to 2400/min (54). High
frequency ventilation (HFV) becomes an "umbrella" term encom
passing HFPPV, HFJV and HFO (54).
A more appropriate approach in defining HFPPV, HFJV and HFO
(Fig. 14) could be based on the specific technology respon
sible for ventilation (54). In HFPPV airways are intermit
tently inflated at rates of 60/min or above with fresh gas
and without gas entrainment (45), while HFJV is ventilation
in which a fresh gas jet introduced into the airway results
20
FIGURE 13. Classification of ventilation modalities on the basis of frequency range (46,54).
FIGURE 14. tion (54).
(lL:EL ratio 1:10) Nc volume wntrol Ncga5entrllinmem
1m Volume-Controlled (System J) Valumeccntrol Nogu..,tralnnte11t
Technical development of high frequency ventila-
Experimental Comparison of HFPPV and HFJV
Normocarbia BronchovenfEil Fluidic Ventilator
"t%~60/22 , PV JIN IC PV JIN IC
9,~ 1229 654 798 1139 936 926
(ml/sec)
Paw ± SO S.2±O.& 4.1±O.6 4.4±O.S 9.3±2.4 6.1±O.7 4.S±O.&
(anH,O)
Y-r±SO 296±148 226±61 188±11& 277±56 263±73 190±87
(mQ
Entrained Gas 26 58 (% ofVT)
PV: Pneumatic Valve; JIN: Jet Injector Nozzle; Ie: Insufflation Une of Double-Lumen Tube. V. max: Maximum Inspiratory Flow; Paw: End-Inspiratory Airway Pressure.
FIGURE 15. Comparative studies of three "open" ventilator systems (PV, JIN and IC) for HFPPV and HFJV in dogs and a lung model (45). With HFPPV there is no gas entrainment (PV and IC), while HFJV depends on entrainment (JIN) of a second gas.
21
ina second gas being entrained simultaneously (Fig. 15).
With HFO, gas in the airway is oscillated back and forth in a
sinusoidal fashion, with a fresh gas flow-by located between
the oscillator and patient (Fig. 10). Classifying on the
basis of technical and functional properties does not infer a
sudden switch from classical to entirely different physiologi
cal methods of ventilation (54).
Experimental work with HFV (HFPPV, HFJV, HFO)
Following the introduction of HFPPV, experimental studies
on dogs (31) verified that adequate ventilation with low
airway pressures and minimal circulatory interference was
possible (Fig. 16). During HFPPV, the intrapleural pressure
was negative and spontaneous breathing was absent. Arterial
blood gas analysis verified that this suppression of spontane
ous breathing occurred even at normoventilation. Further
studies using radiospirometric techniques found that intrapul
monary gas distribution during HFPPV was similar to that ob
served during spontaneous breathing. Lung compliance also
remained unchanged even after 9 hours of HFPPV. During normo
ventilation with HFPPV, cardiac output was not different from
intermittent positive pressure ventilatory patterns. Studies
on diuresis, as an indirect measure of ADH production, indi
cated a lower degree of "stress" during HFPPV than IPPV. This
was evidenced by a more active water excretion during HFPPV.
Early work with HFPPV in cats (30,32) revealed only minor
intrathoracic and transpulmonary pressure variations with ade
quate alveolar ventilation and arterial oxygenation. Detailed
investigation of vagal and phrenic nerve activities (30)
22
Type of ventilation I Span taneaus HF PPV ER
Series 1, 6 dogs 6doU· 6dogl Serie.2· 6 dogs ~
mmHg 12 dog. 1Zdogs 6 dog'
200 ,so '8snH~HHHHH
129.l1V~~~ V ~ ~VV~~ ~~~ 179n H k ~ k k k k ~ ~ k k k 1271 'i~~ ~~ ~ V~ VVVV VV\
'82nH~AA~~H~AA~ '2SDlV n~~~~H~W~\
'00
i mmHg
Ii +,0
~
S -'0
I .. ~ -s -S.6~ ~ ,-i V V i -10 ·9.8
+9.6 fi. 1\ 1\ 1\ 1\ 1\ 1\ 1\ +3.7 = ~ ~ +OgL\J '\I '\J " '\J \J \J " -:J.3~~-
+17.9
SIte 0 6 sec 0
Type of ventilation, spontaneous HF PPV
PA , .. th dog 3 recordings), Dog A Dog A PAWP (nch dog 3 recordings)' Dogs A,C Dogs A.B,C
mmHg . 40
ER
Dog A
Dogs B,C
6.te.
~ -' ~
20 +281\1\/11\.1\1\1\1\/\ 1\ 1\1\1\1\1\. +2S~ +28/\/IJV" A II 1If\1\I\JI. II I\(\ II +7~~"4 - 1111~~ 11 'f" 'f .12 +9~" ... .....,\J~..,~ -... "~~~"l"
E l
i mmHg
~ 20
i '0 ;
+'5.6~ '3.2~ +'3-vr. ••• IA •• A. ............ A .. ' . +6~\N\J-wvt' \"IIN'O"\fAI'Lrww\rY1J +6.8 +4-
~ e ;; ..
6HC. 0 6 sec. 0 SSK.
FIGURE 16. Comparative studies of HFPPV and ER (= IPPV) in dogs (31)
spontaneous breathing,
23
showed that HFPPV modifies afferent vagal nerve activity which
inhibits the respiratory center (Fig. 17). With normal arter-
ial C02 and 02 tensions, efferent phrenic nerve activity is
also abolished resulting in cessation of spontaneous respira-
tion.
afferent nerVi!
efferent nerve
afferent vagal n-erVe activity
SO.
50s
® Lr,
Lr,
@
i.r.
I.r r.
@
Lr.
Lr
50 s
®
Lr,
i.r
50s
FIGURE 17. Efferent phrenic and afferent vagal nerve activities (integrated and directly recorded) during nonroventilation (anesthetized cat). In frame a, spontaneous breathing (88) for 50 sec is illustrated. In band c, HFPPV modifies the afferent vagal activity which inhibits the respiratory center, resulting in no spontaneous breathing movements as the efferent phrenic nerve activity is absent. In d-f, after discontinuation of HFPPV there is a return to SB (30).
Animal studies with HFJV (49,52) also demonstrated adequate
ventilation with low airway pressures and minimal circulatory
interference.
In dog experiments with HFJV (2) and HFPPV (10), ventilator-
synchronous pressure changes in intracranial pressure (ICP)
could be eliminated (Figs. 18 and 19), suggesting that these
forms of ventilation might provide better conditions for the
development of more elaborate microneurosurgical techniques
which require a "quiet" brain. This was first demonstrated
in cats ventilated with HFV (55). Cerebral blood flow (CSF)
during HFPPV (f 100/min) is found to be comparable to flows
24
NormalICP
BP 100 2001
(mmHg) 0
Paw 20j 10
(mmHg) 0
IPPV
Elevated ICP
HFPPV 60 HFPPVIOO
BP ~:l N~~~WWW~~1MNW~~~mfWW\!'~rw-J\M,MMMAMMAmW (mmHg) 0
ICP 0 40
1 (mmHg) 20
Paw 2°1 (mmHg) I~J
IPPV HFPPV60 HFPPVIOO
FIGURES 18 and 19. Comparative studies of IPPV (f 20/min) and HFPPV (f 60 and 100/min) on intracranial pressure (ICP) in dogs with normal (top) and elevated (bottom) ICP (10).
observed during IPPV (14), and nutritive blood flow through
the lungs, kidneys and heart also remain within normal limits.
In 1979, human studies using HFO demonstrated adequate gas
exchange (16). Ventilatory patterns were sinusoidal in nature.
In 1980, animal studies at frequencies of 15 Hz required tidal
volumes less than dead space volume (9).
Theoretical considerations
In 1975, Scherer et ale (39) suggested that axial diffusi-
vity was related to the gas velocity in the trachea and could
25
be as much as 4000 times greater than molecular diffusivity.
Studies by Sjostrand et al. (12,25,54) on low-compressive
ventilators and inspiratory flow patterns of an accelerating-
decelerating character (Fig. 20) all seem to indicate that
intrapulmonary gas mixing in conducting airways is enhanced
by instantaneous high initial inspiratory flow and HFV (Fig.
21). Convection of inspired gas along conducting airways
in the form of eddy flow has been suggested as the probable
cause of improved gas mixing and distribution (23,25).
Recordings of Ventilatory Patterns in a Lung Model
l~ _ 400 /:
:g" 20g / L_____ r------~ -200 ...... \
> -400 -___ i -600 -----
---- SV-20 - H-20
o I 2 3 Time (sec)
Recordings of Ventilatory Patterns in a Lung Model
~" 20g 11/ l---0 r1 , _____ _ ~j -, ~-200 ~ .... ~~
> -400 ---_: -600 ---- __ J
1.0
U 0.5
" ~ 0 W .>
-05
-1.0 ---- SV-20 -H-60
o I 2 Time (sec)
Time in msec Between Onset and 90% of Maximal (VE 90%) Flow
Ventilatory Static Compliance of Lung Model Pattern (ml/cm H2O)
<'7E 90%) 27 S9 90
SV-20 (SV-900) 88 80 84
H-20 (System H) 29 34 34
H-60 (System H) 29 29 34
Acceleration of gas during early inspiration. evaluated as time in msec between onset and 90% of maximal (VE 90%) flow studied in a lung model with 3 linear static compliances.
FIGURES 20 and 21. Ventilatory patterns (top) with a conventional (SV=SV-900) and a low-compressive (H=system H) ventilator, and comparative measures (bottom) of 90% of maximal inspiratory flow (59).
26
The significant decrease in mean airway pressure with HFPPV
is related to at least 3 functional properties of the low-
compression pattern without an inspiratory pause (44,54,58):
First - there is less distension of the lungs and thorax with the smaller effective tidal volme (VT Eff) during HFPPV.
Second - the absence of an inspiratory pause (no-flow period) in the conducting airways means that inspiratory pressures during HFPPV equilibrate with the aveolar space to a lesser extent than at conventional ventilatory frequencies.
Third - at high inspiratory gas flow, airway resistance to the rapidly moving gas provides low distal airway pressure.
Working on HFO systems, in 1980 Fredberg (26) proposed the
hypothesis that enhanced gas exc.hange in airways is controlled
by a mixing process defined directly by the molecular diffusi-
vity of a gas and the root mean square of its oscillatory vel-
ocity (Fig. 22). In other words, gas exchange is enhanced by
high instantaneous flow (12,23,25). To generate high instan-
ntaneous flow with limited volume (42-44,46,54,59), one must
resort to low-compressive systems (Fig. 23) and HFV (Fig. 21).
Therefore, in terms of functional importance, Fredberg sug-
gests that high flow rates with small volume excursions are
the primary factors influencing gas exchange. The associated
low pressure amplitudes have no functional significance in
the gas exchange process but are, none the less, a desirable
factor (42,43,46). Daxial = Dmol + e Unnsd Daxial - Axial Gos DHfUsivity DmoI - Molecular Gas DiHusMliy • - Coefficient of __ Illy
~nns ::: :".:.:"'''' of the Oscillatory Gas Velocity
FIGURE 22. Axial diffusivity according to Fredberg 1980 (26).
Characteristics of Ventilators for Volume-Controlled Ventilation
Characteristics SV-900 System H System J System J+ PEEP of Patient Circuit (Siemens-Elema) (Siostrand) (Sjostrand) (Sjostrand)
Internal Volume (ml) 1650 30 26 26 Internal 5tatic Compli- 2.6 0.06 0.04 0.04
ance (ml/cm H2O) f (breaths/min) 20 60 60 60 I:E Time Ratio 0.49 0.28 0.28 0.28 PEEP (cm H2O) 0 0 0 10 Relative VT 0.46 0.31 0.48 Relative 'ilVENT 1.4 0.92 1.4 Relative Inspiratory 0.45 0.06 0.05
Work
Normoventilation (PaC02 40 mmHg). using FI02 of 0.4 and ventilatory frequencies (f) of 20 and 60 breaths per min. in 8 anesthetized dogs. Relative tidal volumes (Vr). ventilator gas outputs ('ilVENT). and inspiratory work during ventilation with systems H. J and J with end-expiratory pressure of 10 cm H20 (HPEEP) are based on mean values in relation to conditions during ventilation with SV-900.
27
FIGURE 23. Some characteristics of patient circuits of a conventional (SV-900) and two low-compressive (H and J) systems for volume-controlled ventilation (43,47,48).
Alveolar ventilation, as predicted by the Fredberg model
(Fig.22), will increase almost linearly with tidal volume
for a fixed ventilatory frequency. This was shown in the
early experimental studies on HFPPV by Sjostrand et ale (31,
32). Therefore, no optimal tidal volume-frequency relation-
ship appears to exist for maximizing gas exchange. However,
certain configurations may be preferred based on specific
blood gas ranges concomittant to tidal volumes which produce
airway pressures uelow the traumatic level.
From a practical standpoint, with higher frequencies expi-
ratory time shortens and gas trapping occurs, consequently
elevating peak, mean and end-expiratory pressures (44,54).
It was recently demonstrated (3) that, with I:E time ratios
of 0.3, ventilatory frequencies above lOO/min substantially
increased waste ventilation (Figs. 24 and 25). Actually,
higher ventilatory rates (f) than lOO/min did not result in
any decrease in PaC02 or increase in pa02 (3) using three
28
different double-lumen tubes (inspiratory:expiratory lumen
[IL:EL] ratios of 1:1, 1:4 and 1:10). The lowest mean airway
pressure (Paw) and most efficient ventilation and oxygenation
(in terms of PaC02 and Pa02) was obtained using f of 100/min
Double·Lumen Tube 1'10 f = 100 1/E=0.30 f =300 1/E=0.30
Q)
20
10
·-7'-++-7'-7'10 E :J
~ C
"0
20
30 ~ -r---,~"""40 ~
JL,~~~~L..r~'-,Lh4~50 \..~ i= 50 ~~~~~~~~~+-/-7'6000~
)L-,~~4,-/-++7'-;h"-7''-T-7 70 ~ <:>
00 200 400 600 800 1000 1200
Inspiratory Gas Flow (ml/sec)
Double-Lumen Tube 1'10 f= 100 I1E=0.30 f=300 1/E=0.30
Q)
E :J
~ "0 "0 i=
250
20
FIGURES 24 and 25. Comparative studies of a 1:10 inspiratory: expiratory lumen (IL:EL) ratio double-lumen tracheal tube in dogs and a lung model (3).
29
and the IL: EL 1: 10 tube (3). The largest expiratory lumen
tracheal tube (IL:EL 1:10) and f of 100/min are therefore
preferred in HFV.
Clinical applications
In 1972, HFPPV (Fig. 3) gave adequate ventilation and oxy
genation in 15 patients during abdominal surgery under general
anesthesia (28). During HFPPV, adequate ventilation and oxy
genation were achieved with expiratory volumes close to esti
mated dead space. Since 1973, bronchoscopic and laryngoscopic
HFPPV (Fig. 26) have been used as established clinical appli
cations of HFV (ll). In 1977, laryngoscopic HFV (Figs. 12 and
27) was expanded to include HFJV (5,33,53). As ventilation
wi th "open" systems does not permit precise measurement or
control of the tidal volume delivered to the patient, ventila
tion through a rigid bronchoscope, or via specially designed
insufflation catheters require standardized procedures (Fig.
28) •
FIGURE 26. Bronchoscopic HFPPV using Bronchovent® (II, 43) .
30
FIGURE 27. Ventilation with HFJV during fiberoptic bronchoscopy using a fluidic ventilator (53).
Functional Differences Between Bronchoscopic and Laryngoscopic HFPPV in Relation to Injector Techniques
Injector techntqLie in Injoclor tod!nique in Characteristics 8roncho5copic HFPPV bronchoscopy Laryngoscopic HFPPV IaryngosaIpy
Air entrainment (admixture of air) No Yes No Yes Administration of anesthetic gases Y .. No Yes No
of known composition (0,%) Airway pressure during Positive Positive Positive --insufflation (low) (highe<) (low) (higher)
Airway pressure at enckxpiration Slightly positive Atmospherk Slightly positive Atmospherk Ventilatory reserve capacity Considerabte Marginal Considerable Marginal
Ventilation during instrumentation Slightly affected Affected Slightly affected Affected Gas flow direction through larynx Outwardly directed Outwardly directed OUtwardly directed Inwardfy directed
during insufflation (outside the (outside the ("sucks" with it bronchoscope) bronchoscope) blood, pieces of tissue, etc.)
Standardized technique Yes No Yes No (ventilation nomogram)
FIGURE 28. Functional characteristics of HFPPV and HFJV techniques in endoscopy (11,43).
With fixed frequencies and inspiratory times, ventilation
nomograms based on 'numerous bronchoscopies and laryngoscopies
using HFPPV have been developed for initial ventilator gas
output (VVENT) settings (11). In bronchoscopic and laryngos-
copic HFPPV
31
- ventilation is regulated by the magnitude of the ventilator gas output,
inspired oxygen concentration is adjusted by means of the oxygen concentration in the air/oxygen gas mixture delivered by the ventilator.
Compared with spontaneous breathing prior to general anes-
thesia, in patients undergoing diagnostic bronchoscopy HFPPV
improved gas distribution in terms of lung clearance index
and nitrogen washout delay (23,25).
With HFPPV, using an insufflation catheter and a pneumatic
valve connector it is possible to achieve adequate ventilation
in resection of tracheal stenosis without interference of a
bulky endotracheal tube (24). The trachea can be opened with-
out risk of hypoxia. Peroperative endoscopic examination can
be carried out for exact location of the stenosed area and
immediate checking of the anastomosis.
During open chest surgery, volume-controlled HFPPV (Fig. 7)
produces normocarbia and adequate oxygenation despite low mean
airway pressures (35). With an open chest, the lung shows
only moderate movements, good aeration and no atelectasis.
In some patients, tidal volumes approximately 25% lower than
the estimated anatomic dead space gave normocarbia (35). The
limited lung expansion and insignificant ventilation-synchro-
nous movements provide good conditions for the surgeons. At
the end of surgery, the exposed lung re-expands as readily as
with conventional techniques. Recent reports on HFPPV and HFJV
during lobectomy (21,35,51) and HFPPV during pulmonectomy (35,
48) and one-lung ventilation (21) further demonstrate the
clinical applicability of these techniques.
32
In patients in respiratory failure, HFPPV and HFJV provide
normoventilation at smaller tidal volumes (VT Tot) and lower
mean airway pressures than conventional methods (7,17,18,58,
59) • In recent investigations (58) there were no differences
between the ventilatory patterns with respect to mean values
in central venous, pulmonary arterial, and pulmonary capillary
wedge pressures, but ventilation-synchronous variations in
these circulatory variables were abolished during HFPPV and
HFJV. Even though these var iations were abolished, cardiac
index and oxygen transport were not improved. In most severely
ill patients, long-term HFPPV and HFJV have been successful.
Under long-term treatment with HFPPV (7,58) and HFJV (18) the
requirement of sedatives and respiratory depressant drugs are
reduced in comparison to standard ventilatory modes.
As the incidence of barotrauma during positive pressure
ventilation in acute respiratory failure is high, the lower
mean intratracheal pressure during HFPPV and HFJV may be of
clinical importance, particularly in neonatal and pediatric
respiratory care (54).
In patients with bilateral bronchopleural fistulae standard
ventilator treatment could not maintain adequate ventilation
(18,20). Experimental studies with HFPPV (50) and clinical
experience with HFJV (17,18) suggest the possibility of ven
tilatory support with lower FI02 and airway pressures - it was
also possible to discontinue paralytic agents in many cases
(18) •
33
In a clinical evaluation using HFO, 12 patients ranging in
age from 3 days to 74 years were adequately ventilated, and
a reduction in shunt fraction was also observed (15).
Recent animal studies with HFPPV (Figs. 18 and 19) and HFJV
have shown abolished ventilator-synchronous fluctuations in
ICP (2,10,55), markedly diminished ventilator-synchronous
brain movements (14,55), and CBF to be within normal limits
(14). This may aid the development of more elaborate micro-
neurosurgical techniques which require a "quiet" brain (54).
To date, technical or clinical problems associated with
HFPPV (Fig. 29) and HFJV (18) have not been different from
those present with conventional IPPV/CPPV. There are many
established clinical applications of HFV (Fig. 30), but some
still remain to find their place in patient care (54).
CLINICAL USE OF HFPPV AT THE DEPARTMENT OF ANESTHESIOLOGY
AT THE REGIONAL HOSPITAL OF OREBRO. SWEDEN 1972 - 1981
No. of Anesthesia Patierrts Age Complications
Bronchoscopy 1266 3w-86yr
Laryngoscopy 82A 13m-88yr 3 pneumothorax
Thoracic Surgery 17 23yr-72yr
Other Surgery 57 1 d-84yr
Intensive care
Adults 25 24yr-76yr
Children 7 <1 yr
Neonates (IRDS) 32 <100h 5 pneumothorax
FIGURE 29. Clinical applications of HFPPV (57).
Clinical Applications
Laryngoscopy 1 Micronaurosurgery
Bronc:hoscopy 7 Ventilator waning
Thoracic Surgery ? Flail mast Bronchopleural fistula 7 Respiratory failure
Hyaline Membrane disease
FIGURE 30. Clinical applications of HFV (54).
34
Prospects
HFPPV and HFJV seem to have few adverse effects on the pul-
monary, cardiocirculatory and cerebrovascular physiology, and
this may favor patients with impaired vital functions. In
addition to gas exchange in the lungs, HFV should be evaluated
for patient acceptance, weaning procedures and active physio-
therapy during ventilation (44,46,58). Presently utilizing
low-compressive systems (Fig. 30), the merits of HFJV and
volume-controlled HFPPV are comparable to traditional tech-
niques of IPPV and CPPV (54). Ventilatory frequencies of 2
Hz or less should allow construction of low-compression
systems for volume-controlled ventilation without sophisti-
cated technology (44,46). This will hopefully favor develop-
ment of simple but versatile low-compression ventilators for
volume-controlled IPPV and HFV (54). Thereby, improving
patient acceptance of mechanical ventilation.
REFERENCES
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2. Babinski MF, Albin M, Smith RB: Effect of high frequency ventilation in ICP. Crit Care Med 9:159, 1981.
3. Babinski MF, Bunegin L, Sjostrand UH, Smith RB: Animal and lung model studies of double-lumen tracheal tubes for high frequency ventilation. Resp care 28, 1982.
4. Babinski MF, Bunegin L, Smith RB, Hoff BH: Application of double lumen tracheal tubes for HFV. Anesthesiology 55:A370, 1981. '
5. Babinski M, Smith RB, Klain M: High frequency jet ventilation for laryngoscopy. Anesthesiology 52:178, 1980.
6. Bendixen HH, Hedley-Whyte J, Laver MB: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. A concept of atelectasis. New Engl J Med 269:991, 1963.
35
7. Bjerager K, Sjostrand U, Wattwil M: Long-term treatment of two patients with respiratory insufficiency with IPPV!PEEP and HFPPV!PEEP. Acta Anaesth Scand (Suppl) 64:55, 1977.
8. Bjork VO, Engstrom CG: The treatment of ventilatory insufficiency after pulmonary resection with tracheotomy and prolonged artificial ventilation. J Thorac Surg 30: 356, 1955.
9. Bohn DJ, Miyasaka K, Marchak BE, Thompson WR, Froese AB, Bryan AC: ventilation by high frequency oscillation. J Appl Physiol 48:710, 1980.
10. Borg UR, Babinski M, Bunegin L, Sjostrand UH, Smith RB: Abolished intracranial pressure fluctuations with high frequency ventilation. Anaesthesia, Volume of Summaries, Sixth European Congress of Anaesthesiology 1982, pp. 407-408.
11. Borg U, Eriksson I, Sjostrand U: High-frequency positivepressure ventilation (HFPPV): A review based upon its use during bronchoscopy and for laryngoscopy and microlaryngeal surgery under general anesthesia. Anesth Analg 59 : 594, 1980.
12. Borg U, Eriksson I, Sjostrand U, Wattwil M: Experimental studies of continuous positive-pressure ventilation and high-frequency positive-pressure ventilation. Resuscitation 9:1, 1981.
13. Briscoe WA, Forster RE, Comroe JH: Alveolar ventilation at very low tidal volumes. J Appl Physiol 7:27, 1954.
14. Bunegin L, Borg UR, Helsel P, Sjostrand UH, Albin MS, Smith RB: Cerebral blood flow during HFPPV and IPPV at normal and elevated ICP. Anesthesiology 57:A465, 1982.
15. Butler WJ, Bohn DJ, Bryan AC, Froese AB: Ventilation by high frequency oscillation in humans. Anesth Analg 59: 577, 1980.
16. Butler WJ, Bohn DJ, Miyasaka K, Bryan AC, Froese AB: Ventilation of humans by high frequency oscillation. Anesthesiology S368:51, 1979.
17. Carlon GC, Kahn RC, Howland WS, Ray C Jr, Turnbull AD: Clinical experience with high frequency jet ventilation. Crit Care Med 9:1, 1981.
18. Carlon GC, Ray C Jr, Pierri MK, Groeger J, Howland WS: High-frequency jet ventilation. Theoretical considerations and clinical observations. Chest 81:350, 1982.
19. Comroe JH, Bahnson ER, Coates EO: Mental changes occurring in chronically anoxemic patients during oxygen therapy. JAMA 143:1044, 1950.
20. Derderian SS, Rajagopal KR, Abbrecht PH, Bennett LL, Doblar DD, Hunt KK: High frequency positive pressure jet ventilation in bilateral bronchopleural fistulae. Crit Care Med 10:119, 1982.
21. EI-Baz N, EI-Ganzouri A, Gottschalk W, Jensik R: Onelung high-frequency positive-pressure ventilation for sleeve pneumonectomy: An alternative technique. Anesth Analg 60:683, 1981.
22. Engstrom CG: Treatment of severe cases of respiratory paralysis by the Engstrom Universal Respirator. Br Med J 2:666, 1954.
36
23. Eriksson I: The role of conducting airways in gas exchange during high-frequency ventilation - a clinical and theoretical analysis. Anesth Analg 61:483, 1982.
24. Eriksson I, Nilsson L-G, Nordstr5m S, Sj5strand U: Highfrequency positive-pressure ventilation (HFPPV) during transthoracic resecton of tracheal stenosis and during peroperative bronchoscopic examination. Acta Anaesth Scand 19:113, 1975.
25. Eriksson I, Sj5strand U: Effects of high-frequency positive-pressure ventilation (HFPPV) and general anesthesia on intrapulmonary gas distribution in patients undergoing diagnostic bronchoscopy. Anesth Analg 59:585, 1980.
26. Fredberg JJ: Augmented diffusion in the airways can support pulmonary gas exchange. J Appl Physiol 49:232, 1980.
27. Giertz KH: Studier 5ver tryckdifferensandning enligt Sauerbruch och 5ver konstgjord andning (rytmisk luftinbl~sning vid intrathoracala operationer). Uppsala lakaref5rening forh (Suppl) 22:1, 1916.
28. Heijman K, Heijman L, Jonzon A, Sedin G, Sjostrand U, Widman B: High-frequency positive-pressure ventilation during anaesthesia and routine surgery in man. Acta Anaesth Scand 16:176, 1972.
29. Henderson Y, Chillingworth FO, Whitney JL: The respiratory dead space. Am J Physiol 38:1, 1915.
30. Jonzon A: Phrenic and vagal nerve activities during spontaneous respiration and positive-pressure ventilation. Acta Anaesth Scand (Suppl) 64:29, 1977.
31. Jonzon A, Oberg pA, Sedin G, Sjostrand U: High-frequency positive-pressure ventilation by endotracheal insufflation. Acta Anaesth Scand (Suppl) 43:1, 1971.
32. Jonzon A, Sedin G, Sj5strand U: High-frequency positivepressure ventilation (HFPPV) applied for small lung ventilation and compared with spontaneous respiration and continuous positive airway pressure (CPAP). Acta Anaesth Scand (Suppl) 53:23, 1973.
33. Klain M and Smith RB: High frequency percutaneous transtracheal jet ventilation. Crit Care Med 5:280, 1977.
34. Lunkenheimer PP, Rafflenbeul W, Keller H, Frank I, Oickhuth HH, Fuhrmann C: Application of transtracheal pressure-oscillations as a modification of "diffusion respiration". Br J Anaesth 44:627, 1972.
35. Malina JR, Nordstr5m SG, Sj5strand UH, Wattwil LM: Clinical evaluation of high-frequency positive-pressure venilation (HFPPV) in patients scheduled for open-chest surgery. Anesth Analg 60:324, 1981.
36. Matas R: Artifical respiration by direct intralaryngeal intubation with a new graduated air-pump, in its applications to medical and surgical practice. Am Med 3 :97, 1902.
37. Meltzer SJ, Auer J: Continuous respiration without respiratory movements. J Exper Med 11:622, 1909.
38. Sauerbruch F: Zur Pathologie des offenen Pneumothorax und die Grundlagen meines Verfahrens zu seiner Ausschal tung. Mitteilungen aus den Grenzgebieten der Medizin und Chirurgie 13:399, 1904.
37
39. Scherer W, Shendalman LH, Greene NM, Bouhuys A: Measurement of axial diffusivities in a model of the broncheal airways. J Appl Physiol 38:719, 1975.
40. Sjostrand U (ed): Experimental and clinical evaluation of high-frequency positive-pressure ventilation HFPPV. Editorial. Acta Anaesth Scand (Suppl) 64:5, 1977.
41. Sjostrand U: Review of the physiological rationale for and development of high-frequency positive-pressure ventilation - HFPPV. Acta Anaesth Scand (Suppl) 64:7, 1977.
42. Sjostrand U: Pneumatic systems facilitating treatment of respiratory insufficiency with alternative use of IPPV/PEEP, HFPPV/PEEP, CPPB, or CPAP. Acta Anaesth Scand (Suppl) 64:123, 1977.
43. Sj5strand U: High-frequency positive-pressure ventilation (HFPPV): A review. Crit Care Med 8:345, 1980.
44. Sjostrand UH: High frequency positive pressure ventilation. In: European Advances in Intensive Care, K Geiger (ed). International Anesthesiology Clinics, 21,2. L:i,ttle, Brown and COTI""0illY, 1983.
45. Sj5strand UH, Babinski MF, Bunegin L, Smith RB: High frequency ventilation: An experimental comparison of HFPPV and HFJV. Perspectives in High Frequency Ventilation (Eds. Scheck PAE, Sjostrand UH, Smith RB). Martinus Nijhoff Publ. BV, The Hague, 1983.
46. Sjostrand UH, Eriksson IA: High rar.es and low volumes in mechanical ventilation - not just a matter of ventilatory frequency. Anesth Analg 59:567, 1980.
47. Sjostrand UH, Koller M-E, Smith RB, Breivik H, Bunegin L: IPPV, HFPPV and HFPPV/PEEP in dogs with acute cardiac tamponade. Resp Care 28, i982.
48. Sjostrand UH, Wattwil LM, Borg UR, Berggren LE: Volumecontrolled HFPPV as a useful mode of ventilation during open-chest surgery - A report on three cases. Resp Care 27; i3aG, 1982
49. smith RB, Cutaia F, Hoff BH, Babinski M, Gelineau J: Long-term transtracheal high frequency ventilation in dogs. Crit Care Med 9:311, 1981.
50. Smith RB, Hoff BH, Bennett EV, Wilson EAt Grover FL, Babinski MF, Sjostrand UH: High frequency ventilation and IPPV in the presence of a bronchopleural fistula. Perspectives in High Frequency Ventilation (Eds. Scheck PAE, Sjostrand UH, Smith RB). Martinus Nijhoff Pub1. BV, The Hague, 198~.
51. Smith RB, Hoff BH, Rosen L, Wilson E, Swartzman S: High frequency ventilation during pulmonary lobectomy - three cases. Resp Care 26:437, 1981.
52. Smith RB, Klain M, Babinski M: Limits of high frequency percutaneous transtracheal jet ventilation using a fluidic logic controlled ventilator. Can Anaesth Soc J 27: 351, 1980.
53. Smith RB, Lindholm C-E, Klain M: Jet ventilation for fiberoptic bronchoscopy under general anesthesia. Acta Anaesth Scand 20:111, 1976.
54. Smith RB, Sjostrand UH (eds): High Frequency Ventilation. International Anesthesiology Clinics, 21,3. Li:ttle, Dra;.m
and Corrpany;- Boston, 1983
38
55. Todd M, Toutant S, Shapiro H: The effect of high frequency positive-pressure ventilation on intracranial pressure and brain movement in cats. Anesthesiology 54:496, 1981 •
. 56. Tuffier T, Hallion L: Operations intrathoraciques avec respiration artificielle par insufflation. Compte Rendu des Seances de la Societe de Biologie 48:951, 1896.
57.· Wattwil LM: Evaluation of HFPPV in experimental and clincal practice. Acta Univ Upsal 416, Almquist & Wiksell International, Stockholm, 1982
58. Wattwil LM, Sjostrand UH, Borg UR: Comparative studies of IPPV and HFPPV with PEEP in critical care patients -a clinical evaluation. Crit Care Med, 11;30, ~983.
59. wattwil LM, Sjostrand UH, Borg UR, Eriksson IA: Comparaive studies of IPPV and HFPPV with PEEP in critical care patients - studies on intrapulmonary gas distribution. Crit Care Med, 11;38 1 1983.
CONVECTIVE DIFFUSION IN OSCILLATORY FLOW AS A GAS TRANSPORT
MECHANISM DURING HIGH FREQUENCY VENTILATION
H.J.van Ouwerkerk (t), P.Gieles and J.M.Bogaard x
Deptm. of Physics, Technical University, Eindhoven
x Pathophysiological laboratory of the Deptm. of Pulmonary
Diseases. Erasmus University, Rotterdam, The Netherlands
1. INTRODUCTION
39
Gastransport in the bronchial tree is caused by a combined
action of several physical mechanisms.
Under different circumstances with respect to respiratory
frequency, tidal volume and flow pattern these mechanisms,
transporting gas molecules from the mouth to the alveolo-ca
pillary membrane, have different relative contributions.
In a system in which an indicator is transported in a solute
the indicator transport can be described by a general one-di
mensional diffusion with drift equation
oc(x,t)
ot
In which
2 D 0 c{x,t) _ v(x) oc(x,12..
ox 2 oX ( 1 )
c(x,t)= mean concentration over a cross section at x on time t
D
v(x)
= effective longitudinal diffusion coefficient
= mean linear velocity of the solute.
Equation 1 describes the transport as a combined action of
convection (v) and a dispersion of the indicator by an effec
tive diffusion (D).
A general solution of equation 1, with the purpose to des
cribe the concentration-time pattern of benzene vapor at a
point in the bronchial tree, after injection of a bolus of
benzene at the mouth is given by Scherer et al. (1)
c(x,'c) M ----J", e
2 (TIDt) 2
(x-ut) 2
4Dt
(t) H.J.van Ouwerkerk died on 4.7.1982.
( 2)
40
in which
x distance from the mouth
M amount of benzene, injected at the mouth
IT mean linear gas velocity.
In a plane moving with the same speed as the mean linear velo
city the indicator transport by the effective diffusion alone
is given by
Q (3)
in which c is the average concentration over a cross-section m
and x 1 is the axial coo.1:dinate in the new system.
When considering high frequency ventilation the tidal volumes
are so small that the plane which moves with the mean linear
velocity remains in the conducting airways.
In figure 1 a schematic model is shown of the bronchial tree,
built up from 23 generations according to the morphological
studies of Weibel (2).
Oem
10
BRONCHI
20
'0
« w
I u « c:: f-
6
I GENERATIONS
XI XII
sa an2
Fig. 1. Schematic presentation of the first 12 generations of
the bronchial tree. Distance from the larynx and to
tal cross-section area is indicated (after Weibel, 2)
41
Using the quantitative data of Weibel for normal adult lungs
it can be derived that a tidal volume of for instance 50 ml
causes a convective movement from the mouth to approximately the
fifth generation. This generation is distant from the 17th ge
neration which is formed by the first order respiratory bron
chioli, being the first airways available for gasexchange by
alveoli in the wall.
During normal breathing(tidal vol. larger)the inspiratory air
will reach into the primary lobuli; the inspiratory gas front
will approach zero velocity at a distance of some millimeters
from the alveolo-capillary membrane. Within the alveolar space
gas equilibration is completed within a few seconds (Paiva,3).
Augmented effective diffusion, a basic process by which gas
transport occurs during high frequency ventilation, may be
caused by different mechanisms:
a. Radial molecular diffusion in connection with a velocity
profile as caused by laminar flow; this type of diffusion
is first described by Taylor (4) and called Taylor diffusion
(TD) .
b. Turbulent diffusion as caused by turbulence in the flow;
in smooth-walled tubes the effective diffusion is dependent
on the Reynolds number (Taylor,S) which is a measure for the
degree of turbulence.
c. Complicated aerodynamic mechanisms, which cause the occurrence
of vortices; this takes place for instance with jet ventilation.
Chatwin (6) developed a general theory for the calculation of
the effective diffusion along the axis of a tube in which the
flow is driven by a longitudinal pressure gradient varying
harmonically with time.
Slutsky et al. (7) used simplified equations, based on the
work of Taylor (4, 5) and Chatwin to predict the ratio between
effective and molecular diffusion in various parts of the lung,
concerning Reynolds number, oscillation frequency in the oscillatory flow and kinematic viscosity. An experimental valida
tion, based on the measurement of CO 2 excretion in expiratory
gas, could be obtained. It is the ~urpose of this paper to
describe in more detail the convective diffusion, known as
42
Taylor diffusion, during oscillatory flow. Assumptions and re
strictions of the approach will be mentioned and some poten
tial fields of further research, based on our preliminary
theoretical approach, will be indicated.
2. Taylor diffusion during stationary flow
In a laminar flow, obeying Poiseuilles law, a parabolic ve
locity profile will occur causing different linear velocities
in a cross section of a tube (fig. 2a).
[I §> -1 a b
c d
Fig. 2. Schematic presentation of the mechanism of Taylor
diffusion in stationary Poiseuille flow.
a. The parabolic velocity profile.
b. Injection of a bolus of indicator.
c. Occurrence of a radial concentration gradient by
the convective dispersion.
d. Molecular radial diffusion occurs both to the cen
t~e (increasing indicator transport) and to the
wall (decreasing indicator transport).
The velocity profile can be described by
r2 = Uo (1 - "2)
a (4 )
where r is the radial place coordinate,uo the maximum velocity in
the centre and a the radius of the tube. If a bolus of indicator i
injected (fig.2b) convective dispersion will occur (fig.2c). This
convective dispersion will be counteracted by a radial molecular
43
diffusion (Dm) which is caused by the radial concentration
gradient (fig. 2d). The resulting effective diffusion was
first described by Taylor (4). A necessary condition, for the
occurrence of this type of diffusion, is that the time for a
radial equilibration is markedly shorter than the convection
time over a tube length L.
Taylor derived that for a condition as mentioned above
L a 2 - » 2 (5) U o (3.8) D
m The effective diffusion coefficient as derived by Taylor
becomes
(6)
in which the factor 192 is associated with the parabolic velo
city profile.
3. Taylor diffusion in oscillatory flow
The mechanism of TD in this case is presented schematically
in fig. 3. As usual in dispersion phenomena displacements in a
cross-section are indicated with respect to the mean velocity.
With respect to a plane, moving with the mean speed of the
flow during the first half period of the oscillation in the
centre a positive and near the wall a reversed flow can be
observed (fig.3a). During the second half period the direc
tionsare opposite. The dispersion of an injected bolus of in
dicator (fig.3b) is shown in fig. 3c. When the condition for
TD, a quick radial equilibration in comparison with the axial
dispersion, is fulfilled a homogeneous radial equilibration
will develop (fig. 3d). During the second half of the period
th.e situation of fig. 3e will occur. In the figures the rela
tive increase or decrease of indicator in a cross section of
the tube, at the place where the indicator is injected, is shown.
In a steady concentration gradient (~~ = constant) the process
shown in fig. 3 can be presented graphically as is done in
fig. 4.
44
; I
~----r----I
---, I
____ J
a
b
8® ~® .® •
Fig. 3. Schematic presentation of Taylor diffusion in oscilla
tory poiseuille flow. a. Simplified presentation of the velocities with respect to
the mean velocity in a cross-section during the first half
period, b. injection of a bolus of indicator,
c. dispersion of the indicator; the directions of the radial
molecular diffusion are indicated,
d. indicator concentration after complete radial equilibration,
e. dispersion during the second half period of the oscillation.
The relative increase or decrease of the concentration in
a cross-section is indicated.
45
C
I "-
'" '-. '-.
'" /j C+ , '" '-.,
I '-.
'" '-......... "" £l,C
'" I '-.
'" I
l..... "" '"
'" .........
Fig. 4. Schematic presentation of the indicator transport by
Taylor diffusion in an oscillatory flow if a steady
and linear concentration gradient is present.
v(r,w)
*' -u
: £l,t I
~
t
Fig. 5. Graphical illustration of the diffusion condition du
ring oscillatory flow. The maximum velocity under which
Taylor diffusion is predominating is indicated by
dashed lines. The shaded areas give the time-interval
near the zero crossings of the velocity during which
Taylor diffusion occurs.
46
As is shown in this figure a constant gradient is present,
which implies a stationary situation in which an increase and
decrease of indicator mass in neighbouring parts of the tube
are matching.
4. The diffusion condition in oscillatory flow
The diffusion condition as formulated in equation 5 for
steady flow has to be translated to oscillatory flow. The dis
tance over which in an axial direction a radial concentration
gradient can be generated is now given by the amplitude of the flow oscillations in the tube. In a small interval of time,
around the zero crossings of the flow, there has to be a ra
dial equilibration of concentration differences over a cross
section. It can be derived for a simplified velocity profile
(v(r,w) = uO(r)sinwt, Gieles, 8) that in that case the dif-
fusion condition becomes
w « ( 7)
where w is the angular frequency of the oscillation.
A graphical illustration of the diffusion condition can be gi
ven in terms of the velocity. From equation 7 a maximum speed
u~(r,w) can be derived. If v>u* convection predominates, other
wise TD. This is shown graphically in fig. 5
If the influence of TD is supposed to be negligeable in a si
tuation in which for 10% of the period v<u· criteria can be
derived indicating a predominantly convective or TD indicator
transport respectively. If a simplified velocity profile and
a constant u* are assumed this can be illustrated as follows.
TD
2 (3.8) 2D m
2 a
TD + convection convection
with f1 and f2 func~ions, associated with the assumptions
mentioned above.
47
5. Gastransport, caused by Taylor diffusion, in oscillatory flow
For the calculation of the effective diffusion coefficient we
chose a general description of the velocity profile of the form
v(r,w,t) = umax.g(r)R(t) (8)
in which g(r) and R(t) describe the radial and time behavior of
the velocity respectively.
The basic equation for the derivation of the longitudinal effec
tive diffusion coefficient (Deff ) is again the diffusion with
drift equation (1) in which now however v is a function of W, r
and t.
The mean velocity over a cross section is given by
v(r, t) = u .R(t).g(r) max (9)
For ease of calculation the independent variables (x, r, t) are
transformed ~o partly dimensionless coordinates as follows
z
T
The
t x -J V(t1 )dt1
o .E. a
wt
diffusion with
82 1 8c c -2 + 8z z 8z
(10), displacement in a system, moving with
mean velocity
(11), dimensionless radial coordinate
(12), dimensionless time coordinate
drift equation now becomes (Gieles, 8)
2 8c a w au 8c max + . R (T) {g ( z) -"g"'{'Zj" }_._ (13 )
D 8T D 8x 1 m m
As argumented in detail by Gieles (8) in the case of TD the term
8c can be 8T (creation
mentarily
neglected because the variations in source strength
of indicator flow) are so small that they can be mo
followed by a complete radial equilibration.
With this assumption an expression for c(x 1 , z, T) can be de
rived. After the calculation of total mass transport over a
cross section by integrating the product of local c and v and
after using the well known diffusion equation
8c (14)
48
an expression for Deff(T) can be derived
Deff(T)
in which
z
2 2 a u max
D m
CR1 satisfies
d dC R1 (z --)
dz dz
the
dC R1 (--) zdzd'f
dz
equation
= g(z)-grzj
( 1 5 )
( 1 6)
This slJ1nmnrized derivation, which is described in more detail by
Gieles (8) shows that the Taylor diffusion coefficient can be
calculated if a velocity profile is known.
In general one can state that
v = L u . m1 i
(17 )
It can be proved (Gieles, 8) that the effective diffusion coef
ficient obeys
DO(T) = 2 L K .. R. (T) R. (T) I .. ( 1 8) ij 1J 1 J 1J
1 [:") C:ii) where 1.. J zdz ( 1 9 ) 1J 0
2 a .u .U ffi. m.
and K .. 1 J (20) 1J 0 m
If we use a pressure gradient, causing the oscillatory flow,
defined by
1 op A cos wt (21 )
p oX with P density
a complex expression for the velocity profile can be found by
applying the principle of the conservation of mass and the
Navier-Stokes relation (Gieles, 8).
49
Finally this expression gives an effective diffusion coefficient
oot)[ a':m,' .I" m
2 2 a u m2
(l-cos 2 wt).
° m
2 1 a u u + 2 ~~ rna .1 12 +
(22)
111' 112 and 122 are according to (19) and being a function of
A ~V~1JI, with 1J = kinematic viscosity.
In general the complex equation 22 can be shortened to
(23 )
in which kT can be defined as a "steady state" Taylor diffusion
factor.
In a first application 00(T) can be calculated for low frequen
cies. Simplified expressions for vx ' umax ' g(z) and R(t) give as
a final result (Gieles, 8) 2 2 a u
DO(T) = max (l+cos 2 T) 192.0m
(24)
It can be concluded that for low frequencies the Taylor diffu
sion coefficient is changing with two times the frequency of the
oscillations which is consistent with previous calculations
(Chatwin, 6).
6. CONCLUSIONS
We have shown that under predefined conditions the transport
of mass in oscillating flow can be described by Taylor diffusion
already recognized as one of the mechanisms causing gas tran
sport during high frequency ventilation (Slutsky, 7). These
conditions are
a. A much shorter radial equilibration time in comparison with
the convection time.
b. Slow variations in source strength in comparison with radial
equilibration times.
c. A stationary linear concentration gradient.
so The advantage of our model is the ease of a structural analy
sis based on the knowledge of a velocity profile. From prelimi
nary calculations, based on simplified conditions (low frequen
cy, laminar Poiseuille flow) a diffusion coefficient could be
derived, which was consistent with results accepted earlier
(Chatwin, 6; Taylor, 4).
Calculations of the diffusion coefficient for high frequencies
are difficult because in that case the assumption of rapid dif
fusion equilibration in comparison with convective dispersion
is violated.
We believe that our model has the opportunity to be integrated
with the approaches of Chatwin (6) and Slutsky (7) in order
to derive a general theory describing the mass transport
during high frequency ventilation.
7. REFERENCES
1. P.W.Scherer, L.H.Shendalman, N.M.Greene, A.Bouhuijs.
Measurement of axial diffusivities in a model of the bron
chial airways. J. Appl. Physiol. 38(4), 719-723, 1975.
2. E.R.Weibel. Morphometry of the human lung. Ac.Press NY, 1963.
3. M.Paiva. Gas transport in the human lung.
J. Appl. Physiol. 36(3), 401-410, 1973.
4. G.I.Taylor. Dispersion of soluble matter in solvent flowing
slowly through a tube.
Proc. Roy. Soc. (London), A 219, 186-203, 1953.
5. G.I.Taylor. The dispersion of matter in turbulent flow
through a pipe.
Proc. Roy. Soc. (London), A 223, 446-468, 1954.
6. P.C.Chatwin. On the longitudinal dispersion of passive con
taminant in oscillatory flows in tubes.
J. Fl. Mech. 71, 513-527, 1975.
7. A.S.Slutsky, J.M.Drazen, R.H.lngram, R.D.Kamm, A.H.Shapiro,
J.J.Fredberg, S.H.Loring and J.Lehr. Effective pulmonary ven
tilation with small-volume oscillations at high frequency.
Science, 209, 609-611, 1980.
8. P.Gieles. Taylor diffusion in oscillating flow. Internal
report, Technical University, Eindhoven, The Netherlands,
1981 (in Dutch).
PRESSURE FLOW PATTERN AND GAS TRANSPORT USING VARIOUS TYPES
OF HIGH FREQUENCY VENTILATION
M.Baum, H.Benzer, W.Goldschmied, N.Mutz
1. Different High Frequency Ventilation (HFV) systems have been
described so far. Cornmon to all methods are frequencies far
above normal respiratory rates combined with tidal volumes in
the range of the anatomic dead space of the lungs. However,
the gas transport mechanisms involved are not yet quite clear
and may well be of different nature for each HFV system. One
way to improve our understanding are measurements on physical
models of the lungs which allow comparisons between the different
methods. In the first instance pressure, flow and volume con
ditions can be derived from such models. For a more detail des
cribtion of the processes a visualisation of flow profiles and
local velocities in the bronchial system seems to be useful.
Gastransport efficiency can be determined by the nartial pressure
gradiance along the conductive airways in a steady state lung
model. Some of the results from this experimental measurements
with 4 different HFV-systems are discussed.
2. Lung model for pressure flow measurements (Fig.1)
It consists of a glass flask of 50 or 25 1 respectively which
represents the compliant element. The flask can be intubated
via a 20 rnm pipe with common cuffed tracheal tubs. A hot wire
flow sensor is built into this pipe measuring the total flow
in and out the compliant element. An additional chanaeable flow
resistance allows adjustment of different luna impedances. Pressure lines for tracheal (Ptr) and pleural (Ppl) pressure
measurements are provided. A further pipe normally closed allows
simulation of a leaking lung.
52
Lung model I for pressure -flow measurments
hot wire
-' flowsensor /-'
501 (251)
3. Results of pressure flow measurements.
3.1. High frequency pulsation (HFP) fig.2
/ resistance
Our HFP-system basically consists of a T-piece attached to
the tracheal tube with a 1,5 mm bore on top. This nozzle is
connected to a solenoid valve which interrupts the flow coming
from an adjustable high pressure source. The T-piece has a
9 mm neck where the jet spreads and produces positive pressure
pulses. An additional fresh gas flow of 10 l/min and a dead
space tube on the opposite side is necessary to avoid the en
trainment of roomair during insniration. Oriqinal records of
the entrance pressure at the tube (Pentr.), the flow to and from
the lungs (VL) and the pressure a~ alveolar level are qiven.
In addition the cross flow (Vcross) in the dead space tube was
measured with a Fleisch-tube. The two most important findings
are: 1. Only a small portion of the pressure swing is trans
mitted to the alveolar space, but mean pressure is high because
53
of the inability of the luna to recoil during the short expira
tory pause. Alveolar mean pressure raises as the impuls pause
ratio of HFP increases. 2. Most of the gas volume entering the
lungs is entrained gas and even with a cross flow a certain
amount of rebreathing will occure. In adult natients this system
allows frequencies of 3 - 7 Hz and tidal volumes between 90-180 ml.
The system is basically open and spontaneous breathing is pos
sible with low system resistances.
JlIl. 2bar . I f\.L 1 t r 0 ~:!\f "'~ · ~ .~. H _ 2Its lc .f~~ 120~
I E
~ .. ·I: ~ ' .. : 1 . ../"V. •. --'-'-..;..---!-. '. . .. .• -: 2 ... 0 m. b
1 ~ i ~ .! ~ ~ ; : :. ; ~
HFP
v..- ~o-"80mL Reo- 3mb
3.2. High frequency oscillation pneumatic (HFOp) fig.3
In contrast to HFP this system provides an active support for
the expiratory phase. This is achieved by an additional nozzle
acting as an ejector. The two nozzles are feed with impulses
180 0 out of phase. Here again a cross flow and a dead space
tube is necessary to avoid entrainment of roomair. The degree
of rebreathing however is less compaired to HFP. Entrance
pressure has a symetrical shape and air-trapping can now be
avoided as can be seen from the alveolar pressure record.
Due to that sufficient tidal volumes can be maintained at
higher frequencies. We do not have clinical experiance with this
type of oscillation so that ventilatory parameters are not yet
54
available.The system does not offer hiqh resistances to spon
taneous breathing.
3.3. High frequency oscillation mechanical (HFOm)
IE ;. • Ii .: ti' I • ,f'o.. !
F'olv IE
---r----~
HFOp
120mb
3.3. High frequency oscillation mechanical (HFOm) fiq.4
In this system oscillatory volumes are disPlaced by a piston
pump. The only fresh gas entry to the system is maintained
by the cross flow. To direct the oscillations towards the
lungs the impedance of the cross flow system must be high.
This is achieved by an impedance tube with the diameter of
8 rom, 8 m in length. The entrance pressures and peak flow
rates are very high (> 150 mb, ? 4 lis). Hean alveolar pressure
depends on theamount of cross flow and the resistance on the
impedance tube. This system tends to create hiqh deqrees of
rebreathing because of volume demands of the the adult patient
(VE = 150 l/min) the crossflow can hardly be matched. Tidal
volumes are about 150 ml at frequencies of 15-30 Hz. The system
does not allow spontaneous breathing because of the hiqh re
sistance (>100 mb),
,
j\ ,\
v
I
J J IJ
100mb
HFOIl1
{-15-30 liz Ri >100 Vr-150-,(KOm/. R. > AOO
3.4. Forced Diffusion Ventilation (FDV) fiq. 5
I E
FDV
f-S-25 Hi' \i:=10-1S L/m 1n Vr= 10-40mL
1 AOm6
55
In this HFV system 2 jets are entering the bronchial system on
carina level. A special tracheal tube with two pressure lines in
its wall brings down the gas pulses to this location. The jets
leaving the nozzles at the tip of the tracheal tube remain focused
until they reach the inner edge of carina. At this point they form
flow sheeds which travel down the lunqs without significant gas
mixing. At the same time a back flow of stale gas is established
in the remaining bronchial cross section and leaves the lungs via
S6
the main lumen of the tracheal tube. Thus a continous wash-out
process is responsible for gas transport during FDV. To verify
this particular flow profile we have developed a spark curtain
technique which allows visualisation of flow potential fields
in an airway geometry (fig.6).
With this HFV system no entrainment of roomair can be measured
and alveolar pressures - swing as well as mean - are very low.
The mayor disadvantage of this method lies in its sensitivity to
tube position. If the tip of the tube is positioned more than 2 CI
57
above carina special flow profile is lost and aas exchange be
comes poor. In an adequate position tidal volumes of 10 - 14 ml
at frequencies up to 25 Hz can be achieved in adult patients. The
system offers no additional resistance to snontaneous breathing.
Due to the absence of gas entrainment there is no need for a cross
flow.
4. Lung model for partial pressure gradients (fig.7)
analyzer
- to analyzer
I
t
~diffuSive
In a rigid container of approximately 30 1 a rubber model of the
bronchial tree is mounted. At the bottom of the container a
diffusive plate delivers a stabilized adjustable flow of 100 -
300 ml pure CO 2/min to the model which renresents the metabolic
rate. A height adjustable Tbar with many sideholes allows samp
ling of a mean CO 2 concentration at different distances above the
diffusive plate. The actual position of the sampling point is
indicated on a scale. The whole model is filled with cotton to
split the gasflow leaving the 21 ends of the rubber bronchial tree
The geometry of the model is chosen to give distances between
58
carina and diffusive plate similar to that met in the lungs
between carina and blood gas barrier.
5. Results of partial pressure gradience (fig.8)
9 %C02
8
"1 'I-'I-'/.
~)(
6 .,..
~ 5 '" . .
Cl
• 3
".
A 2 ".
L A
'6!L;
6 10 20 11 18
Position of the stationary interface at VC02= 280mlfinin
)( x )( y..
. A • oA ! 6
30 40 50 60
)(
70
X," HFP (3bar, 5HZ, VT-180ml, Ve' 37l/min,6 p,7mbi
o HFO (5HZ,VT-240ml,VE'651/min,6p:9mb)
Do FDV (3,4 bar, 5 HZ,VT-90ml, Ve :28I/min,6p:3,5mbl
X X . X •
A A A
disdance from diffusive
80 90 100mm plate
Here the local CO 2 concentrations are plotted against the dis
tance from the diffusive plate for 3 different HFV systems at a
metabolic rate of 280 ml CO 2/min. The better the gas transport
the further down fresh gas should be brought. The steep increase
of CO 2 indicates the actual position of the virtual gas interface
FDV penetrates the largest distance the virtual interface is
approximately 6 mm above the CO 2 inlet. The rest of the distance
has an almost uniform concentration of 1% CO 2 in the whole con
tainer. HFOp is not as efficient it moves the interface to 11 mm
but also gives the same low CO 2 concentration for the remaining
distance. HFP brings the interface up to 18 mm above the diffusivE
plate and does not lead to an uniform CO 2 concentration in the
container. With this model influences of changes in settings of thE
ventilatory parameters can be estimated which is extremely helpful for the optimisation of the various high frequency ventilation methods.
A REVIEW OF EXPERIMENTAL AND THEORETlCAL STUDlES OF HIGH FREQUENCY VENTILATION
A.S. SLUTSKY, R.D. KAMM and J.M. DRAZEN
1. INTRODUCTION
High frequency ventilation (HFV) is a new mode of mechanical ventilation
in which the ventilatory rates are higher and the tidal volumes considerably
smaller than those observed during spontaneous breathing. Using this
technique, investigators from a number of centers have shown that it is pos
sible to maintain eucapnia even when the tidal volumes (VT) are less than
the anatomic dead space (VD). These results are clearly in conflict with
traditional concepts of gas exchange which are based on the principle that
adequate alveolar ventilation is possible only if VT is greater than VD.
In an attempt to further our understanding of the mechanisms by which HFV
is effective, we have developed a theoretical model of gas mixing during
HFV and we have performed experiments in hardware models, animals and humans
to determine the effect of variables thought to be important during HFV.
The purpose of this paper is to summarize some of our theoretical and ex
perimental results relating to the mechanisms of gas exchange during HFV.
2. THEORETICAL CONSIDERATIONS
Since the tidal volumes used during HFV may be substantially smaller
than required to reach the alveolar zone, bulk flow of gas can only account
for a small fraction of the gas exchange ohserved. Similarly, molecular
diffusion cannot by itself provide an adequate explanation for the effec
tive gas exchange since the total cross-sectiona.l area of the larger
airways is quite small and would limit CO2 elimination to less than 1 ml/min
(at a PaC02 of 40 mm Hg) (1). However, the coupling of axial convection
and radial mixing (either by molecular diffusion or convective processes)
can produce effective gas mixing by a process termed "augmented dispersion".
The remainder of this section will review a quantitative model of gas trans
port during HFV which is has.ed on this concept of "augmented dispersion" (2,3).
We will initially present our original model (3) and then we will present
60
modifications of this model to take into account recent experimental results.
Conceptually, we have divided the lung into the following three zones
(Figure 1), each with a specific gas mixing mechanism (4}:
(I) The alveolar region where the gas velocities are Virtually
zero,
(II) The small airways where the flow is thought to be laminar
and free of secondary flows,
(III) The larger airways where turbulence and swirling flows
tend to effectively mix gas.
VELOCITY o Low
FLOW Mol Laminar REGIME Diffusion
High
Turbulent
Airway Opening
FIGURE 1. Schematic diagram of the cross-sectional of the lung from the alveolar region (left) to the airway opening (left}. The gas velocities and associated mlxlng regimea in zones I to III are also
In zone I, the gas velocities are virtually zero due to the large
total cross-sectional area and thus molecular diffusion is the primary
gas exchange mechanism. In this region gas transport is given by the
Fick equation:
Q = -ADmol dF/dx
where Q diffusional volume flow rate of gas, A = total cross-sectional
area; Dmol is the molecular diffusivity of the gas and dF/dx is the con
centration gradient of the gas. For respiratory gases, Dmol is inversely
proportional to the square root of the molecular weight of the gas and
directly .proportional to the absolute temperature.
In zone II, the dominant flow regime is laminar and convection must
also be considered. Taylor (5) developed an analytic solution to deacribe
gas mixing during steady, unidirectional flow. Because of the development
of a parabolic velocity profile across the diameter of the tube the fluid
at the center is traveling faster than the rest of the gas (Figure 2)_.
If the two gases are immiscible then there will be no interchange between
61
the gas in the paraboloid (gas A) and the gas along the walls (gas B). If,
however, the two gases are miscible, then at the same time as the gas is
being transported by convection, gas A is diffusing out towards the wall
and gas B is diffusing into the paraboloid (as shown by the arrows in
Figure 2). For this second case, Aris (6) expanded on the work of Taylor
(5) for laminar flow in a long straight tube and obtained the following
equation to describe the enhanced transport (compared to molecular diffusion):
Deff = Dmol + (l/l92)u2d 2 /Dmol (2)
,.here: Deff = the effective diffusivity (described below);' u = the cross-
sectional average velocity; and d = the tube diameter. The term Deff is
used to take into account the combined effects on gas exchange of convec-
tion and diffusion. Deff can be thought of as the hypothetical value of
the molecular diffusivity that would be required under static conditions
to produce the same dispersion as that observed under conditions of flow.
B
DIRECTION OF FLOW FIGURE 2. ref. 19).
Dispersion during laminar flow. See text for details (From
If one now considers the case of laminar sinusoidal oscillatory flow,
beginning with the discontinuous concentration profile shown in the top
of Figure 3, there are two possible patterns of dispersion. If Dmo1 is
approximately equal to zero, the sequence of events shovm on the left in
the figure (at four equal intervals during the cycle) take place during
a complete oscillation period. At the end of every cycle (hot tom sketch)
each particle returns to its original position, with the result that the
net axial transfer is zero. Thus, under these conditions (laminar flow
with Dmol = 0) oscillating the fluid will produce no dispersion.
62
Dmol; {) -- Dmol> {)
FIGURE 3. Concentration profiles at five points in a single oscillation period. At the left D~ol = ° and on the right Dmol »0. Note that with Dmo1 = 0, at the end of an oscillation period (360°) there is no net mixing.
If Dmol is significantly greater than zero the smearing of the fluid
interface that occurs during the cycle is not revers_ible. As shown
schematically on the right in Figure 3, as the fluid interface distorts,
according to the parabolic velocity profile, rapid radial diffusion
quickly eliminates any radial variations in concentration. Therefore,
at the end of a complete cycle, a net exchange has taken place between
the two fluids. Watson e72 has analytically ohtained a s_olution under
oscillatory, laminar, flov-' conditions which, for gas ~ixtures in which 'V
v = Dmol, depends upon two dimensionless parameters: (12_ the Peclet number
(Pec) ud/Dmol and (2) the dimensionless frequency (~ =(g/21 lW/Dmo12
where w is the oscillation frequency and Dmol is the molecular diffusivity.
The dimensionless frequency represents the ratio of the tube radius to the
penetration depth of the viscous houndary layer fro~ the wall into the
core of the fluid. When a is much greater than 1, the velocity profile
is blunted and exhibits this boundary layer clos_e to the wall and when
a < 1, the flow profile is closer to the parabolic Qne. obs_erved during
steady flow: The equation for Deff is then given by: 2
Deff/Dmol feaL.Pec cn where f(a} varies from 1/192 for a < 1 to (1/S;Z-la-3 for a » 1.
We have recently experimentally verified the validity of thi$ equation
for values of a ranging from 1. 0 to lQ. ° (82.
In zone III turbulence or turhulent-like eddy ~otion$ are created
in steady or oscillatory flow as a result of various flow conditions.
Examples of these flow conditions include: (it flow instabilities that
arise when the transitional Reynolds number exceeds so~e critical value
63
(e.g. 2300 for steady flow in a long uniform circular tube); (ii) secon
dary motions generated as the fluid passes through a bend or bifurcation
and (iii) eddies due to boundary layer separation. Due to these factors
gas mixing is greatly enhanced in zone (JIll leading to gas exchange
which can be described as well mixed.
Taylor (9) also considered enhancement of dispersion in fully de
veloped turbulent flow in a circular, cylindrical duct and obtained a result
that can be expressed as
Deff = (2.Re-l / 8)ud (4)
where Re is the Reynolds number C = ud/v). The product in parentheses
varies only from 1.31 at a Re of 30 to 0.58 at a Reynolds number of 20,000.
The form of this expression is nearly identical to that found by Scherer
et al (10) in measurements of dispersion during steady flow in a branching
network of tubes, but the numerical coefficient is different on inspiration
(1.08) and expiration (0.37). Scherer et al concluded that this expres-
sion was valid to Re as low as 30, far below that necessary for fully de
veloped turbulent flow. This finding suggests that secondary motions at
a bifurcation enhance mixing in a manner similar to turbulent mixing.
During oscillatory flow in Zone III, Fredberg (21 has suggested that
the time required for the development of secondary flows or airway
turbulence is small compared to the oscillatory time period, and thus an
expression for Deff can be obtained as:
Deff = 0.7 ud (5)
where the coefficient 0.7 is selected as an approximate average between
the two constants found by Scherer et al (0.37 and 1.08).
The demarcation between zones II and III is not known with certainty.
However, swirling motions at bifurcation have been observed down to Reynolds
numbers as low as 50 (11) and the results of Scherer and colleagues (10).
suggest that equation (5) is also valid down to a Reynolds number of 30.
Thus, the use of equation (3) or (5) to calculate Deff depends on the
local Re; if Re is less than some critical Re CRec) (Rec ~ 30) equation
(3) is.used; if Re is greater than Rec, equation 5 is used.
To apply the concepts and equations described above to predict the
gas exchange that would occur during HFV, as suggested by Fredberg (2),
we modeled the lung as a network in which each airway is represented by
a resistance to gas transport. The resistance to gas transport is similar
to the commonly used flow resistance which is defined as the change in
64
pressure divided by the change in flow. During HFV, the driving pressure
for gas exchange is the difference in fractional concentration (~F) of the
gas, the flow is the volume flow rate (Q) of the gas and the resistance (R)
'to gas transport is ~F/Q. Now for any given airway, we can calculate Q by
using the modified Fick equation (with Dmo1 replaced by Deff) suCh that:
Q = -ADeff(dF/dx) (5)
For an airway of length (L} this can be simplified to:
Q = -ADeff (~F /Ll ( 6)
Rearranging terms and noting that ~F/Q is by definition equal to the
resistance to gas transport: • L
R = ~F/Q - ADeff (J)
For any given f and V T' the value of R for any generat ion is then
obtained by using the appropriate value for Deff based on equations 0)_ or (5). The total resistance (Rt ), to gas transport of the lung is thep.
determined by summing the resistances of the generations. The volume flow
rate (Q) of gas can then be calculated as:
where Fa1v and FAo represent the volume fractions of gas in the alveoli
and airway opening, respectively.
Although this model makes use of the fact that there are 3 zones,
each with a different mixing mechanism, experimental data we have obtained
recently suggests that a model based on the four zones defined by a and
Re as shown in Figure 4 is more appropriate (121. However, results of
these experiments have not as yet been incorporated into the model and
thus the predictions given below will be based on the original 3 zone
model.
102
Molecular
~ Diffusion
10 o =0 eff mol
0
III 1.0 ~
0,1 LO 10
Unsteady, laminar
Turbulent Steady. laminar
102 103 104
Re == 2Ua 1I
FIGURE 4. Schematic representation of ya,rious. regions in the lung in which specific mixing regimes depend on the dimensionless parameters a and Re. (a = radius and v = kinematic viscosity. 2 Note that the boundaries between zones are not known with certainty (From ref. 12),.
65
3. THEORETICAL PREDICTIONS
To predict the effects of frequency (f), tidal volume (VTl and lung
volume (VL) on gas exchange during HFV we have used the morphometric data
for the dog lung of Horsfield and Cumming (132 and we have assumed that the
airway walls are rigid. Predictions will be presented in terms of COZ elimination (VCOZ) vs the f.V T product.
The model predicts that for values of f less than about Z5 Hz and VT less than the anatomic dead space, VCOZ varies relatively linearly with
:he f.VT product as shown in Figure 5 (32. The model also predicts that
VCOZ vs f.VT will be relatively independent of lung volume, if the lung
increases in size isotropically (lengths and diameters increasing propor
tionally). The explanation for the relative unimportance of VL is that
with an increase in VL there are two competing phenomena occurring simul
taneously. First, the increasing cross-sectional area of the airways
tends to increase VCOZ in regions where molecular diffusion dominates
(zone I). However, at any fVT the Reynolds number decreases as the dia
meter of the tube increases, thus, regions of the lung which were originally 'V
zone III may become zone II. For Re < 1QO, Deff is smaller if deter-
mined by equation (3) (for zone II) rather than by equation (5) (for zone
III). Thus, the net effect is very little change in VCOZ with increasing VL.
150 ....... . s: ~ . ~ 100 . • ~
'00 .-. . ~ '" i.8~· ~' 50 o~ • • '11
\.f' :}. 0 0.5 1.0 1.5 0 0.5 1.0
VOse (L/sec)
4. EXPERIMENTAL RESULTS
1.5
FIGURE 5. Results of theoretical model (left) and experiments in four dogs (rtght) of VCO? versus Vosc (= fxV T). The value of Rec was set equal to zero. (Adapted from ref. 3) .
The circuit used in our experimental studies is shown in Figure 6. The
high frequency oscillator (HFO) consists of either four loud-speakers
coupled in series (3) or a servo-controlled linear magnetic motor coupled
to a piston (142. The flow measured by the specially calibrated pneumota-
66
chograph (14) is equivalent to that entering the subject because of the
mechanics of the high impedance bias flow system. The fresh gas is bled
from a high pressure source across a needle valve, while the vacuum sink
bleeds gas from the airway into a low pressure reservoir. Using this sys
tem the pressure losses across the positive pressure and vacuum sink are
so large that the changes in pressure at the airway opening due to the
oscillations do not significantly alter this pressure drop and thus essen
tially none of the tidal volume is lost to the bias flow (141. This system
also allows rapid assessment of the VC0 2 since all the gas exits through
the vacuum sink. Thus VC02 is equal to the product of the fractional CO2 concentration in the bias flow times the bias flow rate.
1IItCUUIII SOURCE
t
t COMPRESSED AIR
SOURCE
FIGURE 6. Schematic of experiments apparatus used by Slutsky et al (3}. Details are given in the text (~dapted from ref. 32.
Our initial studies were performed in anesthetized, paralyzed dogs
using frequencies ranging from 4-28 Hz and VT's from 2Q-85% of the combined
anatomic plus equipment dead space (3). The results showed that the
most important factor in determining VC02 was the f.VT product and that
VC02 was roughly proportional to f.VT. We subsequently performed experiments
in which we systematically varied f at a number of fixed values of VI.
I 0" (,) .>
0.5 1.0
Voac (l/a)
1.5 2.0
67
FIGURE 7. Mean results for 13 dogs of VC02 vs Vosc (= fxVT) at various constant values of VT (Adapted from ref. 14).
As ~hown in Figure 7, these results showed that VT had an independent effect
on VCQ2 at any f:VT product (H). On average, a doubling of VT at a constant
f.VT, increased VC02 by an average of 35%. These results were not predicted
from the original theoretical model and most likely relates to the fact
that the theory modelled the gas exchange occurring within the lung but
did not take into account the bulk (convective) removal of CO2 at the airway
opening or the convective mixing that may occur at the alveolar region.
These convective processes have been modelled in various ways (14,15), and
when this factor is included, theoretical and experimental results are
in close accord (Figure 8). In this study, as predicted from the theore·
tical model changes in lung volume had no significant effect on VC02 •
.~
i ~ u .>
0.5
100
1.0
Vase [liler/s]
1.5
40
20
2.0
FIGURE 8. Theoretical results of VCO vs Vosc (= fxVT) when convective purging at the airway opening at the alveolar zone is taken into account as described in ref. 14. (From ref. 14).
We also performed experiments in intubated subjects who had been on
chronic mechanical ventilation due to neurological problems (16). As
68
shown in Figure 9, data obtained with f less than 3 Hz showed that the
f,VT product was mos~ important in determining VC02 ; however, above a
critical frequency, VC02 vs f at constant VT reached a plateau (Figure 10).
400 300 2 4T 200 200 200
c: o· 100 ·0 ... o •• . . E 0 0·· 01-0.. I "-
, 0 100 200 0 100 200 0 100 200
E
'L '~L N 0 100 0 • 100 • VT(mlJ u .> . .20-35
50 0 50 0 0 o 45-65 • 0
o ' .0 • .75-90
0 0 100200 300 100 200
f'VT (ml/sec)
FIGURE 9. Plots of VC02 vs f. VT in five human subj ects. Os.cillatory frequency varied from 0.5 to 3.0 Hz (from ref. l6}.
We hypothesized that this difference in results between the
theoretical data (and dog experimentsL and human data was probably related
to the fact that the human subjects had significant small airways disease
and thus their upper airways acted as a shunt compliance (J7) limiting
the oscillatory volume delivered to the respiratory zone. These results
would not have been predicted from our theoretical model since the model
assumed that the airway walls were rigid. We obtained supportive evidence
that this hypothesis of increased peripheral resistance could account for
the plateauing of VC02 , in a study in dogs using an intravenous histamine in
fusion (a peripheral bronchoconstrictorl (182. Following histamine,
VC02 vs f, at constant VT displayed a similar plateau as observed in
the human studies.
~I'L t=~ ,t~ ~J;+;:~ t:·~ 'Ol;-:~ o>o>L L
o 200 400 0 300 600 900 0 200 400
BREATHS/ MIN
FIGURE 1Q. Plots of measured VC02 divided by metabolic CO2 production vs f, at a VT of 50 ml in 6 human subjects (From ref. 16}.
69
5. SUMMARY AND CONCLUSIONS
The results of both the theoretical and experimental studies show
that augmented dispersion, along with convection can account for the
effective ventilation observed ,>lith HFV. The important variabJes in deter
ming VCOZ are the f,V T product and the magnitude of VT used. However,
since the efficacy of HFV is determined by local flow conditions, the me
chanical properties of the lung especially in cases of pulmonary disease
may be a very important factor in limiting the efficacy of HFV. Further
theoretical and experimental studies are required to more closely define
the exact physical mechanisms by which HFV is effective.
REFERENCES
1. Slutsky AS. 1981. Gas mlxlng by cardiogenic oscillations: A quantitative, theoretical analysis. J. Appl. Physiol:Respiratory Environ. Exer. Physio1. 51(5): 1287-1293.
2. Fredberg JJ. 1980. Augmented diffusion in the airways can support pulmonary gas exchange. J. Appl. Physiol. Environ. Exercise Physiol. 49(2):232-283.
3. Slutsky AS, Drazen 3M, Ingram RH Jr, Kamm RD, Shapiro AH, Fredberg JJ, Loring SH, Lehr J. 1980. Effective pulmonary ventilation with small volume oscillations at high frequency. Science 209: 609-611.
4. Slutsky AS, Brown R. 1982. Cardiogenic oscillations: a potential mechanism enhancing oxygenation during apneic respiration. Medical Hypotheses 8:393-400.
5. Taylor GI. 1953. Dispersion of soluble matter in solvent flowing slowly through a tube. Proc. Roy. Soc. A. 219: 186-203.
6. Aris R. 1956. On the dispersion of a solute in a fluid flowing through a tube. Proc. R. Soc. London Ser. A. 235: 67-77.
7. Watson EJ. Diffusion in oscillatory pipe flow. J. Fluid Mechanics (submitted) .
8. Joshi CH, Kamm RD, Drazen JM, Slutsky AS. An experimental study of gas exchange in laminar oscillatory flow. J. Fluid Mech. (submitted}.
9. Taylor GI. 1954. The dispersion of matter in turbulent flow through a pipe. Proc. Roy. Soc. A. 223: 446-468.
10. Scherer PW, Schendalman LB', Greene NM, Bouhuys A. 1975. Measurement of axial diffusivities in a model of the bronchial airways. J. Appl. Physiol. 38: 719-723.
11. Schroter RC, Sud low MF. 1969. Flow patterns of the human bronchial airways. Respiration Physiology 7: 341-355.
12. Kamm RD, Drazen 3M, Slutsky AS. 1983. Pulmonary gas transport in high frequency ventilation. Critical Reviews in Biomedical Engineering (In preparation}.
13. Horsfield K, Cumming G. 19}5. Morphology of the bronchial tree in the dog. Resp. Physiol. 26: 173-182.
14, Slutsky AS, Kamm RD, Rossing TH, Loring SH, Lehr J, Shapiro AH, Ingram RH Jr, Drazen JM. 1981. C02 elimination in dogs by high frequency (3-30 Hz), low tidal volume ventilation: Effects of frequency, tidal volume and lung volume. J. Clin. Invest. 68: 1475-1484.
70
15. Khoo MCK, Slutsky AS, Drazen 3M, Solway J, Gavriely N, Kamm RD. 1982. An improved model of gas transport during HFV (abstractl. The Physiologist 25(4): 282.
16. Rossing TH, Slutsky AS, Lehr JL, Drinker RA, Kamm R, Drazen 3M. 1981. Tidal volume and frequency dependence of carbon dioxide elimination by high-frequency ventilation. N. Engl. J. Med. 305: 1375-1372.
17. Mead J. 1969. Contribution of compliance of airways to frequency dependent behavior of the lungs. J. Appl. Physiol. 26:670-673.
18. Rossing TH, Slutsky AS, Ingram RH Jr, Kamm RD, Shapiro AH, Drazen 3M. CO2 elimination by high frequency oscillation in dogs - effects of histamine infusion. J. Appl. Physiol. Respir. Environ. Exercise Physiol. (in press).
19. Slutsky AS, Kamm RD, Drazen JM. High frequency oscillatory ventilation using tidal volumes smaller than the anatomic dead space. In, International Anesthesiology Clinics. Little, Brown and Co., Boston, MA., Eds., R.B. Smith and U. Sjostrand, in press.
ACKNOWLEDGMENTS
The work presented in this paper resulted from a collaborative effort involving the following individuals from the West Roxbury VA and Brigham and Women's Hospitals, Harvard Medical School, Massachusetts Institute of Technology, and the Harvard School of Public Health: R. Akhavan, R. Brown, E. Bullister, J.M. Collins, P. Drinker, J. Fredberg, N. Gavriely, R.H. Ingram, Jr., C.H. Joshi, M. Khoo, J. Lehr, S. Loring, T.H. Rossing, A. Shapiro and J. Solway.
Supported in part by the Veterans Administration and grants from the National Heart, Lung and Blood Institute, HL 26566 and HL 00542, and the Fluid Mechanics Program of the National Science Foundation Grant No. ENG 76-08924.
EFFECTS OF HIGH FREQUENCY JET VENTILATION DESIGN AND OPERATIONAL VARIABLES UPON ARTERIAL BLOOD GAS TENSIONS
Jerry M. Calkins, M.D., Ph.D., Charles K. Waterson, BSE., Stuart F. Quan, M.D., Heinrich W. Militzer, M.D., Thomas J. Conahan, III, M.D., Charles W. Otto, M.D., and Stuart R. Hameroff, M.D.
INTRODUCTION
High frequency jet ventilation (HFJV) is but one mode of high frequency
ventilation (HFV) that has been utilized successfully to provide respiratory
support. In HFJV, a small pulsating jet of gas flowing from a regulated high
pressure source is introduced into the airway. Pulsations result from precise
regulation of the gas stream by either fluid.ic or electromechanical control
systems.
Although reports have appeared describing successful application, the
physiologic impact of HFJV characteristics has not been completely
investigated. While unanimous in the conclusion of HFJV effectiveness, no
consensus for design principles and operational guidelines required to apply
HFJV in a safe and effective manner exists. "Rules of thumb" that enable the
clinician to determine initial settings for its introduction have not been
developed. Since the effectiveness of the jet does not appear to depend upon
the delivered "tidal volume", the traditional "rules of thumb" for
conventional ventilator settings are not applicable. Thus, available control
variables which affect the physiologic effect need to be identified.
This paper summarizes the results of protocols conducted to investigate
the effect of certain HFJV design principles and operational guidelines upon
arterial blood gas (ABG) tensions (Pa02 , PaC02). Design variables are defined
as ventilator and jet delivery circuit characteristics not under continuous
operational control. They include the location for introducing the jet into
the airway as a function of the distance from the carina, the ratio of jet
lumen area to expiratory lumen area, and jet .pressure-flow waveshapes.
Operational variables are defined as those under direct operator control
while the device is in use. These include frequency, percent inspiratory time
(% I time) and airway pressures [peak, positive end expiratory pressure
72
(PEEP), and airway pressure difference ( 6 airway pressure = peak - PEEP)].
These particular variables were chosen because of practical clinical
usefulness for control and impact on the mechanisms of gas transport.
METHODS
Three high frequency jet ventilators were utilized. A flueric unit which
created jet pulsations as the gas flowed through a single stage flueric
oscillator was used to determine the effect of jet location in the airway. 1
An electromechanical system employing an electronically controlled solenoid
valve to interrupt the gas stream was utilized to assess the effects of lumen 2 areas and waveshapes. A Healthdyne Model 300 high frequency ventilator that
provided a jet pulse with pressure and flow characteristics similar to the
electromechanical unit was utilized for evaluating the operational variables.
Multiple protocols utilizing mongrel dogs (8 to 30 kg) were conducted.
The animals were anesthetized and paralyzed. A femoral artery and vein were
cannulated for monitoring blood pressure, obtaining specimens for measurement
of ABG tensions, and administration of drugs and fluids.
The dogs were intubated with a 9mm low pressure cuff endotracheal (ET)
tube (double lumen endobronchial was used to determine jet location). A 3mm
Ld. polyethylene catheter passed 6cm beyond the distal tip outside the ET
tube was used to measure airway pressures. This catheter was connected to a
transducer and recording system. The jets were delivered via either a similar
catheter passed through the wall of the ET tube to its distal tip or an
extra lumen extruded into the wall of the ET tube (National Catheter
Company). The proximal end of the ET tube was connected to the breathing
circuit of an anesthesia machine.
Design Variables
The flueric ventilator operating from a constant source pressure of 20
psi at a frequency of 144 min-1 and a 50% inspiratory time (I:E = 1:1) was
utilized to determine effects of jet location in the airway. Under these
settings, this unit provided a total flow of 18.5 Ipm. Random lengths from a
premeasured jet catheter were introduced into the airway. After a fifteen
minute period, ABG tensions were determined.
The electromechanical system operating at a source pressure of 1. 25
psi/kg dog weight was utilized to determine the effects of pressure (flow)
waveshapes. A noncompliant 125 ml capacitor (bottle) placed between the
solenoid outlet and the jet nozzle resulted in a damped sinusoidal (sawtooth)
waveshape. Without the bottle, a rectangular waveshape was produced. The
73
effect of waveshape upon arterial blood gas tensions was determined at three -1
frequencies (120, 150, 180 min ) and three pulse durations (0.05, 0.10, 0.13
secs).
Throughout these protocols, the ratio of jet lumen area to exhaust lumen
area varied. Although constant for each protocol, ratios ranged from 1:6 to
1:11.
Operational Guidelines
The Healthdyne unit was utilized to determine the effects of the
independently controlled operational variables of frequency, % I time, and
peak airway pressure (Paw) upon ABG tensions. A ventilation baseline was
obtained at an FI 02 of 0.4, frequency of 150 min-1 , 30% I time with a peak
airway pressure adjusted to produce normocarbia (40±5 torr). After obtaining
the baseline peak airway values, the effects of the control variables upon
Pa02 and PaC02 (measured at 20 minute intervals) were investigated by: a)
randomly varying frequency (100 to 900 min- 1) at a constant 30% I time and
baseline peak Paw; b) randomly varying % I time (10 to 50) at a constant
frequency of 150 min-1 and baseline peak Paw; c) randomly varying peak Paw (0
to 20 cm H20) at a constant frequency of 150 min- 1 and 30% I time.
Statistical Analysis
Multiple statistical techniques were employed. These included Students'
t-test for paired and unpaired data, three-way analysis of variance, one way
analysis of variance and a posteriori technique (Newman Keuls) for intragroup
significance, and linear regression analysis. Significance was defined as
p<0.05 and linearity as r>\0.8\.
RESULTS
Design Variables
Location of Jet In Airway. The effect of jet location within the
airway upon PaCOZ is shown in figure 1. Frequency, % I time, and driving
pressure, hence flowrate, were held constant. PaC02 correlated linearly (r=
-0.862, p<O.OOl) with catheter tip distance from the carina. The introduction
of the jet at the distal tip of the endobronchial tube resulted in a lower
PaCOz than near the proximal opening of 40±3 torr vs 66±5 torr respectively.
Arterial oxygen tension was not significantly altered by the position of the
catheter tip. Fatal barotrauma resulted when the jet tip was passed 5 cm
beyond the carina.
74
~ e.
~ D..
90
r=-.862
80 p<O.OO1
n=51
70
60
50
40
30
~+-~~-.~.-~~-.~.-ro~-,~T-~ _ 45 - 40 - 35 - 30 - 25 - 20 - 15 - 10 - 5 ? + 5
Distance from Carina (em) aboveca,ina -1- belowca,lna
Figure 1. PaCOZ vs Distance from Carina
Jet Pressure Pulse (Flow) Waveshape. The effect of rectangular and
sawtooth pressure pulse (flow) waveshapes upon airway pressures and ABG
tension at a constant inlet pressure at various frequencies and % I time (I:E
ratios) were determined. Significant differences between waveshapes reveal
that higher peak, lower end-expiratory, and greater airway pressure
differences (peak-PEEP) occurred with rectangular compared with sawtooth
waveshapes at a constant driving pressure, frequency, and pulse duration. For
rectangular waveshape, statistically higher peak airway presures (>7.4 cm
H20) occurred at I:E > 0.35 with highest PEEP (3 cm H20) at an I:E of 0.65.
The largest airway pressure differences (5 cm H20) occurred at an I:E of
0.35. With the sawtooth pulse, the highest peak airway pressures (> 6 cm H20)
were obtained at I:E > 0.33 with the largest values for both PEEP (3.6 cm
H20) and airway pressure difference (4.3 cm HZO) occurring at an I:E of 0.65.
In general, rectangular pressure pulse wave forms produced lower
PaC02 values than the sawtooth waveforms at several I:E values (0.Z5, 0.35,
0.43, 0.48). At a constant inlet pressure (1.Z5 psi/kg) with a frequency of -1 150 min , 30% I time, and peak airway pressure of approximately 7 cm H20,
rectangular pressure waveshapes produced PaCOZ values of 33.l±3.7 torr, while
sawtooth waveshapes yielded PaCOZ values of 67.8±11.3 torr.
Pa02 varied only slightly with differing I:E ratios and waveshapes
at FI 02 values of 1.0. Highest PaOZ values (480 torr) occurred at an I:E of
0.65 for a rectangular wave, whereas for the sawtooth shape the highest PaOZ
75
(460 torr) occurred at an I:E of 0.11.
Ratio of Cross Sectional Areas. Comparison between jet lumen cross
sectional areas and exhaust lumen cross sectional areas demonstrated that
lumen area ratios ranging from 1:6 to 1 :11 would provide normocarbia (40±5
torr). Ratios larger than 1: 6 would tend to cause air trapping and produce
higher PEEP values than desired.
Operational Variables
Prior to initiating the protocols for determining the effects of
frequency, % I time, and peak airway pressure upon ABG tensions, baseline
peak Paw's producing normocarbia (40±5 torr) at a frequency of 150 min -1 and
30% I time were determined. These values were utilized at the constant peak
Paw with varying frequencies and % I times. The baseline peak pressure values
ranged from 6 to 9 cm H20.
Frequency The effect of frequency at a constant peak Paw
(baseline) and % I time on PaC02 is shown in figure 2. With % I time and
airway pressures held constant (30% I-time, peak = 7.29±1.25 cm H20, PEEP
=3.3S±0.69 cm H20), the mean PaC02 varied linearly with frequency (r=0.97). -1 Mean PaC02 ranged from 34.5 torr at a frequency of 100 min to SO.3 torr at
900 min-1
Percent Inspiratory Time Effect of % I time, (inspiratory time/to--1 tal ventilator cycle time) at a constant frequency (150 min ) and peak
Paw (baseline) on PaC02 is shown in figure 3. Regression analysis indicates
that PaC02 varies linearly (r=0.95) with % I time at a constant frequency and
peak airway pressure (F=150 min -1, peak =7.29±1.25 cm H20, PEEP =3.38±0.69
cm H20). Mean PaC02 ranged from 33.1 torr at 10% I time to 43.8 torr at 50% I
time.
Airway Pressures The effect of peak
150 min-1 and 30% I time upon PaC02 is shown
linearly as peak Paw increases (r=-0.95).
Paw at a constant frequency of
in figure 4. PaC02 decreases
Higher peak pressures were
associated with lower values of PaC02 (19.0 torr at peak = 20 cm H20 vs 50.6
torr at peak = 4 cm H20).
These protocols were not designed specifically to investigate the
effects of PEEP or airway pressure difference upon PaC02• However, it was
observed that some PEEP (>3 cm H20) was necessary to avoid hypercapnia. When
larger amounts of PEEP (>10 cm H20) were used, an increase in jet driving
pressure was required to maintain normocarbia. Larger airway pressure
differences, usually associated with higher peak pressures, gave lower values of PaC02 (figure 5).
76
100
85
'" 70 O-c-0'-raB Q.~
55
40
r= .970 m=.062 b= 29.424
55 r = .951 m = .295
50 b=28.269
45
(\J
01::'40 0 .... (1l0 a..~
35
30
900 10 20 30 40 50
Percent Inspiratory Time (1%) Frequency of Jet (min -1)
Figure 2 - Jet Frequency
vs PaC02
60
48
24 I
r = - .954 m = -2.043 b=57.262
I 12~----~------~----~----~
4 8 12 16 Peak Pressure (cm H20)
Figure 4 - Peak Airway Pressure
vs PaC02
20
'C'
Figure 3 - Percent Inspiratory
Time vs PaC02
60.50 -•• • F= 150 min- 1
52.75 • 1% =30% (r= -.783, n=29)
• 45.00 •
• • • (; 37.25 • ~
N
0 <c6 29.50 • • • a.. •
• • • 21.75 • • •
• • • 14.00 •
2.20 3.76 5.32 6.88 8.44 10.00
Airway Pressure Difference (cm H2O) (Peak-PEEP)
Figure 5 - PEEP vs PaC02
77
DISCUSSION
Prior to any discussion of design and operational variables of HFJV, an
understanding of certain physical principles inherent in gas transport must
be obtained. The first is an appreciation for the conservation of mass which
simply states that the rate of mass flowing into a system (patient) must
equal the rate of mass flowing from the system (patient). If these rates are
unequal, then the difference between the two must be accounted for by either
accumulation (over-pressurization) or reaction (metabolism). Thus, every high
frequency ventilator must provide a means of getting a quantity of gas into
and out of a patient with a minimal amount of unnecessary accumulation and at
a sufficient rate to meet any metabolic demand.
In HFV, a relatively high flow pulse of inspiratory gas is introduced,
into the airway. This is an active process with the magnitude of the gas
pulse directly dependent upon the % I time, waveshape,(rectangular yielding
highest flows), pressures (inlet, airway) and airway resistance. For a single
pulse, the volume delivered will also depend upon frequency. Hence,
frequency, % I time, and pressure have interdependent effects upon delivered
volumes.
Once the amount of mass from the inspiratory pulse has been introduced,
it must be exhaled. This can be accomplished by either a passive process
using the elastic recoil of the lung and chest wall or by an active process
which introduces a small negative pressure (suction) to augment exhalation
flow. In either situation (passive or active), the time interval for exhala
tion must allow for a sufficient volume to be removed.
In addition to differences in inspiratory and expiratory techniques,
each HFV system must have a minimally impeded exhalation passage. Any type of
obstruction or exhaust resistance will reduce exhalation flow. As the conser
vation of mass predicts, an accumulation will occur and pressurization will
result. With appropriate control, this can provide a beneficial PEEP effect.
Likewise, if the inlet flow is slightly higher than the outlet flow, an
inadvertent PEEP can be obtained. This is the basic reason for the
inadvertent PEEP commonly found with HFJV techniques.
Since HFJV techniques differ among investigators, a lack of standardiza
tion of source pressure (02 supply), flow regulation, site of jet introduc
tion into the airway, jet nozzle size, and expiratory resistance, reported
results of the effects of jet characteristics and their relationships are
confusing. With this series of studies, three design characteristics which
78
influence mass flow rates and the balance between inspired and expired volume
with HFJV were investigated.
The results of these studies indicate that for lower inlet pressures and
flowrates, the jet is most effective when introduced at the distal tip of the
endotracheal tube. The jet can be introduced at other more proximal points in
the airway which may.offer practical and safety advantages, but the loss in
efficiency must be overcome with higher driving pressures and gas consump
tion. Mucosal damage was not observed at any jet locations. However, a
pneumothorax resulted when the jet was passed below the tip of the ET tube.
Pressure waveforms with a rapid rise and negligible internal compliance
(rectangular) proved more effective than those with a gradual rise
(sawtooth). This further suggests the importance of the initial high flow
transient to the effective inspiratory volume. Flows through the jet were not
measured, but higher driving pressures were necessary to achieve the same
peak airway pressure and expiratory minute volumes with the damped waveform.
Inspiratory lumen to expiratory lumen area ratio appears as another
determinant of the mass balance necessary to control PaC02• In these protocols
no problem was presented in controlling the HFJV system for normocarbia as %
I time and driving pressure were adjusted to compensate for the various
inspiratory-expiratory flow resistances. However, at an I:E ratio of 1:1
(SO%I-time), when a larger (12 gauge) catheter was located within a 4mm ET
tube, the tube was greatly occluded which prevented adequate exhalation flow.
This resulted in higher levels of PEEP than desired and an increase in PaC02•
In the same tube, a 14 gauge catheter appeared to provide the optimum balance
between inspiratory and expiratory flow with the available inspiratory flow
driving pressure. Area ratio in this situation was approximately 1:11.
The effect of frequency on PaC02 is probably the most difficult to
understand because of the many effective frequency ranges produced by various
devices. The HFJV device used in this study became less effective at higher
frequencies at a constant 30% I time. However, when % I time was varied at a
cons~ant frequency, PaC02 decreased linearly with decreasing % I time. This
would suggest the need for a longer exhalation time (a passive process) than
that available with 30% I time at higher frequencies. This is not surprising
in considering the mass balance which must be established between inspiratory
and expiratory volumes with greatly different driving pressures, resistances,
and flowrates.
79
Percent inspiratory time also influences PaC02, apparently by altering
the mass flow dynamics of the system. Flow transients have been observed
during the on-time of the jet. Because of these transients, % I time would
determine whether flow reaches a steady state value at a given pulse fre
quency. Inspiratory time also influences airway pressure differences by its
effect on PEEP via control of exhalation time. An effect of % I time on
oxygenation has been casually observed, but not experimentally tested.
However, it appears that lower % I time yield lower Pa02 , while longer % I
times increase Pa02• This is analogous to the effect of I:E ratio in conven
tional ventilation.
The single strongest determinant of ventilatory sufficiency appears to
be airway pressure. Although the experiments described controlled peak
pressures, data analysis suggest that it is actually airway pressure differ
ence (peak-PEEP) which correlates to PaC02• Since PEEP was not independently
varied, airway pressure difference increased in direct proportion to peak
pressure. In addition, airway pressures required for normocarbia are lower
than those associated with conventional mechanical ventilation. Mean airway
pressures may be comparable, but dependent on rates and I:E ratios.
Although PEEP was not independently controlled, a correlation with PaC02 exists. With airway pressure difference held constant, a greater PEEP is
desirable, perhaps to keep airways open at rates too fast and tidal volumes
too small to open them on each respiratory cycle. However, excessive PEEP
should be avoided due to its hemodynamic effects and increase in dead space,
which may require higher driving pressures and greater airway pressure
differences.
SUMMARY
Design characteristics and operational variables for a HFJV system have
been investigated. The results indicate that for optimization of CO2 removal
at lower flows, a jet having a rectangular pressure (flow) waveshape should
be introduced into the airway close to the carina. Jet lumen to exhaust lumen
area ratios ranging from 1:6 to 1:11 are effective. Some PEEP (>3cm H20) is
necessary to prevent airway collapse at rates too fast and volumes too small
to open them during each respiratory cycle. While airway pressures are low
compared to conventional ventilation, airway pressure differences of 5-10 cm
H20 are necessary for adequate ventilation.
Furthermore, these data suggest operational "rules of thumb". Initial
settings of frequency of 150 min-I, a 30% I time and airway pressures
80
adjusted for adequate chest expansion (usually 5 cm H20 PEEP and peak of 15
cm H20) should provide adequate ventilation. For low Pa02 values, increasing
FrOZ or airway pressures should correct the problem. At high PaCOZ values,
at a given frequency and % I time, increasing peak Paw; or decreasing
frequency keeping % I time and peak Paw constant; or decreasing % I time
keeping frequency and peak Paw constant should correct the problem. Of
course, because of the inter-relationships between variables, numerous other
possibilities exist.
REFERENCES
1. Calkins CM, Waterson CK, Hameroff SR, Harris TR, Jones JF: A simple flueric high frequency jet ventilator. Anesth Analg (Cleve) 1982; 61: 138.
2. Calkins JM, Waterson CK, Hameroff SR, Kanel J: Jet pulse characteristics for high frequency jet ventilation in dogs. Anesth Analg (Cleve) 1982; 61:293.
ACKNOWLEDGEMENT
The authors want to acknowledge the assistance and support given to
these projects by V.L. Samoy, H. Militzer, M.D., C. Wiseman, Healthdyne Inc.
and the Parker B. Francis III Foundation.
AIRWAY PRESSURE AS A DETERMINING FACTOR FOR VE~~ILATION A~~ HAEMODYNAMIC EFFICIENCY DURING HFJV.
'M. JIMENEZ LE~~I~~Z, J.A. CAMBRONERO, J. LOPEZ, B. GALVAN, A. GARCIA, R. DENIA. A. AGUADO.
SERVICIO C. INTENSIVOS AND SERVICIO DE CIRUGIA EXPERIME~~AL (DR. DE MIGUEL), CSSS "LA PAZ", MADRID/SPAIN.
1 • I1~RODUCTION
During t,he use of HFJV normocarbia is achieved with frequencies near
to 100 b.p.m. creating minimum pressure in the airway passage and using a
volume discretely superior to dead volume (1,2).
Recently T. H. Rossing et, al (3) demonstrated t,hat wit,h HFOV the
efectiveness in eliminating C02 is a funct,ion of the product, of t,idal
volume and a frequency almost, reaching a critical stage, t,he use of t,he
same lat,eral flow makes t,he pressure in the airway passage s.imilar at
different frequency levels.
During t,he use of HFJV t,he pressure generated in t,he airway passage
is dependent both on t,he t,idal volume and also the expiratory time. The
select,ion of these paramet,ers t,o obtain an elevated pressure in the air
way passage in cert,ain circumst,ances is achieved by proport,ioning an in
crease in FCR and a better oxygenation (4,5) but the effects might not
be beneficial t,o the ventilation or t,o the haemodynamic efficiency.
With a view to evaluating the haemodynamic changes and the eliminat,ion
of C02 during HFJV at different pressure levels in the airway passage, we
designed the following experimental study.
2. METHODS AND MATERIALS
For this experiment with HFJV we used a Jet-Ventilator similar to
design to that of Carlon et al (6) based on electronic activation by means
of a solenoid valve to which the gases from the hospital's general instal
lation reach and are freed in the endotracheal tube through a needle with
a diameter of 1.9 mm. which is placed in the swivel connector (7). The
placing of a non-returnable valve in the lateral connection permits the
expiration and impedes the intake of air by means of a venturi effect.
With this system we made a study on twelve anaethezied dogs.
82
The dogs were vent, i1 ated wit,h a const,ant tidal volume (6 mI/Kg.) and
liE rat,io (1 : 2); respirat,ory rat,e was increased from 100 t,o 150, 200 and
300 c.p.m. at, 30' int,ervaJ s. Blood analysis were carried out, at, t,he end
of each period. The expired air was collect,ed in a Douglas bag and the
CO2 was analysed using a capniograph. Wit,h this data t,he Vn/VT and VD
was calculat,ed. The cont,rol of t,idal volume was carried out wit,h an
u1t,rasonic spirometer (Burns LS 75) modifying t,he driving pressure. Airway
pressure was measured by a cathet,er advanced past, the carina and connect,ed
to a water column.
To minimise the inn uence of the increase of the pressure in the
airway passage t,he above experiment was repeat,ed at 100 and 200 b.p.m.
using t,he same t,idal volume but modifying the liE rat,io. The I/E rat,ios
used were 1:1 at 100 b.p.m. and 1:6 at 200·b.p.m.
In a parallel experiment, we measured the haemodynamic changes (TA,
CO, PAP and PCP) induced by changing t,he airway pressure, modifying the
frequency, volume and I/E ratio; using a Swanganz t,hermodilution catheter.
First ly the t ida 1 volume and liE rat, io were rna intained constant at
(125 cc and 1 :3) respectively, increasing the frequency t,o 100, 250 and
SOO b.p.m. Haintaining t,he t,idal volume and frequency const,ant, (200 b.p.
m. ), measurement.s were t,aken' at, liE rat ios of 1: 1, 1: 3 and 1: 6. Finally
t,he hap--Illodynamic st,udies were carried out at, a constant, frequency of
(200 b.p.m.) and liE ratio of (1:3) with increases in volume from 100,
150 to 200 mI.
The control of t,he pressure in the airway passage was achieved in
t,he same way as described in t,he previous experiment.
3. RESULTS
While rnaint,aining const,ant t,he volume and liE ratio, t,he increase
of the frequency was followed by an increase in the pressure of the air
way passage. Under these circumstances we always found an increase in
vD/vT. The values are shown in Table 1.
The C02 values obtained with the increase in frequency are not
predict,able as t,he alveolar vent,ilat,ion is influenced by the increase in
VD produced as t,he frequency is elevated.
83
100 150 200 300 b.p.m.
Paw 3.5 :t 5.5 ± 2 10 ± 2.5 21 ± 10
vD/vT 0.75 :t 0.1 0.78 :t 0.1 0.84 ± 0.1 0.93 ± 0.04
pC°2 45 ± 18 46 ± 27 44 ± 31 53 ± 40
Table 1. Obtained values with increases in frequencies at constant VT
and II E rat,ios.
When the liE rat,ios were selected with the object of minimising the
pressure in the airway passage, we observed no significant changes in
VD/VT' (Figure 1).
em H2O 25
Paw 15
5
0.9
Vd/Vt
0.7
Figure A
T
~, ... 1.21 'T' .l..
._. .~.
-3.5 .... T 5
~: .. [.0.93 0.9
T T ! p<.QO, i !! Vd /Vt
:0.73 ! 1. 0.7 : • .i_
7 Paw
.1..
40
, ,
200 300
Figure B
-
Floa !
I:E 1:1
-
F ?DO I:E 1:6
Figure 1. a) Changes with constant r/E and b) Changes in vD/vT and
pC02 when r/E rat,io was modified.
84
Vt 125,1:E 1:3
F 100 250 500 em H20 , ...................... _, 20
Paw 10 --0
o
F 200,1:E 1:3
em H20 Vt 1O'Q .... J~:Q.Jqo 20 •..... " ......... \.
... ....
Paw 10
o
Llmin 4
3 C.O.
2
Llmin 4
3 C.O.
2
F 200, Vt 125
em HzO 20
I:E 1;1 .. JJ.L,6 L/min
4 ...................... M ••••
..•
Paw 10 3 e.o.
o 2
Figure 2. Relation of airway passage pressure obtained using different parameters and CO r<esu1t ..
Cardiac out.put. was similar with HFJV (3.6 ± 1.2 b.p.m.) and IPPV
(3.4 ± 1.1 lop.m.) at. airway pressure lower t.han 13 C[.1S. of H20. When
airway pressures increased t.o higher values, t.he cardiac out. put fell to
2.9 ± 1.3 .l.p.m. The relation between the pressure in the airway passage
reached with the use of different parameters and also the CO result is
reflected in Figure 2.
4. DISCUSSION
The syst.em we used for HFJV was based on t.he electronic activation
of a solenoide valve which gives both security and accuracy for the
frequency and liE ratios programmed.
These charact.erist.ics together wi.t.h the use of a known volume, not.
influenced by t.he out. put flow on avoiding t.he int.ake of air by means of
a venturi effect. -with t.he use of a non-ret.urnable valve- makes us believe
t.hat. t.he experiment. is valid for the det.ermination of the vD/vT during HFJV.
85
The increase in the dead space observed with frequency when constant
liE ratios were.used, can only be attributed to the rise of the pressure
in the airway passage as there was no modification in the dead space when
the experiment was repeated using different liE rat,ios, in order to minimise
the pressure increase in t,he airway passage secondary to t,he rise in frequency
(liE ratio of 1:1 at 100 b.p.m. and 1:6 at 200 b.p.m.). This increase in
the VD is produced both by t,he increase in FRC and t,he interference t,hat,
a rise in the intrapulminary pressure has on the pulmonary circulat,ion wit,h • an increase in v/Q•
We give this fact, great, import,ance during the use of HFJV, as the
increase in the minut,e volume on producing an increase in the pressure of
t,he airway passage and therfore a rise in VD, might, not necessarily be
followed by a greater alveolar ventilation and so it is possible that, an
increase in ventilatory volume is followed by a greater pC02. This
information suggests t,he necessity for the creat ion of nomograms with the
variation of parameters in HFJV (8).
On t,he other hand, we also observed a decrease in CO when the pressure
in the airway passage rose, eit,her because of an increase in frequency (9)
at const,ant VT and II E rat,ios or because of an increase in VT. However,
when the pressure values in the airway passage are maintained low, the
CO is discretely higher in HFJV t,han in CV.
In conclusion, we think t,hat, the pressure generat,ed in t,he airway
passage during HFJV plays an important role both for vent,ilat,ory efficiency
and also for haemodynamic tolerance and so for t,his reasons, we see the
necessit,y of determining which is the best, met,hod for measuring t,his
pressure and also t,he necessity t,o adapt an a] arm to the systp..ffiS used,
for t,he cont,rol of this parameter.
REFERENCES
1. Klain M, Smith RB: High frequency percutaneous t,ranstracheal jet ventilation. Crit. Care Med. 5:280, 1977.
2. Bjerager K, Sjost,rand U, Wat,twil M: Long-t,erm t,reatment of two pat,Lents wit,h respirat,ory insufficiency 'with IPPv/pEEP and HFPPV/ PEEP. Acta Anaest,h. Scand. (supple 64): 55, 1977.
3. Ross.ing TH, Slutsky AS, Lehr JL, Drinker PA, Kamm R, Drazen JM: Tidal Volume and frequency dependence of Carbon Dioxide el iminat, ion by High-frequency vent,ilat,ion. N. Engl. J. Med. 305:1375,1981.
4. Shust,er DP, Snyder JV, Klain M, Grenvik A: High-frequency Jet, Ventilat,ion during the t,reat,ment, of Acute Fulminant, Pulmonary Edema. Chest, 80:682, 1981.
86
.5. Jimenez M, Lopez J, Cambronero JA, Palma MA, l,apuesta JA, Aguado A: Early clinical experience wit,h HFJV in our UCI. S. High Frequency Vent,ilat,ion, Rott,erdam, Sept,ember 1982.
6. Carlon GC, Miodownik S, R."ly Jr. C, Kahn RC: Technical aspect,s and clinical implicat,ions of I1FJV wit,h a solenoide valve. Crit,. Care Med. 9:47, 1891.
7. Jimenez M, Cambronero J A, Lopez J, Lapuert,a J A, M i gue 1 de E, Aguado A: Vent,ilacion a alta frequencia. Estudio preliminar. M. Int,ensiva 6.4, 1982.
8. Carlon GC, Ray Jr. C, Pierri MK, Groeger J, Howland WS: HFJV theoret,ical considerations and clinical observation. Chest 81:3.50, 1982.
9. Klain M, Smit,h RB, Babinski M: Limit,s of high frequency percutaneous transtracheal jet ventilation using a fluidic logic controlled ventilator. Can. Anaesth. Soc. J. 27:351:56. 1980.
B. EXPERIMENTAL STUDIES AND MECHANICS
HIGH FREQUENCY VENTILATION: AN EXPERIMENTAL COMPARISON OF HFPPV AND HFJV
U.H. Sjostrand, M.F. Babinski, U.R. Borg, R.B. Smith
Department of Anesthesiology, The University of Texas Health Science Center, San Antonio, TX 78284, USA
Most of the currently used high frequency ventilation (HFV)
systems are of open character (1,2). HFV creates a demand for
tidal volumes delivered in a short time and with high inspira-
tory flow (1-5). Systems with insignificant compression vol-
ume can fulfill such requirements (3,6). Presently, three
modes of open systems are being used for HFV: a. Insufflation
catheter, or double-lumen tube, £. pneumatic valve, and £. jet
injector nozzle (1). This study evaluates these modalities in
healthy dogs and in a lung model (Figure 1).
METHODS AND PROCEDURES
Seven mongrel dogs (mean BW 22.4 kg) were anesthetized
with thiopental, and intubated with a double-lumen endotracheal
tube (Hi-Lo Jet, National Catheter Corporation, Div. Mallin
ckrodt, Argyle, NY) with an inspiratory:expiratory lumen [IL:EL)
ratio of 1:10. The dogs were ventilated to normocarbia (PaC02
40.1+0.9 "mrnHg) with a Bronchovent® (Siemens-Elema AB, Solna, S-
17195 Sweden~ Siemens-Elema Ventilator Systems, Elk Grove Village
IL 60007) or a fluidic ventilator (7~ FV~ Medical Kit, Corning)
at a frequency (f) of 60/min, with inspiratory time (t%) 22%
of the ventilatory cycle. Both ventilators were used (Figure
1) with the pneumatic valve (PV), the jet injector nozzle
88
(JIN) or the insufflation line (insufflation catheter [IC])
of the double-lumen tracheal tube.
Double Lumen Tube IL:EL
1:10
Pneumatic Valve
Bronchovent or
Fluidic Ventilator f60/min
FIGURE 1. Experimental design of the studies in the lung model using the IL:EL 1:10 double-lumen tracheal tube with pv, JIN and IC, and ventilator settings as in the seven anesthetized dogs.
Figure 1 shows the experimental design, using a lung model
(static compliance 72 ml/cm H20). A rigid 12 mm internal di-
ameter plastic tube, which simulated the trachea, was intu-
bated with the double-lumen tracheal tube as in the dogs.
Ventilation was delivered by the Bronchovent® or the FV in
the same way as in the dog experiments. Gas velocity was
measured using a linear pneumotachograph (Model 3800, Hans
Rudolph, Inc., Kansas City, MO) located between the trachea
and the model lung. For every HFV modality, gas velocities
and integrated tidal volumes were recorded on a pressurized
ink recorder (Gould 2200S, Gould Inc., Cleveland, OH). The
results were calculated from the recordings and combined
with gasometric values obtained in the dog experiments.
89
RESULTS
At normocarbia (Table 1), there were few systematic dif-
ferences in end-inspiratory airway pressures (Paw) between
ventilators or modes of ventilation (Table 2).
with both ventilators, PV provides the highest peak inspi
ratory flow (Vlmax) without air entrainment. Similar to the
original technique for HFPPV (3), with an IC it was possible
to ventilate without air entrainment using both ventilators
(IC=inspiration through the insufflation line of the double-
lumen tube). Ventilation with IC reduced dead space and
tidal volume (VT)' creating normocarbia (Table 1) with less
"waste ventilation" and lower Vlmax than with PV (Table 2).
Using IC or JIN, Vlmax obtained at the distal end of the
tracheal tube was higher with the fluidic ventilator. With
JIN air entrainment contributed to the VT' 26% with Broncho-
vent® and 58% with FV.
Experimental Comparison of HFPPV and HFJV
BronchoventJl Fluidic Ventilator
PV JIN Ie PV JIN Ie
pHa 7.37±0.03 7.36±0.02 7.35000.06 7.3400 0.1 7.37000.02 7.3700 0.04
Pae02 40±1.2 40±1.5 40±1.3 42± 8.1 4O±O.O8 39± 1.2 (mmHg)
Pa02 79±7.4 77±8.4 78±9.6 77±11 81±8.0 77±11 (mmHg)
FI02 0.21. Mean values ± SO are given.
TABLE 1. Mean values (+ SD) of arterial blood obtained in seven anesthetized dogs. -
CONCLUSIONS
PV and IC techniques provide ventilation without entrain-
ment of a second gas, while the JIN technique depends on jet
entrainment of a second gas (1). With JIN, entrainment is
90
related to the jet flow patterns of the jet produced by the
two ventilator systems. This is illustrated by the differ-
ences observed with Bronchovent® (26% of VT entrained) and
FV (58% of VT entrained). Without entrainment of a second
gas, with PV and IC, inspiratory gas can be conditioned and
its composition controlled (4-6). Experimental Comparison of HFPPV and HFJV
Normocarbia Bronchovent" Fluidic Ventilator f/t%=60/22
PV liN Ie PV liN Ie
Ill .... 1229 654 79B 1139 936 926 (ml/sec)
Paw ± SD 5.2±O.8 4.1±O.6 4A±O.5 9.3±2A 6.1±O.7 4.5±O.8 (cmH2O)
v,-±SD 296±148 226±61 188±118 277±56 263±73 190±87 (ml)
Entrained gas 0 26 0 0 58 0 (% of lIT)
PV: Pneumatic Valve; liN: let Injector Nozzle; Ie: Insufflation Une of Double-Lumen Tube. VI max: Maximum Inspiratory Flow; Paw: End·lnspiratory Airway Pressure.
TABLE 2. Mean values (+ SD) for end-inspiratory airway pressures and tidal volumes providing normocarbia in 7 anesthetized dogs. Peak inspiratory flow and entrainment were measured in the lung model (Figure 1).
In this study, PV, IC and JIN were "open systems" and
therefore delivered tidal ventilation is highly dependent
upon lung-chest compliance and inspiratory airway resistance
(3-5). For the same reasons as in volume-controlled IPPV, in
order to guarantee delivery of preset tidal volumes (5,6) op-
timal ventilator design in HFV also requires volume-controlled
tidal ventilation (4-6). Volume-controlled HFV additionally
demands higher inspiratory flow (1,4-6) than with"conventional
systems" for IPPV. If the patient circuit during inspiration
functionally is a "closed system" (1) with negligible com-
pression volume (1,4-6,8), volume-controlled HFV is provided
(5,6). Two low-compression systems for volume-controlled ven
tilation (systems Hand J) are described elsewhere (1,5,6,8).
REFERENCES
1. Sjostrand UH, Bunegin L, Smith RB, Babinski MF: Development and clinical application of high frequency ventilation. Perspectives in High Frequency Ventilation (Eds. Scheck PAE, Sjostrand UB, Smith RB). Martinus Nijhoff Pub!. BV, The Hague, 1983 ..
2. Babinski MF, Sjostrand UH, Smith RB and Bunegin L: Animal and lung model studies of double-lumen tracheal tubes for high frequency ventilation. Resp Care 28, 1983.
91
3. Jonzon A, 5berg pA, Sedin G, Sjostrand U: High-frequency positive-pressure ventilation by endotracheal insufflation. Acta Anaesth Scand (Suppl) 43:1, 1971.
4. Sjostrand U: Review of the physiological rationale for and development of high-frequency positive-pressure ventilation - HFPPV. Acta Anaesth Scand (Suppl) 64:7, 1977.
5. Sjostrand U: High frequency positive pressure ventilation (HFPPV): A review. Crit Care Med 8:345, 1980.
6. Sjostrand U: Pneumatic systems of respiratory insufficiency IPPV/PEEP, HFPPV/PEEP, CPPV, Scand (Suppl) 64:123, 1977.
facilitating treatment with alternative use of
or CPAP. Acta Anaesth
7. Klain M, Smith RB: Fluidic technology. Anaesthesia 31: 25-32, 1976.
8. Sjostrand UH, Koller M-E, Smith RB, Breivik H, Bunegin L: IPPV, HFPPV and HFPPV/PEEP in dogs with acute cardiac tamponade. Resp Care 28, 1983 (in press).
ALVEOLAR PRESSURES DURING HIGH FREQUENCY VENTILATION
P. R. FLETCHER
We have previously suggested (1), on the basis of an analysis of the behavior of a very simple single-compartment
lung model (Fig. 1) consisting of a single compliance
(corresponding to the alveoli), a single resistance
(corresponding to the "lumped" non-elastic resistance of the
airways and lung tissue), and a single inertance (corresponding
to the "lumped" inertance of the lungs and chest wall), that
high-frequency ventilation might be associated with the
development of considerable levels of positive end-expiratory
pressure at the alveolar level despite the maintenance of
n9rmal (atmospheric) end-expiratory pressure levels at the
airway.
FIGURE 1. Simple Lung !1odel
I//~ V .~ .' ~'~_ ~T_
FIGURE 2. Behavior of 'perfect' lung/ventilator system
Our analysis also predicted that the constancy of physiological
dead space with increasing frequency which we have observed in
rabbits, with the consequent, almost linear, increase in
ventilatory requirement as ventilatory frequency is increased,
should result in a commensurate increase in end-expiratory
alveolar pressure at the higher frequencies. Since our model
93
has come under considerable criticism as being far too simple
to be of any value, we have attempted to validate it by
measuring alveolar pressures in rabbits during HFV.
Although, given pressure measuring equipment with an
adequate overall frequency response, proximal airway pressure
can still be recorded with a fair degree of accuracy during
HFV, the measurement of alveolar pressure presents many more
problems. Intrapleural pressure and esophageal pressure have
both been used in the past as surrogates for alveolar pressure
in investigating the physics of respiration at conventional
frequencies but the accurate recording of phasic changes in
these parameters at rates in excess of I Hz would present
severe technical problems and the validity of the assumption
that they continued accurately to reflect alveolar pressure
changes at these frequencies would be open to question. We
felt that the use of proximal airway pressure, measured under
"stop-flow" conditions, as an estimate of the instantaneous
alveolar pressure was open to fewer theoretical objections.
In order to use this approach at conventional frequencies in
animals with normal lungs it is necessary only to use a
ventilator which has a low compressible volume and whose cycle
includes short inspiratory and expiratory holds. Pressures at
the airway and in the alveolar compartment during the various
phases of the respiratory cycle will then be as shown in Fig. 2
(for an idealized system with a ventilator which acts as a
constant flow generator during inspiration). Since the
compressible volume of the ventilator and airway has a
compliance that is small relative to that of the alveolar
compartment, the pressure in the airway will fall at the
beginning of the inspiratory hold, very rapidly approaching
alveolar pressure, and, if expiration is incomplete, will rise
equally rapidly to approach end-expiratory alveolar pressure
during the expiratory hold. Fig. 3 shows actual pressure
waveforms recorded in a mechanical model lung with static
compliance and resistance similar to that of a normal rabbit
while it was being ventilated by our ventilator (which does
have short inspiratory and expiratory holds) at a frequency of
94
.... 20 0
~ 15
C\I - Airway pressure l: 15
-- Airway pressure
--- Alveolar pressure
% E ! 10 S 10
~ 5 !
:::I 5 0 II)
.t II) CD
0.5 10 ... 0 IL Time (sec)
0 50 100
Time (msec) FIGURES 3 & 4. Behavior of mechanical lung model at 1 Hz and approximately 7 Hz
approximately I Hz. The correspondence between "hold"
pressures and "alveolar" pressures remains very close. At
higher frequencies, however, the effects of inertance and
resonance within the system make the correspondence much less
clear (Fig. 4). Tn order to make the necessory measurements at
these higher frequencies, it is necessary to have a "hold"
period which is sufficiently long to allow pressures to
equalize. This requires that ventilation be temporarily
interrupted, which was done by abruptly clamping the connection
between the ventilator and the animal's airway and holding it
clamped for 0.5 - I sec. The pressure transducer is connected
to the airway on the animal's side of the clamping point.
FIGURE 5. Experimental Setup
CD 15
= ..... ~~ 10 ILl: :>OE II u ~~ 5 :c
O~--.-~.---~--~--o 100 200 JOO 400
Time (msec)
FIGURE 6. Pressure tracina for end-expiratory pressure recording
95
Our apparatus and experimental methods were otherwise as
previously described (2,3) (Fig. 5). Anesthetized, curarized,
New Zealand White rabbits were ventilated with a rotary valve
ventilator at a number of frequencies in the 1 to 15 Hz range
and pressure measurements were made after the inspiratory flow
had been adjusted to produce a steady-state PaC02 in the range
of 34 to 42 mm Hg. Three studies have been carried out - the
data shown is representative.
The "plateau" pressure from tracings such as that shown in
Fig. 6 (frequency = ± 7 Hz) was taken as being equal to the
end-expiratory alveolar pressure and that from tracings such as
that shown in Fig. 7 was taken as being equal to
end-inspiratory alveolar pressure.
0 15 C\I
:r E
..2 10 ~ " .. .. ~ 5 11.
'" .. ! <
Time (msec)
FIGURE 7. Pressure tracing for peak pressure recording
30
25
iii J: 20 §
o
ALVEOLAA PAESSUAE DUAING HFV
I!l nEflSUfED VALUES ___ Fll.e MODEL _fit IDJEL
/
J o 2 4 6 8 10 12 14 16 18 20
FAEQUENCT (HZ)
FIGURE 8. Changes in peak pressure with ventilatory freq.
Values for total lung compliance and airway resistance were
measured in the individual rabbits by analysis of the airway
pressure waveform during ventilation at a frequency of
approximately 1 Hz and were substituted in the analytical
solution of the simple lung model with and without making
allowance for the effects of inertance. When inertance was
taken into account, it was assumed to be sufficient to give the
system a (LC) resonant frequency of 5 Hz. The substituted
solution was then used to predict expected end-inspiratory and
end-expiratory alveolar pressures at the frequencies which had
96
been used in the experimental study.
As is shown in Fig. 8 (for another study), end-inspiratory
pressure, as measured by the stop-flow technique, corresponded
very well with that predicted from the simple model, if the
effects of inertance were included in the latter. Measured and
predicted values of end-expiratory pressure (Fig. 9) also
corresponded quite well, although the measured values would
have been more consistent with a system inertance rather
smaller than that assumed by the model. This sort of minor
inconsistency is not unexpected when a simple model is compared
with a complex, real, system and undoubtedly represents some
non-linearity in the behavior of the real system. In general,
our experimental findings were consistent with the effects of
inertance playing a significant but not overwhelmingly
important role in limiting gas-transfer under our experimental
circumstances.
30
~ 25
9 ",20
~ "' IE 15
~ ~ 10
~ Sl 5 "'
ALVEOLAA PRESSURE OURING HFV
I!JI'EASlJREO VflUJES _ALe rcoEL _RCIIXlEL
/ 1m /m
/
O~~~-------------o 2 4 6 6 10 12 14 16 16 20 FREOUENCT 1HZ)
FIGURE 9. Changes in end-expiratory pressure with ventilatory frequency
We conclude that, during high-frequency ventilation,
end-expiratory alveolar pressures may be substantially above
atmospheric, even when there is no positive end-expiratory
pressure at the airway. Some of the beneficial effects of HFV,
in terms of improved oxygenation and reduced intrapulmonary
shunting of blood may depend on its ability to induce PEEP at
the alveolar level with lower mean and peak alveolar pressures
97
than are possible with more conventional types of ventilation.
Since the relationship between ventilatory frequency and
alveolar pressure aoserved in the experimental animals was
qualitatively and quantitatively similar to that predicted by
analysis of our model, simple though it is, it probably
represents a good first approximation to a functional model of
the overall mechanical behavior of the rabbit lung during HFV.
REFERENCES
1. Fletcher PR, Epstein MAF, Epstein RA. Alveolar pressures during high frequency ventilation (HFV). Fed. Proc. 39: 57~, 1980.
2. Fletcher PR, Epstein MAF, Epstein RA. A new ventilator for physiologic studies during high-frequency ventilation. Respir. Physiol. 47: 21-37.
3. Fletcher PR, E?stein RA. Constancy of physiological dead space during hlgh-frequency ventilation. Respir. Physiol. 47: 39-49.
CARBON DIOXIDE CLEARANCE DURlNG HIGH FREQUENCY JET VENTILATION (HFJV)
J.L. J3()(JR;AIN - A.J. MORTIMER - M.K. SYKES
Nuffield Department of anaesthetics, OXford Uni versi ty, Oxford
Several studies have shown that alveolar ventilation
could be maintained with tidal volume less than anatomical
dead space if the respiratory frequency was high enough (2, 5, 8,
9, 10, 11). However mechanisms by which effective gas exchange
occurs are not well understood.
Methodological problems encountered in the measurement
of tidal volume and CO 2 clearance can explain this lack of under
standing. It is the reason why we studied at first CO 2 elimina
tion on high frequency ventilation on a model lung. We took a
particular care in the determination of the linearity and the
frequency response of different systems of measurements. This
study was carried out to determine the relationship between
tidal volume, respiratory frequency and CO 2 elimination.
METhODS
An artificial lung (MANLEY, Resistance = 5 cm H20/1/sec,
compliance 20 or 50 ml/cm H20) was connected to a high frequency
jet ventilator (3) built in the department. Frequency and I/E
Ratio could be varied independently. 4 solenoid valves were
arranged in parallel so that tidal volume (VT) could be changed
without modification of the driving pressure (3 Atm). Pulsed
gas was delivered through an uncompliant tube (I.D. 4 mm) to an
injector (1.8 mm I.D., 2 em in length). This injector was situa
ted at the middle of a T piece directly connected to the Tracheal
tube (9 mm I.D.). The volume between the top of the endotracheal
tube and the lung was 35 mls.
EXPERIMENTAL DESIGN
MANLBY T_t iuDI'
All .... /'o,. ... a.t .. -!:::. Compllanoe
Experimental design
99
Accurate measurement of VT during HFJV is difficult.
We were unable to estimate VT from the flow because of the lack
of linearity of screen pneumotachograph or vortex flowmeter.
VT was measured as the pressure swings of 125 1 closed plethys
mograph by an high fre:JUency, low pressure transducer (EMT 33)
and recorded on anink jet recorder. The flat response of the
system was above 15 Hz. Plethysmograph was calibrated by injec
ting air into the box 100 mls steps, the lung being inside the
box. As the time constant of the box was long (50 sec), the
compression in the box was considered as adiabatic (1).
Continuoms flow of CO 2 was added into the lung. The
amount of CO 2 added was adjusted in order to obtain a stable
mean fraction of CO 2 in the lung (6 %). This FC0 2 was continuous
ly recorded (capnograph Gould MARK III) and the CO 2 flow was
read on a calibrated rotameter. Before this study, we found
100
that CO2 clearance was linearly correlated to the mean CO 2 fraction at any setting of the respirator.
Changlng the frequency, decreased the VT in the same
proportion, so that minute ventilation remained constant. 3 fre
quencies were studied (1 - 3 - 5 Hz) and at each frequency, tidal
volume was varied by changing the number of opened solenoid
valves or I/E Ratio. Simultaneously VT and CO2 cleared were
measured and the results were expressed as the slopt of the
relationship between these two parameters.
RESULTS
Because of loss of tidal volume at high frequency, we
have failed to demonstrate a better CO2 elimination at high
frequency. At all frequencies, we had a positive linear rela
tionship between VT and CO 2 clearance (fig. 2). Change in com
pliance from 50 to 20 mIs/em H20 did not affect this curve.
At 5 Hz, it has been possible to clear CO2 from the
lung althouglt VT was smaller than anatomical dead space (fig. 2).
When CO2 clearance was plotted against minute ventilation,
there was a significant difference between the slopes of the
relationship at 1 hz and 3 HZ. On the other hand, the slope~
at 3 Hz and 5 Hz were not significantly different (fig. 3).
On this model, we can define "alveolar ventilation"
as the product of the frequency and the difference between tidal
volume and anatomical dead space. There was a curvilinear rela
tionship between alveolar ventilation and CO2 clearance at any
frequency (fig. 4) without discontinuation.
1400
1200
.1000
Z 800 :E
~ oJ :e C 600 w I.: « w oJ 0
400 ON 0
200
CO2 CLEARED/ Vt SMALL Vd
3Hz ~fc
.i
....
... /'"
if ~:.
"'/·0 0-:
1'Hz ...•
....... /
0,/;'
.. ).'k 5Hz':
: ..... / 'I.'
./i" 4 .•
,.If '!-.
100 100 300 400 TIDAL VOLUME (MLS)
101
Fig. 2 : Relationship between tidal volume and CO 2 cleared.
Least squares regression lines are shown (doted line).
The hand shows the anatomical dead space. Tidal volume was
varied by affecting number of solenoid valves in the circuit
and liE Ratio.
102
RELATIONSHIP BETWEEN
CO 2 cleared mis/min
1000
500
MINUTE VOLUME AND C~ CLEARED
5hz
1hz
3hz
I r,.<~""T=ci2;;=~_~_:,:""""_~_~minute ventilation '14 10 16 '/mln
Fig. 3 : Relationship between minute ventilation and CO 2 cleare
Least squares regression lines are shown. Slopes at 1 Hz and 3 H
are significantly different, but there is no difference between
3 and 5 Hz.
1200
IJuU
,.;oc
CLEARANCE C~ ML/MN
10
rl. '" 5 R." 20
1 - , - 5 Hz C. ,. 10 (=- 50
12 1Lt 16 18
Fig. 4 : Relationship between "alveolar ventilation" and CO 2 cleared at different resistances, compliances and frequencies.
103
DISCUSSION
Although we have not found any report about CO 2 elimina
tion during HFJV, our results agree with those of the litera
ture using oscillator (2, 8, 10, 11) or special design respira
tor (4, 5). When frequency was increased tidal volume decreased
but CO 2 clearance decreased proportionnaly more.Therefore, minute
ventilation required to maintain a level of CO 2 elimination was
greater at 3 or 5 Hz as ccmpared at 1 Hz. This finding is cons is
tant with the increase in VD/vT when respiratory rate is increa
sed (4, 5, 7). At frequencies lower than 3 Hz, convection can
be a mechanism of gas exchange.
At the opposite, the lack of difference between the
slopes of the clearance and minute ventilation at 3 and 5 Hz
implicates that other mechanisms must play a role in CO 2 elimi
nation. We only speculate about these mechanisms. Enhanced
diffusion (6)is aclassical explanation but Slutsky has found
the limitation of this theory. Theory of organ pipe can suggest
that the fluidic properties of gas must change with frequency.
If we accept this model, we can imagine that the
CO 2 elimination can be influenced by changes of frequency.
For instance, to set the respiratory rate at the resonant fre
quency of the system increase airway pressure swings and
can change the amount of CO 2 eliminated.
Further studies are needed to distinguish different
effects of enhanced diffusion and mechanical changes when
respiratory rate is increased.
104
REFERENCE
1. Bargeton 0, Barres G. 1969. Time characteristics and frequency response of body plethysmograph; in Body Plethysmography, ed. by AB Dubois and KP Van de Woestijne, pp 2-23 (S. Karger, Basel, New-York).
2. Butler WJ, Bohn OJ, Bryan AC, Froese AB. 1980. Ventilation by high frequency oscillation in humans. Anesth. Analg. 59 : 577-584.
3. Carlon GC, Miodownik S, Ray Jr C, Kahn RC. 1981. Technical aspects and clinical L~plications of high frequency jet ventilation withasolenoid valve. Crit Care Med 9 : 47-50.
4. Chakrabarti MK, Sykes MK. 1980. Cardiorespiratory effects of high frequency intermittent positive pressure ventilation in the dog. Br. J. Anaesth. 52 : 475-481.
5. Fletcher PR, Bpstein RA. 1982. Constancy of physiological dead space during high frequency ventilation. Respir Physiol 47 : 39-49.
6. Fredberg JF. 1980. Augmented diffusion in the airways can support pulmonary gas exchange. J. appl. physiol. : Respirat, Environ, Exercise Physiol. 49 (2) : 232-238.
7. Jonzon A, Oberg PA, Sedin G, Sjostrand U. 1971. High frequency positive pressure ventilation by endotracheal insuffla tion. Acta. Anaesth. Scand (suppl 43), 43 : 1-43.
8. Schmid bR, Knopp TJ, Rehder K. 1981. Intrapulmonary gas transport and perfusion during high frequency oscillation. J. Appl. Physiol. Respirat, Environ, Exercise Physiol. 51 (6) 1507-1514.
9. Sjostrand U. 1980. High frequency positive pressure ventilation (HFPPV) a review. Crit Care Med 8 : 345-364.
10. Slutsky AS, Drazen JM, Ingram RH, Kamm RD, Shapiro AH, Fredberg JJ, Loring SH, Lehr J. 1980. Effective pulmonary ventilation with small volume oscillations at high frequency Science 209 : 609-611.
11. Slutsky AS, Kamm RD, Rossing TH, Loring SH, Lehr J, Shapiro AH, Ingram RB, Drazen JM. 1981. Effects of frequency, tidal volume and lung volume on CO elimination in dogs by high frequency (2-30 Hz), low tidaf volume ventilation. J. Clin Invest. 68 ; 1475-1484.
HEMODYNAMIC EFFECTS OF HIGH FREQUENCY VENTILATION
F.R. GIOIA, A.P. HARRIS, R.J. TRAYSTMAN, AND M.C. ROGERS DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE MEDICINE,
JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE
1. INTRODUCTION
Over the past decade, high frequency ventilation (HFV)
has been shown to produce adequate respiratory gas exchange
in laboratory (1-5) and clinical (6-11) trials. Although
the mechanism of gas exchange operative during HFV is unclear,
this technique of ventilatory support presents several potential
advantages in clinical settings relative to conventional positive
pressure ventilation (CV) (12), including diminished pulmonary
barotrauma, improved ventilation/perfusion matching, and
suppression of asynchronous respiratory efforts during mechanical
ventilation.
In addition, a major potential benefit of HFV lies in its possible diminution of cardiorespiratory interactions that
lead to the adverse circulatory effects of CV. HFV is performed using lower peak airway pressures relative to CV. Because the
circulatory effects of CV are closely linked to elevated airway
pressure (13), these responses might be attenuated during HFV.
However, specific knowledge of the circulatory effects of HFV,
particularly at the peripheral organ level, is limited. Using the radiolabeled microsphere technique, we compared
overall hemodynamics and blood flow to multiple peripheral
organs during HFV and CV. Because circulatory changes during CV are more pronounced at elevated airway pressures (i.e., with positive end-expiratory pressure), experiments were conducted
at both low and high mean airway pressures.
106
2. METHODS Studies were performed in 12 healthy adult mongrel dogs
weighing 15 ~ 1.5 kg. The animals were anesthetized with intravenous pentobarbital (20 mg/kg), intubated with an 8 mm ID cuffed endot~acheal tube, and allowed to breathe spontaneously. Catheters were placed in the femoral and axillary arteries for lower and upper body reference withdrawal
sampling, respectively, during microsphere injections and
for systemic arterial pressure (SAP) monitoring. A pigtail
catheter was passed retrograde into the left ventricular
cavity for radiolabeled microsphere injections. A 7Fr thermo
dilution catheter (American Edwards Laboratories, Santa Ana, CA) was positioned with the distal tip in the pulmonary arterial system for monitoring pulmonary artery pressure (PAP),
pulmonary capillary wedge pressure (PCWP), and central venous
pressure (CVP) , and for periodic determination of thermodilution cardiac output (CO). A 17 gauge blunt edged needle
was placed in the right lateral ventricle to monitor intracranial pressure (Iep). Mean airway pressure (Paw) was monitored using a 0.75 mm ID polyethylene catheter attached
to the side of the endotracheal tube and connected to a Statham
gas pressure transducer (model PM5ETC). All other pressures
were monitored continuously using Statham fluid transducers (model P23) coupled to a Gould 8-channel recorder. Core
temperature was maintained between 36.5-37.5°C using a heating
blanket.
Each animal underwent a randomized trial of CV and HFV.
Anesthesia was maintained with periodic bolus infusions of pentobarbital (5mg/kg), and paralysis was maintained with intravenous pancuronium bromide (0.1 mg/kg/hr). CV was performe using a Harvard animal volume ventilator (model 613) at a rate of 14-16 breaths/min and a tidal volume of 12 ml/kg. HFV was performed using a prototype high frequency ventilator consisting of a motor-driven rotating valve that interrupted inspiratory
flow from a high pressure gas source and simultaneously
allowed exhalation into a manually adjusted vacuum source.
107
HFV was delivered at a rate of 10 Hz, and tidal volume was adjusted to maintain PaCO Z within normal limits by altering
the inspiratory flow from the high pressure gas source. The actual tidal volume during HFV was estimated by subsequently collecting the volume delivered by the ventilator over a 3-minute period into a spirometer. Using this technique, the tidal volume during low Paw and high Paw trials was determined
to be no greater than Z.5 ml/kg and 3.5 ml/kg, respectively. Because of air leakage in the valve mechanism associated with
the addition of the negative pressure exhalation source, and
because of the impedence to inspiratory flow added by the
animal preparation, the actual delivered tidal volume during
HFV trials was probably substantially less than the estimated
value. During each trial of CV and HFV, FiOZ was maintained
at 0.4 to ensure PaOZ greater than ISO torr.
The animals were divided into two groups on the basis of
the Paw employed during the experiment. In the first group of 6 animals, Paw was maintained at 3 cm HZO during CV and HFV. The second group consisted of 6 animals in which Paw was elevated to 13 cm HZO. During CV, Paw was elevated by adding 10 cm HZO of PEEP. In the HFV group, Paw was elevated
by manual adjustment of the exhalation vacuum source. Before the ventilatory trial periods began, a bolus of intravenous
crystalloid solution was administered in sufficient quantity to elevate the PCWP to 5.0 + 0.5 torr and the CVP to Z.O +
0.5 torr; In.'t'h.e lOW Paw group, PCWP and CVP were maintained
at: thes.~: lev"t4t~"li(~b~I\igh Paw group, the PCWP and CVP roseto 9:0' L6~:8·<t6~k:~n.a~;S:.\}'~ 0.6 torr, respectively, with
the addition of ' PEEP, and were maintained at these levels
throughout the experiment. Following the initiation of each ventilatory trial, at least, Dne hour was allowed to reach steady-state conditions. At this time, physiologic parameters
were recorded, specimens of arterial and mixed venous blood
were obtained for blood gas and oxygen saturation (SOz) determinations, and the radiolabeled microsphere injection was performed. After randomly selecting one of four isotopes
108
(Sn, Ru, Gd, and Nb), 0.6 ml of silicone radiolabeled micro
sphere suspension (New England Nuclear, Boston MA, IS u
diameter, 4 X 10 6 microsphcres/ml) was injected into the left
ventricular cavity at a constant rate over 60 seconds.
Simultaneously, blood was collected from the reference with
drawal sites by means of a constant rate withdrawal pump;
collections of blood reference withdrawal specimens were
extended an additional three minutes beyond the injection
period. Subsequently, the animal was placed on the alternate
mode of mechanical ventilation, and the experimental sequence
was repeated. Following the experiment, tissue specimens were
obtained from multiple systemic organs and analyzed for their
weighted blood flow using standard analysis for the radiolabeled
microsphere technique (14). In addition, after five days of
formalin fixation, the brain was dissected into neuroanatomic
regions and analyzed for total and regional blood flows.
Data obtained during CV and HFV trials within each Paw
group were compared using the t-test for paired data. When
applicable, low and high Paw groups were compared using the
t-test for non-paired data after pooling values for CV and
HFV within each Paw group.
3. RESULTS
Values for the cardiorespiratory parameters monitored
during the experiment are shown in Table 1. No differences
were found in these variables within either of the Paw groups.
However, when data for the CV and HFV trials within each Paw
group were pooled and compared, significant differences were
found. The high Paw group showed a higher mean PAP and
hemoglobin concentration (Hgb), and lower SVO Z relative to
the low Paw group. In addition, CO was significantly lower
at the elevated Paw.
109
Table 1. Values of monitored cardiopulmonary perameters, expressed as mean + S.E. Asterisk (*) indicates significant difference between-low Paw vs high Paw groups for pooled ev and HFV data at p < 0.05.
LOW Paw HIGH Paw
ev HFV ev HFV
pH 7.34+0.01 7.35+0.02 7.34+0.02 7.34+ 0.02
Pae0 2 34.8+0.6 34.3+0.8 34.3+ 0.6 35.0+0.8
Sa0 2 (%) 99.6+0.3 99.5-11).4 99.6+0.2 99.7+0.3
*SvO 2 (%) 74.2+2.9 71.0+1.1 64.5+3.2 61.8+2.5
*Hgb (gm/dl) 10.9+1.0 11.8+0.7 13.4+1.4 13.5+1.2
HR -1 (min ) 158+10 168+9 145+13 161+15
SAP (torr) 128+12 128+13 144+7 138+9
*PAP (torr) 12.8+1.1 13.8+1.3 17.4+0.9 18.4+1.3
Iep (torr) 13.8+1.1 13.5+1. 3 15.2+1.4 15.2+1.4
*eo (l/min) 1.66+0.12 1. 77+0.11 1.32+0.14 1.34+0.13
Table 2 shows the systemic organ blood flow values measured during the ventilatory trials. No differences were noted
between ev and HFV in any of the peripheral organ flows within
each Paw group. Data pooled from the ev and HFV trials within
each Paw group revealed a significant fall in renal cortical
blood flow during ventilation at the elevated Paw. Although the differences did not achieve statistical significance, a distinct trend toward decreased perfusion of abdominal visceral organs (i.e., hepatic artery, adrenal gland, pancreas, jejunum, and kidney medulla) was observed in the high Paw groups. On
the other hand, blood flow to the brain, skin, skeletal muscles, and myocardium were spared during ventilation at the elevated
airway pressure.
110
Table 2. Systemic organ blood flow values expressed as mean + S.E. Asterisk (*) indicates significant difference between low Paw vs high Paw groups for pooled CV and HFV data at p < 0.05.
Brain
Skin
Skeletal Muscle
MyocardiuF
Hepatic Artery
Adrenal
Pancreas
Jejunum
Kidney Medulla
*Kidney Cortex
Systemic Organ Blood Flow Values (ml/min/lOO gms) LOW Paw HIGH
CV HFV CV
30.5+2.7 30.2+1.9 28+ 3.5
2.0+0.4 2.4+0.7 2.9+0.4
3.6+0.7 3.6+0.7 2.7+0.2
115+22 124+20 102+15
16.9+6.0 17.1+5.9 7.3+3.2
203+26 199+20 143+23 -39.0+15.3 35.5+12.2 24.1+3.8
58.2+18.2 62.6+19.1 32.3+4.3
11.5+4.1 10.4+3.7 4.0+0.9
491+42 521+54 348+37
Paw HFV
24+2.5
2.4+0.3
3.1+0.5
108+20
7.2+3.7
140+27
20.2+3.8
39.4+5.6
4.2+1.0
377+46
In addition, regional cerebral blood flows to the cerebral cortex, diencephalon, cerebellum, brain stem, areas of pure
white matter, and areas of pure grey matter were compared. No differences were found in these flows during CV and HFV
in either of the Paw groups.
4. DISCUSSION
The deve lopment of Jncre90~~d in~rathoracic pres sure with .. ~' .. '-':-"'~:-':.;,- .. ~,,:l;. ... ,..-·· ~-":.".
positive pressure ventilation is associatedJ'fith a multitude '. ,. h:,!.. r .-. ..: ~
of hemodynamic changes. Depression of cardiac output during
positive pressure ventilation was described in the early
studies of Cournand et al (13). This effect is particularly
pronounced when positive pressure ventilation is coupled with
PEEP, a frequent practice in the management of acute
respiratory failure. The fall in cardiac output resulting
from positive pressure ventilation has been attributed to
several mechanisms (15-18), each linked closely to the level
111
of positive airway pressure generated during mechanical ventil
ation. In addition to the effects on overall cardiac output,
changes in the function of a number of peripheral organs
have been described during positive pressure ventilation that
are partially or completely explained by secondary regional
circulatory alterations. Positive pressure ventilation with
PEEP has been shown to decrease urine output and elevate
plasma antidiuretic hormone (19). Subsequent studies revealed
that positive pressure ventilation with PEEP reduced creatinine clearance and sodium excretion t20). Using high tidal volume positive pressure ventilation, Johnson (21) found an elevation
in splanchnic venous pressure and mesenteric vascular resistance associated with depressed mesenteric oxygen consumption. Head trauma patients exposed to positive
pressure ventilation with PEEP experienced elevated intracranial
pressure (22) with potential adverse effects on cerebral
perfusion. Because large swings in positive airway and intrathoracic
pressure are avoided, it has been postulated that HFV might diminish the adverse circulatory effects at positive pressure
ventilatory support. The effect of HFV on cardiac output reported in previous studies is inconsistent. Klain and Smith (2), using the technique of high frequency jet
ventilation, reported increased cardiac output in dogs during HFV. Other investigators found no change in cardiac output
during HFV in normal animals (3) and in acutely ill patients
(8)". These preliminary results, however, are based on small numbers of observations.
Knowledge concerning the response of peripheral organs to
HFV is' scanty. The earliest reports on HFV described spon
taneous diuresis following its initiation in dogs (1). HFV
also produced reductions in respiratory-induced fluctuations
of peak intracranial pressure in experimental animals relative
to CV (23). Additional details of peripheral circulatory responses to HFV are nonexistent.
112
Our study was designed to identify specific cijculatory
effects of HFV, either in terms of overall central hemodynamics
or peripheral organ circulation. Because circulatory changes
during CV are most dramatic at elevated airway pressure (i.e.,
with PEEP), experiments were also conducted at high levels of
airway pressure. The experimental trials of CV and HFV were
conducted at the same mean airway pressure in order to identify
specific changes attributable to the diminished swings in airway
pressure associated with HFV. Both mechanical ventilatory
techniques depressed overall cardiac output at the elevated
airway pressure to equal degrees. In addition, the decrease
in cardiac output accompanying ventilation at the elevated
airway pressure appears to occur at the expense of the same
peripheral circulatory beds with each mode of mechanical
ventilation; both HFV and CV produced equal diminution of
blood flow to abdominal visceral organs at the elevated
airway pressure.
In summary, our results do not indicate a specific
circulatory sparing effect of HFV relative to CV when the two
techniques are performed at equal mean airway and, presumably,
intrapleural pressures. If HFV proves to be more effective
at eliminating ventilation/perfusion mismatching relative
to CV, lower mean airway pressures may be required to maintain
adequate gas exchange, thereby providing an indirect salutary
effect on hemodynamic function. Support of this hypothesis,
however, must await further study.
REFERENCES
1. Jonzon A., Oberg P.A., Sedin G., and Sjostrand U.: Highfrequency positive-pressure ventilation by endotracheal insufflation. Acta Anaesth. Scand., Suppl. 43, 1971.
2. Klain M., and Smith R.B.: High frequency percutaneous transtracheal jet ventilation. Crit. Care Med. 5:280, 1977.
3. Bohn D.J., Miyasaka K., Marchak B.E., Thompson W.K., Froese A.B., and Bryan A.C.: Ventilation by high-frequency oscillation. J. Appl. Physiol. 48:710, 1980.
4. Wright K., Lyrene R.K., Truog W.Eo, Standaert T.A., Murphy J., and Woodrum D.E.: Ventilation by high-frequency oscillation in rabbits with oleic acid lung disease. J. Appl. Physiol. 50:1056, 1981.
113
5. Kolton M., Cattran C.B., Kent Go, Volgyesi G., Froese A.B., and Bryan A.: Oxygenation during high-frequency ventilation compared with conventional mechanical ventilation in two models of lung injury. Anesth. Analg. 61:323, 1982.
6. Heijman K., Heijman L., Jonzon A., Sedin G., Sjostrand U" and Widman B~: High frequency positive pressure ventilation during anaesthesia and routine surgery in man. Acta Anaesth. Scand. 16:176, 1972.
7. Bjerager K., Sjostrand U., and Wattwil M.: Long-term treatment of two patients with respiratory insufficiency with IPPV/PEEP and HFPPV/PEEP. Acta Anaesth. Scand. Suppl. 64, 55, 1977.
8. Butler W.J., Bohn D.J., Bryan AoC., and Froese A.B.: Ventilation by high-frequency oscillation in humans. Anesth. Analg. 59:577, 1980.
9. Malina J.R., Nordstrom S.C., Sjostrand U.H., and Wattwil L.M.: Clinical evaluation of high-frequency positive-pressure ventilation (HFPPV) in patients scheduled for open-chest surgery. Anesth. Analg. 60:324, 1981. .
10. Turnbull A.D., Carlon Go, Howland W.S., and Beattie, Jr. E.J.: High-frequency jet ventilation in major airway or pulmonary disruption. Ann. Thoracic Surg. 32:468, 1981.
11. Carlon G.C., Ray, Jr. C., Pierri M.K., Groeger J., and Howland W.S.: High-frequency j~t ventilation: Theoretical considerations and clinical observations. Chest 81:350, 1982.
12. Slutsky A.S., Brown R., Lehr J., Rossing T., Drazen J.M.: High-frequency ventilation: A promising new approach to mechanical ventilation. Medical Instrumentation 15:220, 1981.
13. Cournand A., Motley H.L., Werko L., and Richards, Jr. D.W.: Physiological studies of the effects of intermittent positive pressure breathing on cardiac output in man, Am. J. Physiol. 152:162, 1948.
14. Heymann M.A., Payne B.D., Hoffman J.I.E., and Rudolph A.M.: Blood flow measurements with radionuclide-labeled particles. Prog. Cardiovas. Dis. 20:55, 1977.
15. Hubay C.A., Waltz R.C., Brecher G.A., Praglin J., and Hingson R.A.: Circulatory dynamics of venous return during positive-negative pressure respiration. Anesthesiology 15:445, 1954.
16. Liebman P.R., Patton M.T., Manny J., Shepro D., and Hechtman H.B.: The mechanism of depressed cardiac output on positive end-expiratory pressure (PEEP). Surgery 83: 594, 1978.
17. Robotham J.L., Lixfeld W., Holl~nd L., MacGregor D., Bromberger-Barnea B., Permutt S., and Rabson J.L.: The effects of positive end-expiratory pressure on right and left ventricular performance. Am. Rev. Respir. Dis. 121: 677, 1980.
18. Jardin F., Farcot J.C., Boisante L" Curien N., Margairaz A., and Bourdarias J.P.: Influence of positive end-expiratory pressure on left ventricular performance. N. Engl.
114
J o Med. 304:387, 1981. 19. Baratz R.A., Philbin D.M., and Patterson R.W.: Plasma
antidiuretic hormone and urinary output during continuous positive-pressure breathing in dogs. Anesthesiology 34: 510, 1971.
20. Hall S.V., Johnson EoE., and Hedley-Whyte J.: Renal hemodynamics and function with continuous positivepressure ventilation in dogs. Anesthesiology 41:452, 1974.
210 Johnson E.E.: Splanchnic hemodynamic response to passive hyperventilation. J o Appl. Physiol. 38:156, 1975.
22. Shapiro H.M., and Marshall L.F.: Intracranial pressure responses to PEEP in head-injured patients. J o Trauma 18:254, 1978.
23. Todd M.M., Toutant S.M., Shapiro H.M., and Smith N.T.: Intracranial pressure effects of low and high frequency ventilation o Anesthesiology 53:Sl96, 1980 0
CARDIOVASCULAR CONSEQUENCES OF HIGH FREQUENCY VENTILATION
CHARLES W. OTTO, M.D., JERRY M. CALKINS, M.D., PH.D., STUART F. QUAN, M.D., THOMAS J. CONAHAN, M.D., CHARLES K. WATERSON, B.S.E., STUART R. HAMEROFF, M.D.
INTRODUCTION
The potential adverse cardiovascular effects of positive pressure
ventilation (decreasing venous return to the right heart leading to a fall in
cardiac output) are well known to modern physicians. Since the magnitude of
these hemodynamic effects is directly related to the amount of positive
pressure applied to the airway, efforts have generally been made to maintain
airway pressures as low as possible during mechanical ventilation. High
frequency ventilation (HFV) can provide adequate alveolar ventilation at much
lower peak airway pressures than conventional ventilation. Consequently, it
has been widely expected that HFV would have less adverse effects on the
cardiovascular system than conventional ventilation. Early work by Eriksson,
et al (1) in healthy dogs supported this view. They found a higher cardiac
output and stroke volume, lower peripheral resistance, and lower peak and
mean airway pressures with high frequency positive pressure ventilation
(HFPPV) compared to conventional ventilation. More recent investigators have
reported improved, unchanged, and impaired hemodynamic function with HFV
under a variety of experimental conditions (Table 1).
TABLE 1. Studies Comparing Hemodynamic Effects of HFV and Conventional Ventilation
Author Subjects Eriksson, 1977 (1) Dogs Butler, 1980(2) Patients Dedhia, 1981(3) Patients Carlon, 1981 (4) Patients Schuster, 1981(5) Patients Hoff, 1981 (6) Dogs Szele, 1981(7) Dogs Carlon, 1981(8) Dogs Otto, 1982 Dogs
* ++ improved; unchanged;
Type of HFV
HFPPV HFO HFJV HFJV HFJV Emerson HFJV HFJV HFJV
impaired
PAW With HFV
Lower ? ? ?
Higher ?
Lower Higher Lower
Hemodynamic Effect of HFV* ++
or ++
++
116
In early patient trials, Butler, et a1(2) using high frequency
oscillation (HFO) and Dedhia(3) using high frequency jet ventilation (HFJV)
found no change in cardiac output between HFV and conventional ventilation.
Carlon, et a1(4) using HFJV found cardiac output unchanged or increased from
conventional ventilation. In these studies peak airway pressures were lower
with HFV but mean airway pressures were not compared. Schuster, et a1(5)
studied 4 patients using HFJV and found higher mean arterial pressures but no
change in stroke or cardiac index. Peak airway pressures were lower but mean
airway pressures were higher with HFJV than conventional ventilation.
In animal experiments, Hoff, et a1(6) reported a decreased cardiac
output using the Emerson HFV system. Sze1e and Shahvari(7) found no
differences in cardiac output, mean arterial pressure or heart rate between
HFV and conventional ventilation in dogs made hypovolemic by hemorrhage in
spite of lower mean airway pressures with HFJV. Carlon, et a1(8) found that
asynchronous HFJV with a higher mean airway pressure than conventional
ventilation caused a decrease in cardiac output. He noted similar findings
when the jet pulsation was synchronized so that peak airway pressures
coincided with mid-diastole. However, synchronizing peak airway pressures
with aortic valve opening resulted in no change in cardiac output when HFJV
was compared to conventional ventilation. This suggests that airway
pressures during HFV may not only alter cardiac output by effects on venous
return but that increasing airway pressure during systolic ejection may aid
left ventricular emptying by decreasing transmural aortic pressure.
Given this array of somewhat contradictory results, we have attempted to
further compare the effects of HFJV and conventional ventilation on the
hemodynamic function of healthy dogs. Our first study was a simple paired
study comparing conventional ventilation to HFJV with and without PEEP. The
second study examined the hemodynamic performance when the high frequency jet
pulse was synchronized with particular parts of the cardiac cycle.
METHODS
Barbiturate-anesthetized dogs were paralyzed with pancuronium except for
spontaneous ventilation studies and monitored with ECG and thoracic aortic
and pulmonary artery thermodilution catheters. Tracheas were intubated with
a 9.0 mm endotracheal tube incorporating an HFJV lumen in the side wall and
orifice at the distal tip (NCC Division/Mallinckrodt, Inc.). FI 02 was 1. 0
for all experiments. Conventional ventilation was delivered by a Bird Mark
117
VII ventilator driving a bellows in a box with a tidal volume of 15-Z0 ml/kg
and rate to maintain PaCOZ of 40 ± 5 torr. HFJV was provided by a previously
described electromechanical jet ventilation system(9). An electronically
controlled solenoid valve periodically interrupted flow from an oxygen
source. Solenoid gas output was delivered via a 3 mm tubing to the
endotracheal tube side lumen. Ventilation was begun with rates of 150 min-1
and driving pressure regulated to give airway excursions of 5-6 cmHZO as
measured 6 em beyond the tip of the endotracheal tube and driving pressure
then adjusted to maintain PaCOZ at 40 ± 5 torr. PEEP was applied by
spring-loaded valves on the exhalation limb of breathing circuits attached to
the endotracheal tube. Solenoid pulses were fixed at 0.1 sec duration. The
solenoid was electronically controlled so that any fixed rate could be given
or the valve could be triggered by the ECG QRS complex with a variable delay
so that peak airway pressure could be made to fall at any pre-selected point
in the cardiac cycle.
In all experiments, the following varibles were measured or calculated:
respiratory rate (RR), tidal volume (conventional ventilation modes only),
peak inspiratory airway pressure (PIP), end expiratory airway pressure (EEP),
mean airway pressure (PAW)' arterial blood gases (PaOZ' PaCOZ' pH), heart
rate (RR) , systolic (SAP), diastolic (DAP) , and mean (MAP) aortic pressure,
systolic (PAS), diastolic (PAD), and mean (PAM) pulmonary artery pressure,
mean pulmonary artery occlusion pressure (PAOP), mean central venous pressure
(CVP) , thermodilution cardiac output, cardiac index (Cl), stroke index (SI),
systemic vascular resistance index (SVRl) and pulmonary vascular resistance
index (PVRl).
Paired Study
In 6 dogs, conventional ventilation (lPPV) was begun and RR adjusted
until PaCOZ was 40 ± 5 torr. The animals were changed to HFJV at a rate of
150 min-1 and driving pressure adjusted until PaCOZ was 40 ± 5 torr. With
ventilator settings thus predetermined, lPPV or HFJV was randomly selected
and the study begun. Following 5 min of ventilation, pressures were recorded
and cardiac ouput and arterial blood gases measured. The opposite mode of
ventilation was immediately begun and measurements repeated after 5 min.
PEEP of 15 cmHZO was then added to both modes of ventilation and the process
repeated including initial ventilator adjustments, randomization and
118
measurements. Results were analyzed using Student's t-test for paired data
with significance accepted as p < 0.05.
Synchronization Study
In 2 groups of 6 dogs each, hemodynamic measurements were made during
spontaneous ventilation, conventional ventilation and HFJV. In the first
group, measurements were made in 9 ventilatory modes without PEEP:
spontaneous ventilation (SV) , conventional ventilation (IPPV), HFJV at 120
min-1 (ASYN-LO), HFJVat 180 min-1 (ASYN-HI), and HFJV at QRS coupled delays
such that peak airway pressure occurred at 0, 0.2, 0.4, 0.6, and 0.8 of the
R-R interval (SYN-O to SYN-0.8). In the second group, measurements were made
in the same ventilatory modes but with 15 cmH20 PEEP added. Spontaneous
ventilatory modes were always studied first or last and all other modes were
studied randomly. Results of the two groups were analyzed separately using a
two-factor analysis of variance and a Newman-Keuls multiple range test with
significance accepted as p < 0.05.
RESULTS
Paired Study
Both with and without PEEP, PIP and PAW were lower during HFJV than
conventional ventilation (Table 2). Without PEEP, there were no significant
differences in any hemodynamic variables or arterial blood gases, probably
because neither ventilation mode was having a significant effect on cardio
vascular function (see below). In the presence of impeded venous return
caused by PEEP, cardiac index and stroke index were 25% higher during HFJV
than conventional ventilation (p < 0.05) but other hemodynamic variables and
"Jlrter~blood"gases were not ,,~<::.,,';-":"" ··i..,>;it:::~~~,: . . ;.::~.?; . .'~:
different (Fig 1).
", .. ~.-<.::·~fi.~-~· ::~5ji:~ ."" .4,~ .. ·"·:. TABLE t. , Pai1;ed, Study - Respiratory Variables
IPPV HFJV
, -1 O-PEEP O-PEEP RR (min ) Tii'±l'" * 143±3 PAW (cm H2O) S.1±0.4 * 3.3±0.4 PIP (em HyO) 14.S±0.9 * S.6±0.S PaC02 (torr 43±1 38±1
* HFJV significantly different from conventional All values mean ± SEM
IPPV HFJV IS-PEEP IS-PEEP 17±1 * 144±3
24.0±0.S * 18.1±0.6 42.3±2.0 * 21. 6±1.1
43±2 41±2
ventilation (p < 0.05)
Hemodynamic Variables CPPV va HFCPPV
HR(mln- 1) 160
f (0 ) 150 I 140
130
I 120 MAP(mmHg) 110
I (0 ) 100 90 eo 70
SI (dyne." sec" em -5) 221 (.o) 20
18 16 14 r f
CI Qlmln/m2) (0 ) ~:~~ 2.8
2.6
2.4 i" 2.2 2.0
CPPV HFCPPV
HR(mln- 1)
Co)
MAP(mmHg) Co)
SI (dynes. sec-em -5) C·)
CI(l/mln/~ Co)
'Slgnlllc8J1tdlllerence lrom other veluee(p<O.05)
119
Homodynamlc Yariablas with PEEP 170
100 f f 150
140
r I I I ! 130
120
110
100
r 90 80 70
~l Ilffllf! 10 5
·Slgnlflcant difference from HFCPPV (p<O.05)
Figure 1 Figure 2
Synchronization Study
Without PEEP. PIP and PAW were significantly higher with IPPV than with
any HFJV mode. However, hemodynamic variables and arterial blood gases were
not different among SV, IPPV, or any of the HFJV modes, indicating that
neither conventional ventilation or HFJV were having significant cardio
vascular effects in these healthy animals.
With PEEP. PIP and PAW were again significantly higher with CPPV than
any HFJV mode (Table 3). There were no differences in airway pressures among
TABLE 3. Synchronization Study with PEEP - Respiratory Variables
RR(/min) PAW (cmH20) PIP (cmH20) PaC02(torr)
CPPV 17 1* 21.9 1.2* 37.0 4.4* 51 9 ASYN-LO 120 0 17.9 0.3 21.S 0.2 40 5 ASYN-HI ISO ° 17.9 0.3 22.0 0.3 41 4 SYN-O 154 4 17 .5 0.2 21.4 0.2 37 4 SYN-0.2 153 4 17.5 0.3 21.3 0.5 37 3 SYN-O.4 164 9 IB.O 0.3 22.0 0.3 39 4 SYN-O.6 153 5 17.S 0.2 21.9 0.2 45 3 SYN-O.B 153 9 17 .S 0.2 21.9 0.3 39 4
* Significantly different from all HFJV modes (p < 0.05) All values mean ± SEM
120
HFJV modes. These anesthetized animals breathing spontaneously with 15 CmHZO
CPAP were unable to maintain a normal PaCOZ• Consequently, the CPAP group
was not used in hemodynamic comparisons. Mean arterial pressure was Z5%
lower and heart rate 15% lower during CPPV than HFJV (p < 0.05) but other
hemodynamic variables and blood gases were not different (Fig Z). Synchron
izing peak airway pressure to any specific part of the cardiac cycle did not
appear to provide any additional advantage since no differences were detected
among the HFJV modes studied.
DISCUSSION
A number of previous studies have demonstrated no change in cardiac
output between HFV and conventional ventilation. This does not necessarily
mean that neither mode has an advantage over the other. As shown in the
synchronization study without PEEP, it is quite possible to have no effect on
hemodynamic function by either mode of ventilation. In order to demonstrate
a difference, a model must be used in which one or both modes of ventilation
will cause a decrease in cardiovascular function. For this model, we chose
functional hypovolemia caused by PEEP since it has been shown that this
preparation is stable over several hours with minimal physiologic
compensation for the decreased cardiac output(10). Our studies clearly
demonstrated that HFJV can have less adverse effects on hemodynamic function
than conventional ventilation under these circumstances.
The reason that HFV can provide a hemodynamic advantage over conven-
tional ventilation has not been unequivocally demonstrated. However, it
seems likely that it is related to differences in mean airway pressure.
Studies in which mean airway pressure is lower with HFJV (including the
present ones) have found improved or unchanged hemodynamic function. Studies
in which mean airway pressure is higher with HFJV have found cardiac output
to be impaired or unchanged. This hypothesis is supported by a recent report
by Tyson, et al(ll) on HFV studies in chronically-instrumented dogs demon
strating a proportional decrease in left ventricular end diastolic volume and
stro'ke volume with increasing mean airway pressures. An increased cardiac
output which might be attributable to improved left ventricular emptying
caused by synchronizing the airway pressure pulses to a specific part of the
cardiac cycle could not be demonstrated in the present synchronization study.
Similarly, Tyson, et al(ll) found no changes in left ventricular systolic or
diastolic function with ventilation synchronized to systole or diastole.
121
CONCLUSIONS
Given the current state of our knowledge, we can conclude that HFV has
the potential to provide adequate alveolar ventilation with less possibility
of adverse cardiovascular side effects than conventional ventilation.
Whether this potential is realized will be dependent upon the HFV system
used. Any advantage will probably be directly related to the extent that
HFJV can provide adequate ventilation at significantly lower mean airway
pressures than conventional systems. Synchronization of airway pressures to
a specific part of the cardiac cycle appears to provide little additional
advantage.
REFERENCES
1. Eriksson IA~ Janzon A, Sedin G, ~j6strand U: The influence of the ventilatory pattern on ventilation, circulation, and oxygen transport during continuous positive pressure ventilation. An experimental study. Acta Anaesthesiol Scand (Suppl) 1977; 64:149.
2. Butler WJ, Bohn DJ, Bryan AC, Froese AB: Ventilation by high frequency oscillation in humans. Anesth Analg (Cleve) 1980; 59:577.
3. Dedhia HV: Hemodynamic effect of high frequency ventilation in open heart surgery patients. Crit Care Med 1981; 9:158.
4. Carlon GC, Kahn RC, Howland RS, Ray C, Turnbull AD: Clinical experience with high frequency ventilation. Crit Care Med 1981; 9:1.
5. Schuster DP, Snyder JV, Klain M, Grenvik A: The use of high frequency jet ventilation during respiratory failure. Crit Care Med 1981; 9:162.
6. Hoff BH, Robotham 31, Smith RB, Cherry D, Bunegin L: Effects of high frequency ventilation (300 to 2400/min) on cardiovascular function and gas exchange in dogs. Anesth Analg (Cleve) 1981; 60:256.
7. Szele G, Shahvari MBG: Comparison of cardiovascular effects of high frequency ventilation and intermittent positive pressure ventilation in hemorrhage shock. Crit Care Med 1981; 9:161.
8. Carlon GC, Pierri MK, Ray C, Kretan V: Hemodynamic and respiratory variables with high frequency jet ventilation (HFJV) synchronized with heart rate. Crit Care Med 1981; 9:163.
9. Calkins JM, Waterson CK, Hameroff SR, Kanel J: Jet pulse characteristics for high frequency jet ventilation. Anesth Analg (Cleve) 1982; 61:293.
10. Qvist J, Pontoppidan H, Wilson RS, Lowenstein E, Laver MD: Hemodynamic responses to mechanical ventilation with PEEP: the effect of hypervolemia. Anesthesiology 1975; 42:45.
11. Tyson GS, McIntyre RW, Maier GW, et al: The mechanical effects of high frequency ventilation on cardiac function in intact dogs. Crit Care Med 1982; 10:212.
PNEUMATIC CONTROLLED CIRCULATION PCC
W.L.den Dunnen, MD, T.Mostert, physicist
Erasmus University Rotterdam, the Netherlands.
1) Introduction
During spontaneous breathing inspiration causes subatmospheric thoracic
pressure which helps blood to flow back to the heart. The interaction
between the circulation and respiration is in the healthy patient reduced
to minimal level. In the patient with chronic bronchitis expiration can
be impaired causing high alveolar pressure during forced expiration. This
phenomenon might lead to compression of the capillaries in the alveolar
septa. If this occurs higher right ventricular stroke work is necessary
to overcome the higher vascular resistance of the lung capillaries. This
lungdisease might lead to chronic pulmonary hypertension and tendency to
right sided decompensation. Intermittent positive pressure ventilation (IPPV)
causes a disturbance of the relationship between respiration and circula
tion in the thoracic cavity because of the continuous mean positive pres
sure. Every clinician can observe the slight increase in pulmonary artery
and aortic pressure when the gases inflate the lungs during LPPV. However,
venous return is decreased so cardiac output remains unchanged. The inter
action between circulation and respiration is predictable,: directly related
to the ventilator frequency. IPPV is applied with low dP!dt of the insuf
flated gases. Because of this low dP! dt the pressure in the trachea is
higher than more distal in the airway~tract. Due to the low dP!dt the thorax
is enlarged by the insufflated volume causing acceptable interaction with
the circulation. This interaction might lead to serious problems when the
mean intrathoracic pressure is increased by positive end-expiratory pres
sure (PEEP). Lung perfusion can be reduced and venous return can be reduced
to unacceptable level. Fortunately most patients can autoregulate the,in
fluences of IPPV leading to tachycardia etc. The interaction of "pneumatics"
and "hydraulics" in the thoracic cavity is represented in fig.!, which
triple communicating vessels also show the individual compliances leading
to total thoracic compliance.
air
1 A B
123
The displacement of the pistons can
-----===~~~~--be used to indicate the individual
(
compliance. During spontaneous brea
thing the pistons A and C go down
but piston~B is going upward caused
by the force of inspiration. Movement
of piston B causes "suction" on the
gas and blood compartment. The diffe
rence in viscosity between air and
blood causes more air to enter the
fig.1 thoracic cavity compared to blood.
During IPPV piston A is forced downward. Pistons B and C are going upward
and the displacement of piston B depends on the elasticity of the thorax.
Most of the energy of the insufflated tidal volume is used to displace the
masses of the thorax itself. There is only little influence on the displa
cement of piston C.
If a patient is treated with high frequency positive pressure ventilation
(HFPPV) one should consider the differences compared to conventional IPPV.
One of the greatest differences between_:HFPPV and IPPV is the high dP/dt
of the ventilatory gases in HFPPV. The tidal volume is reduced sometimes
to even less than the patient's dead space, while the insufflation frequen
cy is increased to at least 60 breaths per minute. The preset working
pressure of a high frequency ventilator is much higher compared to IPPV
(between 2 and 4 Bars approximately). The greater the inner diameter of the
insufflation catheter the higher the dP/dt of the jet-system. If we look
again to figure 1 the displacement of the pistons during HFPPV is as follows:
When piston A is pressed downward there is hardly time to displace the
thorax because of the inert ion of masses~ This results to a high energy
transport to piston C which might lead to obstruction of the circulation
in the alveolar septa, stopping the blood-flow. In fig.1 this can be repre
sented pushing piston C as high as possible. In the literature many authors
state that the mean airway pressure is much lower in HFPPV compared to
IPPV (ref. 1). Also peak pressures appear to be lower depending on the
ventilator settings. We doubt whether this is the real advantage of high
frequency ventilation. To our opinion it is not the peak-, mean- and
lowest airway pressure which are important but the first derivative (dP/dt)
of the insufflated gases. It is important to realize that this high dP/dt
124
causes completely different influences on the lungs. Next diagram shows
an oscillation applied onto the trachea. The airway resistance is repre
sented by the upper line (F=ln.ex1.The slope of the dotted line depends
on the frequency of the oscillation. This line has to be drawn moreverti
cally when higher frequencies are applied. This diagram shows that the
mean pressure in the alveoli is higher compared to the intra-tracheal mean
pressure. The maximum pressure in the alveoli might be higher than the
intra-tracheal mean pressure~ If we apply HFPPV we have to realize that
this physical property of a closed-end narrowing tube is involved. In
lung physiology we are used to talk about reducing airway resistance the
more we enter the lungs, but this statement is not true if we apply HFPPV
with high dP/dt of the insufflated gases !
AIRWAY.RESISTANCE F=ln.ex
IpEEP
ALVEOLAR PRESSURE FLUCTUA110NS
"
fig.2 Airway pressure during HFPPV with different insufflation frequencies
If PEEP is added to this pressure it might lead to serious accidents be
cause of the higher alveolar pressures: overdistention, blocking the cir
culation. In this HFPPV-technique the insufflation of ventilatory gases
depends on the liE ratio. The longer the inspiration time and the greater
the size of the insufflation catheter the more gas is insufflated (and
the greater are the risksinvolvedl. May be this is the reason why some
authors emphasize the application of 22% insp.duty cycle only (ref.2l.This
insufflation time is dependend of the_ventilator properties and provides
an electronic setting but the real insufflation time is much longer when
the tubing dead-space volume is calculated at the working pressure. If
some investigator sets his HFPPV-ventilator in the same setting it might
lead to completely different percentage insp.duty cycle, when measured
in the trachea. As always clinical experience with the ventilator involved
is very important. It is only very difficult to compare each other's results.
If we apply HFPPV to a patient in asynchronous mode we can observe an
125
obvious interference with the heart-duty cycle. Harmonic oscillations can
be observed. The frequency of the oscillations can be predicted and cal
culated from: Harmonic oscillation frequency = Heart rate minus jet-venti-
lation rate (or vice versa). The harmonic oscillations can be said to be
the "beat-frequency" if we compare this phenomenon occurring in music
instruments. Where can this harmonic oscillations be observed? First the
pulmonary artery pressure waves show this phenomenon but they also can be
observed during body plethysmography. Apparently it is very important on
which moment of the heart cycle the ventilatory gases are insufflated.
Harmonic oscillations also occur, if the ventilation frequency is a multiple
of the heart frequency: first and second harmonics. In our experiments the
second harmonic was not powerful enough to cause obvious oscillations.
Next computer diagram shows two sinus-waves and their interaction.
A
.11 II II II II Il JI.II II III ~ V VIV V V V V VIV V V VM VIV V V V B
AfAA AAIAA I\(IIIA AAAII V \/ \11 \/ \/11 \/ II II II II II 11111 V II II II
A f\ f A \1 ,vII II IV II II III
fig.3 Harmonic oscillations: "beat-frequency"
Although this diagram is calculated by the computer it shows the principles
of our observations during the experiments. The interaction of "pneumatics"
and "hydraulics" in the thoracic cavity during asynchronous HFPPV made us
decide to synchronize the heart rate and the insufflation rate as a function
of the patient's ECG and pulmonary artery pressure. If we synchronize on
the heart beat we can insufflate at different moments. Triggering should
be performed in such a way, that the alveolar gas pressure goes low at
the moment that the heart sta~ts the ventricular systole. Insufflation
can be started when the ventricular ejection phase has been finished.
However in our technique expiration takes place on a fixed interval with
fixed time settings, while insufflation depends on the patient's heart
rate. We called this new technique, derived from high frequency ventilation
(ref.3,4): Pneumatic Controlled Circulation.: PCC. Why controlled circulation?
126
To explain this control function we should consider next diagram.
RIGHT VENTRfCLE alveolar Q3 spressure
PRINCIPLE FOR P.Ce.
® HI! ,~ ........ > ~<f~---:reaSed RY.stroke-volume
fig.4 Jet-insufflation during the heart duty cycle.
In this diagram it is quite easy to understand that the insufflation
of ventilatory gases with high dP/dt can be performed on different moments
of the heart beat: during right ventricular systole or diastole. If we
build up an alveolar gas pressure during the right ventricular systole
the lungcapillaries around the alveoli are compressed by overdistention
of the alveoli. This causes impairment of the lung-capillary bloodflow.
(One has to realize that all lungcapillaries are parallel vessels in which
the pressure almost equals the alveolar gas pressure in normal lung phy
siology !) However, if the alveolar gas pressure is higher than the blood
pressure in the capillaries it can cause an immediate stop of the pulmo
nary blood flow. If such a ventilator setting is continued for longer
periods the patient might not survive. If we insufflate the ventilatory
gases during right ventriaular diastole alveolar gaspressure causes com
pression onto the lungcapillaries which are well filled with blood, so
forced accelleration of blood to the left atrium will be the result. This
does not mean that the jet valve opens at the beginning of the diastole.
It depends on the patient's airway resistance. Optimal settings are per
formed if the alveolar gas pressure and lung capillary blood pressure are
in counter phase. If we ventilate in this mode we observe an enormous
change of the area enclosed by the pulmonary artery wave curve; optimal
synchronisation shows an almost true sinusoidal wave curve without dicro-
tic notch. The question may rise: if there is no dicronic notch, is there
any function left for the pulmonary artery valve? However the increase
of the pulse-contour of the pulmary artery wave curve suggests an increase
in right ventricular stroke volume. If we set the ventilator in phase
with the right ventricular systole a straight line is observed by pressure
measurement in the pulmonary artery when the workingpressure of the venti-
127
lator is high enough. In fig.5 the simultaneous registration of ECG (trace
1), oesophageal pressure (2nd trace) ,pulmonary artery pressure (3rd.trace),
intra-tracheal pressure(4th.trace), central venous pressure (5th.trace),
intra-arterial pressure (6th. trace) and peripheral finger-plethysmograph
is shown.
fig.5 Asynchronous HFPPV using our PCC-ventilator.
In this experiment the ventilator was set in such a way that the insuffla
tion rate almost equals the heart rate. An obvious harmonic oscillation
is shown in the oesophageal pressure, pulmonary artery pressure and cen
tral venous pressure. The beat frequency can be calculated from the dif
ference of heart-/jet rate • There is not much influence on the arterial
pressure. Does this mean that there is no influence on the body circulation?
To our opinion this statement is wrong. As long as the patient is able
to "oscillate" he has an escape mechanism to survive high frequency venti
lation. During our research we observed that all patients involved tried
to escape from our ventilator settings if we synchronized heart frequency
and ventilator insufflation frequency completely. Iri all patients an
higher heart rate appears if we try to synchronize in phase. This auto
regulation mechanism seems to be very important. The body tries to escape
the effects of a dangerous modeoof jet-ventilation. If we check
128
cardiac output using the thermo-dilution technique we observe a constant
cardiac output. We also can imagine that if somebody studies organ perfu
sion during HFPPV he gets very constant values, but this observation can
never lead to the conclusion that HFPPV does not interfere with the body
circulation. Both techniques : TD cardiac output and radioactive labeled
perfusion observatio~s. cannot be used to study the effects of HFPPV on
the circulation. We need better techniques observing the changes in cardiac
output beat by beat So may be some investigators have to reconsider
their conclusions. To our opinion there is an enormous influence of HFPPV
on the body circulation. Only, as long as the body can protect itself by
autoregulation mechanisms HFPPV seems to be a useful (but potentially
hazardous) technique. However, if the ventilation does not lead to accep
table blood gases of a patient we change .the insufflation rate. The great
risk of HFPPVis when the insufflation rate completely equals.the patient's
heart rate. We observed that in such settings harmonic oscillations dis-
appear. If we do not monitor the pulmonary artery pressure and other para
meters as mentioned in fig.5 it~never can be predicted in which phase of
the heart cycle synchronisation is obtained. This might lead to sudden
death if synchronisation is obtained in "counter-pulse" setting: intersti
tial lung capillaries might be compressed beat by beat and a complete stop
of the lung circulation can be the result (see fig.1). On the other hand
if synchronisation is obtained in counter-phase the insufflation of the
gases ·might aid the pulmonary blood flow and reduce the right ventricular
stroke work. (Counter pulse setting means in-phase setting: high alveolar
gas pressure simultaneous with high capillary blood pressure. Counter-
phase setting means: high alveolar gas pressure and simultaneous low capil
lary blood pressure). This calculated/more or less counter-phase setting
is the principle of our PCC-technique. The respective membrane pressures
in the alveoli should be counter-phased. If we ventilate in such a wayan
optimal alveolar gas exchange can be achieved. This must be the optimal
setting of HFPPV because the momentaneous transmembraneous pressures corres
pond with the specific gas exchange: oxygen will be easily transported to
the blood with high alveolar gaspressure and low capillary blood pressure
and CO2 can be easily transported from the capillaries to the alveolar gas
space if the blood pressure is higher than the alveolar gas pressure. In
this setting an optimal ventilation/perfusion ratio is obtained. Insuffla
tion of the ventilatory gases should be performed with high dP/dt at the
129
lowest working pressure of the ventilator to obtain acceptable blood
gases.
2) Methods
For our PCC-technique a special ventilator was developed based on the
principle of earlier designed HF-jet ventilators (ref. 3,4) .In this ventila
tor (Pneumocontroller, T.Mostert~BV, physical laboratory,Emmeloord,Holland)
gas mixing is electronically set using electro-magnetic valves specially
designed for the purpose. The gas mixing is time cycled. Any pressure
setting can be obtained with the same reproducible accuracy of gas mixing
(N20/02 or 02/Air) independent of built up back pressures and requested
minute volumes. An humidification system is built-in providing the gases
at body temperature with maximal humidity. An anti-condensation chamber
prevents water droplets to pass .. the jet-valve which is mounted near the
patient. Placing this valve near the patient reduces tubing dead space in
this design to less than 3,5 ml, the 10 Charriere insufflation catheter
included (Unoplast,Denmark). The jet-valve was specially designed for the
purpose. The electronic settings which can be made with this ventilator
are: continuous flow interupted by calculated expiration periods or
insufflation cycles from about 20 ms to 1 sec. I/E ratio can be set in
multiple settings of 10% duty cycle. The jet valve can be triggered by
an external trigger signal or as a function derived from the pulmonary
artery pressure and ECG. Pressure and temperature monitoring are built-in.
(intra-tracheal measurements). The ventilator can be set using an optional
microprocessor to calculate and control the function. Also a digital hand
setting is possible. The insufflation of the ventilatory gases was through
a 10 Charriere suction catheter as mentioned above, placed with the tip
half-way in a routine endotracheal tube. On the endotracheal tube a spe
cial T-piece was mounted (Bronchoscop_-Aid,Dryden Comp.U.S.A.)with an
extra one way valve on the expiratory port preventing the suction of
room air during insufflation.
All the patients selected (6) were undergoing operative procedures
with minimal blood loss, such as peripheral vascular surgery. During rou
tine anaesthesia (neurolept technique) short runs were made with our jet
ventilator (immediate change from IPPV to PCC). During those runs all
patients were well oxygenated before. The longest run was about 2 minutes
and provided us so much information that we decided first to study the
130
results. Monitoring was performed with a routine Hewlett Packard monitoring
device (78000 series). All patients had Swan Ganz TD catheter in place as
well as an arterial line and oesophageal balloon catheter. Intra-tracheal
pressure measurements were obtained using a modified Swan-Ganz TD catheter.
The thermistor of this catheter was used to monitor intra-tracheal tempe
rature. Those measurements were made just near the carina, distal from the
tip of the jet-cannula. A Gould Brush 481 multi-channel recorder was used.
3) Discussion and Conclusions
Although much research needs to be done to confirm our statements the expe
riments onwards established a high interference rate of cooperation and
counteraction periods during HFPPV. The occurence of interaction is as
high as possible during ventilation synchronized with the heart beat.
Fixation in counteract or cooperate mode is determined by the relation
of pulmonary artery pressure and intratracheal pressure. Partial or total
blocking of the pulmonary blood flow appears during more or less equally
phased transmembraneous pressures in the alveoli and surrounding capillaries.
The quantitative interaction depends on the patient's histological lung
status and the physical properties of the heart and lungs. We therefore
caution against uncontrolled HFPPV because of the risk of sudden death
or severe right sided decompensation. In clinical practice HFPPV appears
to be a useful technique. It appears that healthy patients can use their
autoregulation mechanisms to protect themselves against in-phase jet
insufflations. During our experiments all the patients developed tachy
cardic heart rhytms during in-phase ventilation.
To our opinion very sick patients treated with HFPPV should
have Swan Ganz catheter in place, arterial line, oesophageal and CVP
monitoring at least. Special care has to be taken if the oscillations
in the pulmonary arterY pressure wave curve seem to disappear.
We hope that we can prove in the near future that this PCC
technique will be the most beneficial method of artificial ventilation,
when a jet-technique is used. An optimal ventilation/perfusion ratio is
obtained with minimal volumes of insufflated gases at the lowest working
pressure.
131
4) References.
ref.l) Sjostrand VH, Eriksson IA. High rates and low volumes in mechanical
ventilation- not just a matter of ventilatory frequency. Anaesth.
Analg.1980 ; 59:567-76
ref.2) Eriksson IA, Sjostrand VH. Experimental and Clinical Evaluation
of High Frequency Positive Pressure Ventilation (HFPPV) and the
Pneumatic Valve Principle in Bronchoscopy under General Anaesthesia.
Acta Anaesth.Scand. ,1977, Suppl. 64, 83-100
ref.3) Jonzon A,Oberg PA, Sedin G, et al. High frequency positive pressure
ventilation by endotracheal insufflation. Acta Anaesth.Scand.1971;
(suppl.43).
ref.4) Heijman G, Heijman L, Jonzon A. et al. High frequency positive
pressure ventilation during anaesthesia and routine surgery in man.
Act.Anaesth.Scand. 1972; 16:176-87
C. MECHANICS AND BLOODGASES
MICROCOMPUTER-BASED SIGNAL AVERAGER FOR ANALYSIS OF PULSED GAS STREAMS INTENDED FOR USE IN HIGH FREQUENCY JET VENTILATION
L. Deen, Theo Dijkhuis.
1 Introduction
During the last decade few advances have been made in the use of artificial
ventilation to treat infants suffering from the Idiopatic Respiratory
Distress Syndrome (IRDS), (Deen, L. 1981).
In the period from 1967 to 1979 ca. 800 babies with IRDS treated at the
Neonatology Department of the Amsterdam University Hospital, have been
,studied. In the group of 350 artificially ventilated patients 65 % died.
In that period use was made of the same apparatus (the Amsterdam Infant
Ventilator, AIV) working in about the same regime. The impression was
settled that the ventilation method failed sometimes, but up to now no
essentially different technique is fully developed.
High Frequency Jet Ventilation (HFJV) might be an alternative ventilation
method for young children suffering from IRDS.
We have therefore been investigating the use of HFJV in rabbits. In
order to satisfactorily apply this technique, it is essential to be able
to monitor gas flow rates and other ventilation parameters.
We make it our object to apply this technique for clinical use, in parti
cular for use in IRDS patients.
The mode of HFJV we have applied on rabbits is promising. As far as we
are aware no commercial apparatus which is capable of register gasflows
of short duration and computing tidal volumes is available. We have
developed such a system which we report here.
2 System Description
A block diagram of the experimental setup is sho~m in fig. 1.
air
•• :. • •• • •• • •
Printer
Pressure reducer o -3ata
<> • •• • • .. ...
•• • ••
APPLE microcomputer
FIG. 1.
hot wire sensor
DRAGER
spirolog
133
Airflow pulses are created by means of an elctronically controled
solenoid valve (Martonair), switching on and off the background pressure
to a nozzle (1.3 mm i.d.) delivering jet flow into the airpath. The flow
rate is detected and analysed by a combination of two commercially
available apparatus:
1 A Drager Spirolog-1 intended for use with anaesthetic and ventilation
intrurnentation.
2 An Apple-II-plus microcomputer.
The Spirolog-1 measures flow on the principle of a Constant Temperature
Anemometer (.CTA).
The streaming gas is led through a venturi-tube sensor containing two
thin (12,7 urn) platinUm filaments, held at different temperatures. To
gether with two, high precision resistors they form a bridge. The cold
wire (600 C) is included to compensate for heat-loss due to local,
ambient temperature changes. The hot wire (1800 c) is held at constant
temperature. The electrical power needed to compensate for temperature
loss caused by the streaming gas ±$ dependent on the gas flow rate.
(Jansen, J.M.L. 1959). The relationship is non-linear. A linearizing
network reshapes the bridge-output to a proportional relation to gasflow.
134
Because of the nature of the measurement, a noisy output signal is
obtained which ~an not be directly interpreted when monitored on an
oscilloscope.
Noise reduction is necessery to visualize the pulsed flow.
The microcomputer is used as a signal averager, displaying the averaged
signal during a present, software implemented, number of cycles.
The flow diagram 0f the program is shown in fig. 2.
~art
Fig. 2
135
The microcomputer is expanded by the addition of:
1 "A lowpass-filter to reshape the analog signal to avoid the aliasing
effect. \ To obtain sharp cut-off we used a 4-th order
Butterworth filter (cascading two AF 100, Nat. Semicond.) with cut-
off frequency of 1 KHz. (Sampling frequency 2.55 KHz). (Yanikowski, 1981).
2 An analog-digitai ,converter to transform the inpuDsignal, using a
single Ie (AD7581 IN, Analog Devices) and a microprocessor compatible
8-bit, 8 channel memory buffered data-acquisition system accepting
inputs from 0 to 10 Volt. Each channel has updated data after 8 times
80 usec. We read 8 channels succesively at present, software implemented
interval time.
3 Game-paddle pushbutton.
We use this single-bit input facility of the microcomputer for trigger
signal detection. The trigger signal is supplied by the solenoid-valve
stimulator.
4 A floppy-disk system for loading the program into the random acces
memory (RAM) of the microcomputer. The program provides data input
from the AID converter memory, averaging procedure and data transfer
to the picture buffer. In order to get a time extended picture of
precisely 100 msec (256 sample points), a sample frequency is used
o~ 2550 Hz (0.1/255) When averaging is finished the program computes
the tidal volume and integrated flow (displaced volume) in 1/min.
5 A monitor and/or graphic printer for visualizing the flow rate and
for printing some quantative data (tidal volume, minute volume).
Fig. 3.
DRAGER
spirolog-1 ----hot wire sensor solenoid valve
anti-aliasing filter
stimulator
JL
Fig. 3
APPLE video display
microcomputer
graphic printer
136
3 Calibration
Standard flow rates ranging from 10 to 100 l/min (Godard, type 59007)
were used to calibrate the system and to check for linearity. Calculated
flow rates were within + 10 % of standard input flow rates.
A typical calibration curve is shown in fig. 4.
-;: 100 "e ;; Co
~ ~
80
~ 3 g .., " :;
60 Co E 0 u
40
20
4 Results
•
o 20 40 60 80 100 standard flow rate (liter per min)
Fig. 4.
Pulsed gas streams produced by an electronically controled solenoid
valve, with pulse duration from 15 to 40 m/sec at fixed 3 Hz repetition
frequency and different background pressures (1 to 3 ata) are shown in
fig. 5.
137
• 80
E • 3.0 • 2.5
CD & 2.0 ata E 0 1.5 • :::J
[J 1.0 "0 >
60 • & iii ~ - •
0
&
• 40 [J
0 •
• & [J
• & 0
20 0 [J
[J
o 10 20 30 40
pulsduration (msec)
Fig. 5 •
Tidal volume is computed for different parameter settings. Tidal volume
as a function of pulse duration is shown in fig. 6 and 7. Tidal volume
ranging from 15 mi. to 100 mi. can be computed.
138
C 100 'f ... Q) a. ... 80 Q)
:: ... Q) ... l! 60
~ .2 ....
40
20
o
C 100 'f ... Q) a.
40
20
o
10 30
10 30
"
...... ..
pulse duration: 15 msec
pressure: 1 ata
tidal volume :18 ml
50 70 90
Fig, 6 time (millisec)
pulse duration: 40 msec
pressure: 1 ata
tidal volume: 45 ml
-~ ... :'-- l"'-. .,"...,. ....... • ....... : ... " ...... :" 0" ,
50
Fig. 7,
\,
70 90
time (millisec)
139
5 Discussion
We were not able :to measure the frequency respons of the sensor system
because a well defined alternating gasflow was not in store, while the
Spiro log manual did not provide detailed physical information. But, from
literature (Jansen and al., 1959) we conclude that the sampling frequency
we used (2550 Hz) was far within the bandwith limits typical of Constant
Temperature Anemometers (up to tens of KHz) .
The CTA, in fact a mass flow sensing wire of very small size to satisfy
heat transfer and frequency respons, measures mass flow only locally in
a small region of the streaming gas. Tis region must be representative
for the average mass flow through the entire cross section of the venturi
tube the hot wire is located at
6 Conclusions
The experiment setup we present here has enabled us to register in a
reproducaThle way, the flow rate at the input to the ventilatory system.
Because it is the simplest method to use in practice, we have up to now
only investigated this system using pulsed gas streams. However it is
possible to use the apparatus with any waveform having a frequency
content less than 12.5. KHz (limited by the 80 msec. convertion time
of the D/A converter).
It is our intention to use our apparatus in vivo to enable us to define
the parameter settings (flow wave form, pressure and frequency) which
will give optimal gas exchange with minimal circulatory effects.
Ultimately this should prove a useful tool in furthering research into
the ventilatory treatment of infants;sU:ffeting from IRDS.
References
Deen, L. 1981, Artificial Ventilation in Babies with IRDS Thesis.
Jansen, J.M.-L., Ensing, L. and Erp , J.B. van (1959)
A constant-temperature-operation hot-wire anemometer.
Proc. IRE April, 555-567.
Yanikowski n 981) in: Desfgn of microcomputer based medical instrumentatIon
(chap. 2)
Tomkins, W.J. and Webster, J.G. (Eds)
Prentice-Hale, inc. Englewood Cliffs, N.Y.
EVALUATION OF A NEW VALVELESS ALL PURPOSE VENTILA'IOR: EFF.ECI' OF VENTILATING FREQUENCY PEEP, PAC02 AND PA02 ON PHRENIC NERVE ACTIVITY
M K CHAKRABARI'I ESc MPhil, J G WHITWAM MB ChB PhD MRCP FFAReS DEPARI'MENT OF ANAESTHETICS, roYAL POSTGRADUA'IE MEDICAL SCHOOL, HAMMERSMITH HOSPITAL, LONOON, ENGLAND.
n: ·INTIDDl]CIf.[ON
In recent years there has been considerable interest in the use of
ventilation with low tidal volumes at high frequency in patients with
low pulrronary corrpliance and the subject has been reviewed by Sjostrand
(1980).
One claim by Jonzon (1977) is that high frequency ventilation CHIN)
will al:olish efferent phrenic nerve activity, (PNA). This has important
implications for controlling the respiratory activity of patients on
ventilators. This author describes the developnent of a PEEP of 2 an
H20 during REV but makes no reference to changes in blood gas tensions
induced by changes in ventilation other than to state that these were
nonnal. In the clinical reports where beneficial effects have been
described on central respiratory control as a result of introducing HFV
(eg, Davey and Leigh, 1982; Carlon et aI, 1981; Bland et aI, 1980) there
has been a reduction in PaC02 and an improvanent in Pa02 .
The present study was undertaken to detennine the contribution of
ventilation frequency per se on central respiratory acti vi ty, and was
made possible by the developnent of a new ventilator.
2. METHODS
2.1. New Ventilator
The principle underlying this ventilator is to use a single breath
ing tube in which the respiratory gas is introduced near the airway while
a jet in a rrore distal part of the tube drives the respiratory gas into
the lungs. The jet driving gas is independent of the respiratory fresh
gas used for patient ventilation. The distance between the respiratory
gas inlet and the jet is sufficient to prevent the driving gas taking
part in gas exchange in the lungs. There are no valves, or other
obstructions in the breathing circuit which remains open to atrrosphere
air O 2
INSP
IRAT
OR
Y G
AS
anae
sthe
tics
---:, -=
r-l ~ -=
===--
. ->
=:::
J "
-1
-,-
--,1
m
ixer
qa
s flo
w m
onito
r -"
'&
alar
m
brea
thin
g tu
be
DR
IVIN
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GAS
)
-==':;:
:' ==
freq
uenc
y =
=-
<:..-
.-t -
cant
rol
r--
Ie;
''''''''
'ER
tidal
-t
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FIG
. 1.
V
en
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tor
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~
142
at all times. (Fig. 1).
Apart fran the primary driving jet J l t.YJo other jets (J2 and J 3)
can be activated. They provide a oontinuous flaw of gas thereby generat
ing standing pressures up to 2kPa, J 2 in the direction of the inspiratory
flow and J 3 in the reverse direction to produce PEEP and NEEP respectively.
For an adult patient any oonventional standard disposable tubing with
an internal diarreter and length of approx:irnately 22 nm and l.5M respectively
is adequate for tidal volumes up to 500 ml. For chilClren and neonates the
tube size can l:e reduced for convenience but this is not essential.
The respiratory fresh gas is delivered at the connection between the
patient's airway and the breathing circuit. However, to reduce anatomical
dead space, eg, during HFV the respiratory gas may be delivered through a
narrow tube placed either in the lumen of an endotracheal tube or in the
trachea itself. A fresh gas flow of only 1 minute volume (ie approximately
100 ml kg-l in the adult) is required. This gas can be fran any source
eg, anaesthetic, air, oxygen, and is humidified and wanned before entry
into the patient's circuit. Because its flow is constant, conditioning
of the respiratory gas is simple.
Any driving gas, eg, air, oxygen or nitrogen, fran any high pressure
source (ie, 4 bar) is suitable. To provide the variable frequency of
ventilation and variable inspiratory-expiratory time ratios
(I:ji! ratio) a device for "chopping" the driving gas is required which may
be mechanical, electrical or pneumatic.
This machine allows ventilation with any chosen gas, the carposition
of which can be accurately controlled, at both nomal and high respiratory
rates. It also allows the application of NEEP, so that the PEEP developed
during HFV, can be removed and the end expiratory pressure returned to
zero. It can operate from nonnal to high frequencies rrerely bY changing··
the rate control. After a change to high frequency ventilation (HFV)
in the dog there is a small but significant reduction in PaCD2 which
was corrected to control values by decreaf>ing the ventilation volume, and
vice versa. M:!asurerrents of phrenic nerve activity (PNA) v.ere made either
in steady states or in dynamic situations before any change in PaCD2 could occur.
143
2.2. AninlalEApe!iments
Observations ~e made on 8 mongrel dogs. Anaesthesia was induced
with methohexitone 10-12 m:J kg -1 administered as a bolus intravenously,
and maintained with a 1% solution of ex chloralose, initially as a bolus
of 3ml kg -1, and subsequently by a continuous intravenous infusion
(1-2 ml kg -1 hr -1) • They ~ artificially ventilated via an endotracheal
tube and muscular relaxation was provided with suxamethonium (1-2 m:J kg -1 hr -1).
Catheters ~e inserted into the inferior vena cava via a ferroral
vein, and a fenoral artery.
The left phrenic nerve was exposed in the neck, part of which was
dissected free fran surrounding tissues, desheathed and cut distally,
:imrrersed in mineral oN and rrounted on bipolar silver electrodes to
record efferent activity which was processed through a pre amplifier
(Tektronix 122) rectified and integrated (Neurolog NL 703).
Pa02, PaC02 , arterial pH and core t:.eIrperature ~e within the ranges
10.6-33.3 kPa, 4.6-7.0 kPa, 7.31-7.38 and 37oC-380 C respectively. In any
one preparation these values ~e maintained within 5% of control values
throughout the exper:imental period. The ecg,beat by beat heart rate,
intravascular pressures, and intratracheal pressure were recorded. The
phrenic nerve activity and its integrated signal ~ displayed on an
oscilloscope (Tektronix 265) an ultraviolet recorder (SE Laboratories
type 2112) and a pen recorder (Devices MX2).
Quantitative measurements of PNA were obtained in arbitrcuy units by
multiplying the peak height of the integrated signal by the burst
frequency min-I:
Statistical analysis was perfonned by using a 2 way analysis of variance
fol1~ by paired t tests where appropriate. A probability of less than
5% was considered to be significant.
The animals ~ ventilated with a new ventilator.
3. RESULTS
3.1. PaC02 In The Range 6.0-7.0 kPa. Pa02 In The Range 30-35 kPa (ie IDnnal - high CO2' high 02~.!..)':". __________ _
Increasing the ventilation frSllJel1CY fam 12 .bfm to 80 bfm caused a
reduction in PNA of approxiInately 30% and this was ccmparable to the
reduction caused by a PEEP of 0.5 kPa. A PEEP of 1.0 kPa caused a further
large reduction in PNA which returned to control values on return to NFV
144
witlDut PEEP. Under these conditions of blood gas tensions it was never
possible to abolish PNA during the application of either HFV or PEEP.
During HFV the peak airway pressure was reduced by approximately
40% but PEEP developed which in sane preparations was as high as 0.2 kPa
and in others was very small.
3.2. PaCD2 In The Range 4.6 kPa to 5.3 kPa, Pa02 In The Range 30-35 kPa. {Nonnal - low CD2 - High 02 . .:...),;.... ________________ _
When the paCD2 was reduced both HFV and PEEP had a much greater
effect on PNA. Increasing the ventilation frequency to 80 bj;:m decreased
the PNA by over 70% and a PEEP of 0.5 kPa caused a reduction of a similar
order of magnitude. In sane preparations in this group both HFV and PEEP
completely abolished PNA.
3.3. PaCD2 In The Range 4.6 kPa to 5.3 kPa, pa02 In The Range 10.6 kPa -13.3 kPa (Nonnal - low CO2 - normal 02:.:...),;.... __________ _
Decreasing the Pa02 fran over 30 kPa to under 13 kPa caused an increase
in PNA of approxiroately 27% which is due to peripheral chemoreceptor
activity(eg Duffin, 1971). Changing fran NEV to HFIT in air ventilated
animals caused a reduction in PNA of only 2P, ie, the smallest effect
observed in this series of experirrents.
3.4. The role of PEEP generated by HFV on PNA
Changing the ventilation frequency fran 12 to 80 bpn had no more
effect on PNA than applying a PEEP of 0.5 kPa at NEV.
Using the NEEP facility provided by the new ventilator used in this
study it was possible to reduce the PEEP generated by HFIT and thus examine
the effect of HFIT alone.
For example in a dog with a pa0)2 of 5.1 kPa and a Pa02 of 31 kPa
where, on changing from NEV to HFV, PNA was Virtually abolished. When
the PEEP generated by HFV was rerroved PNA returned.
Another example in another preparation shows that during HFIT rerroval
of PEEP restoring and expiratory pressure to zero, increased the rate of
PNA, whereas the application of 0.8 kPa of PEEP totally abolished PNA
which was restored by rerroval of PEEP.
P.N.A during LM.V was observed. When the animal was
breatfuing spontaneously at approximately 30 bpn and the ventilator was
providing IMi7 at 6 bpn, the positive pressure generated by the ventilators
145
inspiratory phase immediately terminated spontaneous respiratory activity
which returned as soon as the airway pressure fell during the ventilator's
expiratory phase. When the ventilator frequency was in=eased to 60 br:ro
thereby reducing the peak inflation pressure, (in this particular animal
very little end expiratory pressure was generated) , PNA continued without
interruption at 30 bpn. After the administration of suxamethonium and a
return to a ventilation frequency of 10 bpn the PNA becarre locked to the
ventilator cycle in expiration in the normal way. In this preparation the
Pa02 was 12 kPa and the Paill2 5.5 kPa during the period of observation.
In these experiments no significant change was allowed in pa02,
PaC02 and pH nor was there any significant change in heart rate and mean
arterial pressure throughout any relevant period of observation.
4. CCNCLUSION
The exmclusion to be drawn from this study is that PaC02, Pa02 and
PEEP are the most important factors which will influence central
respiratory activity. The beneficial effects of high frequency ventilation
in controlling this activity are probably due to more efficient pubnonary
ventilation causing a rise in Pa02 and a fall in PaC02 rather than a
specific effect of the higher frequency. The prinCipal contribution of
high frequency ventilation in depressing central respiratory activity,
apart from changes in' blood gas tensions, may be to exceed the response
time of the lungs thereby generating a positive end expiratory pressure
in the distal airways, where pubnonary stretch receptors are located.
REFERENCES
1. Bland RD, Kim MH, Light M and Woodson JL. 1980. High frequency mechanical ventilation in severe hyaline rrembrane disease. Crit. Care Med., 8, 275.
2. Carlon-OC, Kahn RC, Harland WS, RAY C and Turnbull AD. 1981. Clinical experience with high frequency jet ventilation. Crit. Care M:!d., 9, 1.
3. Davey A:r and Leigh JM. 1982. High frequency venture jet ventilation. Adult respiratory distress syndrare - a case report. Anaesthesia, 37, 670.
4. Duffin J. 1971. The chemical regulation of ventilation. Anaesthesia, 26, 142.
5. Jonzon A. 1977. Phrenic and vagal nerve activities during spontaneous respiration and positive pressure ventilation. Acta Anaesth. Scand., (Suppl.), 64, 29.
6. Sjostrand U. 1980. Hiqh frequency positive presSure ventilation (HFPPV). Crit. Care Med., ~, 345.
HUMIDIFICATION OF THE RESPIRATORY TRACT IN HFJV
w. FUCHS, R. FECHNER, E. RACENBERG
Humidification and heating of the inspired air are abvious
prerequisites for the long-term use of high-frequency venti
lation in patients with respiratory insufficiency. Reports
on successful application (1, 2) as well as the own clinical
experience, that high-frequency ventilation with cold dry
gas results in restlessness and discomfort of awake patients
within 2 to 3 hours of application, initiated the development
of a heater-humidifier-system to be used in conjunction with
a VS 600 high-frequency jet ventilator, Acutronic Medical
Systems, Switzerland~ for which such an equipment is not yet
on sale (3,4).
The requirements with respect to humidity and temperature of
inspired gas when the upper respiratory tract is by-passed
by intubation or tracheostomy are well documented and there
exists a wide variety of technical realizations to achieve
"physiological atmospheric conditions" in conventional
mechanical ventilation (5). However, all classes of existing
equipment - heat- and moisture exchangers, gas-driven or
mechanically actuated nebulizers, water-bath humidifiers -
add a substantial compressible volume to the insufflation
part of the patient circuit and, thereby, reduce the pressure
rise during the insufflation phase. The basic characteristic
of high-frequency ventialtors, i.e. the gas pressure remains
constant regardless of the ventilation phase, is impaired.
The use of conventional humidifiers in combination with high
frequency:ventilators does not comply with the principle that
the internal compressive volume and the internal compliance
of the patient circuit be minimal (6).
147
Our approach to add about 30 mg water per liter of insufflat
ed gas and simultaneously rise the temperature to 33 to 36°
Celsius without changing the gas-flow characteristics of the
high-frequency ventilating unit is depicted diagrammatically
in Fig. 1.
8
FIGURE 1. 1 wet gas warming spiral, 2 thermostat-regulated boiler, 3 servQunit, 4 one-way valve, 5 warm water bath, 6 microinfusion pump, 7 water-warming spiral, 8 patient.
The gas which is delivered by the jet ventilator is warmed
up by passing the delivery tube in form of a spiral through
a water bath, the temperature of which is thermostatically
kept at 57° Celsius. About 30 ml of water are pumped per
hour through a second coil in the water bath by means of a
148
microinfusion pump which delivers the heated water through a
one-way valve into the patient's limb of the jet ventilator
immediately before its entrance into the water bath.
The rationale of this arrangement is simply that - with
correct choice of the dimensions - small amounts of heated
water are fed into the delivery tubing, become nebulized by
the jet stream, the resulting aerosol is warmed up and the
larger particles are baffled out when the stream passes
through the coil. The temperature of the delivered gas at the
patient's end depends, aside from the material and the thick
ness of the wall, on the distance between the water bath and
the connecting piece of the endotracheal tube.
In our system a tube length of 60 cm resulted in a temperature
of 33 to 36° Celcius, reduction of the length to 45 cm in
creased the temperature to 37 to 39° Celsius. In the useful
temperature range of 33 to 36° Celcius condensation shows up
in the tubing close to the patient's end, which is assumed to
indicate a relative humidity of the inspired gas of almost
100 %. The extension of the delivery tube to allow for the
coiling in the water bath results in a pressure loss, which
can be compensated for by choosing a working pressure which
for a given minute volume is 0.5 bar higher than that re
commended by the manufacturer.
Although the described system was considered to be a first
prototype, the parts of which should be improved in design
and combined with a feedback mechanism between gas temperature
and heating power as well as with alarm systems both for the
water-bath temperature and the microinfusion pump, the system
happened to come into clinical use in its preliminary state
in management of a patient with progressive ARDS. After a
period of 9 days of conventional mechanical ventilation, the
arterial blood-gas conditions of this patient became more and
more unsatisfactory in spite of increasing ventilatory volumes
and increasing oxygen fractions in the inspired gas, finally
up to a FI02 of 0.9. Eventually a situation arose where it
149
appeared sufficiently indicated to try HFJV even though the
humidifying system was estimated to be still in a develop
mental stage. Under jet ventilation the Co2-retention improved
and the pa0 2 increased to acceptable values such that the
fractional concentration of the inspired oxygen could be de
creased transitorily to a FI02 of 0.4. However, although a
period of 5 days with more or less acceptable blood-gas
values could be maintained, the fatal progression of/the ARDS
could not be stopped.
REFERENCES
1. Bjerager K, Sjostrand U, Wattwil :1. Long-term treatment of two patients with respiratory insufficiency with IPPV/ PEEP and HFPPV/PEEP. Acta Anaesthesiol. Scand. suppl. 64: 55-68.
2. Carlon GC, Ray C, Klain M, Mc Cormack PM. 1980. Highfrequency positive-pressure ventialtion in management of a patient with bronchopleural fistula. Anaesthesiology 52: 160-162.
3. Racenberg E, Fechner R. 1981. Humidification of the respiratory tract in HFJV. Symposium on "Clinical application of high-frequency ventilation". Pittsburgh, U.S.A. April 10th.
4. Fechner R, Racenberg E. 1982. Befeuchtung der Luftwege bei Beatmung mit hohen Frequenzen, in press.
5. Chamney AR. 1969. Humidification requirements and techniques. Anaesthesia 24: 602-617.
6. Sjostrand U. 1977. Review of the physiological rationale for and development of high-frequency positive-pressure ventilation - HFPPV. Acta Anaesthesiol. Scand. suppl. 64: 7-27.
EFFICIENCY OF INTRAPULMONARY GAS DISTRIBUTION DURING HIGH-FREQUENCY VENTILATION
Ivan Eriksson, M.D. Department of Anaesthesiology and Intensive Care, Regional Hospital, Urebro, S-701 85, Sweden.
The type of high-frequency ventilation developed by our group, highfrequency positive-pressure ventilation (HFPPV), is characterized by a ventilatory frequency of 60/min and a relative insufflation time of 22% of the period time (1). So far, it has been used clinically mainly for bronchoscopy and for laryngoscopy under general anaesthesia (2) and in a limited number of patients with adult respiratory distress syndrome (3). Recent studies of central and peripheral circulation in dogs and in patients have not shown any hemodynamic differences between HFPPV and conventional mechanical ventilation (3).
On the other hand, studies conparing HFPPV with other forms of ventilation have shown a more efficient washout of N2 during HFPPV. In patients undergoing diagnostic bronchoscopy because of suspected or verified pulmonary disease, intrapulmonary gas distribution showed im~rovement during HFPPV as compared with spontaneous breathing (SB; 4). In patients requirin~ mechanical ventilation because of respiratory failure the intrapulmonary gas distribution improved as compared with mechanical ventilation at a frequency of 20/min (5).
The aim of this paper is - on the basis of those studies (4, 5, 6) - to analyze the methods and indices used and the mechanisms which may explain the differences in gas exchange and intrapulmonary gas distribution between ventilation at high and at low ventilatory frequencies.
Nine patients scheduled for diagnostic bronchoscopy were examined by means of a non-rebreathing multiple breath nitrogen washout technique (4). The experimental arrangements are shown in Fig. 1. Each investigation started with the patient awake and breathing spontaneously, then under general anaesthesia, endotracheal intubation and muscular relaxation with HFPPV. A momentaneous change from air to oxygen breathing was made and oxygen breathing was then continued until end-expired N2-concentration had reached 2%.
151
Fig. 1. Experimental arrangement. E = endotracheal tube. N = needle for gas sampling. Pv = pneumatic valve connector. Vent = ventilator attachment. V = valves. P-t = pneumotachography flow head. Db = Douglas bag.
The efficiency of nitrogen washout was higher during HFPPV as compared
with SB (Fig. 2). Nitrogen washout delays (NWOD) were 21S.6 ~ 112.1% during SB and decreased to 85.S ± 70.5% during HFPPV. This measure of efficiency of intrapulmonary gas distribution is obtained from resolution of semilogarithmic plots of NWO-curves into compartments with different ventilatory
rates, i.e. different alveolar dilution factors (Fig. 3). However, those compartments are not anatomical realities but functional compartments with
different nitrogen clearance rates. If there is only one compartment, the method of analysis gives no delay at all (NWOD = 0%) no matter how fast or slow the actual clearance rate of nitrogen is. When there are two or more
compartments with different clearance rates, the delay percentage expresses
" c ~
~ -.; "0
, 0 -" ~ ~
3 c ~ 0>
~ "
'/,
500
400
300
200
100
NZWOD
~ tSD
S8 HFPPV
Fig. 2. NWOD during SB and during HFPPV. p< 0.01. From Eri ksson & Sjostrand 1980.
152
a percentage of the ideal situation, i.e. as if the tidal volume was ventilating only one compartment with a size equal to the sum of the different compartments. Further, the method of analysis treats washout data as if the different compartments were ventilated in parallel, all other forms of ventilatory inequality being excluded by the original assumption. This is a weakness as there is currently a general agreement that both series (stra
tified) and parallel (regional) inhomogeneities exist although their relative importance remains undefined (7).
10 20
No of breaths
30
Fig. 3. Resolution of semilogarithmic plot of NWOcurve into compartments.
A simpler index which is considered to measure the overall efficiency
of intrapulmonary gas distribution, no matter what type of inhomogeneity
present, is the lung clearance index (LCI) according to Becklake (8);
LCI = ~T FRC where n is the number of breaths. The observed LCI is lower during HFPPV than during SB (Fig. 4). Thus, also this index gives a more efficient gas distribution during HFPPV as compared with SB. However, in this form, it only tells us the total ventilation per minute necessary to washout the FRC and not much about the efficiency in relation to the size of the tidal
volume (VT) as compared with the anatomical dead space (VO)'
An ideal situation, according to traditional concepts of pulmonary ventilation, is when the volume (VT - VO) to a full extent takes part in alveolar
gas exchange, i.e. it mixes with alveolar gas so that there are no concen-
50
40
. ~ .
30 u c ~
~ -1l go .3 20
10
'" "'",
tSD
58
LCI
HFPPV
153
Fig. 4. LCI during 58 and during HFPPV. p<0.0005. From Eriksson & 5jostrand 1980.
tration gradients within the alveolar space (Fig. 5). The diluting effect of each tidal volume during washout can then be expressed as an alveolar dilution factor (see Fig. 5). Fig. 5 also shows the basic equation for washout of an inert gas from a uniformly ventilated space.
Inspiration of oxygen
Before gas mixing After gas mixing
Vo - - -lVT
.-----\V - -V
}RC
Alveolar dilution factor w = FRC FRC <(VT - VOl
FA = FA • wn n 0
Fig. 5. The classical concept of gas exchange in the lung .
The ideal or expected, value for n (FN2 decreasing from 80% to 2%) then
is;
n = log 0.025 log w
Using this value for n it is now possible to calculate the ideal or expected LCI for any combination of volume and frequency based upon the concept in Fig. 5. The results calculated for 58 and HFPPV are shown in Fig. 6. In
154
seven of nine patients LCI-observed is thus lower than LCI-expected during HFPPV (n.s.). During spontaneous breathing LCI-observed is higher than LCIexpected in all patients (p<O.OOl).
The fact that LCI-observed can be better than LCI-expected during HFPPV. especially taking into consideration that gas mixing within the alveolar space may not be complete. means that the interface between alveolar and tidal gas is not at its usual position. but extends into the conducting airways (cf Fig. 5). The extent to which this takes place can be calculated
as a functional or physiological dead space for N2 (VO N2 );
V = FRC + V _ FRC DN2 T 1010g O.025/n
For derivation. see Eriksson 1982 (6).
LCI LCI ·obs!-exp
30
20
10
oL---~~--------------------~~~----~ S.B. HFPPV
Fig. 6. The relationship between physiological dead space for N2 (VDN2) and two different lung clearance indices.
To the right in Fig. 6 the dead spaces for N2 thus calculated are plotted together with LCI. There is a highly significant correlation between the slopes of the two lines. The dead space for nitrogen is smaller than the volume of the conducting airways in seven out of nine patients. This cal~ culated dead space for N2 includes every part of the tidal volume which does not fully equilibrate with alveolar gas. Analogous with the physiological dead space for CO2 it constitutes the sum of parallel dead space in the conducting airways and series dead space due to stratified inhomogeneities in the alveolar space. One important difference between N2 and CO2 in this
155
context is that an alveolar dead space for N2 can be secondary only to in
complete diffusion within the alveolar dead space, while for CO2 it can
also be secondary to inadequate alveolar perfusion.
With an axial velocity during HFPPV of 2.500 to 3.000 cm/sec, corre
sponding to 1.5 l/sec, there is turbulent flow not only in the tracheal
tube but probably also some generations down in the conducting airways. It
is therefor likely that the explanation to these findings is increased gas mixing secondary to high gas flO\~ velocity with turbulence and "augmented
diffusion" (9) in the conducting airways. A closer look at the NWO-curves during HFPPV gives support to this theory. Fig. 7 shows two nitrogen washout curves from the same patient. The upper curve was obtained during snontaneous breathing and the lower during HFPPV. N2 is obviously eliminated much faster during HFPPV. This is partly due to hyperventilation. The average VT was 423 ml during SB and 331 ml during HFPPV. There is also another striking difference. The N2-concentration during HFPPV does not reach zero
during inspiration or initially during expiration, in spite of oxygen breath
ing, until most of the N2 is eliminated. During spontaneous breathing there is a classical curve with O2 expired from the conducting airways or anato
mical dead space initially and then an alveolar plateau. During HFPPV, on the other hand, the initial expired gas in this patient contains around 17%
of nitrogen during the first expiration after changing to oxygen breathing. Also at the end of inspiration there is no pure oxygen in the endotracheal tube. During expiration the N2-concentration then rises steeply while the conducting airways are being emptied. Obviously there is an increased mixing
between tidal and alveolar gas in the conducting airways. NWO-curves of
principally the same type have been obtained during HFPPV in patients with ARDS (3).
0/0
ao~ FNz 40
0
%
FN2 eo ~~ 4: 11krr.-.
0 20 40 60 80 100 sec
Fig. 7. NWO-curves during spontaneous breathing and during HFPPV for one patient. From Eriksson 1982.
156
As the amount of N2 that is being eliminated is also proportional to the area under the nitrogen concentration curve in each experiment, one would expect some correlation between initial expired N2-concentration and the efficiency of N2-washout. Fig. 8 thus shows nitrogen washout in terms of LCI-observed plotted against initial expired N2-concentration. A high initial expired N2-concentration seems to be related to an efficient washout of N2. One explanation to the rather low correlation could be that an increased gas mixing in the conducting airways are not the only source of variance in nitrogen washout but the extent of diffusion equilibration in
the distal airways for N2 (alveolar dead space) is also of importance.
'/, r-----..-------,---,..,
N Z
'l;
" 2 20
1 ~ t 10
LClobs
r=0.59 y=0.2640- 0.0136.
°0~--~---170------1~5
lung Clearence Index (observed)
Fig. 8. Initial expired N -concentration plotted against observed lung clearance index (LCI-obs). From Eriksson 1982.
The mean V D/VT- rati 0 for N2 duri ng HFPPV thus becomes 0.38 contrary to a VD/VT-ratio of around 0.75 for CO2 (6). It can be explained by a more even topographical distribution of inspired gas during HFPPV. This is possible if the distribution is not governed by the presence of regional differences in time constants. Several investigators (10, 11, 12) have found such a more even distribution with increasing inspiratory flow rates, although during spontaneous breathing, but they (11, 12) could also show a substantial departure from predictions based on regional time constants alone. The more efficient washout of N2 during HFPPV could then be explained by a better ventilation of poorly perfused non dependent parts of the lung. As N2 - contrary to CO 2 - is not dependent upon alveolar perfusion for washout this may increase washout of N2 and at the same time even decrease washout of CO2,
157
CONCLUSION During high-frequency ventilation at 60 breath/min, the high gas flow
velocity in the conducting airways probably gives augmented diffusion during inspiration. Together with the ordinary diffusion processes and gas mixing, this causes residual gas to be present in the conducting airways at end-inspiration. These findings are compatible with a small functional dead space for N2 (VDN2)' contrary to a considerably larger physiological dead space for CO2, The efficiency of N2-washout during HFPPV can not be used directly as a measure of efficiency of pulmonary exchange of CO2 and of O2,
REFERENCES 1. Sjostrand U. 1977. Summary of experimental and clinical features of high
frequency positive-pressure ventilation - HFPPV. Acta Anaesth. Scand., Suppl., 64:165.
2. Borg U, Eriksson I, Sjostrand U. 1980. High-frequency positive-pressure ventilation (HFPPV): A review based upon its use during bronchoscopy and for laryngoscopy and microlaryngeal surgery under general anesthesia. Anesth Analg. 59:594.
3. Wattwil 14. 1982. Evaluation of HFPPV in experimental and clinical practice. Thesis. University of Uppsala, Sweden.
4. Eriksson I. Sjostrand U. 1980. Effects of high-frequency positive-pressure ventilation (HFPPV) and general anesthesia on intrapulmonary gas distribution in patients undergoing diagnostic bronchoscopy. Anesth Analg. 59: 585.
5. Wattwil M. Sjostrand U, Borg U, Eriksson I. 1983. Comparative studies of CPPV and HFPPV in critical care patients - Studies on intrapulmonary gas distribution. Crit. Care Med. 11, 1983.
6. Eriksson I. 1982. The role of conducting airways and gas exchange during high-frequency ventilation - A clinical and theoretical analysis. Anesth Analg. 61:483.
7. Cumming G, Semple SJ. 1980. Disorders of the respiratory system. Sec. Ed. Blackwell Scientific Publications. p 79.
8. Becklake MR. 1952. A new index of the intrapulmonary mixture of inspired air. Thorax 7:111.
9. Fredberg JJ. 1980. Augmented diffusion in the airways can support pulmonary gas exchange. J. Appl. Physiol. 49:232.
10. Bake B, Wood L, Murphy B, Macklem PT, Milic-Emili J. 1974. Effect of inspiratory flow rate on regional distribution of inspired gas. J. Appl. Physiol. 37:8.
11. Sybrecht G, Landau L, Murphy BB, Engel LA, Martin RR, t1acklem PT. 1976. Influence of posture on flow dependence of distribution of inhaled 133Xe bali. J. Appl. Physiol. 41:489.
12. Fixley f15, Roussos C5, r~urphy B. Martin RR, Engel LA. 1978. Flow dependence of gas distribution and the pattern of inspiratory muscle contraction. J. Appl. Physiol. 45:733.
GAS EXCHANGE IN mGH FREQUENCY VENTILATION: AN EXPERIMENTAL STUDY
M. KLAIN
1. INTRODUCTION
There is a significant disagreement between the results published about
gas exchange in high frequency ventilation (HFV). Different authors advocate
different frequencies as optimal. These conflicting results are often caused by
significant differences in equipment used for high frequency ventilation. In
addition, various theoretical papers try to establish at what frequency there is
no more convection but only diffusion of gases in the lungs.
Disregarding how interesting these theoretical discussions might be, we
have to realize that diffusion exists on every level of gas transport and that we
also have bulk movement of the gases up to the alveoli even during high frequency
ventilation. Simple clinical observation shows that there is chest expansion during
HFV. Movement of the chest wall is decreased, but nevertheless can be easily
observed. Therefore, we should try to explain the gas exchange as in any other
type of artificial ventilation.
We decided to take a look at the gas exchange from a very practical
standpoint. Namely, how should we set the ventilator and what parameter
expresses best the ventilatory support needed?
In high frequency jet ventilation (1), the most widely used method at the
present, most of the authors talk about driving pressure, expressed in PSI or bar.
From the users standpoint this is understandable because this is the control which
is most often adjusted in order to change the level of respiratory support. But
it does not give the full information. The same driving pressure
.... .... 0 -
520
490
460
430 75
50
·25
o o
0
10
M 8
.; ~ 6 .... -.. o .Ci .. .. CD .. Q.
4
~ 2 .> . .. o
159
HIGH FREQUENCY JET VENTILATION
Po 02 • P(O.OI
~t- !---!
Po C02
• 100
'\ , , ,
•
200
~
•
300 400 500 600
RESPIRATORY RATE
FIGURE 1
" ~ . '...x • e---e 150/min,r c -O.836 )to. . X---X IOO/min,r=-O.892 , X X",, •
" X 'X ........ ........
.... ---X -"1c-- ----------o ~~~---~~---~---~---~---~---~---~---~
o 30 60 90 120 150
PaC02 (torr)
FIGURE 2
160
might be related to completely different gas flows delivered to the patient if
different catheters or inspiratory durations are used. Tidal volume alone is also
not sufficient, if not related to the frequency used. We found the minute volume
to be the most useful parameter for adjustment of the ventilator. The volume
of gases delivered by the ventilator in a minute is dependent on 1. the driving
pressure, 2. the catheter size and 3. inspiratory time. Increase of each of
the three parameters will increase the delivered minute volume. Change in
frequency will not change the minute volume but will only divide it in smaller
tidal volumes.
2. TRANSPORT AND ELIMINATION OF CARBON DIOXIDE
The elimination of C02 during high frequency ventilation is minute
ventilation dependent. The higher the minute volume administered the better
C02 elimination will be. In other words, the product of frequency and tidal
volume is the primary determinant of C02 elimination during high frequency
ventilation. Therefore, we can say that the concept of alveolar ventilation is
valid also for HFV. With one qualification, namely that it applies even when
the calculated dead space is bigger than tidal volume.
The high frequency jet ventilator can be considered a flow interrupter.
Therefore, the higher the frequency used the smaller the tidal volumes delivered
but the total flow per minute is unchanged if other parameters remain constant.
If we observe the PaC02 during high frequency jet ventilation at frequencies
between 100 and 600 breaths per minute (Fig. 1) we will see that there is an
increase in arterial PC02 with increasing frequencies. That means that with
higher frequencies the same minute volume is not sufficient. At the same
frequency we can change the level of respiratory support by changing the driving
pressure (Fig. 2). The higher the driving pressure we use, the lower the PaC02
will be. If we compare (Figure 3) the minute volume needed at different
4.0
-~ 3.0 .a -'" '" ~ 2.0
Q.
C' c > \.. 1.0 o
.. , I .,
I " I~' I '\ I \' , " • , .
" "
o ° .,
" ' .. -- ... ......... ~-- .... --.: .......
o. \ -.. • ·0 e. e. -.. -.. -.. . .. e. .. .. . .. -.... . ...
o.
161
- 100/MIN --- 150/ MIN . ...... 250/ MIN
". ..
O.O~--~----~----~--~----~----~--~
o 20 40 60 80 100 120 140
PaC02 (tor r)
FIGURE 3 PaC02
1.0 40torr PaC02 50 torr
.8 60torr
01 70torr ~
"- SOtorr G) .6 E ~
0 > G)
.4 -~ c ::::e
.2
o ~~L-__ L-__ L-__ L-__ L-__ L-__ L-__ L-~~~
50 100 150 200 250 300 RR/min
FIGURE 4
162
frequencies, we will see that a higher minute volume is needed to achieve the
same level of arterial carbon dioxide at higher frequencies. The nomogram in
Figure 4 shows that with increasing frequency the same gas exchange can be
achieved simply by increasing the driving pressure (i.e. minute volume per kilogram
of body weight).
3. OXYGENATION
Even in high frequency ventilation, the oxygenation depends predominantly
on mean airway pressure. In our studies on anesthetized dogs with oleic acid
injury (2) we could show that mean airway pressure is similar to the mean airway
pressure during conventional ventilation. As Figure 5 indicates, the same mean
airway pressure can be achieved during high frequency ventilation with much
lower peak airway pressure. Superimposing the curves of airway pressures
generated by conventional ventilation and by high frequency jet ventilation
demonstrates why mean airway pressure remains the same. Peak airway pressure
is lower during inspiration, but fluctuates higher during the period when in
conventional ventilation the pressure during exhalation decreases.
The results also showed that the mean airway pressure can explain only
about 70% of the changes in oxygenation and that the pressure pulse (i.e. peak
minus PEEP pressure), in other words the tidal volume has additional influence.
That could explain the importance of sighing to prevent collapse of alveoli which
are under lower pressure during high frequency ventilation.
4. CONCLUSION
The gas exchange in high frequency ventilation is after all not so different
from conventional ventilation. Most of it can be explained by the concept of
alveolar ventilation and mean airway pressure. The adjustment of ventilatory
parameters can then be logically explained and needed corrections for different
163
frequencies can be made. The only difference is that we have to acknowledge
that mixing of gases occurs also in conductive airways so that the dead space
serves not only for transport but also for mixing of respiratory gases.
20 16
Powl2
51 HFJV (IIJ CV
torr ~""""'...o.MIiIollllllllllllll I sec,
FIGURE 5
REFERENCES
1. Klain M, Smith RB: High frequency percutaneous transtracheal jet
ventilation. Crit. Care Med. 5(6): 280-287, 1977.
2. Schuster DP, Klain M: High frequency ventilation during acute lung injury. Anesthesiology 55(3): A70, 1981.
GASANALYSIS BY MASSSPECTROMETRY DURING HIGH FREQUENCY
VENTILATION
G. ROLLY and L. VERSICHELEN
High frequency ventilation (HFV) techniques are nowadays
more and more used in experimental and clinical set-ups and seve
ral devices for HFV have become available. Some are claimed
to give a volume controlled ventilation, without air entrain
ment and others are seemingly functioning as a jet injector,
inducing admission of a certain amount of ambient air to the
injected gasmixture. It is self evident that the oxygenation
of the patient can greatly be influenced by the amount of air
entrained. Furthermore the measurement of endtidal CO2 by
sampling at the end of the endotracheal tube during HFV does
not reflect the paC0 2 value and the efficiency of alveolar
ventilation anymore.
To gain better insight in the dynamics of gas exchange
during HFV, the present study was undertaken.
TECHNIQUES
A CentronicR massspectrometer, specially adapted for
anaesthetic gases, was used as it permitted simultaneous
measurement and recording of up to 8 gases. 02' N2 , Argon,
CO 2 and when appropriate N20 concentrations were analysed.
A long small bored catheter was used, permitting gas sampling
at the lower part of the trachea. This flexible catheter was
fixed at the outer wall of the endotracheal tube, the termi
nal end being distal from the tube tip or was slided through
the tube. In some cases an endotracheal tube was used with
a built-in sampling line. When no endotracheal tube was in
165
place, but instead a naso-tracheal insufflation catheter, the
sampling catheter was again fixed to this one, the tip ending
distally.
For sake of convenience, measurements were made on pa
tients anaesthetised by i.v. techniques. In some patients
arterial blood was sampled for bloodgas measurements permit
ting the analysis of the efficacy of HFV.
The effects of ventilatory patterns were studied with
1) an AGA BRONCHOVENTR at a fixed standard frequency of
60/min. and at an inspiratory time of 22 % and 2) an ACUTRONICR
MK 800, at various frequencies. Hundred % O2 was always used
as injecting gas, permitting easy recognition of any air en
trainment (N 2 measurement) .
DRONCHOVIENT
M.P ......... V.
Fig. 1. N2 washout, after connection of Bronchovent via
nasa-tracheal catheter to the patient (at the extreme
left sampling of ambient air) .
166
RESULTS
After application of HFV via a special naso-tracheal
catheter, connected to the Bronchovent, N washout of the pa-2
tient occurs immediately and from than on only a trace amount
of N2 can be recorded (Fig. 1). The Bronchovent ventilator
induces no air entrainment, when a naso-tracheal catheter is
used and functions as a pneumatic valve, as claimed by
Sjostrand permitting true HFPPV at a standard frequency of
60/min. The CO2 concentration recorded permits reliable judg
ment of the depth of ventilation.
When a naso-tracheal catheter is in place, no air entrain
ment is present independent of the HFV apparatus used (Broncho
vent or Acutronic) or of the frequencies used (60 to 600/min.),
so the N2 concentration recorded is virtually zero (Fig. 2).
_IIIEIT I ACUT.IIIC (°2 100 %) IA8AL CATHRTB.
It; C... I. I. 108 200 - ___ " .. fNNtNNfIVW, i AIM I, ,IN"
7.53 7.56 7.55 1.52 1.43 7.36
565 491 575
31
3 3 2.5 1.5 1 1
.J ~Moeac~A"!laa~'"
Fig. 2. Absence of air admission (N 2) when using a naso
tracheal catheter.
-7.30
1
167
This is also reflected in the high but expected values of
Pa0 2 • With progressive increase of frequencies at an insuf
flation time of 20 %, without adapting the insufflation vo
lume, an increase of paC02 , and most importantly a pronounced
increase of the gradient between arterial and measured end
tidal CO2 concentration are noticed. The FAC02 calculated
out of the recorded tracings, is not at all representative
for judging the efficacy of ventilation, as it decreases with
increasing frequencies.
When the Acutronic is connected to an endotracheal tube
by means of a T piece pierced by an AngiocathR as injecting
catheter, air entrainment is always present (Fig. 3). The
apparatus functions as a jet ventilator (HFJV). This is al
ready understandable by looking at the principle of the in
jection through a small bored needle, into a larger space
(venturi effect) • Air entrainment is highest with lower
CP. ACITROIIC
80
143
361
28
137
208
489
42
3.5
311 408
Fig. 3. Air admission (N2) when HFV connected via a T piece and Angiocath.
168
(60-100/min.) frequencies (30 % N2) and lessens with pro
gressively higher (300-400/min.) frequencies (10 % N2). This
is evidenced in the pa0 2 values which are higher at increased
frequencies, but overall the values are lower than when a
naso-tracheal catheter is used. The CO 2 gradient is increa
sing with higher frequencies and again FAC02 is no more re
flecting the adequacy of ventilation at the highest frequencies.
When the Acutronic is directly connected to a special
endotracheal tube (MallinckrodtR Hi-Lo jet insufflation tube),
provided with a particular insufflation line through which
the injection is done, again air is entrained (Fig. 4) and
the Acutronic functions as a HFJV apparatus. This air entrain
ment (N2 measurement) is variable and is least at the highest
frequencies. Ac=ordingly Pa0 2 is highest in these situations.
The CO2 gradient is high and greatest with higher frequencies.
FAC0 2 is low and unreliable at high frequencies.
IALLINOIlROOT
%1: ..... _ 4111
... ·1'.G 1'.11 1'.11' 7.G 7.37 ~'" ... ,
1 .. ~~ !:l~U~t" ~i! .111111 11
'" - ', .. '
ilL~~ !,~t· '.";.;:.
I·' .' ',: ,1 " '1"
401 382 415 412 492
33 20 23 37
1.5 1.25
Fig. 4. Air admission (N2) when HFV connected via a Mallinck
rodt injection tube.
169
When the Acutronic is connected to another patient's
endotracheal tube by means of a T piece and an Angiocath and
a wide range of ventilatory frequencies is used, it can be
seen that air entrainment is lowest at highest frequencies
and it increases with lesser frequencies, but a ceiling effect
is present from 100 cycles/min. on, down to 20/min. (fig. 5).
This is also reflected in the measured pa0 2 values. FAC02 is
again lowest and the CO 2 gradient highest at highest frequen
cies. Seemingly the problem of air entrainment is greatest
at lower frequencies (20 - 100/min.) and somewhat lesser at
higher frequencies (200 - 400/min.) but it is the reverse for
the high CO2 gradient and unreliable FAC0 2 .
AceTI.le (Oa 100~) T ... 808 + ANOIGOATH c..ZI U II • .. III
iar 1.41 ' t~ 7.2, 7.22 .. '300' 433i 488
• 25 ,32 42 59 4' 3.6 :us :2:.5 t25
:"J, 'i ! 1~. ~ ,
~t'MMMa!M~lMI III (IIIIIIHNI_II
Fig. 5. Air admission (N 2) when HFV connected via a
T piece and Angiocath.
.. 123
523
t25
>Itt' hMt!)t':f:".~
170
In clinical intensive care practice one side of the T
piece can be connected to a continuous flow of breathing gas
for patients presenting partial spontaneous breathing. When
a low flow of 100 % 02 is connected to one side of the T piece,
the other end open to the atmosphere, air entrainment (N2) is
greatly reduced during HFJV (Fig. 6). When instead a high
flow of a 50 % °2/50 % N20 mixture is given, N2 disappears
almost completely but N20 concentration is nevertheless only
marginal. The amount of air entrainment is dependent on the
fresh gas flow given at one end of the T piece.
IC.Tlllle 10:z 100 III I
SIDE INLET AIR AIR AIR
% CPM 211 !II 6. -- ... ,-----,,-~ .
o
TPlI!CB O:z 6.
+ INGIOCATH 0:z/N:fJ • ~
¥
"
0:z/N:fJ 211
~
f't~rI' ;'Ii.\\\\+"i'*'~;;l:,jlW ........... I,".11iIIt
Fig. 6. Influence of side inlet gas flow on air admission (N2).
When an 02/N 20 blender is used for the driving force to
the Acutronic, connected to a Mallinckrodt tube, and set at
171
a 50 % °2/50 % N20 mixture, a 30 % N2 concentration is evi
denced as air entrainment (Fig. 7). When the inspiration
time is changed from 30 % to 20 %, it is noticed that air en
trainment is less. Seemingly a higher inspiration time induces
higher air entrainment.
Fig. 7. Influence of driving gases and of inspiratory time on air admission (at the extreme left, change from 100 % 02 to 50 % °2/50 % N20) .
Summarising, at all frequencies injection through a naso
tracheal catheter induces no air entrainment; injection both
through the special injection line of the Mallinckrodt tube and
through" the Angiocath pierced in the T piece, provokes air en
trainment. The recorded N2 concentrations are less at highest
frequencies but are more important at lower frequencies, al
though a ceiling effect is noticed at lowest frequencies.
At a frequency of 60/min. or less at all modes of injec
tion, a normal FAC02 tracing can be recorded, but at higher
frequencies FAC02 is unreliable as these values are too low,
probably due to technical disturbances or to abnormal or yet
uncompletely understood gasdynamics.
DIGITAL VENTILATION
M.Wendt,L.Freitag,F.Dankwart
The rapid development of respiratory therapy techniques in
the last lS years might have come to a standstill.Conventional
ventilators are safe, easy to handle and useful in most cases
of respiratory failure. Nevertheless this form of ventilatory
support has shown its limitations so that a lot of clinicians
and engineers have been looking for new ways.High frequency ventilation is going to be an important tool in several IeUs. In contrast to conventional respirators the high frequency ventilators are usually working with open systems,not calibrate
tidal volumes,very high working pressures with lower airway pressures and without any feed back from the lung to the venti= lator.The most common high frequency ventilator for experiment a
purposes is the piston pump oscillator.This device creates sinusoid pressure waves inside the lung.Mean airway pressure
is low and in a wide range independent from the frequency.
One great advantage is the fact that the same volume is sucked
out which has been pressed in during the former foreward
movement of the piston. The main disadvantage for clinical requirements is the difficulty to regulate the ventilator.
To change for example the tidal volume you have to stop the motor and need a screw driver. In combination with a conventiona respirator for mucolysis the piston pump might play an importan role in the future,as a stand-alone respirator for the treatmen" of adult patients it will hardly be suitable.More popular are
the high frequency jet ventilators.Most of the devices interrup
a high pressure gas stream with a solenoid valve. The t-piece
technique allowes the use of a conventional tracheal tube.
The frequency is limited because the expiration depends on
the elastic retraction forces of the patient's chest.At higher
frequencies a PEEP-effect is unavoidable. Controlling tidal
173
volumes is rather simple by changing the working pressure and/ or the I:E ratio.
Thus on today's market three different forms of ventilation
are in competition. Conventional mechanical ventilation (CMV),
high frequency oscillation (HFO) and high frequency jet venti= lation (HFJV) have there individual advantages and indications.
It seems to be impossable to change from one characteristical
ventilatory pattern to another without changing the machine. There is no manufacturer offering a universal respirator.
in the last years we have developed a new ventilator that is suitable for all known forms of respiratory support.We have to
apologize for creating a new name for this technology.It is called Digital Ventilation,not only because the respirator is digitally controlled .In contrast to analogly working CM venti= lators the solenoid valves of a jet respirator are either completely closed or completely open. The digital ventilator
uses the fact that an increasing pulse time of a jet ventilator results in a PEEP effect and also in a higher mean airway pressure. The intrathoracical volume is also increasing, becoming
a function of the duty cycle.If the jet-pulse frequency is high enough, the big inner compliance of the bronchial tree acts as an integrator of the volume pulses. The lung reacts like a Digital
Analog Converter and the pressure volume responses to the jet
pulses of for example 30 Hz inside the chest look rather "normal". If the solenoid valve of the jet ventilator is controlled by
a generator which can be independently adjusted in frequency and
pulse width one can program a lot of new forms of ventilatory pattern. Picture 2 shows the application of a so called "mixed mode".Line Z below the ECG shows the electrical signal coming
from the generator. The following lines are registrations of the resulting volume (measured by transthoracical impedance), expired COz,airway and pulmonary arterial pressures.The part of superimposed vibration in the slow sinusoid pressure changes depends on the ground frequency of the jet pulses.Realize that only one "either or" valve is working. The amplitude is adjusted by the difference between the lowest and the highest I:E ratio. Though this technique of pulse width modulation allows the
174
Picture The increasing pulse time of a jet ventilator results in a PEEP effect.The int~athoracical volume is also
increasing. Higher frequencies generate a near normal pressure
volume relationship
, , I I lIE<
GENERATOR ~!.~~ .... __ ................ _ ................ _ ........ ..... ___ ............... -"-"""" ... -------, ......... _-_ ......... _-_ ......... __ ........ --_ .... -------
£XPI.ED CO:z
Picture 2 The technique of pulse width modulation allows
the programming of every respiratory pattern. In this case
a sinusoid pressure wave form is generated for the ventilation of a 17 years old man with a thoracical trauma.
175
programming of a great variety of pressure shapes,there is
still a hidden flaw. Like all jet ventilators,also this digital
ventilator has frequency limits for flow dynamic reasons.
To use the advantages of the oscillatory devices we constructed
a special tube adapter with two built in jet cannulas blowing into opposite directions. There is a venturi effect to jet gas stream into and outside the tracheal tube.A complex electronical
circuit guarantees that both cannulas press in and suck out the same amount of gas.In this way the airway pressure can be kept zero or even negative if necessary. The flow of fresh and humidified gas getting into the adapter via a third opening flushes the system and can be used for CPAP or PEEP ventilation.
Picture 3
:ao-/ ! CMV , '-.
~ ~FO •• _ I
~,'\;\\\\, \jl/\I\\\ \,'\ \.~ =====::>" '-c: 1~ i
This picture shows the described adapter. Using this
adapter and a programmable generator all well known pressure
curves like HFJV,HFO and CMV can be applicated.
To fulfill clinical requirements the dimensions of the tube adapter have been chosen so,that spontaneous breathing, coughing and even suctioning is possible without any problems. Two
176
valves are necessary and the control of the frequency generator
is a task for a little single board computer. In the newest
version of a Digital Ventilator the most popular breathing
patterns are stored in an eprom so that this single machine
can imitate and replace all the different types of respirators
that have been described above.
The following registration (Picture 4) was made by switching
over from a conventional respirator to the Digital Ventilator
(arrow).After imitation of the former breathing pattern,
the software controlled machine switched over to HFJV and
later to HFO.Using the choosen frequencies,the blood gases
remained nearly unchanged,effects of the circulation could
not be measured.
Picture 4
See text.
lS
\ N~~~~~~~-~h ___ ~~~~~---~ __ ~~ __ ~~--~_~~~~~~~~~~ __ ~~~~_h
CAPNOGRAM
~'-/'\./' • I ' " \ I' ,', I "
"",,\,-' f,,' \ ' ~ [" - : :. "
- " \ . , I ~ '- •• , \
~~, r-----, ~r"r""-",·""-r,",r"-"t ( t"" "",n""U \ (\ " ,,'\ \'\J'".,' ,'J\',,' 1"',, •.
C02 BRONCH,V ~ ~ MAss SPECTROMETER
Comparison of conventional and Digital Ventilation.
With a computer controlled ventilator savety circuits can be
easily established. Closed loop techniques might be possible
in the future,and,as the software is the only limitation,the
Digital Ventilator might become a powerful tool for experimental
177
studies. Its main advantage is however that it could bring back
the single universal respirator.
Freitag L.,Wendt M.,Dankwart F. ,Lawin P. Digital Ventilation,
an approach to an universal ventilator.Vortrag,gehalten vor
der Association for the advancement of medical instrumentation (AAMI), 17th Annual Meeting 9.-12.5.1982 San Francisco
Freitag 1. ,Wendt M.,Dankwart F.,van Aken H.,Lawin P. Entwicklung eines Respirators und Monitorsystemes flir die High Frequency Ventilation.Vortrag ZAK 1981,15.-19.9.1982 Berlin
D. CLINICAL USE - PART I
ONE-LUNG HIGH-FREQUENCY VENTILATION FOR
INTRATHORACIC SURGERY
N. EL-BAZ, M.D., A. EL-GANZOURI, M.D., A. IVANKOVICH, M.D.
Conventional one-lung intermittent positive pressure
ventilation (OL-IPPV) through a single-lumen cuffed
endobronchial tube has proved to be a valuable technique
during anesthesia for thoracic surgery. This technique
was introduced by Waters in 1932 to prevent the
contamination of the intubated lung during the resection
of the upper infected lung (lung abscess, bronchiectasis,
empyema). Selective one-lung ventilation was also found
essential during major airway surgery. OL-IPPV also
provides optimal surgical conditions during pulmonary
resection and non-pulmonary intrathoracic surgical
procedures. Because OL-IPPV has been associated with
unacceptably low levels of oxygenation in a large number
of patients despite the use of 100% oxygen, the routine
application of this technique to improve surgical
conditions has been unjustified.
Although the hypoxic pulmonary vasoconstriction
reflex has been shown in animal studies to reduce blood
flow to the hypoxic collapsed areas of the lung, this
reflex does not function efficiently during the collapse
of one lung in humans under general anesthesia. This
causes a continuous, unaltered perfusion of the upper
collapsed lung and a large intrapulmonary shunt (Qs/Qt)
measured between 21 to 65% of cardiac output during
OL-IPPV. In addition, Qs/Qt was also found to increase
progressively during OL-IPPV as a result of progressive
development of microatelectasis and ventilation perfusion
abnormalities in the dependent ventilated lung. This led
179
to the evaluation of OL-IPPV at large tidal volumes,
prolonged inspiratory times, and with positive
end-expiratory pressures (PEEP) to improve the
ventilation/perfusion ratio and to prevent the development
of microatelectasis in the dependent lung. Nonetheless,
these techniques were associated with an increase in mean
airway pressure, intra-alveolar pressure, and pulmonary
vascular resistance of the ventilated lung, causing a
significant increase in blood flow through the upper
collapsed lung (shunt), and arterial oxygen desaturation.
Because of this direct relationship between the mean
intra-alveolar pressures in the dependent lung and
perfusion of the upper collapsed lung, we evaluated the
effect of high-frequency ventilation (HFV) at low airway
pressure on shunting and oxygenation during one-lung
ventilation. The technique of high-frequency ventilation
is based on the administration of a small tidal volume at
a high respiratory rate into an open valveless circuit.
HFV has been shown to provide adequate alveolar
ventilation and oxygenation at low mean and peak airway
pressures. Intrapleural pressure was also shown during
HFV to remain continuously negative, causing minimal
impairment to the pulmonary and systemic circulations.
!~~!~!~Q_~~=~~~g_~!g~=~!~9~~~~~_~~~!!!~!~~~_iQ~=~~2~ OL-HFV was ini.tially evaluated in 30 patients during
a variety of intrathoracic procedures (lobectomy,
pneumonectomy, and esophagectomy). Anesthesia was induced
180
in these patients with thiopental 4 mg/kg, and muscle
relaxation was achieved with pancuronium 0.2 mg/kg. The
appropriate bronchus was intubated under direct vision
(Stortz rigid fiberoptic bronchoscope) with an 8.0 mm ID
single-lumen cuffed endobronchial tube. One-lung
ventilation was established with 100% oxygen and each
patient was placed in the appropriate lateral position for
thoracotomy. Anesthesia was maintained in these patients
with IV morphine I to 2 mg/kg and IV diazepam 0.5 - 1 mg/kg. After the pleura was opened, each patient received
OL-IPPV for 45 minutes at a respiratory rate of 12
breaths/min, tidal volume of 10 ml/kg. This was followed
in each patient by another 45 minutes of OL-HFV of the
same lung at a frequency of 150 breaths/min, driving gas
pressure (DGP) 25 psi, and inspiratory time percentage
(IT%) of 40%. Arterial (radial) and mixed venous
(pulmonary artery) blood samples were taken
simultaneously, after each period of ventilation, for
blood-gas analysis and calculation of Qs/Qt.
Our application of OL-HFV after 45 minutes of OL-IPPV
was associated with a significant increase of mean Pa02 and a lower Qs/Qt for all patients.
ONE-LUNG VENTI LA TION FOR THORACIC SURGERY
OL-IPPV OL-HFPPV
Respiratory Rate 12 breath/min 150 breath/min
Pa02mmHg 146 (41-340) 189 (85-420)
PaC02mmHg 38 (32-48) 34 (28-41)
as/at % 32 (17-59) 21 (9-39)
Pa02 below 17 Patients 5 Patients 100 mmHg (57%) (17%)
Os/Ot above 19 Patients 8 Patients 35% (63%) (27%)
PV02mmHg 41 (31-49) 52 (38-61)
OL-HFV was associated with a significant improvement
of oxygenation and reduction of Qs/Qt in 24 patients
(80%), no significant change in 3 patients (10%), and
slightly lower Pa02 and increased Qs/Qt in 3 patients
(10%). Seventeen patients (56%) had an unacceptably low
Pa02 (below 100 mmHg) during OL-IPPV. This was
significantly reduced after establishment of OL-HFV to 5
patients (17%). Table 1 summarizes the results:
This significant improvement of oxygenation and
reduction of Qs/Qt during OL-HFV is the result of an
improvement of gas distribution matched with increased
perfusion of the dependent lung. The low airway and
intra-alveolar pressures during HFV minimally interfered
with the gravity-dependent pulmonary blood flow, causing
the preferential perfusion of the dependent ventilated
lung. This increase in perfusion was also matched with
efficient gas mixing and uniform gas distribution
characteristic of HFV, with significant improvement of
oxygenation in 80% of our patients.
181
Although OL-HFV was associated with a significant
improvement in gas exchange through the dependent lung and
the elimination of the risk of hypoxemia in 12 patients, a
small number of patients (17%) continued to maintain an
unacceptable Pa02 below 100 mmHg during OL-HFV. This
led us to modify the technique of one-lung high-frequency
ventilation to allow for some gas exchange through the
182
upper collapsed lung without compromising the surgical
advantages of one-lung ventilation.
~~~!!!~~_~~~=~~~~_~!~~=~!~9~~~~~_~~~!!!~!!~~_i~Q~=~~2 MOL-HFV is based on the administration of HFV through
an UNCUFFED endobronchial tube to allow for continuous
outflow of gas from the intubated bronchus into the carina
and trachea. This technique was developed on the basis of
our observation of blood gases, and the size of the upper
lung during our evaluation of one-lung HFV through a small
catheter for major airway surgery.
The inefficient function of the hypoxic pulmonary
vasoconstriction reflex in humans under general anesthesia
causes a continuous unaltered perfusion of the upper
collapsed lung. Although the attempt to reduce blood flow
to the collapsed lung by placement of a Swan-Ganz catheter
into the appropriate pulmonary artery for mechanical
narrowing by continuous inflation of the balloon has been
ineffective, surgical clamping of the appropriate
pulmonary artery has been shown to improve oxygenation
significantly and to reduce Qs/Qt during OL-IPPV. Because
of the difficulties and risks of clamping the pulmonary
artery, efforts have been made to utilize the upper
collapsed lung to participate in gas exchange and improve
oxygenation during OL-IPPV. Oxygen insufflation into the
collapsed lung at zero airway pressure during OL-IPPV was
initially evaluated. Although the results of this
1~
technique are controversial, oxygen insufflation at a
continuously positive airway pressure (CPAP) between 5 to
15 cm H20 has been shown recently to be effective in
improving oxygenation during OL-IPPV. Nonetheless, this
high CPAP was also found to cause progressive inflation of
the collapsed lung and impairment of surgical access.
Improvement of oxygenation during one-lung ventilation can
also be achieved with periodic two-lung ventilation
alternating with OL-IPPV, or abandonment of one-lung
ventilation and the re-establishment of conventional
two-lung ventilation.
In an effort to improve oxygenation and at the same
time to maintain the surgical advantages of one-lung
ventilation, we developed and evaluated the new technique
of MOL-HFV in 40 patients aged between 24 and 79 during a
variety of intrathoracic surgical procedures. Anesthesia
was maintained in these patients with morphine 1 to 2
mg/kg, diazepam 0.5 to 1 mg/kg and pancuronium 0.1-0.2
mg/kg. The appropriate bronchus was intubated with 'an 8.0
mm single-lumen cuffed endobronchial tube. Accurate
positioning of the tube was achieved under direct vision
through a rigid fiberoptic bronchoscope (Stortz) placed
inside the tube. All patients were placed in the
appropriate lateral position for a thoracotomy. After the
pleura was opened, each patient received a sequence of
OL-IPPV, OL-HFV, and MOL-HFV. Each modality was used to
ventilate the same lung under the same conditions for
periods of' 30 minutes, each patient serving as his own
control.
Isolated OL-IPPV was administered at a respiratory
rate of 12 br~aths/min and a tidal volume of 10 ml/kg for
30 minutes. Isolated OL-HFV (cuff inflated) was
administered at respiratory rates of 250 breaths/min at a
driving gas pressure (DGP) of 25 psi, and an IT% of 40%
for another 30 minutes. This was followed by the
DEFLATION of the cuff of the endobronchial tube (no
184
isolation) and lowering of the driving gas pressure of HFV
to 15 psi for the administration of MOL-HFV for another 30
minutes. Arterial and mixed venous blood samples were
taken simultaneously after each period of ventilation for
gas analysis and calculation of Qs/Qt. Surgical
interruption of the blood flow to the collapsed lung was
delayed until the completion of the study. All patients
were ventilated with 100% oxygen to minimize the effect of
ventilation/perfusion abnormalities in the ventilated
dependent lung.
593 600
525
500 450
400 369
Pa02 mmHg 300
213 200
139 100 126
89
0 43
60 60
50 44
40 39
OslO! 32
... 30 23
20 16
10 13 10
7 0
I I I OL-IPPV OL-HFV MOL-HFV
ONE-LUNG VENTILATION
We have found that oxygenation improved significantly
after the substitution of HFV for conventional IPPV during
isolated one-lung ventilation (cuff inflated). The number
of patients with unacceptably low Pa02 (below 100 mmHg)
185
was also significantly reduced during OL-HFV, as was shown
in our previous study. The use of MOL-HFV in these
patients, however, achieved the highest Pa02 in all
patients with the successful elimination of the risk of
hypoxemia. MDL-HFV also achieved a Pa02 above 100 mmHg
in those patients with an unacceptable Pa02 during the
periods of OL-IPPV and OL-HFV. 40
30
20
_ Patients with OslO! above 35%
_ Patients with Pa02 below 100 mmHg
23
o 0
100%
58% 53%
25%
18%
o 0% Ol-lPPV Ol-HFV MOl-HFV
ONE - LUNG VENTILATION
HFV is based on the administration of a small tidal
volume, at high velocity, into an open valveless system.
Although deflation of the endobronchial tube cuff does not
influence the efficiency of gas exchange during HFV, this
allows a continuous outflow of gas from the intubated
bronchus through the trachea, larynx, and mouth. This
continuous eddy flow of gas at the carina was found to
generate a low level of continuous positive airway
pressure (CPAP) measured in this group of patients at
between 0.5 to 1.5 cm H20. Although no significant
iticrease in the size of the coll~psed lung results, this
low CPAP successfully recruites some alveoli in the collapsed lung to participate in gas exchange, with
significant improvement of oxygenation. The difference
186
between the Pa02 during MDL-HFV compared to OL-HFV is
the result of oxygenation accomplished through the upper
collapsed lung.
These studies have shown that the substitution of HFV
for conventional IPPV increases the margin of safety of
isolated one-lung ventilation, which is mandatory during
the excision of an infected lung with cavitation.
MOL-HFV through an uncuffed endobronchial tube was
also shown to eliminate the risk of hypoxemia and maintain
the surgical advantages of one-lung anesthesia for routine
intrathoracic surgery. In addition, the use of a small
uncuffed endobronchial tube for MDL-HFV is less traumatic
to the airways and avoids the problems and complications
of double-lumen tubes. We have also found MDL-HFV through
a small tube valuable for one-lung ventilation in young
children. We believe the alternative use of MOL-HFV for
routine intrathoracic surgery will increase the safety and
applications of the valuable technique of one-lung
anesthesia.
REFERENCES
1. Torda TA, McCullock CH, O'Brien HD, et al: Pulmonary venous admixture during one-lung anaesthesia. Anaesthesia; 29:272-279, 1974.
2. Khanam T, Branthwaite MA: Arterial oxygenation during one-lung anaesthesia. Anaesthesia; 28:280, 1973.
3. Kerr JH, Crampton-Smith A, Prys-Roberts C, et al: Observations during endobronchial anaesthesia II: Oxygenation. Brit J Anaesth; 48:48, 1974.
4. Thomas DF, Campbell D: Changes in arterial oxygen tension during one-lung anaesthesia. Br J Anaesth; 45:611-616, 1974.
5. Sjostrand U: Review of the physiological rationale for and development of high-frequency positive-pressure ventilation-HFPPV. Acta Anaesthesiol Scand (suppl); 64:7-27, 1977.
6. Sjostrand UH, Ericksson IA: High rates and low volumes in mechanical ventilation - not just a matter of ventilatory frequency. Anesth Analg; 59:567-576, 1980.
7. EI-Baz N, EI-Ganzouri A, Gottschalk W, Jensik R: One-lung high frequency positive pressure ventilation for sleeve pneumonectomy: an alternative technique. Anesth Analg; 60:683-686, 1981.
187
8. Slutsky AS, Brown R, Lehr J, et al: High-frequency ventilation: a promising new approach to mechanical ventilation. J Med Instrumentation; 15:229-233, 1981.
9. EI-Baz N, Jensik R, Faber LP, et al: One-lung high frequency ventilation for tracheoplasty and bronchoplasty, a new technique. Ann Thorac Surg 34:564-571, 1982.
10. EI-Baz N, et al: One-lung high frequency positive pressure ventilation for intrathoracic surgery, Anesth Analg, 61:180-181, 1982.
11. Mathers J, Benumof JL, Wahrenbrock EA: General anesthetics and regional hypoxic pulmonary vasoconstriction. Anesthesiology; 46:111, 1977.
12. Benumof JL: Mechanisms of decreased blood flow to atelectatic lung. J Appl Physiol; 46:1047-1048,1979.
13. Hill TR, Finley TN, Takamura HJ, et al: The effect of inflation pressure in the contralateral lung on blood flow through an atelectatic lung in the dog. Fed Proc; 21:108,1962.
14. Cap an LM, Turndorf H, Chandrakant P, et al: Optimization of arterial oxygenation during one-lung anesthesia. Anesth Analg; 59:846-851, 1980.
15. Alfrey DD, Benumof JL, Trousdale FR: Improving oxygenation during one-lung ventilation in dogs: the effect of positive end-expiratory pressure and blood flow restriction to the nonventilated lung. Anesthesiology; 55:381-385, 1981.
16. El-Baz N, et al: One-lung high frequency ventilation through a small uncuffed tube for lung surgery, J Cardiovasc Surg December, 1982 (in press).
17. Katz JA, Laverne RG, Fairley HE, et al: Pulmonary oxygen during endobronchial anesthesia: effect of tidal volume and PEEP. Anesthesiology; 56:164-171, 1982.
HIGH FREQUENCY INSUFFLATION TECHNIQUE DURING ENDOLARYNGEAL
MICROSURGERY
L. VERSICHELEN*, G. ROLLY* and H. VERMEERSCH**
INTRODUCTION
An adequate ventilation technique for laryngeal micro
surgery should permit a clear view of the larynx, provide
the ENT-surgeon with a maximum working space, and prevent
the potential hazards inherent to the use of the laser beam
in the presence of more than 21 % 02' such as ignition of
the tube and tracheal and pulmonary burns. For these reasons
we have chosen to perform this type of intervention while
using the high frequency ventilation technique and only air
as insufflation gas (1,2,3). It uses smaller tidal volumes
and much higher rates than conventional methods. This results
in a better alveolar gas exchange (4,5). Moreover, there is
less chance of depressing the cardiovascular system, since
the airway pressure is continuously kept positive with low
peak pressures (6). The present report evaluates in detail
the clinical application and the respiratory parameters
(P02 and PC02) of this new type of ventilation.
Initially we have used the AGA BRONCHOVENTR (7,8).
Since 1981 we have added the ACUTRONICR high frequency jet
ventilator to our equipment.
PATIENTS Sixty-six unselected patients were anaesthetised for
diagnosis and treatment of laryngeal and tracheal disorders.
State University of Ghent (Belgium) * Depa.rt::nent of Anaesthesia (Dir. Prof. Dr G. roLLY)
xx Depart:rrent of otorhinolaryngology (Dir. Prof. Dr P. KLUYSKENS)
189
Out of the 66 patients, 56 were ventilated with the R
AGA BRONCHOVENT at a standard frequency of 60 per minute
and a relative insufflation time of 22 % of the ventilatory
cycle. For intubation and endotracheal insufflation a small
bored nasotracheal catheter was used. Side holes at its
distal end have a dual advantage. They prevent not only
the entrainment of air, but provide also a continuous upwards
directed gas flow which prevents the aspiration of blood and
tissues pieces, while enhancing the evacuation of fumes du
ring laser interventions. The expiration takes place through
the open larynx, around the small catheter. Minute volume
is calculated according to the special appropriate ventila
tion nomogram for the Bronchovent.
The other 10 patients were ventilated with the ACUTRONICR
high frequency jet ventilator, type MK 800 at a ventilatory
frequency of 400 per minute. This rate was prefered over
the frequency of 200 - 300 per minute, since inconvenient
vibrations of the vocal cords occur. This obviously is less
advisable during surgical micromanipulations. A preliminary
trial indicated that a relative insufflation time of 20 %
yielded the best operation condition for the surgeon. Again
a special appropriate nasotracheal catheter with side holes
at its distal end was used for insufflation and intubation.
Arterial blood gas tensions were used as criteria for judging
the adequacy of ventilation.
Age, weight, length and duration of anaesthesia and sur
gery are shown in Table I. The indications for laryngeal mi
crosurgery are shown in Table II.
ANAESTHESIA TECHNIQUE
The evening before operation the patients received lora
zepam (TemestaR) 2.5 mg by mouth. Premedication consisted
of ThalamonalR (fentanyl 0.1 + dehydrobenzperidol 5 mg) or
pethidine according to patients' condition, and atropine 0.01
mg/kg given i.m. 45 minutes before the start of anaesthesia.
190
BRONCHOVENTR ACUTRONICR
n 56 10
if 39 5
~ 17 5
Age y. 45.3 + 2.6 54.2 + 5.8 - -( 6 - 79 ) ( 10 - 72 )
Weight kg 63.5 + 1.9 66.8 + 5.7 - -( 22 - 90 ) ( 28 - 96 )
Length cm 166.7 + 1.6 161.4 + 3.7 - -(122 - 186) (135 - 175)
Anaesth.dur. min. 31.3 + 1.7 41.5 + 2.6 - -( 20 - 60 ) ( 30 - 60 )
Surg. duro min. 22.3 + 1.9 31.0 + 2.7 - -( 5 - 50 ) ( 20 - 50 )
Table I. Anthropometric data and duration of anaesthesia
and surgery (Mean + SEMi range between brackets) .
Laryngeal papillomatosis 14
Granulation tissue resection 7
Glottic web 4
Vocal cord polyp 4
Vocal cord resection 1
Edema post radiation 3
Arytenoidectomy 2
Cordectomy 1
Ectopic thyroid of tongue 1
Cyst in the vallecula 1
Lymphangioma tongue 1
Angioma 2
Diagnostic laryngoscopy 25
Table II. Indications for laryngeal microsurgery.
191
Under local anaesthesia radial artery catheterisation
was performed. Anaesthesia was induced with etomidate
300 ~g/kg and a continuous infusion at a rate of 30 ~g/kg/min.
Alfentanil was given in a starting bolus of 40 ~g/kg and
later-on in increments of 15 ~g/kg according to clinical
parameters of bloodpressure and heartrate.
One minute before induction pancuronium bromide
(pavulonR) 1 mg was given in order to prevent muscle pain
due to succinylcholine. Succinylcholine was given in a do
se of 1 mg/kg allowing the placement of a nasotracheal ven
tilation catheter and later-on in increments of 25 to 50 mg
according to necessity.
In the present study the patients were ventilated with
100 % O2 , except during laser microsurgery when air was used.
Starting values of systolic and diastolic bloodpressure,
heartrate and bloodgases were taken preoperatively while the
patient was breathing room-air and every 5 to 10 min. during
HFV and at the end of surgery, while the patient was awake
and breathing room-air. Systolic and diastolic bloodpressu
res and heartrate were measured using the DinamapR and auto
matically recorded.
RESULTS
Systolic and diastolic bloodpressures and heartrate
(Mean ~ SEM) are shown in Fig. 1. After induction of
anaesthesia and start of HFV with 100 % O2 (I), some de
crease of systolic bloodpressure and heartrate was noticed
in both groups(decrease of systolic bloodpressure : p ~ 0.05
or p ~ 0.02). During HFV with air (II, III, IV) systolic
bloodpressure tended to rise towards the preanaesthetic va
lues and even surpassed them after awakening.Diastolic blood
pressure showed only minor variations. Heartrate changes
were moderate in both groups.
192
ENDOLARYNBEAL MICROSURBERY. H.F.V.
mmHg 1711
150
1211
100
75
50
b/rnln
• pc 0.05
... pc 0.02 MEAN t5.E.M. ~ BRONCHOVENT
c:::::J ACUTRONIC
5yst. B.P.
Diest. B.P.
']iI~tll1ll~ Heart rate
Pre anaesthesia , ii' 1 ]I m III
I 100 % 02 Awake
L du,lngH.F.V. (Inte,val 5-10 min) .J
Fig. 1. Cardiovascular parameters at the different examina
tion moments (Mean + SEM) .
The results of bloodgas measurements are shown in
Fig. 2. During the 100 % oxygen HFV (I) the Pa0 2 increase
was highly significant (p <: 0.02) in both groups. During
air ventilation (II, III, IV) pa0 2 decreased, but was still
significantly increased at some moments compared to the
preanaesthetic moments. This probably reflects the not
yet completely accomplished 02- washout of the body.
Pa02 increased again when switching HFV to 100 % 02' The
postanaesthetic Pa0 2 values when breathing spontaneously
were higher (p<:0.02) than the preanaesthetic ones, as the
patients received 02 by mask.
mmHg 420
400
32
300
280
100
80
60
40
H.F.V. ~ BRONCHOV E NT
MEAN! 5.E.M. c:::J ACUTRONIC
Pae,
~ ~hl
lrn1rim'm~~m PaCe,
Pre anaesthesia i 100 % 02 Awake
Lduring H.F.V. (interval 5-10 min) .....
Fig. 2 Bloodgas measurement at the different examination
moments (Mean + SEM) .
193
D~ring HFV paC02 values were never in an abnormal range
and they decreased significantly (p ~ 0.02) in both groups
compared to the awake values; these preanaesthetic values were
however moderately high in this group of patients with respi-
ratory disturbances. pH r standard bicarbonate and base
excess are shown in Fig. 3. These parameters were in the
normal expected range throughout the different examination
periods.
194
ENDOLARYNGEAL MICROSURGERY. H.F.V. "Pca.os ~ BRONCHOVENT
~t .... p c a.o2 MEANt S.E.M • c::J ACUTRONIC
UB I 136
tl ~ ~ 7.34 fl m pHa
U2 rtl no mEq/1
'l 24
23
~ lID ~ ~ 22
~ ~ Stand.
m Blc. 21
20
mEq/1
-~~ -2 m ~ t; f1fl ~ fitl Base
-3 ~ Excess
-4
I i I , , Preanaesthesla I ]I m III 100%0 2 Awake
~durlng H.F.V.(lnterval 5-10mln) ..J
Fig. 3. Acid-base balance at the different examination
moments (Mean + SEM) .
DISCUSSION
The HFV technique can maintain very adequately a
normal pa0 2 and PaC0 2 for the duration of the endolaryngeal
surgery (9), even in patients with marked respiratory
disturbances. Chan~ing pure oxygen to air only, during
the limited period of the actual use of the laser beam,
solves the problem of ignition of the endotracheal tube
and of tracheal and pulmonary burns. When the nasotracheal
tube was accidently hit by the laser beam in the presence
of air, no combustion occured.
195
For this reason, it was never found necessary to protect
the nasotracheal tube with non-ignitable material, nor to
use metal (10, 11) tubes. When during longer laser sessions,
discrete signs of hypoxia were noticed, surgery was shortly
interrupted and the patient was ventilated with pure oxygen.
Switching again to air permits the laser procedure to be
continued without any danger.
Laryngeal microsurgery is often a short procedure.
The ideal anaesthesia technique therefore should allow the
patient to awake smoothly, without any delay and a rapid
recovery of the cough reflex. Total intravenous anaesthe
sia with etomidate and alfentanil during this type of HFV
for laryngeal surgery fulfilled, in our experience, all
these criteria.
CONCLUSIONS
Combining total intravenous anaesthesia with high
frequency ventilation provides ideal conditions for the
ENT-surgeon. Both techniques of HFV proved to be clini
cally satisfactory, but from a surgical point of view the
lower frequency of 60/min. was prefered.
Muscle relaxation prevents coughing and straining and
allows adequate ventilation with the HFV technique.
Since the oxygen concentration in the breathing gases
can be changed rapidly, the ENT-surgeon can work in per
fectly safe conditions, and because the anaesthesiologist
can eventually easily compensate for a slight tendency
towards hypoxia, the duration of the laryngeal examination
and procedure is never a limiting factor.
196
SUMMARY High frequency ventilation was used for endolaryngeal
microsurgery and lasermicrosurgery with the AGA BronchoventR
and the AcutronicR HFJ ventilator. Either oxygen or an
oxygen/air mixture or air were given via a nasotracheal in
sufflation catheter. Anaesthesia was induced with etomidate 0.3 mg/kg and
alfentanil 40 ~g/kg and maintained with an etomidate infu
sion of 30 ~g/kg/min. and alfentanil increments of 15 pg/kg
when necessary. Preoperative and postoperative measurements were made
while the patient was breathing room air and every 5 - 10
minutes during anaesthesia and surgery.
The results show that adequate oxygenation and CO 2 eli
mination were maintained in nearly all patients. Bloodpressure
and heartrate remain stable during surgery. Satisfactory sur
gical operation conditions were obtained.
REFERENCES
1. Sjostrand U. 1977. Review of the physiological rational for and development of HFPPV. Acta Anaesth. Scand., Suppl. 64, 7::::27.
2. Sjostrand U. 1980. High frequency positive pressure ventilation (HFPPV) : A review. Crit. Care Med., ~, 345-364.
3. Klain M. and Smith R.B. 1977. High frequency percutaneous transtracheal jet ventilation. Crit. Care Med., 5, 280-281.
4. Sjostrand U. and Eriksson I. 1980. High rates and low volumes in mechanical ventilation - not just a matter a ventilatory frequency. Anesth. Analg., 59, 567-576.
5. Slutsky A.S., Drazen J.M., Ingram R."H. et al. 1980. Effective pulmonary ventilation with small volume oscillations at high frequency. Science, 209, 609-611.
6. Klain M. and Keszler H. 1980:-Circulation assist by high frequency ventilation. Crit. Care Med., 7, 232-234.
7. Eriksson I. and Sjostrand U. 1977. A clinical evaluation of HFPPV in laryngoscopy under general anaesthesia. Acta Anaesth. Scand., Suppl. 64, 101-110.
8. Eriksson I. and Sjostrand U. 1977. Experimental and clinical evaluation of HFPPV and pneumatic valve principle in bronchoscopy under general anaesthesia. Acta Anaesth. Scand., Suppl. 64, 83-100.
197
9. Versichelen L., Rolly G., Kluyskens P., Vermeersch H. 1981. Anesthesie generale pour laryngoscopie et/ou bronchoscopie chez l'enfant. Anesth. Analg. Reanim., 38, 463-467.
10. Norton M.L. and De Vos P. 1978. New endotracheal tube for laser surgery of the larynx. Ann. Otol., 87, 554-557.
11. Hirschman C.A., Leon D., Porch D. et al. 1980. Improved metal endotracheal tube for laser surgery of the airway. Anesth. Analg., 59, 789-791.
TOTAL INTRAVENOUS ANAESTHESIA DURING HIGH FREQUENCY
VENTILATION.
C. Mallios, P.A. Scheck.
Our enthusiasm of applying since May 1980, High Frequency
Ventilation as a routine technique for some ENT procedures
was overshadowed by the alarming reports of 10 patients out
of 250 (15.3%) who experienced intraoperative awareness.
The incidence of awareness during general anaesthesia using
nitrous oxide/oxygen/relaxants and narcotic analgesic
techniques is approximately 1% (1,2)
By using an open system of ventilation with oxygen enriched
air (35 - 50% oxygen) we managed to keep the endoscopy room
free of pollution from anaesthetic gases.
In order to avoid pollution, awareness and achieve cardio
vascular stability for the high risk patients such as older
people with cardiac and lung disease and others in poor
condition because of the growing larynx tumor, we started
in Harch 1982 to use a continuous infusion of a mixture
of Etomidate and Alfentanil for Total Intravenous Anaesthesia (3)
This mixture which we called ETAL is popular in our
department for ENT procedures and for high risk surgical
patients in general.
It has proved easy to prepare involving no extra work load
for the anaesthetic nursing staff.
In patients undergoing peroral endoscopies, microlaryngeal
surgery, laser treatment to the larynx and Zenkers
diverticulum and for thoracosopies, anaesthesia was
maintaned by continuous infusion of Etomidate and Alfentanil.
INFUSION: ETAL
1. Endoscopies and micro laryngeal surgery 124
2. Laser surgery to the larynx 44
3. Laser surgery for Zenkers diverticulum 6
4. Thoracosopies 6
Total: 180
The investigation was carried out in 180 patients aged
11-90 years (mean 52.7 years), physical status (ASA I-IV)
and body-weight 50-116 kg (mean 68.4 kg).
The duration of anaesthesia varied between 10 and 150
minutes (mean 34.7 minutes).
The time between the end of anaesthesia and spontaneous
breathing was 5-10 minutes.
199
Forty-five minutes prior to anaesthesia, the patients
received an intramuscular premedication of atropine sulphate
or thiazinamium (multergan(R)) sometimes combined with
narcotic analgesics or diazepam, according to the
requirements.
Once the baseline of cardiorespiratory parameters was
obtained anaesthesia was induced with 1.0 - 1.5 mg
Alfentanil i.v. followed by preoxygenation with a face mask
for two minutes, then slowly injecting Etomidate (0.25 -
0.30 mg /kg ) and suxamethonium chloride 1 mg /kg
ANAESTHESIA FOR INDUCTION
Alfentanil 1.0 - 1.5 m~ Lv.
Preoxygenation (mask) 2 minutes
Etomidate 12 18 mg Lv.
Suxamethonium chI. 60 80 mg Lv.
200
An (AGA) insufflation catheter was then inserted naso
tracheally. This catheter has an external diameter of 4.7 rom
and four side holes to abolish the venturi effect.
A continuous gas flow directed outward through the larynx
prevents aspiration of blood or debris.
Ventilation was effected either by the low pressure venti
lator Bronchovent (Siemens-Elema) or by the riark 800 Jet
Ventilator (Acutronic).
For continuous infusion a solution of 125 mg. Etomidate in
ethanol and 5 mg Alfentanil were diluted in 250 ml glucose
2.5 % and NaCl 0.45 %.
ANAESTHESIA FOR MAINTENANCE
Infusion I
Glucose 2.5 % + NaCl 0.45 %
Etomidate
Alfentanil
Infusion II
Suxamethonium chloride
250 ml
125 mg
5 mg
0.1 %
The average doses of drugs used in our series were:
AVERAGE DOSAGE
Etomidate
Alfentanil
Suxamethonium
chloride
77 (60-90)
mg/per hour
2.75 (2.5 - 4.0)
mg/per hour
400 (300-600)
mg/per hour
After 10 minutes of rapid infusion of 200 ml/h the rate was
reduced to 120 ml/h or less.
The infusion was given through a volumetric pump.
Suxamethonium chloride 0.1%, in a seperate infusion was
used for complete relaxation during the whole procedure.
201
ECG and heart rate were constantly monitored, blood
pressure was measured by an automatic recorder every minute
during induction and every 2.5 minutes during the procedure.
Arterial blood gases were measured before starting
anaesthesia and every 10-15 minutes or whenever necessary.
They remained within the physiological range.
At the end of the procedure the infusions were stopped and
the total amount of ETAL and suxamethonium chloride adminis
tered were recorded together with the duration of anaesthesia.
Following the return of deglutition and spontaneous breathing
the insufflation catheter - which was well tolerated - was
removed under suction and the patient was brought to the
recovery room. At the postoperative interview in the
recovery room all patients seemed surprised to hear that
the procedure had already taken place.
Most of them recalled the application of the mask during
preoxygenation and nothing further until they woke up.
The next day, patients were seen in their room in the ward
and were asked again whether they had heard or felt
anything during the procedure.
All replies were negative: no patient experienced awareness.
Ward nurses and ENT surgeons were asked to question the
patients: there were also no reports of awareness.
During the immediate recovery period 26 patients (15.3%)
became nauseated and/or vomited.
Shivering was observed in 8 patients (4.4 %)
Myoclonia in 5 patients (2.7 %) and
Restlessness in 15 patients (8.3 %) postoperatively.
202
Advantages and disadvantages of the ETAL infusion technique:
advantages:
no awareness
cardiovascular stability
no limit to the duration
good degree of hypnosis
good analgesia
no pollution
rapid recovery
Conclusion
disadvantages:
use of a volumetric pump
nausea and/or vomiting
shivering
myoclonia
restlessness
Total Intravenous Anaesthesia using Etomidate and
Alfentanil in a solution of glucose and sodium chloride
in a monitored drip infusion is pollution free and offers
cardiovascular stability.
Using short acting drugs, awakening after the endoscopic
surgical procedure is very quick. This is of great importance
in the prevention of aspiration of blood or debris into the
lungs.
REFERENCES
1. Wilson, S.L., et al.
Awareness, Dreams and Hallucinations associated with
general anesthesia.
Anesth. Analg. 54, 609-617, 1975.
2. Hilgenberg, C.J.
Intraoperative awareness during high-dose Fentanyl -
oxygen Anesthesia.
Anesthesiology 54, 341-343, 1981.
3. Gepts, E., Camu, F.
203
Total intravenous anesthesia with etomidate for micro
laryngoscopy.
Applicability and short comings.
Acta An. Belg. 32, 177-184, 1981.
HIGH FREQUENCY VENTILATION FOR LASER SURGERY OF THE LARYNX.
P.A. Scheck, C. Mallios, P. Knegt.
Surgery of the larynx via the peroral endoscopic route using
the laser beam has introduced new possibilities in the
treatment of different pathological processes in this area.
Table 1.
Indications:
1. Premalignant pathology.
2. Papilloma.
3. Partial resection of tumor.
4. Small relapse of tumor.
5. Diverticulotomy.
Materials and methods:
Compared to other surgical methods, endolaryngeal surgery
using the laser beam has several advantages on one side
and serious risk on the other side.
The advantages are:
a) minimal bleeding because blood vessels of less than 0,5
rom in diameter are coagulated. Even oedema is minimal as
cells near the impact point are not affected. The conse
quence of these characteristics is that tracheostomy may
frequently be prevented in cases where it would be
necessary.
b) nearly painless healing which is precise and rapid
because there is little damaged tissue and epithelial
migration proceeds rapidly.
c) functional results are very good as there is minimal
contracture or scar tissue formation.
Fig. 1 Equipment for laser surgery, high frequency
ventilation and monitoring.
205
The main risk in the use of the laser beam is the ignition
of the endotracheal tube, the flame and the inhalation of
smoke (2,3,4,5) ~ Therefore, during laser surgery of the
larynx the anaesthetist has to deal with special circum
stances and conditions in ensuring a free airway and
adequate ventilation of the fully paralysed patient. To
prevent lesions of the skin or ocular damage, the patients
face is covered by moistened gauze.
A standard armoured endotracheal tube with an internal
diameter of 7 rom or more fills the glottis to such an
extent that it is difficult for the surgeon to find suffi
cient space to carry out the treatment properly. There are
of course no problems with ventilating a patient with a
tracheostomy cannula. The laser beam can cause ignition of practically all
cannulas and tubes in the upper airway for ventilation or
for maintaining a free airway (6).
In order to demonstrate the effect of the laser beam on
various materials we have irradiated some of the materials
206
commonly used in the upper airway. The carbon dioxide laser
FLF 25, and a beam of 15 watts for 0,2 sec. was used.
Endotracheal tubes react either by bursting in flames (as
armoured tubes do) or by melting of the outer layers, which
happens to red rubber tubes. Portex tubes produce dense
smoke. Vygon endotracheal tubes react in a similar way.
The 14 gauge catheter we are using for HFV produces dense
smoke as well. An alluminium foil covering the same catheter
completely protects against ignition by the laser beam even
when this beam hits the foil several times in the same
place.
The catheter has to be covered by the foil as close as
possible to its tip, leaving at least two side holes of the
catheter free.
A flame in the patients airway is extremely dangerous and
may even endanger his life. A program of the management of
fire or dense smoke in the airways has been suggested (5).
Results:
We had experience with more than a hundred HFV's delivered
by the Bronchovent apparatus with bloodgas monitoring
before we used this technique for laser surgery of the
larynx. Anaesthesia for these procedures is described
elswhere.
The technique of ventilation is as follows:
The 14 FC insufflation catheter is, as a rule, passed
through the nostril and with the aid of a Magill forceps
directed into the trachea. The catheter is then connected
to the ventilator. The Kleinsasser instrument is fixed and
surgery on the larynx can commence. To prevent damage to
the nasal mucosa by the aluminium foil, the nasal catheter
may be introduced through a nasal airway.
The insufflation catheter leaves almost the whole glottis
free and is even out of the surgeons view. A disadvantage
Fig. 2 Armoured tube:bursting in flames (15 watts,
0,2 sec.)
Fig. 3 Red rubber tube: melting of the outer layers,
thin smoke is produced.
207
208
Fig. 4 Porte x tubes: dense smoke.
Fig. 5 Vygon tubes: dense smoke.
209
of the use of this small catheter during HFV is the impossi
bility of protecting the sublaryngeal region or the trachea
before the laser beam with moist cotton or gauze. This
would - of course - impede expiration. If necessary, the
laryngeal structures can be protected by a metal mirror. No
Lesions of the tracheal mucosa caused by the reflected
laser beam have been detected so far.
Another technique which might be useful under difficult
anatomical conditions, is to ventilate through a metal
catheter with an internal diameter of 2,5 mm or more.
Air entrainment occurs during ventilation through this metal
catheter, which is without side holes.
When this technique is used, carbon dioxide yalues as a
rule increase slowly and should be carefully monitored.
In some patients it is even technically possible to measure
e~d-expiratory CO2 continuously or intermittently.
HFV together with laser treatment has been used so far fox
85 treatments in the larynx, for the Zenkers diverticulum
of the oesophagus in 12 patients and for the laser treat
ment of tumors of the tongue base in 8 patients.
The bloodgas values are summarized in table 2. When a
mixture of air with 50% oxygen is used for ventilation,
oxygen saturation remains unchanged.
For evacuation of the smoke during laser treatments, a
second catheter is placed nasally with its tip in the
nasopharynx. A low suction pressure is effective in produ
cing a practically smoke-free surgical field.
Table 2.
Blood
-1 min. 5
pH 7,34 2:0,13
pac02 5,23 + 0,3
Pao2 17,6 + 1,2
Sat. 02 98,7 + 0,6
HFPPV - Laser larynx
gases (KPa) - n = 85
30
7,40 +0', H
4,30 + 0,5
21,1 + 2,8
98,8 + 0,4
7,34
3,7
16,1
98,1
60
+ Ol} 15
+ 0,6
+ 1,3
+ 0,7
90(n=18)
7,36 ... 0,16
4,6 + 0,5 -16,7 + 1,4
97,8 + 0,8
210
SUMMARY
Ventilation using a frequency of 1 Hz or more through a
small insufflation catheter is very well tolerated by
patients with pathology on or close to the vocal cords. The
space in the larynx offers the surgeon the possibility of
free access for treatment with a laser beam.
In several patients laser treatment is effective only
because ventilation through a small catheter leaves suffi
cient space in the glottis region.
References:
1. Borg U., Eriksson I., Sjostrand U.:
High-Frequency Positive-Pressure Ventilation (HFPPV):
A review based upon its use during bronchoscopy and for
laryngoscopy and microlaryngeal surgery under general
anesthesia.
Anesth. Analg. 59, 8, 594 - 603, 1980.
2. Burgess G.E., LeJeune F.E.
Endotracheal tube ignition during laser surgery of the
larynx.
Arch. Otolaryngol. 105, 561 - 562, 1979.
3. Cozine K., Rosenbaum L.M.,Akanazi J., Rosenbaum S.H.:
Laser-induced endotracheal tube fire.
Anesthesiology 55, 583 - 585, 1981.
4. Meyers A.:
Complications of CO2 laser surgery of the larynx.
Ann. Otol. 90, 132 - 134, 1981.
5. Schramm V.L., Mattox D.E., Stool S.E.:
Acute management of laser-ignited intratracheal explosion.
The Laryngoscope 91, 1417 - 1425, 1981.
6. Treyve E., Yarington C.J., Thompson G.E.:
Incendiary characteristics of endotracheal tubes with
the carbon dioxide laser, an Experimental study.
Ann. atol. 90, 328 - 330, 1981.
7. Wainwright A.C., et al :
Anaesthetic Safety with the carbon dioxide laser.
Anaesthesia 36, 411 - 415, 1981.
211
HIGH FREQUENCY JET VENTILATION VIA A NASOTRACHEAL TUBE FOR
SURGERY OF THE LARYNX AND TRACHEA.
W.K. Hirlinger, A. Deller, O. Sigg, W. Dick, H.H. Mehrkens.
Jet ventilation, a method which has been developed over the
past few years, is a major advance which in the field of
laryngeal micro-surgery and also tracheal surgery and
tracheostomies allows a much improved field of vision.
We have studied the use of high frequency jet ventilation
via naso-tracheal tube in 40 cases. 31 Patients underwent
direct laryngoscopy. 3 patients tracheoscopy and 6 patients
tracheotomy and tracheal plastic surgery. The patients
were on average 42 years of age, 14 were female and 26 male.
Body weight averaged 70.2 kg. The duration of surgery was
34 min. on average and that of anaesthesia 59 min.
General anaesthesia was carried out as a modified neurolept
analgesia using flunitrazepam (0.01-0.02 mg/kg body weight)
and fentanyl (0.3-0.5 mg). Succinylcholine was given for
relaxation, or, for the longer procedures, diallylnortoxiferin.
Following induction and relaxation, a Bard-Parker nasal
oxygen catheter was introduced through the nose into the
trachea. In those cases who already had a tracheostomy the
catheter was introduced through this. The jet ventilator
used was a ~1K800 supplied by Acutronic.
Ventilation was generally carried out at a frequency of
150/min, with an inspiration time of between 30 - 40 %.
The flow minute volume was adjusted according to observation
of thoracic excursion and of auscultation. On average we
ventilated with an F1W of 232 ml/kg body weight (range 109 -
365 ml/kg body weight). The FI02 lay between 0.3 - 1.0.
Nitrous oxide was added using a Bird nitrous oxide-oxygen
blender. The quality of ventilation was checked by arterial
blood gas analysis.
Results
Fig. 1 shows the relation ship between the PaC02 values
measured, and the flow minute volume. Most patients were
either normally or somewhat hyperventilated.
213
The relationship. between paC02 and FHV in ml/kg body weight
is shown. No correlation could be found between these values
even when those patients with normal lung function who only
underwent laryngoscopy were analysed·.
Fig. 2 shows that with an FI02 of 0.5 the patients were
adequately oxygenated. The average PaC02 was 202.5 rom Hg.
Discussion
Based on this admittedly, small study of high frequency jet
ventilation we have reached the following conclusions:
1: Provided that the gas insufflated is able to flow away
unhindered, a safe and fully adequate ventilation can
be achieved. We were unable to find a correlation
between the flow minute volume as expressed in ml/kg
body weight and PaC0 2 levels. Further variables, such
as the placing of the tip of the tube, and the quality
of the gas escape must also be born in mind.
2: A major advantage of the method lies in the fact that
the operators visual field is, especially in cases of
laryngeal micro-surgery, much improved.
3: At the selected frequency which we used, there is always
a pressure gradient out of the airways to the outside
and hence a risk of aspirating blood is avoided.
4: In comparison to low frequency jet ventilation, the
reversal of anaesthesia following high frequency is
unproblematic, because the catheter is well tolerated
and can be left in position until the patient is awake
and has an adequate spontanous ventilation.
PaC0
2 fm
mH
g) 70
60
50
40
·30 20
-l -i J
Pa~
-EI
NZEL
WER
TE
IN
ABHl
-ING
IGKE
IT
YOM
FLOW
MIN
UTEN
VOLU
MEN
(F
MV)
n
= 40
""
0"
:"
I . ~
. "
5·
6 7
8 9
10
11
12
13
14
15
16
V
18
19
20
21
22
23
24
25
N
, .....
. .j>
.
FMJ
(L •
MIN
-"I)
Pa02
(mrn
Hg
)
400
150
Pao 2
(~1ITTEUJERTE)BEI
FI0
2 ;::
0 ... 5
IN
t\B
Hi'X
NGIG
KEIT
VO
M FL
OVJM
INUT
ENVO
LUM
EN
(FfW
)
200
250
300
350
FMV
(ML'
KG
-1
KG)
E. CLINICAL USE· PART II
HIGH-FREQUENCY POSITIVE-PRESSURE VENTILATION
FOR MAJOR AIRWAY SURGERY
N. EL-BAZ, M.D., A. EL-GANZOURI, M.D., A. IVANKOVICH, M.D.
Major airway surgery includes resection and
reconstruction of the trachea and carina, and the more
extensive resection of sleeve pneumonectomy which includes
removal of one lung, the carina, and a portion of the other
bronchus. Major airway surgery presents to anesthesia the
problems of providing adequate and continuous alveolar
ventilation and oxygenation during the period of resection
and reconstruction of the airway, without impairing
surgical access to the circumference of the open airway.
Conventional intermittent positive pressure
ventilation (IPPV) through an endobronchial tube has been
described to provide one-lung ventilation during airway
surgery. This technique is based on the advancement of
the endotracheal tube, and its placement inside a main
bronchus for one-lung ventilation. Although conventional
one-lung IPPV may achieve adequate alveolar ventilation
and oxygenation, the large endobronchial tube obstructs
surgical access to the circumference of the open airway.
To improve surgical access, repeated withdrawal and
advancement of the endotracheal tube through the open
airway is required, with a sequence of alternate periods
of one-lung ventilation and apnea. Alternatively, the
open bronchus can be intubated by the surgeon
(transthoracic) with another sterile endobronchial tube.
This also requires another sterile anesthesia circuit to
be connected to the transthoracic tube and passed over to
the anesthesia team for one-lung ventilation. In this
217
technique, after the completion of the posterior portion of
the airway anastomosis, the transthoracic endobronchial
tube must be removed to allow for surgical access to the
anterior and lateral circumference of the airway. One
lung ventilation is achieved, at this stage, by advancing
the endotracheal tube through the partially reconstructed
airway as in the other technique. In our experience both
techniques are cumbersome, traumatic to the airways, and
compromise alveolar ventilation and oxygenation for
surgical access.
--IPPV
Cardiopulmonary bypass has been evaluated as an
alternative method of ventilation during major airway
surgery. Although this technique provides optimal gas
exchange and surgical conditions, the problems associated
with arterial and venous cannUlation, systemic
heparinization, and the use of a perfusion pump limit the
value of this technique for airway surgery.
Injector jet ventilation through a small
endobronchial catheter has also been evaluated during
major airway surgery. Although the small catheter
provides optimal surgical access, thi~ technique also has
been associated with major problems. The delivered large
218
tidal volume during injector jet ventilation causes
exaggerated movement of the mediastinum and frequent
displacement (flagging) of the catheter. Besides frequent
interruption of ventilation and surgery for positioning
the catheter, this technique has been associated with
barotrauma, particularly during one-lung ventilation. The
negative pressure generated above the tip of the catheter
during injector jet ventilation also suctions blood and
debris into the intubated bronchus causing post-operative
pulmonary problems. These major disadvantages led to the
evaluation of oxygen insufflation through a small
endobronchial catheter. Although the small catheter
provided optimal surgical access, this technique is
associated with progressive hypercarbia and respiratory
acidosis, limiting its value to very short surgical
procedures. Oxygen insufflation through a catheter
supplemented with occasional jet ventilation was also
described for major airway surgery. Nonetheless, this
technique is awkward and combines the problems associated
with both techniques.
In an effort to avoid the foregoing problems, we
evaluated the technique of high-frequency
positive-pressure ventilation (HFPPV) through a
small-diameter catheter during a variety of major airway
surgical procedures. HFPPV is based on the
administration of a small tidal volume of approximately
the volume of dead space (50-250 ml), at a frequency
between 1 and 10 Hz (60 to 600 breaths/min). HFPPV was
shown in animal and human studies to achieve adequate
alveolar gas exchange by a combination of convective flow
and acceleration of gas diffusion. The eddy flow
characteristic of HFPPV was also found to improve gas
mixing and achieve a more uniform gas distribution
independent of regional time constant. The airway
pressure during HFPPV is continuously positive with low
219
mean and peak pressures, causing minimal impairment to the
pulmonary and systemic circulations.
ONE-LUNG HFPPV FOR SLEEVE PNEUMONECTOMY
OL-HFPPV was used in 6 patients undergoing right
sleeve pneumonectomy for treatment of right upper lobe
bronchogenic carcinoma involving the right main bronchus,
carina, and trachea. Anesthesia was induced in these
patients with sodium thiopental 4 mg/kg, and muscle
relaxation was achieved with pancuronium 0.15 mg/kg. The
trachea was intubated with an 8.0 mm ID cuffed
endotracheal tube. This was placed under direct vision
(Stortz bronchoscope) above the involved part of the
trachea. Anesthesia was maintained in these patients with
intravenous administration of morphine 1 to 2 mg/kg and
diazepam 0.5 to 1 mg/kg, and conventional two-lung IPPV
with 100% oxygen was initially used in each patient.
After surgical dissection the trachea and left main
bronchus were transsected beyond the tumor area, and the
right lung was removed with the carina. At that time, a 2
mm ID presterilized catheter was advanced through the
endotracheal tube, the transected trachea, and placed
inside the left main bronchus for one-lung HFPPV. The
distal end of the catheter has a single opening at the
tip, and the proximal end has a metal adaptor to prevent
gas leakage and disconnection during the use of
high-pressure gases for HFPPV. The proximal end of the
catheter was connected to the output tubing of our HFPPV
ventilator. Left-lung HFPPV through the catheter with
100% oxygen was used in these patients at frequencies
between 80 and 250 breaths/min, driving gas pressure (DGP)
between 15 and 35 psi, and insufflation time percentage
(IT%) of 40%.
220
HFPPV
Frequency 80-250 breath/min
DGP 15-25 PSI IT'!(, 40%
1.0
ENDOTRACHEAL TUBE
LEFT LUNG HFPPV FOR RIGHT SLEEVE PNEUMONECTOMY
HFPPV maintained adequate ventilation and oxygenation
in these patients for periods of between 1.5 and 3 hours.
Pa02 ranged between 200 and 610 mmHg, and PaC02 between
19 and 40 mmHg. In addition, the small-size catheter
provided optimal access to the circumference of the trachea
and left bronchus, allowing for perfect anatomical
alignment and for reconstruction of an airtight anastomosis. We have also found the delivered small tidal
volume of HFPPV causes minimal movement of the mediastinum,
and the catheter remains stationary in the left main
bronchus. The continuous outflow of HFPPV gas from the
left main bronchus was also found to prevent its
contamination with blood and debris.
After the completion of the trachea-bronchial
anastomosis, the HFPPV catheter was removed and conventional IPPV was resumed through the endotracheal
tube. This was required to achieve a high mean airway
pressure for detection of gas leakage through the
anastomosis. At completion of surgery, muscle relaxant
and narcotics were reversed. The endotracheal tube was
removed in the operating room after each patient had
established adequate spontaneous breathing. All patients
were admitted to the Surgical Intensive Care Unit for
continuous monitoring.
221
The same technique of left-lung HFPPV through the
catheter was also evaluated in three patients during
limited excision of carinal tumors and repair with
pericardial flap, and in another two patients during the
resection of low tracheal tumors involving between 3 to 5
tracheal rings, and tracheal end-to-end anastomosis. Conventional two-lung IPPV was initially used in these patients. This was discontinued after the resection of
the airway and the HFPPV catheter was passed down the
endotracheal tube and placed inside the left main bronchus
for one-lung ventilation. HFPPV was used at frequencies
between 150 to 250 breaths/min, DGP between 15 to 35 psi,
and IT% of 40% at F I02 of 1.0. HFPPV maintained
adequate alveolar ventilation and oxygenation in these
patients, with Pa02 ranging between 190 to 410 mmHg and
a PaC02 between 32 to 44 mmHg. In addi t ion, the small
catheter provided optimal surgical access.
ONE-LUNG HFPPV FOR MAJOR ENDOSCOPIC LASER SURGERY
One-lung HFPPV through a catheter was also valuable
during bronchoscopic laser excision of inoperable carinal tumors in two patients. These tumors caused 70 to 80% occlusion of the right main bronchus. The aim of the surgery is to excise a portion of the tumor to allow for
gas exchange through the right lung for the improvement of
respiratory function. After induction of anesthesia, the
left. main bronchus was intubated wi th a 2 mm (I .D.)
catheter for OL-HFPPV.
222
HFV [F iOO-150]
15-35
30-50
0.21
ONE-LUNG HFPPV FOR MAJOR LASER SURGERY
The small catheter allowed adequate intratracheal
space for the placement of the rigid bronchoscope alongside
the HFPPV catheter. The lumen of the rigid bronchoscope
also functioned as an outlet for HFPPV gases to the
atmosphere. Based on our findings that polyvinylchloride
(PVC) HFPPV catheters, when filled with air are only
punctured but not ignited by laser beams, eliminated the
fire hazard associated with endoscopic laser surgery in
these two patients by using air instead of oxygen. HFPPV
was used in these patients at frequencies of between 100
and 150 breaths/min, DGP between 10 and 25 psi, IT% of 40%.
This achieved a mean Pa0 2 of 65 mmHg in the first patient
and 85 mmHg in the second patient, which was acceptable and
somewhat higher than their preoperative Pa02 of 51 and 59
mmHg, respectively. Besides the elimination of the fire
hazards with this technique, the small catheter gave
optimal unobstructed access to their carinal tumors.
!~Q=~~~g-~!g~-~~~~~~~~~-~Q~!!!~~-~~~~~~~-~~~!!~~!!Q~ i!~=~~~~~2_~Q~_!~~~~~~_~~~~~!!Q~_~_~~~Q~~!~~~!!Q~
TL-HFPPV was also evaluated in five patients during
resection and reconstruction of the cervical portion of
223
the trachea for treatment of tumors and tracheal stenosis.
Because of the site of the tumors and the narrowed tracheal
lumen in these patients, anesthesia was induced with
halothane and the trachea was intubated with a 2 mmID HFPPV
catheter (no endotracheal tube) for TL-HFV. Anesthesia was
maintained with morphine 1-2 mg/kg and diazepam 0.5 to 1
mg/kg, and muscle relaxation was achieved with pancuronium
0.2 mg/kg. To insure a continuous outflow of gas from the
larynx to the atmosphere, nasopharyngeal and oropharyngeal
airways were placed in each patient. A nasogastric tube
was also placed to prevent gastric gas distention as a
result of the continuously positive pharyngeal airway
pressure associated with this technique.
TL-HFPPV
HFV F 100-250 breath/min
I F 100-250 I DGP 15-35 PSI
I DGP IT'll 40'16
20-50 F102 1.0
liT'll 30-50 Pa02 450-580 nwnHg
I FlO, 1.0 PaC02 21-36 nwnHg
TRACHEAL RESECTION AND RECONSTRUCTION
TL-HFPPV with 100% oxygen was used in these five
patients at frequencies between 100-250 breaths/min, DGP of
15-35 psi, and IT% of 40%. This achieved adequate
oxygenation and alveolar ventilation, with a Pa02 between 450 and 580 mmHg and PaCOz between 21 and 36 mmHg. In addition, the small catheter provided optimal
unobstructed surgical access during tracheal excision and
reconstruction.
224
At completion of surgery, muscle relaxants and narcotics were reversed. The HFPPV catheter was removed in the operating room after each patient had established adequate spontaneous breathing
TL-HFPPV was also valuable in another patient with post-tracheostomy tracheal stenosis (60%) scheduled for resection anastomosis of the cervical trachea. After induction of anesthesia the trachea was intubated with an
HFPPV catheter for TL-HFPPV with 100% oxygen.
Intraoperatively, the left recurrent laryngeal nerve was found to be incorporated into a mass of scar tissue firmly
adhered to the stenotic part of the trachea. To maintain the integrity of the laryngeal airway, the surgical procedure was changed to reconstruction of the trachea with a hyoid bone graft. This also required support with
a Montgomery tracheal T-tube to prevent the advancement of
the bone graft into the tracheal lumen. This major change
of surgical plan was easily accommodated during this
technique of HFPPV. The distal end of the HFPPV catheter
was pulled out through the longitudinally incised trachea and passed through the intraluminal lumen of the tracheal
T-tube, and both were placed inside the trachea.
HFPPV CATHETER
Frequency 1150 brealhlrT*1
~----1 DGP 15-25 PSI IT'J(, 40%
Pa02 440-510 mmHg PaC02 42-50 rnmHg
FI02 1.0
HIGH FREQUENCY VENTILATION fOR TRACHEAL RECONSTRUCTION WITH TRACHEAL T -TUBE
TL-HFPPV was continued through the catheter and the
T-tube functioned as an exit for HFPPV gas outflow. In
addition, TL-HFPPV maintained optimal oxygenation with a
mean Pa02 of 459 mmHg, and adequate alveolar ventilation
with a mean PaC02 of 41 mmHg.
At completion of surgery, HFPPV through the catheter
was continued in the Intensive Care Unit to allow for
gradual recovery from muscle relaxants and narcotics.
Although HFPPV has been reported to abolish spontaneous
breathing, nonetheless this patient resumed spontaneous
breathing while receiving TL-HFPPV. Respiratory weaning
was achieved in this patient by gradual reduction of the
delivered tidal volume, by reducing the driving gas
pressure of the HFPPV, and the catheter was removed after
adequate spontaneous breathing had been established.
225
Our application of HFPPV through a small catheter for
one-lung and for two-lung ventilation during these diverse
major airway surgical procedures has achieved adequate and
continuous alveolar ventilation and oxygenation. Our use
of a small catheter also provided optimal and
uninterrupted surgical access to the circumference of the
open airways. Besides avoiding all the major problems
associated with the other methods of ventilation, we
consider this simple and versatile technique of HFPPV
ideal for major airway surgery.
REFERENCES
1. Faber ML, Jensik RJ: The Planning of Tracheal Surgery, Surg Clin North Am 1970; 59:113-122.
2. Goffin B, Bland J, Grillo HC: Anesthetic management of tracheal resection and reconstruction. Anesth Analg 19691; 48:884-890.
3. Jensik RJ, Faber LP, Milloy FH, Goldin MD: Tracheal sleeve pneumonectomy for advanced carcinoma of the lung. Surg Gynecol Obstet 1972; 134:231.
4. Neville WE, Thomason RD, Peacock H, et al: Cardiopulmonary bypass during non-cardiac surgery. Arch Surg 1966; 92:576-587.
226
5. Wood FM, Neptune WB, Palatchi A: Resection of the carina and main-stem bronchi with the use of extracorporeal circulation. N Eng J Med 1961; 264:492-494.
6. Lee P, English ICW: Management of anesthesia during tracheal resection. Anaesthesia 1974; 29:305.
7. Deslauriers J, Beaulieu M, Benzera A: Sleeve Pneumonectomy for Bronchogenic Carcinoma. An Thorac Surg 1979; 28:474-476.
8. Sjostrand D: Review of the Physiological Rationale for and Development of High-Frequency PositivePressure Ventilation-HFPPV. Acta Anaesthesiol Scand (Suppl) 1977, 64:7-27.
9. Sjostrand D, Ericksson IA: High Rates and Low Volumes in Mechanical Ventilation - Not Just a Matter of Ventilatory Frequency. Anesth Analg 1980; 59:567-576.
10. EI-Baz N, EI-Ganzouri A, Gottschalk W, Jensik R: One-Lung High Frequency Positive-Pressure Ventilation for Sleeve Pneumonectomy: An Alternative Technique. Anesth Analg 1981; 60:683-686.
II. EI-Baz N, Jensik R, Faber LP, et al: One-lung high frequency ventilation for bronchoplasty and tracheoplasty. Ann Thorac Surg 1982, 34:564-571.
12. EI-Baz N, Holinger L, EI-Ganzouri A, et al: High-frequency positive-pressure ventilation for tracheal reconstruction supported by tracheal T-tube. Anesth Analg 1982; 61:796-800.
HIGH FREQUENCY JET VENTILATION FOR PULMONARY RESECTION
P. MOULAERT and G. ROLLY
EMERSON was the first to use High Frequency Ventilation
(HFV) more than 20 years ago. He suggested that high fre
quency oscillations could improve gas mixing by applying
small oscillations on the ventilatory pattern developed by
a conventional positive pressure ventilator.
Although the widespread use of High Frequency Jet Ven
tilation (HFJV) for laryngoscopy, bronchoscopy and ENT-proce
dures, other clinical applications remain experimental du
ring anaesthesia. Because of reports on relatively immobile
lungs and a uniform distribution of ventilation (1), we star
ted using HFJV during anaesthesia for pulmonary resection.
HFJV was introduced by KLAIN (2). The gas is delivered
by a fluidic logic controlled ventilator through a small can
nula into the trachea. Small jets of high velocity gas at
frequencies of 1 - 10 Hz. produce a very effective gas ex
change. Coaxial flow probably occurs in the airways.
The cannula (AngiocathR 14 G - with side holes) can be in
serted by cricothyroid puncture or introduced into an ordi
nary endotracheal tube by a swivel adapter. A nasotracheal
cannula and a specially designed endotracheal "Jet"-tube
(MallinckrodtR Hi-Lo jet TM) can be used too. It is basicaly
an open system. Moderate levels of PEEP up to 5 cm H20 and
a variable degree of air entrainment by Venturi effect are seen during HFJV.
State University of Ghent (Belgium) - Department of Anaesthesia (Dir. Prof. Dr G. ROLLY)
228
PATIENTS AND METHODS
Five male patients, aged 62.7 ~ 6.5 (Mean ~ SEM)
(range 54 - 69) years operated for lungcancer were studied,
2 of whom undergoing pneumonectomy and 3 lobectomy. Body
weight was 65.0 ~ 3.7 (range 60 - 68) kg.
All were premedicated with Fentanyl 0.10 mg, Droperidol
5 mg and Atropine 0.5 mg by intramuscular route one hour
prior to surgery. On arrival in the operating room, plastic
cannulae were placed in the left and right cephalic veins. One cannula was used for a continuous infusion of Etomidate
and Alfentanil. The other cannula was used for additional
medication and for blood replacement.
After an Allentest was done, an arterial line was set
up in the radial artery or alternatively in the femoral arte
ry, for pressure monitoring and bloodgas sampling; ECG- and
pulse curve were also monitored.
After preoxygenation anaesthesia was induced with Diaze
pam 10 mg, Alfentanil 2.5 mg and Pancuronium 8 mg. The pa
tient was manually ventilated with pure oxygen. The Etomidate -1 -1 -1 -1
(10 ~g.kg .min. ) - Alfentanil (0.1 ~g.kg .min. ) drip
was started within 2 minutes and the first 10 minutes in a
5 fold rate. The solution given in drip was Hypnomidate pro
Infusione 250 mg and Alfentanil 2.5 mg in 250 ml Dextrose 5 %.
After full muscular relaxation a cuff Hi-Lo Jet MallinckrodtR.
endotracheal tube 9.0 rom I.O. and a gastric tube were intro
duced. High Frequency Jet Ventilation was started. Additio
nal medication was given on clinical judgment: Alfentanil in
bolus doses of 1 mg, Pancuronium in increments of 2 mg and
Oroperidol in doses of 5 mg. The Etomidate-Alfentanil drip
was stopped 20 minutes before the end of surgery.
Ventilation was established by a MK-800 AcutronicR High
Frequency Jet Ventilator driven by pure oxygen. Its output
was connected to the transparant line of the endotracheal
229
Jet-tube ending in an insufflation lumen at its near distal
part. Humidification was acoomplished by infusion of 10 mI.
hour- 1 normal saline with an IvacR pump in the opaque white
line or the tube, ending distally of the insufflation lumen.
The ventilator was initially set at a driving pressure of
1.5 Bar, a rate of 250 cycles.min.- 1 , 30 % inspiratory time
and catheter select knob on position 2, resulting in a minute
volume of 16 l.min.-1 . Further adjustments of driving pres
sure were to be done according to arterial bloodgas determi
nations, but were actually not necessary.
At the end of surgery, muscular relaxation and narcotic
respiratory depression were reversed with Neostigmine 2.5 mgt
Atropine 1.0 mg and Naloxone 0.2 mg. Weaning was established
by diminishing progressively driving pressure. Postoperative
care took place in the Intensive Care Unit, where patients
were extubated after adequate recovery of spontaneous brea
thing and consciousness.
RESULTS
Surgery lasted 3.7 + 0.8 hours; the duration of Etomidate
Alfentanil drip was 3.9 + 0.5 hours and the number of Alfen
tanil bolus doses of 1 mg, was 5.0 ±. 2.1. All patients recei
ved Droperidol 25 mg and one needed a supplementary dose of
Diazepam 10 mg.
Heart rate and arterial blood pressure are shown in Table I.
Heart rate Systolic Diastolic
-1 art.BP art.BP b.min. mm Hg mmH
Awake before induction 72.5+ 9.5 120.2+18.2 65.5+17.3 5min.after intubation 67.5+13.1 130.4+25.8 60.6+11.5 5 min.after incision 67.5+13.1 157.5+29.8 70.2+ 8.1 After 2 hrs of surgery 70.0+14.1 130.6+36.0 75.7+12.9 During skin closure 82.5+17 .0 180.8+16.3 80.1+15.2
Table I. Heart rate and arterial bloodpressures at different examination moments (Mean + SEM) .
230
Cardiovascular parameters were relatively constant during
operation, although blood pressure tended to rise. Individual
differences were however marked.
Arterial bloodgases are shown in Table II.
Awake before induction 5 min.after incision After 2 hrs of surgery After 5 min.open bronch. During skin closure
pHa
7.36+0.05 7.40+0.14 7.33+0.09 7.33+0.12 7.37+0.05
paC02 nun Hg
50.0+14.0 37.2+13.1 43.5+12.3 42.0+15.8 38.6+ 8.0
pa0 2 nun Hg
65.5+ 6.5 313.5+85.5 281.0+103.2 292.4+114.8 314 .6+75.3
Table II. Bloodgas analysis at different examination moments
(Mean ~ SEM) .
Oxygenation was always good by using pure oxygen on the ven
tilator, although the results of pa02 suggest that air entrain
ment took place. PaC0 2 tended to normocapnia indicating a
sufficient gas exchange, probably by convection and diffusion
(3). Ventilation remained still adequate even in the presence
of an open bronchus after removal of a lung or a lobe.
Overall operating conditions were good. Lung movements
were minimal : the only slight vibrations did not impede the -1 surgeon. On lower or higher frequencies than 250 cycles.min. ,
greater lung excursions or faster vibrations were troublesome.
Lung expansion was good and complete, due to a positive air
way pressure during the entire ventilatory cycle.
Recovery after anaesthesia was quick. All patients were
extubated within one hour after the end of surgery. No respi
ratory problems were encountered during the postoperative
period. None of the patients developped postoperative atelec
tasis.
231
Although there is no definite need for an endobronchial
tube when using HFJV, however a cuffed endotracheal tube is
necessary during pulmonary surgery for different reasons.
Secretions can be aspirated through it and the lungs are ea
sily inflated holding temporarily a finger on the open end.
Although calculated tidal volume delivered by the ven
tilator was 60 ml, the real tidal volume exceeds the volume
of gases directly delivered by the ventilator (4). Outside
gases are entrained due to the jet effect and absence of an
air valve mechanism (5). This impl±cates monitoring of oxy
genation and control of ventilation by arterial bloodgas ana
lysis are necessary. As N20 and potent inhalation anaesthe
tics cannot be administrated in a conventional way, total
intravenous anaesthesia is necessary.
For the surgeon the mean disadvantages of the technique
are the noice and the fact that gases are flushed in his face
through an open bronchus by the high driving pressure. These
are amply compensated by the fact that it is possible to keep
the bronchus open without harm during several minutes. On the
other hand the adequate ventilation, minimal lung excursions
and good lung expansion without atelectasis are appreciated.
Although the technique of HFJV with total intravenous
anaesthesia seems appropriate for pulmonary surgery, more stu
dies have to prove it is at least as good as conventional
techniques of ventilation and anaesthesia.
SUMMARY
High Frequency Jet Ventilation has been used for pulmonary resecti~n in five patients, using a cuffed Hi-Lo ~et Mallinckrodt endotracheal tube and an MK-800 Acutronic High_ 1 Frequency Jet Ventilator, with pure oxygen at 250 cycles.min. , in combination with total intravenous anaesthesia, maintained by an infusion of Etomidate and Alfentanil.
Ventilatory and cardiovascular parameters remained relatively stable during operation, recovery was quick and postoperative period without major problems.
Although adequate ventilation and good oxygenation, even with an open bronchus, and minimal lung excursions with a good lung expansion without atelectasis amply compensate the disadvantage of noice with this technique,it remains still controversial.
232
REFERENCES
1. Slutsky A.S. et al. 1980. Steady flow in a model of human central airways. J. Appl. Physiol., Resp. Environ.Exer. Physiol., 49, 417-423.
2. Klain M. e~al. 1977. High Frequency Percutaneous Transtracheal Jet Ventilation. Crit. Care Med. 5 (6), 280-287.
3. Carlon et al. 1982. High Frequency Jet Ventilation: tech.nical and physiologic considerations. Second International Symposium on Intensive Care and Emergency Medecine, Brussels, March 24-26.
4. Scacci. 1979. Air entrainment masks: Jet mixing is how they work; the Bernouilli and Venturi principles are how they don't. Resp. Care, 24, 928.
5. Rolly G. and Versichelen L. 1982. Gas analysis by massspectrometry during High Frequency Ventilation. International Symposium on High Frequency Ventilation, Rotterdam, September 17 - 18.
CLINICAL EXPERIENCE WITH mGH FREQUENCY VENTILATION
M. KLAIN, J. FINE, A. SLADEN, K. GUNTUPALLI, J. MARQUEZ, H. KESZLER
1. ADVANTAGES OF HFV
Indications for clinical application of high frequency ventilation (HFV) are
given by the basic characteristics of the method (1). High frequency ventilation
is capable to achieve a good gas exchange with small tidal volumes. Resulting
low airway pressures and low intrathoracic pressures decrease the incidence of
two main side effects of positive pressure ventilation, namely barotrauma and
circulatory depression. Therefore, barotrauma or prevention of barotrauma and
prevention of circulatory depression are the two main indications for high
frequency ventilation.
The second characteristic of HFV is that it does not interfere with
spontaneous breathing. Because it can be superimposed on spontaneous breathing
it provides very acceptable assisted ventilation and a method of weaning from
ventilatory support.
High frequency jet ventilation (HFJV) offers two additional advantages (2).
First, it can be administered through a small insufflation catheter. Small
catheters not only eliminate competition for the airway with the surgeon but
enable adequate ventilation if the airways are open or even if there is a large
leak. Typical indications are respiratory support during tracheobronchial
suctioning or fiberoptic bronchoscopy or during exchange of endotracheal tubes.
In all these cases no other method can match the advantages of HFJV.
Secondly, uncuffed endotracheal tubes for total or partial ventilatory
support offer an advantage not only during weaning but also do not disturbe
234
mucociliary transport. If the frequency is high enough (100 or higher), HFJV
will prevent aspiration even with translaryngeally introduced catheters (3).
Last not least, HFJV allows transtracheal application of ventilatory support.
Cricothyroid membrane puncture is a simple way of emergency airway
management especially in upper airway or orofacial trauma (4). During
cardiopulmonary resuscitation it is not necessary to interpose ventilation between
heart compressions and cardioresuscitative drugs can be administered directly
in the jet even before an I.V. line is available (5).
2. CLINICAL EXPERIENCE
More than 700 patients were ventilated at the University of Pittsburgh
Health Center Hospitals with high frequency jet ventilation.
Sixty-five percent of the patients were ventilated intraoperatively, 2596
in intensive care units and 1096 in the emergency room and postoperative
recovery room.
Forty-five percent of the patients were ventilated via a cuffed endotracheal
tube. In half of them a "Hi-Low" jet tube was used which has the jet channel
incorporated in the wall of the tube. In the other half a regular endotracheal
tube was used with the jet catheter inserted through a T-connector on the
proximal end of the tube. In 5096 of the patients an uncuffed 14F catheter
was introduced nasotracheally under direct vision and in 596 of the patients a
transtracheal cannula was used. The following indications were found successful:
3. INTRAOPERATIVE USE
Laryngoscopies, bronchoscopies, and microlaryngeal procedures were the
primary indications for HFJV. Even a small uncuffed insufflation catheter
protects the airway from aspiration and assures minimal discomfort during
emergence from anesthesia. Oral surgical procedures can also benefit from
235
high frequency ventilation and was used in 165 patients, especially for
outpatients. The method decreased postoperative discomfort of the patients.
Small tidal volumes which result in less movement in the operative field
simplify surgical dissection in hepatic resection or any operative procedure below
the diaphragm. HFV was therefore used in 147 patients during laparotomy.
Less fluctuation in the surgical field also is beneficial in craniotomies and
thoracotomies. Because the non-dependent lung is in semi-expanded condition
and is not under high pressure, the surgical dissection is facilitated and the gas
exchange is superior to that achieved by one lung ventilation. HFJV can even
be used for differential lung ventilation, for example during surgery on a
bronchopleural fistula (6).
4. POSTOPERATIVE USE
Postoperatively the indications are similar. Prevention of barotrauma
after lung surgery presents one group of indications. The second is given by
tolerance of HFJV by the patient. Weaning of patients from respiratory support
and assisted ventilation facilitates the decision whether the patient should be
extubated or sedated. Especially in patients who are fighting the ventilator
but are not yet fully awake and capable of spontaneous breathing, HFJV offers
a method of respiratory support with avoidance of further sedation. The patient
gradually resumes spontaneous breathing without struggling.
5. LONG TERM VENTILATION
The primary indication in long term ventilation is bronchopleural fistula
(7). HFJV maintains normal gas exchange despite the presence of a leak. In
respiratory distress syndrome it can be used to prevent hypercarbia (8). But
the method can also be used for prevention of barotrauma in patients with low
compliance lungs and resulting high airway pressure. The method was found
236
advantageous for assisted ventilation and weaning of ventilator dependent
patients as well (9). No sedation or muscle relaxant was needed and the patients
gradually resumed spontaneous breathing.
6. EMERGENCY USE OF HIGH FREQUENCY JET VENTILATION
Transtracheal jet ventilation should be the method of choice for emergency
airway management and respiratory support in hospital settings. It was
successfully used to secure the airway and prevent aspiration in cases of oral
and facial trauma or upper airway trauma. In that situation a cricothyroid
catheter allows ventilatory support before anesthesia is started. It is also
possible to displace a foreign body impacted at the level of the cords. In
suitable cases of difficult intubation this method permits avoidance of awake
intUbation.
7. MONITORING OF HIGH FREQUENCY VENTILATION
High frequency ventilation poses some problems in monitoring because of
rapid frequencies and small tidal volumes. In the range of most clinically useful
frequencies up to 600 per minute clinical observation remains an important
method. The observation of chest excursions and a precordial stethoscope give
useful information about ventilation and proper positioning of the endotracheal
tube. This is even more important if uncuffed endotracheal tubes or transtracheal
cannulas are used because in this case it is not easy to monitor the gas delivered.
On the other hand, if a cuffed endotracheal tube or tracheostomy tube is
used, capnography will give useful monitoring information. In our stUdies a
Perkin-Elmer MGAI00 AB mass spectrometer and shared respiratory monitoring
system with 150 feet lines and continuous suction by vacuum pump was used.
A teflon capillary tube allows sampling from a connector attached to the
proximal end of the endotracheal tube. The results are displayed on a remote
237
::~ 11:48
~'~I ,r-; 13:12
14:37
,elWIO IQ 18 16 14 12 10 8 6 4 2 0
TIME (sec)
FIGURE 1
238
monitor on the anesthesia machine. The C02 concentration in respiratory gases
fluctuated around mean exhaled value (2.25%). It never reached zero nor
alveolar gas values. When the patient started to breath high frequency pulses
were superimposed on spontaneous breaths (Fig. 1). The more the patient
breathes on his own, the higher will be the highest PC02 till eventually it will
be close to the arterial PCO 2.
Flow measurements with a Boums L875 ultrasonic flowmeter, a Critikon
A21A respiratory monitor with disposable Osborn pneumotachograph and with a
Perkin-Elmer ultrasonic VMS monitor yielded reproducible results up to 200
breaths per minute. With the VMS system not only the total expiratory minute
volume but aslo the entrainment could be accurately measured. Unfortunately
the flow measurements can be used only if a cuffed endotracheal tube is present
except with the MKSOO ventilator where the flow is measured and displa~
directly in the instrument.
Transcutaneous PC02 measurement in a series of patients performed with
a Narco tcPC02 monitor yielded results comparable to the ones obtained with
conventional ventilators. There was always a gradient but the trend was
identical. As a simple noninvasive method this will probably find more use
intraoperati vely.
The most important parameters, especially in patients with respiratory
failure were of course the arterial blood gases. In this regard the monitoring
of high frequency ventilation does not differ from methods used during respiratory
support in conventional ventilation.
S. CONCLUSION
Clinical experience with more than 700 patients shows that high frequency
jet ventilation is a worthwhile addition to our methods of respiratory support
and should be used in all situations where the patient can benefit from its basic
advantages. They include lower airway and intrapulmonary pressures, better
239
tolerance by the patient and avoidance of large cuffed endotracheal tubes under
certain circumstances. Monitoring of patients on high frequency ventilation can
be accomplished mostly by standard methods.
REFERENCES
1. Klain M: High frequency ventilation. Respiratory Care 26(5): 427-8, 1981.
2. Klain M, Smith RB: High frequency percutaneous transtracheal jet ventilation. Crit. Care Med. 5(6): 280-287, 1977.
3. Klain M, Keszler H, Nordin U: Is jet ventilation without cuffed tube safe? Anesth Analg 61(2): 195-196, 1982.
4. Klain M, Miller J, Kalla R: Emergency use of high frequency jet ventilation: Crit. Care Med. 9(3): 160, 1981.
5. Klain M, Keszler H, Brader E: High frequency jet ventilation in CPR. Crit. Care Med.9(5): 421-422, 1981.
6. Benjaminsson E, Klain M: Intraoperative dual-mode indpendent lung ventilation of a patient with bronchopleural fistula. Anesth Analg 60: 118-119, 1981.
7. Carlon GC, Ray C, Klain M, McCormack PM: High frequency positive pressure ventilation in management of a patient with bronchopleural fisula. Anesthesiology 52: 160-162, 1980.
8. Schuster DP, Snyder JV, Klain M, Grenvik A: High frequency jet ventilation during the treatment of acute fulminant pulmonary edema. Chest 80(6): 682-685, 1981.
9. Kalla R, Wald M, Klain M: Weaning of ventilator dependent patients by high frequency jet ventilation. Crit. Care Med. 9(3): 162, 1981.
PERI AND POSTOPERATIVE APPLICMIrn OF VARIOUS TYPES OF HIGH FREQUENCY VENTILATION < HFV )
H. BENZER, M. BAUM, ST. DUMA, A. GEYER, N. MUTZ
Before I turn to my actual subject, allow me to make a
few brief introductory comments on our "philosophical back
ground," which determined our approach to high frequency
ventilation.
We began studying high frequency ventilation techniques
in experiments in 1978 in order to come closer to our idea of
ventilation of the diseased lung with simultaneous immobilization
Our research in this field was there-
fore always focused on the search for methods of high frequency
ventilation which make ~~~~_!~~g~~~£~~~ and small tidal volumes
possible.
High frequency ventilation with high frequencies <> 300/min.
may be superior to lower frequencies «300/min. ) for the
following reasons:
1. ~~!!~~_~~~£~~~~~~!~£~ of the diseased lung.
High frequencies with a relatively stable mean airway
pressure, jet minimum inspiratory pressure, and PEEP may
lead to a type of "immobilization of the affected lung."
2. ~~~~_~i~~~~~_~!!~£!~_£~_!~~_~~~!~£~=~£!~~~_~Z~!~~. Prevention of rhythmic overexpansion of the alveoli will
decrease the turnover of surfactant, and thereby, safe
surfactant, which would be very important in ARDS.
3. ~~~~_~~~g~~~~!Z_£!_~~~!~~~!~£~' less mismatching.
It may be assumed in high frequency ventilation with high
frequencies that the diffusion component is activated.
4. !~£~~~~~i_~~£~~!£~Z~~~ and better lung clearance.
During high frequency ventilation, there is increased
secretolysis, and hence, improved clearance function.
241
Until today, our clinical experience with high frequency
ventilation includes 103 patients ( Table 1 ).
Table 1. High Frequency Ventilation ( F> 300/min. ): Clinical Experiment
Reason for using HFV No.of patients Method of HFV Duration of HVF
Intensive Care patients
Intraoperative application
Postoperative ventilation in cardiac patients
Total
43
26
34
103
(HFJV)FDV,HFP gh _ 16 days
FDV, HFP x 125 min.
HFP x 213 min.
During intra and postoperative application of high frequency
ventilation, we used two types of high frequency ventilation:
forced diffusion ventilat,ion
HFP ).
In forced diffusion ventilation, mixed gas with 5 bar is
available at the outlet of an oxygen blender. The required
initial pressure is adjusted via a reducer. The jet's pulsations
are controlled via a solenoid valve which is regulated from an
impulse generator with variable frequencies and variable inspira-
tion/expiration ratios. The jet is conveyed to the distal end
of the tube via 2 jet canals integrated into a specially designed
jet tube. The positioning of the tube is very important; the
location of the nozzles should be 1 1/2 cm over the carina.
This method allows frequencies of up to 1,500 in man with
very low tidal volumes of about 10:30 mI.
In high frequency pulsation, the nozzle at the proximal
end of the endotracheal tube extends into a transversely flowing
current of fresh gas. On the one hand, this fresh gas flow
serves moistening, but also mainly prohibits rebreathing, and
enables better elimination of CO 2 . This again allows, in
comparison to high frequency jet ventilation, the use of higher
frequencies with lower tidal volumes.
242
We used high frequency ventilation for intraoperative venti-
lation on 26 patients.
Forced diffusion ventilation was used on 7 patients during
abdominal surgery at frequencies from 300 up to 1,500 per minute
and an average duration of 144 min.
Forced diffusion ventilation was then used in lung surgery
on 7 patients at frequencies of 350/min. and an average duration
of 109 min.
12 patients were ventilated during lung surgery with high
frequency pulsation at a frequency of 300/min. and an average
duration of 121 min. Table 2).
Table 2. High Frequency Ventilation -- Intraoperative Applicatic
Diagnosis Operation No. of Pat. Method f/min.
gastroin- abdominal 7 FDV 300-1500 ----------testinal ~!!.!:.~~!:.L tumors
lung tumors !!!.:2.~ 7 FDV 350 lung cyst, ~!!.!:.~~::'l pleural thickening
" !~:2.~ 12 HFP 300
~!!.E:K~_E:l
Total 26
Duration of HF\ (min. :
x 144
x 109
x 121
243
Po02 [mmHs] Fi02=1ZI.5 Pa02 [mmHs] Fi02=1ZI.5
LUNG. SURG. 3121121 ABDOM. SURG. 3 121 IZIT
25121 25
2121121 2121
15121
11Z11Z1l
5~ l 5121
CMV F 0 V CMV F 0 V
,FIGURE 1. Pa0 2 in the FDV group.
Fig.1 shows the values of Pa0 2 in the FDV group. After
transition from conventional ventilation to forced diffusion
ventilation, there was a drop in arterial oxygen pressure in
the thoracic surgery group, especially during the stage of lung
surgery. It rose again after chest closure. In the abdominal
surgery group, there were, all in all, only slight changes in
arterial oxygen pressure.
244
PaC02 [mmHg] PaC02 [mmHg]
60 LUNG SURG. 60 ABDOM. SURG.
50 50
40
30
20 CMV F o V CMV F 0 V
,FIGURE 2. PaC0 2 in the FDV group.
In this group the arterial CO 2 pressure ( Fig. 2 ) rose in
the !~~~~~~~_~~~~~~r group at transition from conventional
ventilation to forced diffusion ventilation. However, it remaine,
within the tolerance range.
CO 2 pressure remained in normal range. At transition from con-
ventional ventilation to forced diffusion ventilation, it dropped
in some cases.
31'J1'J
251'J
288
158
188
58
P02 IN% OF CONTROUCMV]
IV P02 193
HIGH FREQUENCY PULSATION IN LUNG SURGERY[F=31'J1'J/min] [Fi02=iI.5]
[mmHgl
~ CMV HFP HFP HFP
8 2 3
fIGURE 3. Pa0 2 in the HFP group.
245
In the patient group on which we used HFP during lung surgery
with frequencies of 300/min. and an Fi02 pf 0.5, the arterial
oxygen pressure ( Fig. 3 ), shown in percent of control (CMV)
showed essentially no change in comparison to the control range
during all stages ( closed chest - 1 - open chest - 2 - and
closed chest - 3 - ).
246
HIGH FREIlUENCY PULSATION IN LUNG SURGERY [F=300/minl PC02[mmHgl
5'"
4'"
3'"
2'"
10
CMV HFP HFP HFP
2 3
FIGURE 4. PaC0 2 in the HFP group.
The arterial CO 2 pressure ( Fig. 4 ) also remained essential 1
unchanged after transition from conventional ventilation (CMV)
to HFP.
CONCLUSION
It is possible to maintain ~~~g~~!~_~~~_~~£~~~~~ with HFV
during major surgical procedures and even lUng surgery. An
improved exposition of the operation field can be acheived be
cause of the extensive resting position of the lungs caused by
high frequencies in connection with very small tidal volumes.
Small tidal volumes and, thereby, low peripheral pressure can
reduce gas volume loss in cases of pleural leakage. In using an
open system, there are other advantages in comparison to con-
247
ventional mechanical ventilation:
load during coughing manoeuvres.
There is no high pressure
Suction manoeuvres are possible
at any time without interrupting ventilation.
The weaning process is very easy, because there is no inter
ference with spontaneous breathing.
A combination with other techniques of ventilation like
IPPV, IMV, or ~E~E can be installed easily.
We do think that HFV will gain some significance in the
future in ventilating patients in the operating theater.
On patients following general surgery, we observed that
short-term postoperative ventilation with high frequency venti-
lation was advantageous. In using an open system, especially
the weaning process went very well, because high frequency
ventilation acts as a type of augmented ventilation.
Having this experience, we then used high frequency pulsation
in postoperative ventilation of postcardiac patients after extra
corporeal circulation.
First, 28 adult patients were ventilated postoperatively
with high frequency pulsation after aortocoronary bypass opera-
tions, valve replacement, and closure of septum defects. Fre-
quencies of 300 to 480/min. were used. The duration of post-
operative ventilation was an average of 230 minutes. This method
was then used on a group of 6 children. Here, the ventilation
frequency was 300 to 420; duration of postoperative ventilation
an average of 195 minutes
went well in all patients.
Table 3 ). The weaning procedure
Table 3. High Frequency Pulsation (HFP) in Postcardiac Patients
Group A:Adults Operation Diagnosis No.of.Pat. f/min.Duration Age of HFP, 'year~ (min.)
EKG(ACB, coronary 28 300-480 x 230 x 49 valve re- dis.valve placement, disease, closure) sept. defects
Group B:Chil- EKG sept.defect 6 300-420 x 195 x 5 dren (closure)
Total 34
248
Immediately after the patient's arrival at the intensive
care unit, he is ventilated for 20 minutes in a conventional
mode. After acquiring blood gas analyses, the ventilation is
changed to high frequency pulsation.
Pa02
400
300
200
100
HIGH FREQUENCY PULSATION IN POSTCARDIAC PATIENTS
PaC02
50 CMV HFP[300J CMV HFP[300J
40
FIGURE 5. Blood gases during postoperative HFP
Fig. 5 shows that in the transition from controlled venti
lation to high frequency pulsation, the arterial oxygen pressure
rose on the average.
unchanged.
Arterial CO 2 pressure stayed essentially
249
HIGH FREQUENCY PULSATION IN POSTCARDIAC PATIENS
Pa02 PaC02
400 50
300 0 200
::::::::::=
-----llZllZI
~
IZI 5 6 7 8 5 6 7 8 F [HZ]
<FIGURE 6. Blood gases in HFP and frequency of HFP.
Fig. 6 shows that arterial oxygen pressure improves with
increasing frequency, shown here in Hertz.
However, at the same time, it was shown that arterial
CO 2 pressure rises with increasing ventilation frequency.
CONCLUSION
In postcardiac patients, gas exchange could be maintained
well during controlled ventilation and the weaning period. In
all patients, the weaning procedure was favorable; there was
no interference with spontaneous breathing because of using an
open system.
Even in cases of severe secondary lung alterations, especially
in patients with mitral valve diseases, ventilation could be
controlled with high frequency ventilation.
250
The arterial oxygen tension improves with increasing fre-
quencies. Increasing the frequency was followed by decreased
efficiency of CO 2 elimination.
The arterial oxygen tension progressively improved as mean
airway pressure increased.
During high frequency pulsation, hemodynamics are very
stable. The counteraction to hemodynamics depends on the
frequency, inspiration/expiration ration, and t~ primary pressure
HIGH FREQUENCY JET VENTILATION IN THE POSTOPERATIVE PERIOD
A. SLADEN, K. GUNTUPALLI, M. KLAIN, AND C. MCCONAHA
Mechanical ventilation frequently is required for patients in the
postoperative period.
We elected to evaluate the feasibility and practicality of high frequency
jet ventilation as an alternative to mechanical ventilation during the initial
twenty-four hour postoperative period.
Our goals were to
1. devise an effective system,
2. define optimum initial jet ventilation settings,
3. assess ventilation and oxygenation,
4. observe the use of HFJV in endotracheal suctioning; and
5. assess HFJV as a weaning technique.
Ninety-four unselected patients admitted to Surgical and Neurosurgical
Intensive Care Units were ventilated with high frequency jet ventilation.
The patients' ages ranged from 10-92 years; 75% being 65 years and older.
There were 58% males and 42% females.
The operations included craniotomies 6%, thoracic procedures 17%
(pulmonary resections and esophagectomies), abdominal procedures 47% (porta
systemic shunts, gastrectomies, bowel resections, pancreatic resections,
adrenalectomies, nephrectomies and cystectomies with ureteral diversions), and
major vascular procedures 26% (abdominal aortic aneurysmectomies and aorto
bifemoral bypa,sses). There were 4% trauma patients who had no operative
procedures but received ventilatory support with the jet.
252
Jet System
Patients were ventilated with a VS 600 ventilator, an electronically
operated, high frequency jet ventilator which uses air or oxygen at 45 psi (Fig. 1).
FIGURE 1. Air-oxygen blender with high pressure tubing connecting blender outlet to rear of VS 600. .
253
At this pressure, a blended mixture of oxygen and air enters the ventilator
and exits at a selected regulated pressure through a plastic tube, about 100 cm
in length, to a Y piece attached to the jet port of a Ri-lo endotracheal tube
(Fig. 2).
FIGURE 2. Blended gases, at selected driving pressure, entering Y piece attached to jet port of RHo endotracheal tube.
254
This endotracheal tube incorporates a jet lumen in its wall, and the lumen
terminates about 5 cm above the tip (Fig. 3).
FIGURE 3. RHo endotracheal tube with jet lumen incorporated into the wall of the tube.
255
Into the other limb of the Y piece, half normal saline is infused at 5-6
ml/hour. This fluid is nebulized and hydrates the dry jetted gases. An additional
smaller lumen, built into the wall of the endotracheal tube terminates at the
tip of the tube and is connected to either a low pressure alarm device or a
pressure module (Fig. 4).
FIGURE 4. Infusion of fluid for nebulization into the other limb of the Y piece.
256
Entrainment System
An oxygen enrichment entrainment system is essential at the proximal end
of the endotracheal tube because of the "carburetor effect" of the jetted gases.
Oxygen, at the same FI02 as the jet mixture, flows through a heated nebulizer
to a 3 liter reservoir bag, and then through tubing to the proximal horizontal
limb of a T piece (Fig. 5).
FIGURE 5. Nebulized heated gases flow to a 3 liter reservoir bag and then to a T piece connected to an endotracheal tube.
257
The vertical limb of the T piece is connected to the endotracheal tube
while the distal horizontal limb is connected to another corrugated tube which
terminates with a PEEP valve (Fig. 6).
FIGURE 6. Afferent and efferent limbs of endotracheal tube with PEEP valve.
258
When the electric power supply to the ventilator is discontinued, jetting
ceases, and the system constitutes a continuous positive pressure (CPAP) system
(Fig. 7).
FIGURE 7. Continuous positive pressure (CPAP) system.
Settings
Our initial HFJV mode for a patient admitted to the ICU either is to
match the jet mode used in the operating suite or if HFJV has not been used
immediately prior to admission to use the following settings.
Driving Pressure 35 psi, Jet Rate 100/min, I:E Ratio 30:70, FI02 0.9,
PEEP 5 cm H20.
259
At a jet rate of 100/min and a pressure of 35 psi, a PEEP of 2-3 cm is
inherent in the system and only a 2.5 cm PEEP value is necessary, to provide
the initial required 5 cm PEEP. Absolute PEEP values are documented on a
strip recorder.
After 15-20 minutes of jet ventilation, arterial blood is sampled for blood
gases and ventilator adjustments are made to satisfy the patient's needs.
Ventilation. In the majority of patients, the driving pressure will need to
be reduced because of hyperventilation. At a frequency of lOO/min the driving
pressure appears to be the primary mode of C02 elimination. If hypercarbia
is present the pressure can be increased or the IE ratio changed. We have
observed increased efficiency of C02 elimination when the IE ratio is changed
from 30:70 to an IE ratio of40:60 or 50:50.
Oxygenation. FI02 can be titrated, by adjustment of the blender, to
provide optimum arterial oxygen tension. When a high FI02 is required because
of an increase in intrapulmonary shunting, additional PEEP is added to the system.
HFJV and PEEP in Acute Respiratory Failure 35 psi, frequency 100/min.
Physiologic Profile:
ZEEP CI 3.39 L/M2, P 93/m, SI 37 ml/M 2, TPRI 2412 dyne.sec.cm-5.M2,
Qsp/Qt 17%.
PEEP 10 cm H20 CI 2.81 L/M2, P 95/m, SI 30 ml/M2, TPRI 2813
dyne.sec.cm-5.M2, Qsp/Qt 12%
Cardiorespiratory profiles using HFJV, initially without and then with PEEP
showed a decrease both in cardiac index and intrapulmonary shunt. The effect
of PEEP on cardiac index and Qsp/Qt is similar to that seen with conventional
ventilation.
260
Suctioning without Hypoxemia
With a jet endotracheal tube, jetting can be continued during suctioning
and hypoxemia prevented. In a study of 15 patients, the mean decrease in
Pa02 with suctioning and jetting was 15 (404 to 389) mm Hg compared to
suctioning without jetting when the decrease was 90 (417 to 327) mm Hg. The
relevance of this study is the prevention of a fall in Pa02 in the patient who's
initial Pa02, is marginal.
Weaning
With resolution of postoperative respiratory failure or awakening from
anesthesia the jetting pressure was gradually reduced resulting in patients
breathing spontaneously and simultaneously with jet ventilation (Fig. 8).
FIGURE 8. This demonstrates a patient initiating spontaneous ventilation with superimposed high frequency jet ventilation.
261
Patients reported they were comfortable spontaneously breathing, while
jetted at 100 per minute.
They did not complain of the sudden breaths which occur with the IMV mode
of ventilation.
When the jetting pressure had been reduced to 10-15 psi, and arterial
blood gases were satisfactory, jetting was discontinued and the patient
allowed to breathe spontaneously with a CPAP circuit. Following
satisfactory arterial blood gases with CPAP they are extubated.
Complications and extubation
In the 94 patients reported, there were no complications associated with
HFJV.
85% were extubated within a 24 hour period, 15% demonstrated persistent
criteria consistent with acute respiratory failure and required HFJV for up to
14 days.
Conclusion
Our goals were aChieved,
1. high frequency jet ventilation for the postoperative patients is both
feasible and practical,
2. an effective system to oxygenate and ventilate was devised to which
PEEP could be added
3. optimum settings were defined
4. a significant fall in Pa02 with suctioning, could be prevented and
5. the potential for weaning was assessed.
We believe that HFJV offers a new and improved technique for venilatory
support of postoperative patients.
F. INTENSIVE CARE
HIGH FREQUENCY JET VENTILATION COMPARED TO VOLUME-CYCLED VENTILATION: A PROSPECTIVE RANDOMIZED EVALUATION
Graziano C. CARLON, Jeffrey S. GROEGER
INTRODUCTION
High Frequency Jet Ventilation (HFJV) is substantially different
from other forms of mechanical ventilation. The physical principle on
which HFJV operates is that of jet mixing and entrainment. Animal experiments
clinical case reports2- 4 and small serles feasibility studiesS ,6 have
demonstrated clinical applicability of HFJV. Results as expected in any
uncontrolled evaluation of a new teChnique have been controversial.
It is recognized that present clinically acceptable forms of ventila
tory management although based on sound physiological principles have not
been compared in a prospective. randomized manner in the critically ill.7
Volume Cycled Ventilation (VCV) with Intermittent Mandatory Ventilation
(IMV)7-1D has not been compared to controlled ventilation and different
end-points of Positive End Expiratory Pressure (PEEP) therapyll (best
compliance,12 pulmonary venous admixture of cardiac output,13 oxygen
delivery14) have not been compared for clinical efficacy.
As there is no technique of mechanical ventilation which is universally
accepted and specific contraindications of HFJV have not been identified,
a comparative study of its efficacy appears well justified.
MATERIAL AND METHODS
Patients admitted to the ICU of Memorial Hospital were assigned to
VCV or HFJV according to a table of random numbers if they were in respiratory
failure defined as the clinical inability to spontaneously maintain adequate
arterial oxygenation and/or alveolar ventilation. Postoperative patients
requiring respiratory support were not randomized as long as progressive
weaning from the ventilator was possible. If respiratory function worsened,
requiring increased support, they were then entered into the randomization.
Patients who died or improved enough to be extubated within 12 hours from
initiation of mechanical ventilation were excluded from the study. In
263
such cases the next patient was assigned to the same randomized from of
ventilation as the patients eliminated from the protocol.
VCV was delivered with IMV and PEEP.ls,16 Bear Medical Bear I
ventilators were used. Tidal volumes of 10-12 ml/kg, respiratory rate S
breaths/min, PEEP 5 cmH20 and Fi02 O.S were the initial settings. PEEP
was increased as need to provide a Pa02 2 70 mmHg with Fi02 S .40 and IMV
adjusted to maintain a pH 7.35-7.45 units. Weaning commenced when PEEP
was decreased to 5 cmH20 and was accomplished by progressively decreasing
IMV rates.
HFJV was delivered with six ventilators built at our Institution. 17
Gases are gated through a solenoid valve with a response time of ~ 10
msec. Inspiratory line is made of Teflon, 100cm long and 0.6cm in
diameter. A Scm injector cannula with an internal diameter of 1.62mm 1S
used.
Humidification with normal saline (15-30 ml/hr) is administered
through a parallel cannula, whose distal port opens in front of the jet
injector and is nebulized by the jet itself.
HFJV was administered at rates of 100 breaths/min with an Inspiratory/
Expiratory (I:E) ratio of 1:2. Driving pressure was initially adjusted
to provide a tidal volume of 3.5 ml/kg. PEEP was initially 5 cmH20 and
Fi02 0.8. Respiratory rate and I:E ratios were never changed. PEEP was
adjusted to provide a 8a02 ~ .90 with Fi02 ~ .45. Driving pressure was
increased or decreased to maintain PaC02 35-45 mmHg. Weaning was attempted
when PEEP was decreased to Scm and driving pressure was decreased to 10
psig. The patient would be taken off the ventilator and placed on CPAP
for 5-10 min. As clinically tolerated the length of spontaneous
breathing was progressively lengthened.
In all patients, intravascular volume expansion and/or inotropic
drugs were used as necessary to maintain cardiac index> 3.5 L/min/m2.1S
Patients were crossed from one form of ventilation to the other if
target goals ,were not achieved within 24 hours from initiation of ventila
tion. Crossover was continued for 24 hours and they remained on new form
of ventilator if they improved; otherwise they were returned to the
initially randomized ventilator type.
Patients who were randomized to HFJV were initially placed on VCV
until informed consent could be obtained. If at three hours informed
consent could not be obtained; they were excluded from the study.
264
Patients were monitored as follows:
1. ECG was continuously displayed on an oscilloscope (Abbott Medical
Electronics). Heart rate was read from the digital display of the
monitoring equipment.
2. Systemic blood pressure was monitored through a 20-gauge indwelling
arterial line. Transducers were calibrated against a reference mercury
column at least three times a day. Blood pressure tracings Were dis
played on an oscilloscope (Abbott Medical Electronics).
3. Pulmonary artery pressure was monitored through a balloon-tipped cath
eter (Edwards Laboratories) inserted percutaneously from a jugular,
subclavian or femoral vein. The trace was displayed on an oscilloscope
(Tektronix Physiologic Monitor 410). Systolic, diastolic and mean
pulmonary artery pressures were read from the digital display of the
monitoring equipment. Pulmonary artery wedge pressure was obtained by
planimetry from the oscilloscopic tracing during end expiration.
4. Cardiac output was measured in triplicate by thermodilution (Edwards
Laboratories 9520 A Cardiac Output Computer). Only values which did
not differ more than 20% from each other were accepted. Cardiac index
was calculated from cardiac output and body surface area.
S. Peak inspiratory pressure was obtained from the manometer of the
ventilator (Bear Medical BEAR I) on VCV. In the first four patients
randomized to HFJV, airway pressure was measured through an air-filled
catheter inserted into the alrway. The tip of the catheter was placed
at 30cm from the proximal port of the tracheal tube. As the results
exactly duplicated those of many previous animal studies, it was decided
to eliminate this aspect of monitoring which complicated airway toilette. 19
6 .. Arterial and mixed venous blood gases were collected as clinically
indicated and analyzed with a Corning 1L-175 blood gas analyzer. Hemo
globin concentration and saturation were measured with a IL-278 co
oxymeter. Methemoglobin and carboxyhemoglobin were also measured by
cooxymetry, and used in the computation of pulmonary venous admixture. 20
Fi02 was measured by mass-spectrometry (Perkin-EImers RMS-III Medical
Mass Spectrometer). To normalize PaOZ for different Fi02' the arterial/
alveolar index (Pa02 divided by FiOZ) was used. 2l
Total ventilatory time, individual patient duration of full support,
weaning phase and survival was recorded, as were hemodynamic and vent
ilatory variables (PEEP, tidal volume, PaC02, Pa02, Fi02' PaOZ/Fi02,
265
cardiac index, mean systemic and pulmonary artery and wedge pressure and
Qsp/Qt).
Whenever a statistical test was applied, P value < 0.05 was accepted
as significant.
RESULTS
Technical: 112 patients were ventilated with six high frequency jet
ventilators for a total time of 548 days without any technical complication.
The average consecutive duration of each episode of ventilation was 2.5
days. The longest time of continuous ventilation was 14.8 days. 109
patients were ventilated on VCV for a total of 528 days. The average
consecutive ventilatory period was 2.25 days, while the longest
continuous support was 18.75 days.
Clinical: 44/112 patients on HFJV (39%) survived as compared to 36/109
on VCV (33.3%). This does not represent a statistically significant
difference in survival. Duration of respiratory support for survivors of
HFJV and VCV are shown in Table 1.
TABLE 1
Full Support (days) Total Survived All Patients Survivors Weaning (days)
HFJV 112 44 (39%) 4.3 + 1.8 3.3 + 2.1 2.2 + 0.8
VCV 109 36 (33%) 4.9 + 4.2 4.9 + 2.3 1.1 + 0.2
All data expressed as mean ~ SEM.
Of 109 patients randomized to VCV, 29 (22%) could not be ventilated
or oxygenated well enough to reach the selected end-point. When crossed
to HFJV 21/29 (72%) improved initially and remained on HFJV for 3.5 + 2.8
days. All 29 patients expired.
Of 112 patients randomized to HFJV, 10 (9%) were crossed to VCV.
8/10 (80%) initially improved and 2/10 (20%) survived. They remained on
mechanical support 1.0 ~ 0.5.
Peak airway pressure was 20-70 cmH20 higher than PEEP on VCV, while
on,HFJV peak inspiratory pressure was never more than 8 cmH20 above PEEP
(Tab. 2).
Arterial oxygenation expressed as arteriolar/alveolar index (Pa02/Fi02)
was greater in VCV than HFJV. Oxygenation was better in all survivors.
Qsp/Qt was higher on HFJV in all patients compared to VCV (Tab. 2).
In all patients alveolar ventilation as indicated by PaC02 was
better on HFJV than VCV. Survivors on HFJV had PaC02 significantly
lower than those that expired (Tab. 2).
266
Variable
PEEP
cmH20
TABLE 2
HFJV Outcome No. Value
Survived 592 t* 7.63 + 0.16
Died 2202 * 10.28 + 0.12
Driving Pressure Survived 559
2038
t 14.0 + 0.16
17.0 + 0.1 psig Died
Tidal volume
(ml/kg)
Peak inspiratory
Survived
Died
611 t* 3.35 + 0.05
1801 * 4.0 + 0.03
pressure Survived * 3 - 5 cmH20 ) PEEP cmH20
Pa02/Fi02
units
Pa02
mmHg
Fi02
fraction
PaC02
mmHg
Cardiac Index
L/min/m2
Qsp/Qt
%
Died
Survived
Died
Survived
Died
639
2356
t* 196 + 3.1
*169+1.5
639 t* 81.7 + 1.1
2362 * 74.6 + 0.6
Survived 639 t* 0.44 + 0.0
Died 2359 * 0.47 + 0.0
Sur~ived 639 t* 38.3 + 0.3
Died 2358 * 40.8 + 0.2
Survived 215 t* 3.51 + 0.1
Died 901 * 3.87 + 0.04
Survived 215 t* 0.13 + 0.01
Died 830 * 0.18 + 0.00
* P < 0.05 HFJV compared to VCV
VCV No. Value
543 + 5.39 + 0.13
1306 8.29 + 0.13
517
1171
12.4 + 0.08
12.6 + 0.07
487 t 36.6 + 0.5
1117
598
1401
598
1404
605
1402
601
1402
148
406
185
452
46.0 + 0.4
t 250 + 3.6
194 + 2.2
t 97 + 1. 5
82 + 1.0
to.40 + 0.0
0.45 + 0.0
42.0 + 0.3
43.0 + 0.2
4.1 + 0.1
4.3 + 0.08
0.11 + 0.01
0.14 + 0.01
t P < 0.05 Patients who survived compared to those who died
All data expressed as mean + SEM
Fi02 recorded was consistent with selected end-points of therapy (Tab 2).
Tidal volume on VCV was 12.5 ~ 0.8 ml/kg in all patients. Tidal
volume required to provide desired alveolar ventilation on HFJV was 3.4 +
0.05 ml/kg in survivors and 4.0 ~ 0.03 ml/kg in those that expired. Driving
pressure required to achieve these tidal volumes were 14.0 + 0.17 psig
and 17.0 ~ 0.1, respectively (Tab. 2).
Correlation of tidal volume to driving pressure can be established
267
on HFJV with an increase of 10.5 ml/psig (driving pressure) in both
patients who lived or died. The y-intercept was 98ml for survivors and
101 for those that expired.
500
400
-g 300 (I)
E ::I (5 > ~ 200 i=
Figure 1
TIDAL VOLUME vs. DRIVING PRESSURE
---Patients who died y = 100 + (10.46 ± 0.6)x -Patients who survived y = 98 + (10.75 ± 0.5)x
O~----~----~----~-----L-----J
Driving pressure (psig)
Changes of tidal volume for changes of driving pressure in patients who died and in patients who survived after HFJV support. For each outcome, three slopes are provided (mean + SD).
DISCUSSION
Mortality in the immunosuppressed pancytopenic patient with systemic
malignancy and respiratory failure requiring mechanical ventilation is
usually very high (70-80%).22,23 In this homogenous group improvement
associated with· different techniques may therefore become more apparent.
Utilizing IMV with PEEP and setting clinical end-points for both VCV
and HFJV, we compared not only two methods of ventilation but also two
management strategies. With HFJV end-point was maximization of oxygen
transport and with VCV maximization of lung compliance, spontaneous
268
ventilation and oxygen transport.
Data provided shows that available technology for HFJV can safely
provide prolonged respiratory support with the same ease as VCV. The
highest driving pressure required by an individual patient was 38 psig;
well within the capabilities of centralized gas distribution systems;
mean driving pressure values were quite lower.
Severity of lung disease did not have any effect on delivery of
tidal volume. Resistance to jet flow is determined by cannula diameter
and length; thus the slope of tidal volume/driving pressure is identical
in patients who lived and died (Fig. 1). PEEP, causing a few cmH20
increase in airway pressure cannot significantly effect resistance and
had no influence on driving pressure.
Clinically patients did equally as well on HFJV as VCV. Survival
rate and total respiratory support time were identical. Full mechanical
support was longer on VCV, but weaning was longer on HFJV due to different
techniques employed. There were five episodes of barotrauma on VCV and
five on HFJV; an incidence well below other reported series. Z4
More patients required changes from VCV to HFJV, than vice versa,
and survived longer after the cross-over. This may be due to the strategy
of management, which on VCV requires re-expansion of lung volume to improve
compliance, thereby decreasing work-of-breathing, and to reduce shunt.
Functional residual capacity may have to increase to 150-Z00% of
predicted if shunt must decrease to the arbitrary value of 15%.Z5 Initial failure to ventilate patients with VCV or HFJV is a function
of the severity of pulmonary pathology, rather than mechanical support
used; all patients who were crossed over ultimately expired.
Reflecting different end-points chosen for HFJV and VCV, PaOZ was
higher on VCV both as an absolute and more so if FiOZ was considered.
Cardiac index was higher on VCV because purposeful intervention to sustain
that value was more common by a factor of 3:1. An increase in cardiac
index is necessary to reach a higher mixed venous PvOZ to minimize effects
of shunt fraction on arterial PaOZ' Shunt was only 3% higher on HFJV as
compared to VCV.
Substantial differences are seen between the mode of action of the
devices. COZ clearance occurs with tidal volumes of 4 ml/kg or less on
HFJV, one third as high as those required on VCV.Z6 On HFJV tidal volume
in patients who expired was 0.5 ml/kg higher than those who survived, a
269
small but statistically significant difference. These findings indicate
that alveolar ventilation can be fully maintained with very low tidal
volumes and suggest that diffusion cannot be the only mechanism of C02
clearance on HFJV. Gas convection must increase when lung function
deteriorates with greater mismatch of ventilation with perfusion.
Progressive improvement of arterial oxygenation with HFJV is In line
with the expected mechanism of action and natural history of acute
respiratory failure. When a constant and continuous distending airway
pressure lS applied to animals in respiratory failure, functional residual
capacity progressively increases. 27 ,28 Lung hysteresis favors continuous
recruitment of alveoli without the need for large breaths at high peak
inspiratory pressures. When HFJV is applied at rates of 100 breaths/min,
collapsed lung segments re-expand and remaln distended despite low tidal
volumes. 29 Application of continuous distending airway pressure is
protective of alveolar surfactant,30 while VCV with elevated peak pressures
damage the surfactant layer. 3l Dysfunction of alveolar surfactant by
hyperventilation with VCV may be greater in the critically ill patient as
the alveolar pool of surfactant may be reduced if nutrition is not
adequate. 32 HFJV with small tidal volumes and continuous airway pressure
should be ideal to protect surfactant.
The overall implications of this study are numerous. HFJV with
tidal volumes of no more than 4 ml/kg is practical and safe for prolonged
periods of support in patients with respiratory failure. Conventional
goal-oriented therapy with VCV where attempts are made to minimize shunt
with PEEP and to favor spontaneous ventilation with IMV did not improve
morbidity or mortality nor reduce duration of ventilatory assistance.
Pharmacologic intervention to maintain cardiac index above 3.5 L/m2/min
was needed three times as frequently on VCV as on HFJV, further investiga
tion is needed to define the exact mechanism whereby peak pressure or
other aspects of VCV interfere with hemodynamics.
HFJV does not increase survival but is effective In the management
of acute respiratory failure. The population studied normally has a very
high mortality with multisystem failure. Further study is indicated to
evaluate specific forms of respiratory failure, which may benefit from
HFJV.
270
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2. Carlon GC, Ray C Jr, Klain M, McCormack PM. 1980. High frequency positive pressure ventilation in management of a patient with bronchopleural fistula. Anesthesiology 52:160.
3. Schuster DP, Snyder JV, Klain M, Grenvik A. 1981. High frequency jet ventilation during the treatment of acute fulminant pulmonary edema. Chest 80:682.
4. Kiszler H, Klain M. 1980. Tracheobronchial toilet without cardiorespiratory impairment. Crit Care Med 8:298.
5. Carlon GC, Kahn RC, Howland WS, Ray C Jr, Turnbull AD. 1981. Clinical experience with high frequency jet ventilation. Crit Care Med 9:1.
6. Carlon GC, Ray C Jr, Pierri MK, Groeger J, Howland WS. 1982. High frequency jet ventilation. 81:350.
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8. Downs JB, Klein EF Jr, Desautels D et al. 1973. Intermittent mandatory ventilation: a new approach to weaning patients from mechanical ventilators. Chest 64:331.
9. Petty TL. 1981. Intermittent mandatory ventilation reconsidered. Crit Care Med 9:620.
10. Sahn SA, Lakshminaryan S. 1973. Beside criteria for discontinuation of mechanical ventilation. Chest 63:1002.
11. Ashbaugh DG, Bigelow DB, Petty TL, Levin BE. 1967. Acute respiratory distress in adults. Lancet 2:319.
12. Suter PM, Fairley HB, Isenberg MD. 1975. Optimum end-expiratory pressure in patients with acute pulmonary failure. N Eng J Med 292:284.
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14. Civetta 3M, Barnes TA, Smith LO. 1975. Optimal PEEP and intermittent mandatory ventilation in the treatment of acute respiratory failure. Resp Care 2:551.
15. Rinaldo JE, Rogers RM. 1982. Adult respiratory distress syndrome. N Eng J Med 306:900.
16. Hudson LD, Ed. 1981. Adult respiratory distress syndrome. Semin Resp Med 2:99.
17. Carlon GC, Miodownik S, Ray C Jr, Kahn RC. 1981. Technical aspects and clihical implications of high frequency jet ventilation with a solenoid valve. Crit Care Med 9:47.
18. Shoemaker WC, Pierchala C, Chang P, State D. 1977.Prediction of outcome and severity of illness by analysis of the frequency distribution of cardiorespiratory variables. Crit Care Med 5:82.
19. Carlon GC, 'Ray C Jr, Goetz WS, Groeger J. 1981. High frequency jet ventilation in respiratory failure: infuence of driving pressure and cannula size. Crit Care Med 9:159.
20. Cohn JD, Engler PE. 1979. Shunt effect of carboxyhemoglobin. Crit Care Med 7:54.
21. Keighley GR. 1974. The arterial/alveolar oxygenation: an index of gas exchange applicable to varying inspired oxygen concentrations. Am Rev Resp Dis 109:142.
22. Carlon GC. 1978, Respiratory failure in cancer patients. Curr Prob in Cancer 4:3.
23. Hewlett RI, Wilson AF. 1977. Adult respiratory distress syndrome
CARDS) following aggressive management of extensive acute lymphoblastic leukemia. Cancer 39:2422.
24. Kirby RR. 1979. Ventilatory support and pulmonary barotrauma. Anesthesiology 50:1981.
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25. Rose DM, Downs JB, Heenan TJ. 1981. Temporal response of functional residual capacity and oxygen tension to changes in positive end-expiratory pressure. Crit Care Med 9:79. .
26. Carlon GC, Ray C Jr, Kvetan V, Groeger J. 1981. High frequency jet ventilation in oleic acid injured lungs. Crit Care Med 9:161.
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28. Faridy EE, Permutt S, Riley RL. 1966. Effect of ventilation on surface forces in excised dogs' lungs. J Appl Physiol 21:1453.
29. Carlon GC, Turnbull AD, Alexander JD, Howland WS, Beattie EJ: High frequency jet ventilation during tracheal surgery. Crit Care Med 1981; 9:163.
30. Webb HH, Tierney DF. 1974. Experimental pulmonary edema due to intermittent posLtLve pressure ventilation with high inflation pressures: protection by positive end-expiratory pressure. Am Rev Respir Dis 110:556.
31. Wyszogrodski I, Kyei-Aboagye K, Taeusch HW Jr, Avery ME. 1975. Surfactant inactivation by hyperventilation: conservation by endexpiratory pressure. J Appl Phyiol 38:461.
32. Thet LA, Alvarez H. 1982. Effect of hyperventilation and starvation on rat lung mechanics and surfactant. Am Rev Resp Dis 126:286.
272
COMPARATIVE STUDIES OF CPPV AND HFPPV IN CRITICAL CARE PATIENTS: CLINICAL EVALUATION AND STUDIES ON INTRAPULMONARY GAS DISTRIBUTION
U.H. SJOSTRAND*t, U.R. BORG*, LA. ERIKSSON*, R.B. SMITHt, L.M. WATTWIL*
*Department of Anesthesiology and Intensive Care, Regional Hospital of Orebro, Orebro, S-70185 Sweden; tDepartment of Anesthesiology, The University of Texas Health Science Center, San Antonio, Texas 78284, USA
During recent years, the introduction of low compression
ventilator systems (1-3) has increased the use of high fre-
quency positive pressure ventilation, HFPPV (4). The present
study was motivated by the need to compare clinical data on
conventional positive pressure ventilation and HFPPV in cri-
tically ill neonates and adults (2,5,6,7).
In the first part (8) of this study on patients with re-
spiratory failure (RF), comparisons were made between a con-
ventional "volume-controlled" ventilator (SV-900) and a pro-
totype of a low-compressive system for volume-controlled ven-
tilation (system H). In the second part (9) of this study,
ventilatory patterns (pneumotachography) and intrapulmonary
gas distribution (nitrogen washout) were studied in patients
during continuous positive pressure ventilation (CPPV) and
HFPPV.
METHODS AND PROCEDURES
The procedures of this investigation were approved by the
Ethics Committee of the Regional Hospital in Orebro (RHO).
273
The clinical evaluation was performed during December, 1980
through May, 1981 at RHO. All patients were treated for RF
and received therapy according to established routines within
the ICU.
Patients
Part 1. Twelve patients (8 men and 4 women; mean age 66
years) with RF were studied. The criteria for RF was the need
for high FI02 (~0.4 despite adequate PEEP) in order to obtain
an acceptable arterial oxygen tension with respect to the
patient's clinical condition.
Part 2. Ten patients (8 men and 2 women; mean age 63 years)
with respiratory failure (RF) were studied. 7 required an
initial FI02 of 0.4 or more.
Measurements and procedures
Arterial pressure and blood samples for gas analysis were
obtained from a radial artery catheter. A pulmonary artery
catheter was inserted percutaneously for measurements of cen
tral venous (CVP), pulmonary arterial (PAP) and pulmonary cap
illary wedge (PCWP) pressures and sampling of mixed venous
blood. Cardiac output (CO) was measured by the thermodilution
technique.
Tracheal intubation was performed with a Deane tube no. 8
(National Catheter Corp., Inc., Argyle, NY) with a special
lumen for intratracheal pressure measurement or respiratory
gas sampling. For direct measurement of the intrapleural
pressure (Ppl), a previously described technique was used (8).
All catheters were filled with saline and connected to
saline-filled transducers. In two patients, intratracheal
274
pressure (ITP) was measured with two systems, one through the
saline-filled channel of the Deane tube connected to a trans
ducer EM 751A (flat amplitude/frequency response of DC-12 Hz),
and the second via a catheter tip transducer (DC-20,000 Hz)
inserted 2 cm distal to the end of the Deane tube. Similar
measurements were also made in a previously described lung
model (10) with adjustable linear static compliance.
Arterial and mixed venous blood samples were immediately
analyzed for gas tensions and acid base balance in an auto
matic analyzer with all values corrected for patient's temper
ature. FI02 was measured by means of a quadropole mass-spec
trometer. The average tidal volume settings giving normoven
tilation (normocarbia, PaC02 40 mmHg) were studied in a lung
model(lO) with static compliances of 30, 60 and 90 ml/cm H20.
The uniformity of distribution of inspired gas, measured by
a mul tiple-breath NWO technique (11), was not studied until
the patient was managed with an FI02 of 0.3 at a PEEP of 10
cm H20. Fractions of inspired (FIN2) and expired (FEN2)
gases were obtained via the separate channel in the Deane
tube and measured by means of a quadropole mass-spectrometer.
Oxygen ventilation was continued until FEN2 had decreased to
less than 2% above gas impurities. The NWO curves were
resolved into their components and single or multiple lung
spaces were defined, an index of deviation of the observed
pattern of gas distribution from the ideally uniform pattern,
denoted nitrogen washout delay (NWOD), was obtained for
each condition studied, using the equation:
275
NWOD%= X 100
Ventilators and procedures
Comparisons were made between a conventional "volume-con
trolled" ventilator, SV-900 (Servo Ventilator 900, Ventilator
Division, Siemens-Elema AB, Solna, S-17195 Sweden~ Siemens
Elema Ventilator Systems, Elk Grove Village, IL 60007), and
a prototype (2,3,6) of a low-compressive system (Siemens-Elema
AB, Sweden) for volume-controlled ventilation (system H).
The temperature (36°C) and the relative humidity (98%) in the
upper part of the tracheal tube/cannula were the same in both
systems.
Three ventilatory patterns were studied~ two at f of 20
breaths/min (SV-900 and system H), denoted SV-20 and H-20, and
one at f of 60 breaths/min (system H), denoted H-60 (H-60
HFPPV) • The ventilator settings were the same (6) as in a
preceding experimental study (SV-900: inspiration time [t%]
25% with an end-inspiratory pause of 10% of the ventilatory
cycle~ system H: t% of 22%).
The patient circuit of system H includes a pneumatic valve
connector (1,2), which permits suctioning during ventilation
(2,3,12). In system H, the internal volume of the patient
circuit is only 3%, and the internal static compliance only
2%, of the total values of SV-900 (3). A number of alarm and
safety functions are included in system H (2).
In order to counteract the reduction of functional residual
capacity (FRC) that normally takes place during mechanical
276
ventilation (3), all patients were ventilated applying PEEP,
usually at a level of 7.5-10 ern H20.
In the supine position, ventilation was provided with both
SV-900 and system H in all patients, but alternatively com
menced with SV-900 (at f of 20/min) or system H (at f of 20
or 60/min, respectively). All measurements were performed
after a period of at least 20 min of normocarbia and steady
state of cardiovascular functions (6,13).
All ventilatory volumes were determined with an ultrasonic
volumeter and in some patients also by means of a Tissot tank
spirometer. For calculation of the delivered total tidal
volume (VT Tot) of the ventilators, the expired gas volume was
divided by the number of ventilatory cycles during the collec
tion period. The compression volume (Ve) was calculated as
the product of measured internal pressure at end-insufflation
and the internal static compliance (ISC) of the patient cir
cuit (2,3). The effective tidal volume (VT Eff) was obtained
by subtracting Vc from VT Tot (VT Eff = VT Tot - Ve)·
All differences were tested for statistical significance
by means of the non-parametric Wilcoxon matched-pairs signed
ranks test (13).
RESULTS
The three types of ventilation could be performed in all
patients. In no case was the immediate cause of death due
to either hypoventilation or hypoxia, although 5 of the 12
patients in the first part of the study died (mortality 42%).
No complications related to the procedures of the investiga
tion were observed.
277
There were no differences in systemic arterial pressure or
heart rate during ventilation with the three ventilatory modes.
With H-60, the delivered tidal volume for normoventilation was
290 (~ 102) ml, which was approximately 46% (SV-20; 539 ~ 153
ml) and 50% (H-20; 576 ~ 191 ml) of that required at f of 20/
min. There was a reduction of mean airway pressure (ITPmean )
with H-60.
Two simultaneous airway pressure recordings in a patient,
one with the aid of the catheter tip transducer and the other
via the separate channel of the Deane tube connected to a
transducer, showed no major differences. The results exclude
the presence of excessive pressures or oscillations during
H-60.
The amount of sedatives and respiratory depressant drugs
were calculated (12) in 4 patients.
ventilation with H-60 was 20-50% of
The requirement during
tha t with SV-20. At
normocarbia and with the same FI02, our impression was that
that H-60 provided less "discoordination" than SV-20 and
H-20.
The ventilatory patterns of SV-20, H-20 and H-60 were
studied by using a previously described lung model (10) with
a linear compliance similar to the clinical setting. Obvious
differences in ventilatory patterns are present during the
inspiratory phase (Fig.l). System H delivers an instanta
neous, while SV-20 del ivers a delayed, accelerating flow,
which in both cases turns into a decelerating flow during
the major part of
between onset of
the inspiratory phase. The time in msec
inspiration and 90% maximal inspiratory
278
flow rate was measured in a lung model with 3 linear static
compliances during ventilation with SV-20, H-20 and H-60
(Table 1). With H-20 and H-60, the average delay is about
30 msec, but with SV-20 the delay is almost 85 msec, irrespec-
tive of lung compliance.
Recordings of Ventilatory Patterns In a Lung Model
---- 5v-20 -H-20
I 2 Time (sec)
Recordings of Ventila10ry Patterns," a Lung Model
~: ~----, ~ ~ ~ ollJ1k}.--V .~ -05 L-/-------- l
-10 .--- sv-20 -H-60
o I 2 Time (sec)
FIGURE 1. Gas flow in upper end of tracheal tube (VE) and the delivered tidal volume (VT Tot) with SV-900 and system H in a lung model (linear compliance 59 mljmin H20). During ventilat ion with H-20 and H-60, VT Tot is equal to the effective tidal volume (VT Eff)' providing there is no leakage (reproduced from 9 ) • Left: SV-20 and H-20. Right: SV-20 and H-60.
Time in msec Between Onset and 90% of Maximal (VE 90%) Flow
Ventilatory Static Compliance of Lung Model Pattern (ml/cm H2O)
(~E 90%) 27 59 90
SV-20 (SV-900) 88 80 84
H-20 (System H) 29 34 34
H-60 (5ystem H) 29 29 34
TABLE 1. Acceleration of gas during early inspiration, evaluated as time in msec between onset and 90% of maximal (VE 90%) flow studied in a lung model with 3 linear static compliances.
Studies on NWOD% (Fig. 2) show improved intrapulmonary gas
distribution with H-60 (R ~ 0.05). Taking uneven gas distri
bution into consideration (in patients with severe pulmonary
dysfunction), the corrected NWO curves give the same result.
i
70 60
.0
i 10
l! • 8 ~ Ii 6
i 5 Z 4
279
NWOD % = no ~ini It 100
~H- 60" 74.2% NWOD H- 20' 87.6%
SV- 2O-1CXi.9%
FIGURE 2. Average nitrogen washout curves (solid lines) during SV-20, 8-20 and 8-60 (average of all patients). Corrected nitrogen curves are indicated by dotted lines. The NWOD% values calculated according to Fowler ~t ale (11) display a significant difference (£ ~ 0.05) between 8-60 and SV-20.
DISCUSSION
Controlled mechanical ventilation aims to achieve gas
exchange without "cliscoordination" (out of phase problems)
between the patient and the ventilator. In RF this is often
accomplished by a combination of hyperventilation, high FI02,
PEEP and use of sedatives, respiratory depressants, and some-
times neuromuscular blocking agents. Despite this, in severe
RF discoordination between patient and ventilator sometimes
is a prominent problem during controlled mechanical ventila-
tion. The experimentally and clinically documented inhibition
of spontaneous respiration during 8FPPV (14,15) has the impli-
cation of less need for sedation and better acceptance of mech-
anical ventilation (12).
280
Circulation and oxygen transport
There were no differences in variables associated with cir-
culation and oxygen transport. Appropriate levels of PEEP
were used to reduce airway closure and ventilation/perfusion
mismatch. In most patients, arterial oxygenation was rela
ted to mean airway pressure during all three modes of venti
lation. Although the ventilation-synchronous variations in
CVP, PAP and PCWP were abolished during normoventilation with
H-60 (1,3,13,14), cardiac index did not improve. The reason
for unchanged cardiac index is probably that the differences
in transpulmonary pressure were too small to influence cardiac
filling and performance.
Ventilators and ventilatory patterns in conducting airways
In conventional systems there is a significant compressible
volume and the delivered total tidal volume (VT Tot) and ef
fective tidal volume (VT Eff) are not equal (1-3,6). System H
is a low-compressive system and VT Tot is almost equal to
VT Eff if there is no leakage within the patient circuit (3,6).
System H provides volume-controlled ventilation in its proper
sense (2), with volume as the preset ("independent") variable
and pressure as the measured ("dependent") variable. During
H-60, maximal inspiratory gas flow was almost twice as high
as during SV-20 (Fig. 1), and with system H maximal flow
rate was attained much earlier (Table 1).
The linear velocity of gas during HFPPV was calculated pre
viously (16). It is in the order of 2,500-3,000 em/sec, cor
responding to peak Reynold's numbers of well above 10,000 and
thus turbulent flow (16). With H-60, the zone of turbulent
281
flow reaches further down in the conducting airways and the
ventilatory pattern (Fig. 1) may therefore increase gas mix
ing, secondary to turbulence in conducting airways. The ab
sence of a "no flow" period during HFPPV further facilitates
intrapulmonary mixing of gas.
Patient's acceptance
The three types of ventilation could be administered in all
patients, but it was not possible to find a suitable method
for comparis~n of the patient's acceptance. However, under
long-term t'teatment .. 4 patients showed less need for analge
'sic and sedative drugs during ventilation with H-60 than with
SV-20. Even if such comparisons are questionable, the results
are in keeping with our previous (12) and present impressions.
Also, the patients accepted ventilation with H-60 better as
there was less "fighting the ventilator" than with H-20 or
SV-20.
CONCLUSIONS
This study found H-60 (HFPPV) to be equally efficient in
regards to cardiac performance and oxygen transport, and as
well accepted by the patient as conventional controlled
ventilation (SV-20). As the incidence of barotrauma during
positive-pressure ventilation is high, the lower mean ITP
with H-60 may be of clinical importance. In critically ill
patients, continued mechanical ventilation with oxygen dur
ing suctioning through the pneumatic valve is an important
feature of system H (2,3,8).
In terms of NWOD%, the present study shows that H-60
(HFPPV) gives more efficient intrapulmonary gas distribution
282
than a conventional ventilator (SV-20). During NWO with
oxygen, high concentration of N2 in the initial expiratory
gas with H-60 indicates enhanced transfer and/or mixing of
gas in the conducting airways. Studies in the lung model
show that a ventilator with minimal compressible volume
(system H), contrary to a conventional ventilator system
(SV-900), generates high flow and delivers VT Tot equal
to VT Eff. Without the delay present in conventional ven-
tilator systems, system H delivers the effective tidal vol-
ume with high linear velocity, increasing gas mixing second-
ary to turbulence. It is important to note that the enhanced
gas mixing and improved gas distribution in HFPPV are accom-
plished with lower mean airway pressure.
REFERENCES
1. Sjostrand U: Review of the physiological rationale for and development of high-frequency positive-pressure ventilation - HFPPV. Acta Anaesth Scand (Suppl) 64:7, 1977.
2. Sjostrand U: Pneumatic systems facilitating treatment of respiratory insufficiency with alternative use of IPPV/ PEEP, HFPPV/PEEP, CPPB, or CPAP. Acta Anaesth Scand (Suppl) 64:123, 1977.
3. Sjostrand U: tion (HFPPV):
High-frequency positive-pressure ventilaA review. Crit Care Med 8:345, 1980.
4. Hattox JS: Editorial Contempo '81: Anesthesiology. JAMA 245:2182, 1981.
5. Sjostrand UH, Eriksson IA: High rates and low volumes in mechanical ventilation - not just a matter of ventilatory frequency. Anesth Analg 59:567, 1980.
6. Borg U, Eriksson I, Sjostrand U, Wattwil M: Experimental studies of continuous positive-pressure ventilation and high-frequency positive-pressure ventilation. Resuscitation 9: 1, 1981.
283
7. Carlon GC, Howland WS, K1ain M, Go1diner PL, Cole R Jr: High frequency positive pressure ventilation for ventilatory support in patients with bronchop1eura1 fistulas. Crit Care Med 7:128, 1979.
8. Wattwi1 LM, Sjostrand UH, Borg UR: Comparative studies of IPPV and HFPPV with PEEP in critical care patients -a clinical evaluation. Crit Care Med, 11, 30, 1983.
9. Wattwi1 LM, Sjostrand UH, Borg UR, Eriksson IA: Comparative studies of CPPV and HFPPV with PEEP in critical care patients - studies on intrapulmonary gas distribution. Crit Care Med, 11, 38, 1983.
10. Borg U, Eriksson I, Lyttkens L, Nilsson L-G, Sjostrand U: High-frequency positive-pressure ventilation (HFPPV) applied in bronchoscopy under general anaesthesia - an experimental study. Acta Anaesth Scand (Suppl) 64:69, 1977.
11. Fowler WS, Cornish ER, Kety SS: Lung function studies. VIII. Analysis of alveolar ventilation by pulmonary N2 clearance curves. J Clin Inv 31:40, 1952.
12. Bjerager K, Sjostrand U, Wattwil M: Long-term treatment of two patients with respiratory insufficiency with IPPV/ PEEP and HFPPV/PEEP. Acta Anaesth Scand (Suppl) 64:55, 1977 •
13. Eriksson I, Jonzon A, Sedin G, Sjostrand U: The influence of the ventilatory pattern on ventilation, circulation and oxygen transport during continuous positive-pressure ventilation - an experimental study. Acta Anaesth Scand (Suppl) 64:149, 1977.
14. Jonzon A, Oberg P~, Sedin G, Sjostrand U: High-frequency positive-pressure ventilation by endotracheal insufflation. Acta Anaesth Scand (Suppl) 43:1, 1971.
15. Jonzon A: Phrenic and vagal nerve activities during spontaneous respiration and positive-pressure ventilation. Acta Anaesth Scand (Suppl) 64:29, 1977.
16. Eriksson I: The role of conducting airways in gas exchange during high-frequency ventilation - a clinical and theoretical analysis. Anesth Analg 61:483, 1982.
ALTERNATIVES TO CONVENTIONAL VENTILATION
T. JAMES GALLAGHER
Over the last two years in the United States interest
in high frequency ventilation (HFV) has surged. The technique is not really new, having been introduced in Sweden
almost fifteen years ago. The original idea was to provide adequate oxygenation and alveolar ventilation during rigid bronchoscopy and laryngeal surgery. Sjostrand and his colleagues generated frequencies of 60 to 120 positive pressure
breaths per minute.
Compared to conventional ventilatory modes, HFV offers several distinct advantages. The principal characteristic,
allowing a tidal volume less than dead space, reduces both
mean airway and peak inflation pressures. That translates
into a less impaired cardiac function, particularly venous return and right ventricular afterload. Additionally, pul
monary barotrauma, which relates to both distending pressure
and to lung volume, should also be lessened. Delivery systems for HFV are highly variable. The var
ious terms, high frequency positive pressure ventilation (HFPPV), high frequency jet ventilation (HFJV), and high frequency oscillation (HFO), are not interchangeable 7 each system is distinct and, physiologically, the results are not
the same. The original concepts of Sjostrand provided us with
HFPPV. The ventilator delivers positive breaths at frequen
cies greater than 60 per minute and uses the low-compliance,
non-distensible circuitry common to all high frequency sys
tems. This is necessary because the small volumes delivered
make humidification a problem. The circuit is directly at
tached to an endotracheal tube, originally to either an un-
285
cuffed tube or to a trans laryngeal catheter. Both permitted
exhalation around themselves. Since the development of sen
sitive exhalation valves, cuffed endotracheal tubes are more
often used.
Conventional ventilators with frequency capabilities of
up to 150 breaths per minute can be adapted for HFPPV. New
ly developed systems can operate at rates of at least 900
breaths per minute (15 hertz). The advantages of HFPPV in
clude easy adaptability of present conventional machines to
it and simple circuitry. However, tidal volume and even
frequency are increased at the expense of mean airway and
peak inflation pressures, which also increase. Additional
ly, humidification during long-term use remains a problem.
High frequency jet ventilation uses a different system
of delivery. A small-bore, low-compliance inspiratory tube
is mated to a catheter with an even smaller diameter. An
endotracheal tube is previously fitted with a three-way
swivel adapter (Portex) usually fitted for fiberoptic bron
choscopy. A 14- or 16-gauge angiocath fits with an airtight
seal through one limb while a third limb attaches to a con
tinuous-flow gas source. When in place, the catheter aligns
in the center of the tube near the connection to the
adapter. with each cycle, gas is accelerated through the
narrower lumen of the angiocath. The increased rate of flow
creates an area of negativity at .right angles to the angio
cath. The low-flow (20 L/min), previously-humidified gas is
then entrained into the airway. Not only is tidal volume
enhanced, but gas is humidified.
It is unclear whether the relationship of the catheter
tip to the carina is critical. Some evidence suggests that
the closer the injector is to the carina, the more efficient
the ventilation. However, entrainment becomes more diffi
cult. Further studies are needed in this area.
Modifications of delivery systems for HFJV also have
involved the endotracheal tube. Attempts have been made to
incorporate the angiocath into the tube~ thus, a second nar
row lumen is added. Early designs have the gas delivered to
286
the tip of the tube just above the carina while later modi
fications have the injector tip moved back to the midpoint
of the endotracheal tube.
High frequency jet ventilation delivers gas through a
narrowed orifice to effect a jet. The entrainment of gas
ensures both that gas is humidified and that tidal volume is
augmented. Rates vary but usually exceed 80 breaths per
minute.
High frequency jet ventilation has heralded a new sys
tem to generate flow, the present configuration of which
largely resembles an interrupter to flow. Usually a sole
noid comprises the principal component. The solenoid reacts
like a sensitive switch with the additional capability to
time the flow of gas. Most jet ventilators are powered by
an air-oxygen source at 50 psig. The fraction of inspired
oxygen can vary and the actual pressure can be manipulated
to as low as 5 to 10 psig. Some ventilators permit flow
rather than pressure to be controlled; the results are the
same.
At high frequencies, inspiratory time must also be con
trolled precisely. Very short times, as brief as 0.01 sec
onds, are important. Otherwise, at the high rates, inspira
tion occupies too much of the respiratory cycle and curtails
passive exhalation. Air becomes trapped, inadvertent posi
tive end-expiratory pressure develops, and arterial oxygen
tension may increase. Optimal inspiratory time appears to
be between 20% and 30% of the entire respiratory cycle.
There are still questions about the best methods for
jet ventilation. A new tube wi th an injector incorporated
into the tip can deliver gas just above the carina. In com
parison to a tube with an injector located at the distal
end, gas exchange may be better. However, the car ina as
well as the right and left mainstem bronchi are all exposed
to much higher flows and pressures with possible detrimental
effects. Also, with this system, entrainment is less effi
cient because the port at which humidified flow has access
is located further away.
287
Significant clinical differences are not apparent among
the more conventional 18-, 16-, or 14-gauge jet injector
systems. All have the same influence on airway pressure,
gas exchange, and cardiac performance. The larger the lumen
is, the greater the tidal volume~ but, if the lumen is too
large, entrainment becomes less effective.
High frequency oscillation involves the continuous
movement of the same volume of gas in and out of the airway.
Unlike other systems, new volumes of gas are not continually
introduced into the airway. The same volume moves in a to
and-fro manner and oxygen flows in at a rate consistent with
metabolic demands. Carbon dioxide can be removed by several
methods including an in-line carbon dioxide absorber. How
ever, the soda lime exhausts quickly, which increases cir
cuit resistance, and the absorber must be frequently
changed. A more sophisticated approach involves a bypass
circuit. A tube connected at right angles to the delivery
circuit permits exhalation and the elimination of carbon di
oxide. As airway pressure increases, the gas takes the path
of least resistance - out the bypass - and does not flow to
the patient. Lengthening the tube or adding an expiratory
resistance valve ensures a greater flow of gas to the pa
tient. Although still unproven, the more physiologic sinu
soidal wave pattern developed by the piston pump may be
beneficial. In general, HFO operates at low airway pres-
sure. Best results have been reported at frequencies
greater than 900 breaths per minute.
To date, no definitive explanations answer how HFV pro
vides adequate oxygenation and alveolar ventilation. Suc
cess with tidal volume less than dead space implies a pro
cess altogether different from that with conventional methods. We know HFV differs from apneic oxygenation. with that method, the lungs do not continually expand and deflate
but are kept at resting functional residual capacity with
oxygenation remaining adequate. However, during HFV, carbon
dioxide tension does not rise as in apneic methods so that
288
other changes must be occurring in addition to oxygen simply being added to meet metabolic demands.
A coaxial type of flow has been advanced as one alternative explanation. During HFO, the profile of the gas moving down the airway resembles that of laminar flow. Gas in the center of the airway moves faster than that along the edge. When the flow is reversed, the leading edge is blunted and the gas at the center and the periphery moves at the
same rate. The net effect is that gas at the center of the airway moves into the terminal airways while exhaled gas
moves in the opposite direction, along the edges. Recently,
several different models of double-lumen endotracheal tubes for HFV have been introduced. In several studies, carbon
dioxide has been more efficiently eliminated when the double-lumen replaces the conventional single-lumen tube.
This may refute the coaxial flow model because improvement
with a double-lumen tube indicates inspiratory gases may in
fluence expiratory gases. Recently the theory of augmented diffusion or enhanced
diffusivity has been developed to explain the workings of
either HFPPV or HFJV. The high rates of flow, the small
diameter circuitry, and the narrow orifices all contribute to turbulent flow. We normally think of turbulent flow in
the larger airways and laminar flow in the distal units.
The high velocity and turbulence combine to excite mole
cules, which, in turn excite more distal but still neighbor
ing particles. Therefore, the effect of the blunt profile
of turbulent flow occurs along the entire length of the airway. The diffusion gradients are such that oxygen moves in
to the gas exchange units and carbon dioxide exi ts in the opposite direction. Hence, delivery of new volumes of gas with small tidal volumes can maintain normal gas exchange.
Newer investigative methods have provided other possible explanations. Lehr has oscillated excised intact
lungs and, with the aid of stroboscopic lighting, has photographed their movement. At very high frequencies, the lung
does not move as a unit7 in fact, considerable asynchrony
289
develops. He theorizes that, if different units ventilate
in different phases, then the same volume of gas may be
shared, especially if intra-alveolar flow occurs. The
explanation resembles a Pendeluft type of flow.
What patients would especially benefit from HFV? In
Sweden, the technique has been amply proven for bronchos
copy, laryngoscopy, or laryngeal surgery. The small volumes
and low pressures would seem suitable for neonates with hya
line membrane disease. Work in this area has been encourag
ing: but few data are yet available.
Since the lung moves minimally during HFV, it may offer
advantages during certain thoracic surgical procedures. It
may not be necessary to collapse the lung out of the
surgeon's way for the procedure to be performed in a rela
tively quiet operating field and problems with re-expansion
are then eliminated.
Several case reports have demonstrated the effective
ness of HFV to treat bronchopleural cutaneous fistula. The
reduced peak and mean airway pressures most likely provide a
better environment for pulmonary healing. Presently, there
are few data on the effect of HFV on adult respiratory dis-
tress syndrome. Positive end-expiratory pressure is still
required and the mean airway pressures developed usually
equal those developed with conventional methods. The asso
ciated reductions in peak inflation pressure may reduce the
incidence of pulmonary barotrauma. Additionally, the re
duced peak inflation pressure may influence pulmonary artery
pressure and, subsequently, the right ventricular afterload
may be affected less.
Reports that HFV succeeded when conventional techniques
"failed" must be carefully evaluated. One recalls the EeMO
studies: a failure of conventional support meant inadequate
oxygenation at a minimal PEEP level of only 5 to 10 cm H20.
Recently, HFV has been applied in new directions. The
technique may be useful to control elevated intracranial
pressure. Reports have indicated that both mean intra
cranial pressure and peaks in it may be reduced by HFV, most
290
uikely, again, secondary to the reduced peak inflation and
mean airway pressures. Klain has demonstrated that HFV can
prevent the aspiration of at least liquid. This could be
beneficial in conjunction with cricothyrotomy. During emer
gency situations, when skilled help is not available, HFV
may be the safest method to secure the airway. Finally, HFV
during cardiopulmonary resuscitation precludes the need to
synchronize ventilation with cardiac massage. In fact, the
rapid changes in intrapleural and intrathoracic pressures
may actually promote blood flow during resuscitation.
As with any technique, complications may develop. At
the present, little information on the long-term effects of
high pressure in the airway exists. These effects need to
be identified and their impact delineated before HFV can be
accepted clinically. We have a technique and a mechanism of
action we do not understand and side effects that remain to
be identified. Also, the most suitable patients and
diseases have yet to be identified. until these major ques
tions can be answered satisfactorily, HFV must remain the
province of the investigator. The answers cannot be found
without precise selection of homogeneous populations of
patients and well-designed clinical and laboratory
investigations.
291
BIBLIOGRAPHY
1. Butler WJ, Bohn DJ, Bryan AC, Froese AB. high-frequency oscillation in humans. (Cleve) 59:577, 1980.
Ventilation by Anesth Analg
2. Carlon GC, Ray C Jr, Klain M, McCormack PM. Highfrequency positive-pressure ventilation in management of a patient with bronchopleural fistula. Anesthesiology 52:160, 1980.
3. Borg Uf Eriksson I, Sjostrand U. tive pressure ventilation (HFPPV): its use during bronchoscopy and for crolaryngeal surgery under general Analg (Cleve) 59: 594, 1980.
High frequency posiA review based upon laryngoscopy and mianesthesia. Anesth
4. Fredberg JJ. Augmented diffusion in the airways can support pulmonary gas exchange. J Appl Physiol 49:232, 1980.
5. Kirby RR. High-frequency positive-pressure ventilation (HFPPV): What role in ventilatory insufficiency? Anesthesiology 52:109, 1980.
COMBINED HIGH-FREQUENCY VENTILATION FOR TREATMENT OF SEVERE RESPIRATORY FAILURE
N. EL-BAZ, M.D., A. EL-GANZOURI, M.D., A. IVANKOVICH, M.D.
Adult respiratory distress syndrome (ARDS) describes
complex pulmonary changes as a result of a variable
etiology. ARDS is associated with widespread damage to
alveoli, airways and pulmonary capillaries. This causes
inefficient gas exchange as a result of high airway
resistance, low lung compliance, pulmonary edema and alteration of pulmonary perfusion. These complex changes of
ARDS cause failure of the normal mechanics of breathing to provide adequate tidal volume, proper gas distribution, and
efficient gas diffusion, resulting in progressive hypoxemia and hypercarbia.
Conventional intermittent positive pressure ventilation (IPPV) was developed 30 years ago to duplicate the natural
pattern of breathing by delivering a large tidal volume at a
low respiratory rate. Although this approach has been safe
and effective in treatment of mild and moderate ARDS, this
technique frequently fails to achieve adequate gas exchange
in severe ARDS despite the addition of high levels of
positive end expiratory pressure (PEEP). In addition,
conventional mechanical ventilation has been shown to impair
pulmonary blood flow and venous return with deterioration of
cardiac function and tissue perfusion. Although cardiac
output can be maintained in most patients with adjuvant administration of inotropic drugs (dopamine) and large
volumes of intravenous fluids, this approach can be
inefficacious and deleterious to the critically ill patients
with severe ARDS. Conventional ventilation has also been
293
associated with a high level of antidiuretic hormone (ADH) ,
causing oligurea and renal shut down. Besides, it has been
associated with a high incidence of barotrauma, particularly
during the application of PEEP. Conventional ventilation is
also traumatic and uncomfortable to patients, and requires
the frequent administration of muscle relaxants and
sedatives. This causes severe psychological trauma to the
patient's family having an unconscious, unresponsive
relative.
Because of these major disadvantages and limitations of
conventional mechanical ventilation, extracorporeal membrane
oxygenators (ECMO) have been evaluated as an alternative
approach. Although ECMO has been successful in providing
adequate gas exchange in patients with severe ARDS and
allowing time for the diseased lungs to heal, the problems
associated with arterial and venous cannulation, systemic
heparinization, and prolonged use of a perfusion pump has
limited the value and applications of this technique for
treatment of respiratory failure.
In an effort to avoid the problems described with
conventional mechanical ventilation and ECMO and to provide
adequate gas exchange in patients with severe ARDS, we
developed and evaluated the new technique of combined high
frequency ventilation (CHFV). CHFV is based on the
administration of high-frequency positive-pressure
ventilation (HFPPV) simultaneously with high-frequency
oscillatory ventilation (HFOV), each at separate and
independent parameters.
High-frequency ventilation (HFV) is a new method of
artificial ventilation which is based on the administration
of small tidal volumes (between 5 to 250 ml) at a high
respi'ratory rate (between 60-6000 breaths/min). HFValso
differs from conventional ventilation in having a small
tidal volume delivered at high velocity, into an open
valveless circuit with a continuous outflow of gases to the
atmosphere. High-frequency ventilation has been shown in
294
animal and human studies to provide adequate alveolar
ventilation and oxygenation with minimal impairment to the
cardiovascular system. The use of a small tidal volume and
an open circuit during HFV explains the associated low mean
and peak airway pressures, continuously negative
intrapleural pressure, and the minimal impairment to the
venous return and pulmonary circulation. The frequent
administration of HFV small tidal volumes, at high velocity,
into the center of a continuous outflow of gas generates an
eddy flow characteristic of high-frequency ventilation.
This has been shown to improve gas mixing in the airways and
achieves a uniform gas distribution independent of regional
airway resistance and compliance. Because of the different systems, methodologies, and
terminology used by various investigators, we have suggested
a simple classification of HFV according to the frequency
used: A) high-frequency positive-pressure ventilation
(HFPPV), which utilizes a frequency between 1-10 Hz (60-600
breaths/min) and delivers a tidal volume of more or less the
volume of dead space (50-250 ml). HFPPV achieves adequate
alveolar ventilation and oxygenation by a combination of
convective flow and improved gas diffusion. B) High
frequency oscillatory ventilation (HFOV) , which utilizes a
faster frequency between 10-100 Hz (600-6000 breaths/min)
and delivers a much smaller tidal volume beween 5 to 50 ml.
HFOV achieves alveolar ventilation and oxygenation by pure
acceleration of gas diffusion.
Our early application of HFV as a resuscitative measure
for treatment of intractable hypoxemia in patients with
severe ARDS after the failure of maximal conventional IPPV
and PEEP to maintain oxygenation was associated with two
major problems: inadequate humidification, and CO2 accumulation with respiratory acidosis during the use of
high-frequency oscillatory ventilation. We have solved
these two problems by incorporating humi,dification in our
system by nebulization of water, and developed combined
295
high-frequency ventilation (HFPPV plus HFOV) , eliminating
the problem of CO2 accumulation.
HUMI>IFICATION DURING CHFV
To Patient
TI£RMOSTAllC CONlROLlED WAlERBATH
HFPPV
.. " ......... TIME (SECONDS)
COMBINED HIGH FREQUENCY VENTILATION
CHFV was initially evaluated in ten adult patients,
aged between 15 to 59. These patients developed ARDS as a
result of various causes (pneumonia, massive transfusion,
aspiration pneumonitis, disseminated vasculitis, and
necrotising alveolitis). They developed terminal
respiratory failure and severe progressive hypoxemia (Pa02 below 50 mmHg) during maximal respiratory support with IPPV
and PEEP. Our criteria for terminal respiratory failure,
and for the application of HFV were a Pa02 below 50 mmHg
at F I02 of 1.0, tidal volume above 20 ml/kg, and a PEEP of
more than 15 cm H20. All patients were admitted and
managed in our surgical intensive care unit (SIT) with
continuous monitoring of intraarterial pressure, pulmonary
artery and wedge pressure, cardiac output (thermodilution),
and arterial and mixed venous blood gases. These patients
required frequent administration of for muscle relaxation
(pancuronium) and for sedation (diazepam) to facilitate the
administration of IPPV and PEEP. Large doses of dopamine
10-20 mcg/kg/min were also received by each patient during
IPPV to maintain an acceptable cardiac output
CHFV was evaluated in these patients after they met the
296
criteria of terminal respiratory failure and was compared to
IPPV and PEEP, HFPPV and HFOV. The three modalities of HFV
were administered in each patient at a sequence based on the
frequency used, HFPPV, HFO, and CHFV, from low to higher
frequencies. These three modalities were delivered to each
patient through the same ventilator, tubing, and HFV
endotracheal tube adaptor for standardization. Each patient
served as his own control.
HFPPV was used in these patients during the first day
at a rate of 250 breaths/min, driving gas pressure (DGP) of
20 psi, insufflation time percentage (IT%) of 40% and F I02 of 1.0. HFOV was used on the second day in each patient at
a frequency of 2000 breaths/min, DGP of 35 psi, and IT% of
50% at F I02 of 1.0. On the third day CHFV was
administered to these patients and continued for a period fo
5 to 21 days. The HFPPV component of CHFV was administered
at a frequency of 60 breaths/min, DGP of 20 psi, and IT% of
40% at F I02 of 1.0. This was synchronized with an HFOV
component of CHFV at a frequency of 3000 breaths/min, DGP of
20 psi and IT% of 50% at F I02 of 1.0. These parameters of
HFV were chosen on the basis of our early experience with
this system, and standardized for the purpose of this study.
Our criteria for reestablishment of conventional
mechanical ventilation in these patients receiving combined
high-frequency ventilation were:
1. Pa02 above 100 mmHg, at F I02 of 0.4 maintained
during CHFV for a period of 24 hours.
2. The development of any complication directly related to
any modality of HFV.
3. Inability to improve oxygenation within one hour of
establishment of HFV.
The parameters chosen for reestablishment of IPPV
PEEP were a tidal volume of 10 ml/kg, respiratory rate
breaths/min, and a PEEP of 10 cm H20 with an F I02 of
0.4.
and
of 12
The three modalities of HFV were administered in these
patients after they had met the criteria of terminal
respiratory failure. These patients maintained a mean
297
Pa02 of 45 mmHg (35-50 mmHg) and a mean PaC02 of 40 mmHg
(35-60 mmHg) during their last day of conventional IPPV and
PEEP. The application of HFPPV for one day was associated
with a slight improvement of oxygenation to a mean of 75
mmHg (58-89 mmHg) and adequate CO2 elimination with a mean
PaC02 of 38 mmHg (30-50 mmHg). The administration of
high- frequency oscillation the following day was associated
with a significant improvement of oxygenation to a mean
Pa02 of 227 mmHg (150-319 mmHg). Nonetheless, HFOV was
associated with hypercarbia and respiratory acidosis with a
mean PaC02 of 78 (45 to 99 mmHg). The application of CHFV
on the third study day in these patients achieved the
highest oxygenation with a mean Pa02 of 298 mmHg (190-350
mmHg). CHFV was also associated with efficient CO2 elimination with a mean PaC02 of 32 (24-42) mmHg.
400
300
Pa02 200 mmHg
100
0 HFPPV HFOV CHFV
100
80
PaC02 60 mmHg
40
20
0 IPPV+PEEP HFPPV HFOV CHFV
298
Besides the significant improvement of gas exchange
during these modalities of HFV, cardiac output improved
significantly in each patient. The patients maintained a
cardiac output at a mean of 3.2 L/min (between 2.1 to 4.3
L/min)supported with large doses of dopamine 10-20
mcg/kg/min during conventional mechanical ventilation.
HFPPV was associated with a significant increase of cardiac
output to 4.9 L/min (between 3.7 to 6.1 L/min). Cardiac
output was also well maintained during HFOV at a mean of 5.9 L/min (between 3.9 to 6.3 L/min) and during CHFV at a mean
of 5.7 L/min (between 3.7 to 6.4 L/min).
IPPV+PEEP
HFPPV
HFOV
CHFV
TERMINAL RESPIRATORY FAILURE (10 PATIENTS)
Pa02 PaC02 C.O.
mmHg mmHg Llmin
45 (35-50) 40 (35-60) 3.2 (2.1-4.3)
75 (58-89) 38 (30-50) 4.9 (3.7-6.1)
227 (150-319) 78 (45-99) 5.9 (3.9-6.3)
298 (190-350) 32 (24-42) 5.7 (3.7-6.4) All patients tolerated these three modalities of HFV
well and were able to breath spontaneously through the open
system of HFV. Because muscle relaxants and sedatives were
not required during the use of HFV, this allowed for return
of consciousness and each patient was able to communicate
with his family and nursing staff.
Despite these significant improvements in respiratory
and cardiac functions, eight patients (80%) died as a result
of multisyste~ failure and cardiac arrest, with a Pa02 above 50 mmHg. These patients received combined high
frequency ventilation for a period between 2 to 21 days.
Postmortem lung examination in these patients showed red
hepatization and disseminated necrotizing alveolitis. The
other two patients (20%) continued to improve during CHFV
299
and on the fifth day of CHFV met the criteria for
reestablishment of conventional ventilation. One of these
patients required repeated abdominal surgical procedures,
while receiving IPPV and PEEP. He developed septic abdomen,
hepatic and renal failure and died of a cardiac arrest
postoperatively three months after our use of CHFV. ,The
other patient progressively improved and was successfully
weaned and extubated, and left the hospital alive.
This study showed that CHFV successfully treated in all
patients the intractable hypoxemia of terminal respiratory
failure which had developed during maximal support with
conventional IPPV and PEEP. Although the mechanism by which
HFV provides effective gas exchange is not known with
certainty, we believe CHFV provides a new approach for
management of severe respiratory failure. CHFV provides a
differentiated gas exchange; oxygenation is achieved by
acceleration of gas diffusion by the HFOV component. This
is shown by the slight difference between Pa0 2 during HFOV
and CHFV; while CO2 elimination is achieved independently
by convection through the HFPPV component of CHFV. This is
also shown by the slight difference between PaC0 2 during
HFPPV and CHFV.
We also found CHFV valuable in five children aged
between 2 months to 4 years. These patients developed
terminal respiratory failure and progressive hypoxemia
despite the use of IPPV at respiratory rates between 40 to
80 breaths/min, tidal volumes between 20 to 35 ml/kg at
F 102 of 1.0 and PEEP between 15 to 25 cm H20. They also
maintained a mean Pa0 2 of 32 mmHg (28 to 41 mmHg) and a
PaC0 2 of 43 (between 38 to 61 mmHg). These five children
received CHFV after death appeared eminent as a result of
severe progressive hypoxemia. The HFPPV component of CHFV
was administered at a frequency between 40 to 60 breath/min,
driving gas pressure between 5 to 15 PSI, inspiratory time
of 0.1 second. This was synchronized and combined with HFOV
componate at a frequency between 1000 to 3000 breath/min,
300 :
DGP between 10 to 20 PSI, IT% of 50% both at F I 02 of
1.0. CHFV achieved adequate oxygenation in these patients
with a mean Pa0 2 of 112 mmHg (86 to 193 mmHg), and
efficient CO 2 elimination with a mean PaC0 2 of 39 mmHg
(23 to 41 mmHg). CHFV was also associated with significant
improvement of cardiac function, with a mean cardiac index
of 1.94 L/m2/min compared to a mean of 1.2 L/m2 /min.
Nonetheless, three patients progressed into a multisystemic
failure and died as a result of cardiac arrest within 2 to 5
days. The other two patients, however, developed
progressive hypoxemia despite maximal support with CHFV for
3 and 5 days. Conventional IPPV and PEEP was reestablished
in these two young patients. This was associated with
significant deterioration of oxygenation and both progressed
into cardiorespiratory failure and died within one hour
after IPPV and PEEP.
Although our application of CHFV in patients with
severe ARDS and terminal hypoxemia was a challenge, it
showed the efficacy of this new method to achieve adequate
gas exchange after the failure of our conventional methods
of ventilation. We believe the early application of CHFV in
patients with mild and moderate ARDS will prove its value in
our clinical practice not only by avoiding all the side
effects of conventional mechanical ventilation but also by
its ability to provide a more efficient alveolar gas
exchange.
REFERENCES
I. Kirby RR, Downs JB, Civetta JB, et al: High Level Positive End Expiratory Pressure (PEEP) in Acute Respiratory Insufficiency. Chest 1975; 67:156-163.
2,. Downs JB, Klein EF, Jr., Modell JH: The Effect of Incremental PEEP on Pa0 2 in Patients With Respiratory Failure. Anesth Analg 1973; 52:210-215.
3. Lyager S: Ventilation/Perfusion Ratio During Intermittent Positive-pressure Ventilation. Acta Anaesthesiol Scand 1970; 14:211-232.
4. Kirby RR, Downs JB, Civetta JB, et al: High Level Positive End Expiratory Pressure (PEEP) in Acute Respiratory Insufficiency. Chest 1975; 67:156-163.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Gallagher J, Civetta JB: Goal-Directed Therapy of Acute Respiratory Failure. Anesth Analg 1980; 59:813-834.
301
Qvist J, Pontoppidan H, Wilson R, et al: Hemodynamic Response to Mechanical Ventilation With PEEP: The Effect of Hypervolemia. Anesthesiology 1975; 42:45-55. Kirby RR, Pery JC, Calderwood HW, et al: Cardiorespiratory Effect of High Positive End-Expiratory Pressure. Anesthesiology 1975; 43:533-539. Kumar A, Pontoppidan H. Falke KJ, et al: Pulmonary Barotrauma During Mechanical Ventilation. Crit Care Med 1973; 1:181-186. Kirby RR: Ventilatory Support and Pulmonary Barotrauma. Anesthesiology 1979; 50:181-182. Zapol WM, Snider MT, Schneider RC, Extracorporeal Membrane Oxygenation for Acute Respiratory Failure. Anesthesiology 1977; 46:272-285. Ratliff IL, Hill JD, Fallat RJ, et al: Complications Associated With Membrane Lung Support by Venoarterial Perfusion. Ann Thorac Surg 1975; 19:537-539.
Sjostrand UH, Eriksson IA: High Rates and Low Volumes in Mechanical Ventilation - Not Just a Matter of Ventilatory Frequency. Anesth Analg 1980; 59:567-576. Sjostrand U: High-Frequency Positive-Pressure Ventilation (HFPPV): A Review. Crit Care Med 1980, 8:345-364. Butler WJ, Bohn DJ, Bryan AC, Froese AB: Ventilation by High-Frequency Oscillation in Humans. Anesth Analg 1980; 59:577-584. Fredberg JJ: Augmented Diffusion in the Airway Can Support Pulmonary Gas Exchange. J Appl Physiol 1980; 49:232. . Kirby RR: High-Frequency Positive-Pressure Ventilation (HFPPV): What role in ventilatory insufficiency? Anesthesiology 1980; 52:109-110. Kolton M, Cattran CB, Kent G: Oxygenation during high-frequency ventilation compared with conventional mechanical ventilation in two models of lung injury. Anesth Analg 1982; 6:323-332. Goldstein DH, Slutsky AS, Ingram RHJr, et al: CO Elimination by High Frequency Ventilation (4 to 10 Hz) in Normal Subjects. Am Rev Respir Dis 1981; 123:251-255. Rossing TH, Slutsky AS, Lehr JL, et al: Tidal Volume and Frequency Dependence of Carbon Dioxide Elimination by High-Frequency Ventilation. N Engl J Med 1981; 305:1375-1379. E1-Baz et al: Combined High-Frequency Ventilation for Treatment of Teminal Respiratory Failure; A New Technique. Anesth Ana1g (in press) 1983.
HIGH FREQUENCY JET AND INTERMITTENT POSITIVE PRESSURE VENTILATION, WITH PEEP: A COMPARISON OF PEAK AND MEAN AIRWAY PRESSURES
A. SLADEN, K. GUNTUPALLI, M. KLAIN AND R. ROMANO
Conventional intermittent positive pressure ventilation produces barotrauma
on the basis of high peak airway pressures. Complications include pneumothorax
and subcutaneous emphysema, pneumomediastinum and pneumopericardium. The
incidence further is increased with the addition of PEEP, which usually results
in the generation of higher peak airway pressures. Aside from this, barotrauma
in association with conventional mechanical ventilation is highly likely in the
presence of pneumatoceles, or a lung abscess with an air fluid level. Here,
the lung tissue is tenuous and requires relatively low pressure to disrupt the
parenchyma.
Following pulmonary resection, the sutures or staples should prevent an
air leak when moderate airway pressures are applied. However, if infection is
present or developes at the suture or staple line, and conventional ventilation
is used, disruption of the suture line, and its sequelae can occur. Finally, the
production of a tracheobronchial cutaneous fistula by barotrauma, results in a
constant leak of tidal volume with each inspiratory cycle of the mechanical
ventilator. Application of PEEP further increases volume loss. Failure of the
tom lung margins to heal is perpetuated because of the generation of high
airway pressures and constant gas flow between the disrupted surfaces.
The generation of high airway pressures, particularly with PEEP has been
shown to reduce cardiac index on the basis of a reduction in preload. The
hypothesis is that the high ~ airway pressure rather than the high peak
airway pressure effects preload.
303
High frequency jet ventilation has been recommended as a ventilation
technique to avoid the generation of high airway pressures and thus prevent
their sequelae; barotrauma to the lung and reduction in preload and stroke index_
With this prologue in mind, we elected to compare peak airway pressures,
PAP, and mean airway pressures, Paw, with high frequency jet ventilation and
PEEP, HFJV, and conventional intermittent positive pressure ventilation with
similar PEEP, CPPV_
Eleven patients, without chronic obstructive lung disease, admitted to the
Surgical Intensive Care Unit with postoperative respiratory failure, initially were
ventilated with CPPV using a tidal volume of 10 ml/kg, PEEP 2-3 mm Hg and
the intermittent mandatory ventilation was adjusted to provide normocarbia_
Airway pressures then were recorded on a strip chart recorder using a
scale of zero to 40 mm Hg and a speed of 25 mm/second_
Ventilation was changed to high frequency jet ventilation at a rate of
100/min, inspiratory time 30% of the respiratory cycle and PEEP similar to
CPPV_ The jetting pressure was adjusted to provide a PaC02 similar to that
obtained with CPPV and, again, airway pressures were recorded_
The similarity in PaC02 using both systems is essential in order to compare
airway pressures at comparable minute alveolar ventilations_ There were no
changes either in fluid or drug administration between the studies_
Results:
CPPV HFJV P
PaC02 5-24+0-2 5-27+0-2 kPa NS
PEEP 2-7+0-2 2-4+0-2 mm Hg NS
PAP 15-4+0-9 9-1+0-9 mm Hg <0-001
Paw 4-41+0-29 4-99+0-39 mm Hg NS
304
The study demonstrates in a clinical setting, with high frequency jet
ventilation at 100/min and at the same alveolar ventilation as conventional
ventilation, peak airway pressure is statistically different and less with HFJV
than CPPV. Equally important is the observation that there is no significant
difference in mean airway pressures.
Comments
Three issues arise from this study.
The first is that using High Frequency Jet Ventilation at 100/min and an
inspiratory time of 30%, peak airway pressure is reduced by 59% compared to
CPPV at a tidal volume of 10 ml/kg. Therefore, HFJV is the technique of
choice to prevent pulmonary barotrauma, to reduce air leaks in generated
tracheobronchial cutaneous fistulae and promote healing of these fistulae.
Because of the reduction in PAP it is an ideal mode of ventilation in the
postoperative patient with a pulmonary resection.
The second is that although peak airway pressures ~ different, mean
airway pressures were not statistically different. Since there was NO change
in cardiac index, stroke index or after load (see study of cardiorespiratory
parameters) it appears that it is the mean rather than peak airway pressures
that affect cardiac function. We recommend monitoring of mean in addition
to peak airway pressures.
Thirdly, mean airway pressure rather than peak airway pressure is believed
to be the factor which is related to oxygen delivery. The decrease in Pa02
and increase in Qsp/Qt without change in cardiac function with HFJV leads us
to question the theory that mean airway pressure is a primary factor in oxygen
delivery.
HIGH FREQUENCY JET VENTILATION AND CONVENTIONAL VENTILATION: A COMPARISON OF CARDIORESPIRATORY PARAMETERS
A. SLADEN, K. GUNTUPALLI, M. KLAIN AND R. ROMANO
High frequency jet ventilation frequently is suitable as an alternative to
conventional ventilation when ventilatory support is indicated.
We have observed that when patients who have been ventilated with
conventional volume limited ventilators have their mode of ventilatory support
changed to high frequency jet ventilation, there is an initial decrease in arterial
oxygen tension. With continued high frequency jet ventilation, the decrease in
Pa02 usually is transitory and returns to the pre jet ventilation level within a
time period of sixty minutes.
This prospective study was designed to obtain and compare cardiorespiratory
data with conventional volume limited ventilation, and PEEP, CPPV, and high
frequency jet ventilation and PEEP, HFJV, and to determine the etiology for
the decrease in Pa02'
Method
A heterogeneous group of nine consecutive, non cardiac surgical patients,
who required postoperative ventilatory support, were admitted directly from the
operating room to the surgical intensive care unit. Initially, each patient was
ventilated with CPPV at a tidal volume of 10 ml/kg, PEEP 2-3 mm Hg and
IMV was adjusted to provide normocarbia. Subsequently, when a steady state
was reached a cardiorespiratory profile was obtained.
306
CPPV was discontinued and HFJV begun at the same FI02 and PEEP as
CPPV. The jet ventilator was adjusted to deliver a frequency of 100 per minute
and a driving pressure of 35 psi. After 20 minutes, arterial blood gases were
obtained and the driving pressure adjusted, if necessary, to produce normocarbia.
Again, with the patient in a steady state the cardiorespiratory profile was
repeated. No changes were made, either in fluid or drug administration, between
the two profiles.
Results:
CPPV HVJV P Value
CI 2'5+0'2 2'6+0·1 L.min.-1.M-2 NS
P 98+7 100+4 min-1 NS
SI 26'4+1'8 26'5+1'5 ml.M-2 NS
LVSWI 34'1 +3'S 36'12:2'4 gm.M.M-2 NS
TPRI 2846+321 2923+276 dyne.sec.cm-S .M-2 NS
a-V02 4'6+0'2 4'6+0'3 ml.dl NS
Q02 113'8+6'1 118'5+6'7 ml.min-1.M-2 NS
Pa02 27'64+2'99 19'96+2'37 kPa <0'003 . . Qsp/Qt 6·9+1·S 10'9+1'5% <O'OOS
PaC02 5'24+0'2 S'27+0'2 kPa NS
This study demonstrated, at the similar alveolar ventilation, there was no
significant difference in CI, P, SI, LVSWI, TPRI, a-V02 and oxygen consumption
between CPPV and HFJV at 100 per minute. . . There was a significant decrease in Pa02. P < 0'003 and increase in Qsp/Qt,
P < O·OOS.
The etiology for the decrease in Pa02 was increase in intrapulmonary
shunting and was not associated with change in cardiac index.
Discussion
Hemodynamics
307
The physiologic profiles indicate that hemodynamic stability was maintained
with HFJV at 100 per minute compared to CPPV. Ejection volume, work and
resistance were unchanged as was a-V02 and oxygen consumption.
Pulmonary
Headly-White demonstrated that repetitive small tidal volumes result in
decrease in Pa02 and increase intrapulmonary shunting, the latter the result of
microatelectasis. PEEP splints open alveoli, recruits collapsed alveoli and
maintains functional capacity. High frequency jet ventilation introduced by
Klain and Smith in 1977 consists of the delivery of small tidal volumes at rapid
frequencies Perhaps, the terminology "tidal volume" is not appropriate, because
the delivered gas volumes are small and, in fact, may be less than the patients
dead space. It would appear that high frequency jet ventilation, the delivery
of rapid but small volume, neither causes alveoli to blossom, nor distends alveolar
walls. In fact, it is likely to lead to a reduction in the production of surfactant,
the generation of microatelectasis, decrease in function residual capacity and
increase in intrapulmonary shunting. However, similar levels of PEEP were
used in HFJV as in CPPV and should have recruited alveoli, maintained FRC
and prevented an increase in Qsp/Qt.
In this clinical study with matching alveolar ventilation, FI02 and PEEP,
a decrease in Pa02 occurred with HFJV. The most likely explanation for this
is nonexpansion of alveoli and decrease in surfactant production. The result,
microatelectasis and increase in intrapulmonary shunting.
However, the paradox is, if we accept this hypothesis, why does the Pa02
subsequently retum to a level similar to that obtained with conventional
ventilation.
308
Two questions remain unanswered
1. What is the FRC with HFJV compared to CPPV at the same PEEP?
and
2. What is the surface tension of lung fluid with HFJV compared to CPPV?
The results of this study indicate that prophylactic PEEP is recommended
when HFJV is used for respiratory support and that it is prudent to initiate
HFJV with a high FI02 and decrease FI02 as indicated by arterial oxygen tension.
EARLY CLINICAL EXPERIENCE WITII HIGH FREQUENCY IN OUR UCI.
DRS. M. JIMENEZ LENDINEZ, J. LOPEZ DIEZ, J.A. CAMBRONERO GALACHE, M.A. PALMA GAMIZ, J.A. LAPUERTA, A. AGUADO MATORRAS.
UNIDAD DE CUIDADOS INrENSIVOS CSS "LA PAZ" MADRID-SPAIN.
1 • INTRODUCTION
The fact that mechanica1 venti1ation at Conventiona1 Frequencies
(CV) is not, exempt, of risk (1) is the reason why, that, aft,er pub 1 icat, ions
by t,he Scandinavian Schoo 1 ( 2, 3,4) t,he app 1 icat ion of II igh Frequencies
(HFV) in Intensive Care Unit,s was put, int,o use.
Although t,he main indicat,ion for t,he use of this method appears t,o
be airway or pulmonary disrupt ion <'5,6,7) HFV cou1 d however, prove t,o be
an auxiliary met,hod of vent,ilat,ion for all t,hose clinical sit,uat,ions (4,8)
where for different reasons, an efficient, vent,i1at,ion cannot, be obt,ained
using CV. Inspit,e of t,he advant,ages that, HFV offers, it is not, widely
used due t,o various fact,ors, among which is the apprehension towards using
a form of vent,ilat,ion ot,her t,han t,he commonly known; t,he adsence of standard
syst,ems for its use and the fact, that, t,here exist, no efficient, alarm or
humidificat,ion syst,ems.
In t,his art,icle, we disclose our ear1y c1inica1 experience wit,h 7
crit,ically ill patient,s being CV t,reated and for whom we considered the
possibility of using HFJV.
2. MATERIALS AND METHODS
The use of HFJV was carried out with a Jet-Venti1at,or (9) we built
in our Unit and similar to the design of Carlon G.C et al (10) based on
a solenoide valve t,o which the mixture of gases (Air/02) reaches at, a
high pressure coming from the general conduct of the Hospital inst,allat,ion.
The valve is activat,ed by an elect,ronic timer wit,h an independent, select,or
both for t,he frequency and for t,he liE ratio. The mixt,ure of gases is
freed in the swivel connector through a needle with a diameter of 1.9 mm.
The placing of a non-ret,urnable valve in t,he lat,eral of t,he swivel permit,s
the expiration impeding the intake of air by means of a venturi effect.
310
Using this systp.lll, we ventilated seven pat,ients aged between 14 and
76. The change from CV t,o HFJV in two pat,ients was mot,ivat,ed by a rupture
in the airway passage, in another two cases, the change was motivated by
hypercarbia inspit,e of being vent,ilat,ed at high volumes and frequencies
reaching danger pressure peaks. The remaining three pat,ients were found
to be septic and inadapted and in whom the presence of hypotension was
making sedation dangerous. The time they remained under HFJV varied
between 90' and z6 hours. In two of the patients, the change from CV
to HFJV was carried out on several ocassions.
Once they were subjected to IIFJV with a range of frequencies of 1Z0-
ZOO b.p.m. and an I/E ratio of l:Z, blood gases were analyzed and the
volume was regulated whereby modifying the driving pressure in order to
obtain normocarbia, a second blood sample was taken 60' later. All of
the pat,ient-s were ventilat,ed with a mixture of air/Oz, except in one
patient suffering from severe hypoxp.mia where FiOZ of 1 and Peep + 10
ems. of HZO was used by means of placing an Ambu valve in the lateral
connection of the swivel.
The control of t,he volume was carried out wit,h a Vent,ilation Monitor
Bourns LS-7.5. In all of the cases the airway pressure was measured wit,h
a catheter advanced past the carina and connected to a water column.
In three cases, because of the hap.lllodynamic situation a Swan-Ganz
catheter had to be used and pressures and cardiac out, put were determined
bot,h in CV and HFJV.
3. RESULTS
After readjusting according to t,he data obtained from t,he first blood
analysis, we always achieved pCOZ levels of bet-ween 30-40 torr after 60'
on HFJV. The results obtained together with the parameters employed
using a constant I/E ratio of l:Z are summarised in Tabl~ 1.
Breath/m 160 ± 30 b.p.m. pH 7.34 :<:: 0.09
minute volume 3.5 :!: .5 L.p.m. pCOZ 3Z :!: 4.3
driving pressure 1.8 + 0.7 Kg/cm2 C03H2 20 :<:: 1.3
airway pressure 11 :<:: 4 ems.H20 paO/Fi02 202 :!: 132
Table 1 shows the ventilatory pattern and gasometric data of our patients
dur ing HFJV.
311
A comparative study of our patient,s on CV and IIFJV is reflect,ed in Figure
1.
50
42 PaC02 40
~2 30 A graph ie respresent,at ion
250 of blood gases i.n CV and
HFJV.
PaO/~02 200 ~02
150 162
t i IP PV HFJV
Indepf'ndf'nt,ly of having aehif'vf'd normacarbi.a, Wf' obtained a bet,t,er
oxygenation going from a pa02/Fi02 of 162 to 202 with HFJV. This improve
ment, was more not,able in pat,ients wit,h severe hypoxemia where t,he para
met~ers were modified t,o obtain a grf'atf'r pressure in the airway passage
(Figure 2).
IPPV f 12 I:E 1:2 Vt 1000 F: 120
J 1 torr
90
70
.(I •••••
.... .. ""
50 0." - 55 48
2h
uu'HFJV
I:E 1:1 F:150
~ .... , ..
.............
"'//'/'/
.......
1 .. Il~ ..
I:E 1:1 F:120
,/108 "'"
. ......... , ......... .
8h
.....
83
HR time 12 h
Figure 2: Reflects the changes in p02 in one pat, ient, using different,
parameters with HFJV.
312
In three patient,s haf'.JIlodynamically monitored, no significant changes
were found in the cardiac output (an average of 6:3 LIM on CV and 6.z LIM
on HFJV.
4. DISCUSSION
With our first clinical experience with HFJV, we established the
utility of our syst,em and consequentially val id for delivering stable
volumes, frequencies and liE ratios and which can be modified. The prelimi
nary result,s obt,ained with our pat,ient,s confirmed that it is possible to
give an adequate ventilation at volumes discretely higher to the VD with
variable TIE ratios and frequencies. These paramet,ers, however, produce
a variation in the pressure of the airway passage, which is charact,eristic
of t,his type of vent,ilat,ion both for its ventilat,ory and haemodynamic
efficiency (11).
Independently of the physiological mechanisms which contribute t,o
the gas int,erchange during HFJV, t,here is no doubt what,soever t,hat with
HFJV normocarbia can be achieved in clinical situations where CV proves
t,o be inadequat,e, such as rupture of t,he a irway passage, or when high
pressure peaks in IPPV implicate the risk of pulmonary barotrama (5,6).
The improvement in t,he paOz/FiOZ ratio observed in our patient,s
could be att,ribut,ed to the increase in pressure produced during HFJV, wit,h
or withour PEEP, which result,s in a decrease in shunt (8). Alt,hough during
HFJV, the peak pressure is minimum, in most cases however, t,he average
pressure is higher t,han that, achieved in IPPV and therefore we obtain an
increase in FRC.
Insofar as the haemodynamic performance is concerned, we observed no
significant differences in CO using CV and HFJV, however, HFJV does pro-
vide an efficient ventilat,ion without having to resort, to sedation (avoiding
therefore the risk of hypotension) as was the case with three of our patients.
This means t,hat the situation of unadaption in patients with septic shock
using mechanical ventilation could be an indication for the use of HFJV.
Because we had to limit the duration of our IIFJV experience with each
pat,ient due to t,he lack of an efficient humidification and alarm system,our
results are therefore also limit,ed. However, we do believe that, HFJV should
be considered as an alternative for all those patients, who for different
reasons, an efficient, gas interchange is not achieved using mechanical
ventilat,ion.
313
REFERENCES
1. Kirby RR: Ventilatory support, and pulmonary barotrama. Anaest,!lPs iol ogy 1979, 50:181.
2. Sjost,rand U: Review of the physiological rat,ionale for and development of high frequency posit,ive-pressure vent,ilation IIFPPV. Acta Anaesth. Scand. (supple. 64):7, 1977.
3. Bjerager K, Sjost,rand U, Wattvi 1 M: Long term treatment, of t,wo pat, ients with respiratory insufficiency wit,h IPPV fPEEP and HFPPV / PEEP. Ada Anaesth. Scand. 1977, 64: 55.
4. Sjostrand U: High Frequency positive-pressure vent,ilat,ion (HFPPV). A Review Crit,. Care Med. 1980, 8:345.
5. Carlon GC, Ray C, Klain M et al: lIigh-Frequency posit,ive pressure vent, ilat ion in management, of a pat, ient, wi th br'Cmchop 1 eural [i stu 1 a. Anaest,hesiology 1980, 52: 160.
6. Turnbull fl., Carlon G, Howland W, Beatt,ie E: High-Frequency Jet Veni;ilation in Major Airway or Pulmonary Disruption. Am. Thor. Surg. 1981, 32:468.
7. Derderian S. et al: High Frequency positive pressure Jet, Ventilat.ion in bilateral bronchopleural fistula. Crit. Care Med. 1982, 10:110.
8. Schuster D, Snyder JV, Klain M, Grenvik A: High Frequency Jet Ventilation during the treat,ment, of Acut,e Fulminant Pulmonary Fdema. Chpst, 1981, 80:682.
9. Jimenez M, et, al: Vent,ilacion a a1t,a frequencia. Estudio Ppel iminar. M. Intensiva 1982, 6:4.
10. Carlon G, Miodownik S, Ray C, Kahn R: Technical aspects and cl inieal implicat,ions of high frequency jet, vent,ilat,ion wit,h a solenoide yah'e. Crit. Care Med. 1981, 9:47.
11. Jimenez M, Cambronero JA, Lopez J, Galvan B, Garcia A, Denia R, Aguado A: Airway Pressure as a det,ermining factor for vent,ilation and haemodynamic efficiency during IIFJV. loS. High Frequency Vent i lat ion. September 1982 (Rotherdam).
WHAT IS THE ROLE OF TRANSTRACHEAL VENTILATION IN EMERGENCY AND LONG-TERM RESPffiATORY SUPPORT?
M. KLAIN, H. KESZLER
High frequency jet ventilation (HFJV) is capable of providing total
respiratory support through a 14 gauge catheter introduced by cricothyroid
membrane puncture (1). This method offers distinct advantages for emergency
use. It can be performed even in conscious patients under local anesthesia
without muscle paralysis. In such a way sometimes traumatic attempts at
intubation in emergency situations can be avoided and the need for extensive
neck hyperextension eliminated. Because cricothyroid membrane puncture is
usually easy we can secure the airway in a short time.
We have shown previously that as long as respiratory frequency is 100 per
minute or higher and the inspiratory duration is at least 33% but preferrably
50% we are able to prevent aspiration even under adverse conditions (2). In
experiments on dogs a fluid level of 5 cm in the upper airways did not cause
aspiration as long as ventilatory support was maintained by transtracheal HFJV.
In addition, during cardiopulmonary resuscitation it is not necessary to
interrupt cardiac compressions to administer mechanical breath because there
is no concern that pressure would be unnecessarily high. Also, it has been
shown by isotope scanning that cardioresuscitative drugs administered into the
jet were within 12 seconds dispersed not only in the periphery of the lungs but
were already in the cardiac pool (3).
The advantages in emergency application should lead to the use of HFJV
in situations where rapid control of the airway is necessary with prevention of
aspiration. Further the fact that we can administer drugs even before an IV line
315
is established should lead one to consider transtracheal puncture and ventilatory
support by HFJV as one of the first steps needed for CPR (4). In advanced
life support it should be taught to emergency medical technicians.
However transtracheal ventilation should be considered beyond its use in
emergency airway management. Considering the damage produced by
endotracheal tubes to the surface of the tracheal wall and to the function of
normal mucociliary transport (5) transtracheal ventilation may offer an
alternative even for medium and long range ventilation. The discomfort produced
by a large, cuffed endotracheal tube requires often sedation or muscle paralysis
to permit ventilatory support. Transtracheal ventilation would allow the
conscious patient to be more comfortable, and even to speak and eat.
Existing catheters are not suitable yet for long-term use because they can
easily kink when the patient starts to use his auxilliary respiratory muscles or
moves his head. For short term use, especially if the head can be kept slightly
hyperextended, even currently available catheters are satisfactory. For long-
term ventilation better designed catheters which can be easily secured to the
skin are necessary. When these problems will have been solved, long-term
ventilatory support by transtracheal jet ventilation, should be considered feasible.
REFERENCES
1. Klain M, Smith RB: High frequency percutaneous transtracheal jet ventilation. Crit. Care Med. 5(6): 280-287, 1977.
2. Keszler H, Klain M, Nordin U: High frequency jet ventilation prevents aspiration during cardiopulmonary resuscitation. Crit. Care Med. 9(3): 161, 1981.
3. Klain M, Keszler H, Nordin U: Intrapulmonary drug administration during high frequency jet ventilation. Abstr. of 2nd World Congress on Emergency and Disaster Medicine, p. 189, Pittsburgh, P A, 1981.
4. Klain M, Keszler H, Brader E: High frequency jet ventilation in CPR. Crit. Care Med. 9(5): 421-422, 1981.
5. Nordin U, Klain M, Keszler H: IDectron-microscopic studies of tracheal mucosa after high frequency jet ventilation. Crit. Care Med. 10(3): 211, 1982.
HIGH FREQUENCY VENTILATION AND IPPV IN THE PRESENCE OF A BRONCHOPLEURAL FISTULA
R.B. SMITH, B.H. HOFF, E.V. BENNETT, E.A. WILSON, F.L. GROVER, M.F. BABINSKI, U.H. SJ5STRAND
Department of Anesthesiology, The University of Texas Health Science Center, San Antonio, TX 78284, USA
Alveolar ventilation during IPPV depends on the bulk move-
ment of gas through the conducting airways in volumes that
exceed the anatomical dead space. Inhalation is a discrete
interval during which inspired gas enters the airway and pro-
ceeds to the alveolar gas exchange pool. Exhalation is also
a discrete period during which the bulk volume of the inspired
gas exits the lungs. During IPPV there is a phasic variation
in tne airway pressure which is transmitted to the thorax
resul ting in respiratory variations in the pulmonary artery
and systemic arterial pressures.
ventilation after the creation of an experimental broncho-
pleural fistula at conventional and high frequency rates pro-
duces markedly different results. A bronchopleural fistula
causes inspired gas to bypass the alveoli. During mechanical
ventilation using IPPV, alveolar ventilation may be inadequate
resulting in hypercarbia, acidosis and death. Increasing the
tidal volume or the addition of positive end-expiratory pres-
sure may only increase the volume of inspired gas that is
shunted through the fistula.
In the dog, a median sternotomy thoracotomy was performed
to allow creation of bilateral bronchopleural fistulae by
placing 4.5 mm inner diameter cannulae into each main stem
317
bronchus. The fistulae are clamped and the phasic movements
of the lung during IPPV are visualized. There are discrete
inflations and deflations with each respiratory cycle caused
by the large tidal ventilation. During high frequency venti
lation (HFV) at a rate of 300/min with a 10 psi driving pres
sure, the vibratory movement of the lungs is demonstrated.
The lungs remain constantly inflated but there are oscillatory
movements.
The fistulae are opened and the paucity of inspiratory lung
movement with IPPV is noted. There is a continual increase
in paC02 which exceeds 120 mmHg at 30 min. A mixed metabolic
and respiratory acidosis also develops. The fistulae are
closed for a period of recovery, and then opened again. With
a 10 psi driving pressure, the dog is ventilated with HFV at
a rate of 300/min. There is constant inflation of the lungs
compared with IPPV. Within 10 minutes at a rate of 300/min,
the arterial PC02 will decline to levels below 20 mmHg. The
stabili ty of airway and vascular pressures with HFV during
the ventilatory rate of 300/min is illustrated (1).
In recent studies in 7 anesthetized dogs (2), continuous
positive pressure ventilation (CPPV: Engstrom ventilator) at a
frequency (f) of 20/min, volume-controlled high frequency pos
itive pressure ventilation (HFPPV: Bronchovent® Special) at f
60/min and HFV of a vibratory pattern (EHFV: Emerson prototype
ventilator) at f 300/min were compared. With bilateral fistu
lae open, airway pressure decreased 3-4 mmHg during all three
modes of ventilation. With HFPPV and EHFV paC02 was unchanged,
but with CPPV it increased with time. Pa02 decreased with all
318
three modes of ventilation, but with HFPPV it was maintained
at a sufficient and constant level during the 30 min test
period. Adequate short-term ventilation and oxygenation of
these dogs with large bilateral bronchopleural fistulae was
possible with CPPV, HFPPV and EHFV. However, volume-con-
trolled HFPPV was the most efficient.
In summary, the presence of large bronchopleural fistulae
may result in life-threatening hypercarbia, acidosis and
hypoxia during ventilation with IPPV. When IPPV has proven
inadequate in terms of arterial P02 and PC02' HFV (HFPPV or
EHFV) may provide adequate gas exchange and allow a normal
cardiac output in the presence of bronchopleural fistulae.
REFERENCES
1. Hoff B, Smith RB, Wilson E, Babinski M, Phillips W, Bennett E: High frequency ventilation (HFV) during bronchopleural fistula. Anesthesiology (Suppl) 55:A71, 1981.
2. Wilson EA, Hoff BH, Sjostrand UH, Borg UR, Smith RB, Bennett EV: Conventional and high frequency ventilation in dogs with bronchopleural fistula. Crit Care Med 10:232, 19-82.
HIGH FREQUENCY VENTILATION WITH TOPICAL ANAESTHESIA AS AN AID TO PHYSIOTHERAPY.
C.J.J. WESTERMANN, 11.D.; C.D. LAROS, M.D.; J.M. DOLK, PHYSIOTHERAPIST - PULMONARY DEPARTMENT, ST. ANTONIUS HOSPITAL, UTRECHT, THE NETHERLANDS.
INTRODUCTION.
High frequency ventilation (HFV) with topical anaesthesia
and without tracheal intubation has been used in our
hospital in patients with chronio obstructive lung disease
and progressive CO2-retention, due to exacerbations.
In these patients conventional mechanical ventilation has
several disadvantages. It often requires general anaesthesia
or sedation, is associated with additional risks and usually
it takes several days to wean the patient off the
respirator. 1) It was thought that in this kind of patients
HFV with topical anaesthesia might improve alveolar
ventilation and reduce the need for conventional mechanical
ventilation. However, HFV led to excessive mobilization of
sputum and these patients with severely compromised
pulmonary function and flaccid lungs had serious difficulty
in handling large quantities of sputum. 2)
The observation that HFV mobilized sputum was the reason
for the application of HFV in a patient, in whom retained
secretions were thought to form a clinical problem and
whose pulmonary function and lungcompliance seemed
acceptable.
PATIENT.
The patient was a 38 year old housewife with chronic asthma
since the age of 15, and extensive peripheral bilateral
bronchiectasis. There were no indications for the presence
of allergy, cystic fibrosis, ciliary dysfunction or
allergic aspergillosis. In 1961 the left basal segments
320
and the inferior segment of the lingula had been resected
because of recurrent left sided infections. In 1978 the
left hypertrophied aa. bronchiales were embolized because
of recurrent massive hemoptysis. In 1979 the apical segment
of the left lower lobe was resected because of recurrent
left sided infections and hemoptysis.
Nevertheless a chronic Pseudomonas infection persisted and
in spite of extensive medical treatment including daily
physiotherapy and inhalation therapy she had to be hospitalized
with increasing frequency because of febrile episodes,
hemoptysis and dyspnea. During these admissions, adding
up to 4 months a year, daily sputum volume was between
100 and 300 ml.
The pulmonary function was as follows:
METHODS.
VC
VCpredicted
VCpredicted, corrected
FEV1 % VC
RV % TC
P.F.R.
Pa , 02, rest
Pa , C02, rest
2,5
3,8
2,8
59
45
170
8,8
3,5
L, BTPS
L
L
- 69 %
%
L/min.
- 11 kPa.
- 5,5 kPa
HFV was used in 8 weekly sessions of 40 - 50 minutes on an
out patient basis during two months. During this period
maintenance therapy was kept constant, but minor adjustments
to prednisone requirements had to be made.
Daily sputum volume was recorded and peak flow rate (P.F.R.)
using the mini Wright Peak Flow Meter was measured three
times a day.
HFV was administered through a straight Metras sonde, ch. 19,
which was positioned halfway the trachea after topical
anaesthesia (0.5 % tetracaine) had been applied to the
mucosa of pharynx, larynx and trachea. No premedication
was used. A selfmade high frequency device (techn. A.H.
321
Strohmsdorffer) delivered pulses of 70 - 100 mI. of ambient
air to the trachea with a frequency of 100 - 150/min., a
working pressure of 4 Atm. and an inspiratory time of 30 %.
The patient was in the semirecumbent position and during
the initial sessions bloodpressure, pulse rate and arterial
blood gasses were monitored; once bronchoscopy was performed
before and directly after HFV to see, if damage to the
tracheal mucosa resulted from HFV. After each session of
HFV the patients was put in Trendelenburgs position and
recieved vigorous physiotherapy during several hours.
RESULTS.
HFV with topical anaesthesia was well tolerated except
for an increasing cough, not responding to additional
intratracheal tetracaine towards the end of the procedure.
No periods of apnea occurred and bloodpressure, pulse
rate and arterial blood gasses remained stable.
Bronchoscopy immediately after HFV revealed no mucosal
damage of the tracheobronchial mucosa and no hemoptysis
was precipitated by HFV.
Although the constant cough and expectoration during
and shortly after HFV were tiring, the patient felt
better afterwards and less dyspneic. This subjective
sense of well-being lasted 1 - 3 days after HFV, slowly
decreasing afterwards.
In the first hours following HFV large amounts of mucoid
and subsequently purulent sputum were expectorated. The
daily sputum volume on the day of HFV averaged 960 mI.
(range: 840 - 1060 mI.) and decreased in the following
week to an average of 270 mI. (fig.) Cultures of sputum
continued to grow Pseudomonas Aerfiginosa.
P.F.R. showed a tendency to follow the variations in daily
sputum volume. This is shown for P.F.R., measured at
21.00 hours (fig.). Between day "0" and day "3" after HFV,
P.F.R. increased with an average of 64 L/min. (range: 25 -
80 L/min.) or 36.5% (range: 14 - 67%) of the P.F.R. before
322
HFV. In most periods between HFV, P.F.R. decreased
subsequently. The average of the P.F.R. of the three days
following HFV was 184 L/min., compared with an average of
158 L/min. of the three days before HFV.
~ 38YRS. PEAK L/MIN FLOW RATE 220
1000
800 DAILY
SPUTUM VOLUME 600 IN ML
.... H.F.V.
DISCUSSION.
.... .... .... .... H.F.V. H.F.V. H.F.V. H.F.V.
IN L/MIN
200
180
160
140
120
100
1982
.... .... H.F.V. H.F.V. H.F.V.
HFV with topical anaesthesia during 40 - 50 minutes per
week was well accepted. However, it should be realized,
that this patient had a long history of hospital admissions
and surgical and medical treatment. She was on the one
hand accustomed to invasive procedures concerning the
airways and on the other hand well motivated. In other
patients HFV administered in this way might encounter a
smaller compliance.
HFV was also physically well tolerated. Circulatory and
ventilatory parameters remained stable during the procedure,
and no apnea occurred. With bronchoscopy immediately after
HFV no mucosal lesions of the tracheobronchial tree were
observed resulting from swaying of the flexible Metras
sonde or from the air-jet itself.
323
In the first hours after HFV an average of 960 mI. of
sputum was expectorated. Enhanced secretion by the bronchial
glands could be the result of stimulation and irritation of
these glands by HFV. In our patient this mechanism does not
seem to be the major cause of the increased expectoration,
because bronchoscopy after HFV did not reveal mucosal
irritation or damage, and because the expectorated sputum
was largely purulent. Moreover, pulmonary function tended
to improve after the procedure, whereas in the case of
enhanched bronchial secretion a decrease of pulmonary
function would be expect.ed. We favour the opinion that
HFV loosened and liquified retained secretions.
The mechanism by which HFV in our patient mobilized the
sputum is probably a complex one. Prior to the HFV only
moderate amounts (100 - 300 ml/day) of sputum were
expectorated during postural drainage and physiotherapy.
After HFV large quantities were recovered by the same
measures. Apparently the small volume of the air-jet,
enlarged by entraining air, had two effects on retained
secretions:
Firstly a liquifying effect on sticky sputum,
that could not be mobilized by conventional
means of physiotherapy,
Secondly HFV loosened sputum from the walls
of the bronchial tree.
This loosening may be the result of two different, but
co-operating mechanisms:
a) vibration of the bronchial walls. High frequency
air pulses cause vibration, particularly of the
stiff elements of the lung i.c. the bronchial
walls. During a normal cough a similar mechanism
has been demon stated with a high resolution
pneumotachograph. 3)
b) shearing forces acting on the sputum adherent
to the bronchial mucosa. HFV will cause turbulency
and vibration of the gas in the bronchial lumen,
both causing shear forces at the periphery of the
324
gasstream.
If this theoretical model of the action of HFV on retained
bronchial secretions is correct, a smaller effect of HFV
may be expected in emphysema. In these lungs vibration dies
out, due to the flaccidity of the structures.
Whereas the influence of HFV on daily sputum volume in our
patient is clear, the relation between HFV and pulmonary
function is less conspicuous. Because of the variability
of pulmonary function in asthmatics this relation may be
clouded. Yet in most periods an increase of P.F.R. can be
observed in the first days after HFV, followed by a decline.
The increase in sputum volume occurred within several hours
after HFV, whereas the improvement of P.F.R. occurred later.
We therefor think, that the primary effect of HFV is not on
pulmonary function but on expectoration. Retention of large
amounts of sputum has a deleterious influence on pulmonary
function. Mobilization and expectoration of retained sputum
will improve pulmonary function.
HFV with topical anaesthesia proved to be a valuable tool
in the management of the presented patient. The period of
observation has been too short to detect any benificial
influence of HFV on the frequency of hospital admissions.
HFV was well tolerated on an out patient basis. It should
be realized that the motivation of the patient must be good,
because co-operation during the sessions is essential.
In our opinion HFV may be a useful aid to physiotherapy in
selected patients with difficulty in expectoration, such as
patients with bronchiectasis, mucoviscidosis of ciliary
disfunction.
REFERENCES.
1. Sluiter H.J., Blokzijl E.J., van Dijl W., van Haeringen J.R., Hilvering C. and Steenhuis E.J. Amer. Rev. Resp. Dis., 1972, 105, 932.
2. Bateman J.R.M., Newman S.P., Daunt K.M., Sheahan N.F., Pavia D. and Clarke S.W. Thorax, 1981, 36, 683.
3. Douma J.H. Progress Report, Inst. Med. Phys., The Netherlands, 1976, 5, 200.
INDEX
Acidosis, respiratory, 294 Adapter
swivel, 285 tube, 175
ADH production, 21 Afterload, right ventricular, 284 Air entrainment, 89, 164 Airway tube compartments, 5 Airway volume, 3 Alluminium foil, 206 Alveolar compartment, 5 Alveolar mean pressure, 53 Amsterdam infant ventilator, 132 Anaesthesia, total intravenous,
195, 198 Andersson, 12 Angiocath, 285 Antidiuretic hormone, 111, 193 Apple-II, 133 Arbitrary units, 8 ARDS, 292 Aris equation, 61 Aspiration, 314 Auer, 12 Awareness, 198
Bard-Parker catheter, 212 Barotrauma, 14, 32, 73, 218, 233,
235, 268, 281, 284, 302, 312 Becklake, 152 Bendixen, 12 Bjork, 12, 13 Blood flow
cerebral, 23, 110 organ, 109
Brain movements, 33 Bronchial tree generations, 40 Bronchiectasis, 23, 24 Bronchoscopy, 150
diagnostic, 31 procedure, 234
Bronchovent, 88 Bulk flow, 59
Bulk movement, 316 Bypass, cardiopulmonary, 217
Capillaries, lung, 122 Capnography, 236 Carbon dioxide
elimination, 160 transport, 160
Carboxyhemoglobin, 264 Carburetor effect, 256 Cardiac compressions, 314 Cardiac index, 32, 118, 259, 268,
300 Cardiac output, 21, 84, 110, 116,
120, 264, 298 Cardiac performance, 281 Cardiovascular system, 115 Carina, 285 Carinal tumors, 221 CBF, 33 Ceiling effect, 169 Chamber, anti-condensation, 129 CHFV, 293 Children, 247 Circuit, low-compressive patient,
16 Clearance
carbon dioxide, 98 function, 240
Clearance lung index, 31 Co and a or wall effect, 14 Coefficient, diffusion, 3, 39, 47,
48 Compartments, 5 Compliance
inner, 173 internal, 14
static, 276 linear static, 274, 278 lung, 21 lung-chest, 90 static, 274 total lung, 95
326
Compliant element, 51 Compression, low, 272 compression volume, 87, 90 Computer, board, 176 Concentration cascade, 4 Concentration gradient, 4, 152 Condensation, 148 Convection
axial, 59 of inspired gas, 25
Converter, digital analog, 173 Coordinate
radial, 47 time, 47
Coughing, 247 CPAP, 120, 183, 258 CPPV, 120 Crafoord,12 Craniotomy, 235 Cricothyroid membrane, 234
puncture, 314 Cross flow, 52, 54 Cylinder of air, 4, 7
Dead space, 7 anatomical, 152 functional, 154, 157 physiological, 154, 157
Deane tube, 273 Decompensation, right sided, 122 Definitions, 19 Design principles, 71 Diffusion
augmented, 155, 157 convective, 3, 39 effective, 39, 41 enhanced, 103 gas, 294 molecular, 10, 18, 59 radial, 2
molecular, 41 Taylor, 1, 10, 41, 42, 43 turbulent, 41
Diffusion coefficient, 3, 10, 39, 47, 48
Diffusive plate, 58 Diffusivity, molecular, 25, 26 Dilution factor, 153 Dispersion, 39
augmented, 59 axial, 43 longitudinal, 1
Distress syndrome, 132 Diuresis, 21 Diverticulotomy, 204 Dopamine, 292
Douglas bag, 82 Drugs, respiratory depressant, 277
Elimination of CO2' 259 Emerson prototype ventilator, 317 Emphysema, 324 Engstrom, 12, 13
ventilator, 317 Entrainment, 238, 286
of roomair, 56 Equilibration, radial, 43 ETAL, 198 Exhalation time, 78 Expectoration, 321 Expiratory holds, 93
Feed back, 172 Fell, 12 Fick equation, 60, 64 Fistula
bronchopleural, 32, 235, 316 tracheobronchial cutaneous, 302
Flames, 206 Fleisch tube, 52 Flow interrupter, 160 Flow profiles, 51 Flow
accelerating, 277 convective, 218, 294 decelerating, 277 high instantaneous, 26 laminar, 2, 41 oscilatory, 39, 43, 46
laminar sinusoidal, 61 stationary, 42 swirling, 60 turbulent, 60, 155, 280
Flow sensor, 51 Fluidic ventilator, 89 Fredberg, 26 Frenckner, 12
Gas distribution, intrapulmonary, 21, 150
Gas exchange, 150 Gas transport, 51 Gas trapping, 27 Gas velocity, 24, 88 Giertz, 12
Haemodynamic changes, 82 Hallion, 12 Healthdyne, 72 Hedley-White, 12 Hemodynamic effects, 105 Hemodynamic function, 115
Hi-low jet tube, 234 High frequency oscillation
mechanical, 54 pneumatic, 53
High frequency pulsation, 52 Histamine, 68 Hooke, 12 Humidification, 129, 146, 229, 263,
285, 294
ICP, 33 Ignition, 194, 205 Immobilization of lung, 240 IMV, 143 Inertion of masses, 123 Inspiratory holds, 93 Inspiratory time, 75 Insufflation catheter, 87 Interactions, cardiorespiratory,
105 Interference, circulatory, 21 Interview, postoperative, 201 IRDS, 132
Jet injector nozzle, 87 Jet location, 73
Klain, 14
Laparotomy, 235 Laryngoscopy, 150 Laryngoscopy procedure, 234 Laser, 221 Laser microsurgery, 191 Laser surgery, 204 Laver, 12 LCI, 153, 154 Linear pneumotachograph, 88 Lobectomy, 31 Long-term treatment, 32 Longitudinal dispersion, 2 Lung clearance index, 31, 152 Lung model, 57, 92 Lung movements, 31 Lunkenheimer, 17
Mass, conservation of, 77 Mass-spectrometer, 274 Meltzer, 12 Methemoglobin, 264 Microatelectasis, 178 Microlaryngeal procedure, 234 Microprocessor, 129 Microsphere technique, 105 Microsurgery
endolaryngeal, 188
laryngeal, 212 laser, 191
Mismatching, 240 perfusion, 112 ventilation, 112
Mixing, radial, 59 Mode, asynchronous, 124 Models, hardware, 59 Modulation, pulse width, 173 Motor, magnetic, 65 Movement, convective, 41 Mucosal damage, 78 Mycoviscidosis, 324
Nebulizers, 146 NEEP, 141 Neuroleptanalgesia, 212 Newman-Keuls, 73
327
Newman-Keuls multiple range, 118 Nitrogen washout, 151, 272 Nitrogen washout delay, 31, 274 Nomogran, 162
ventilation, 30 Non-movable gas, 7
Oberg, 14 Obstructive lung disease, 319 O'Dwyer, 12 Oleic acid, 162 Open systems, 90 Oscillations, harmonic, 125 Oscillator
flueric, 72 piston-pump, 172
Oscillatory cycle, 8 Oscillatory frequency, 8 Oscillatory volume, 7, 8, 10 Overexpansion of alveoli, 240 Oxygen blender, 241 Oxygen transport, 32, 281 Oxygenation, apneic diffusion, 19 Oxygenator, extracorporeal
membrane, 293
Papilloma, 204 Partial pressure gradient, 57, 58 Patients, postcardiac, 247, 249 Pause, inspiratory, 26 Peak flow rates, 54 PEEP, 92, 96, 107, 118, 120, 141,
172, 179, 262, 292, 295, 302, 305 inadvertent, 77
PEEP valve, 257 Perfusion, organ, 128 Phrenic nerve, 140 Phrenic nerve activity, 21, 23
328
Physical models, 51 Physiotherapy, 34 P i.s ton-pump, 54 Plots, semilogarithmic, 151 Pneumocontroller, 129 Pneumonectomy, 219
sleeve, 216 Pneumotachography, 272 pneumothorax, 78 Poiseuilles law, 42 Pollution, 198 Pressure, 172
airway, 14, 93 alveolar gas, 126 distal airway, 26 driving, 158, 160 end-expiratory alveolar, 96 end-inspiratory airway, 89 entrance, 54 esophageal, 93 intracranial, 23 intrapleural, 21, 93 intrathoracic, 21, 110, 233 low airway, 21 low peripheral, 246 lung capillary blood, 126 mean airway, 27, 285, 302 peak airway, 115, 265, 302 peak inflation, 284, 285 peak inspiratory, 265 rectangular, 79 transpulmonary, 21, 280
Pressure flow measurements, 51 Pulmonary resection, 227 Pulmonectomy, 31 Pulsation, high frequency, 241
Radial diffusion, 2 Radial dispersion, 3 Radial mixing, 59 Rebreathing, 54 Rectangular pressure, 79 Reservoir, low pressure, 66 Resistance
airway, 26 inspiratory airway, 90
Respiratory distress syndrome, 150, 235
Respiratory failure, 273, 292 Retraction forces, 172 Reynolds number, 41, 62, 63 Rotary valve ventilator, 95
Sauerbruch, 12 sawtooth pressure pulse, 74 Scherer, 24
Secretolysis, 240 Shunt compliance, 68 Shunt fraction, 33 Shunt, intrapulmonary, 259, 306 Sighing, 162 Sjostrand, 14, 25 smith, 14 Smoke, 206 Space, anatomic dead, 31 Spirolog-l, 133 Spirometer, Tissot tank, 276 Sputum, 319 stenosis, tracheal, 31 Stroke index, 118 Stroke volume, 120 Suction manoeuvres, 247 Suctioning, 260 Surfactant, alveolar, 269 surgery
abdominal, 242 airway, 216 lung, 242
Swivel connector, 309 System H, 15, 16 System J, 16, 17 Systems, low-compression, 90
Temperature, core, 142 Thoracotomy, 235 Tracheal pressure, 51 Tracheal resection, 222 Tracheal tube, double-lumen, 88 Transcutaneous PC02, 238 Transport
backward, 5 convective, 2, 3 diffusive, 3 forward, 5 mucociliary, 234, 315
Transtracheal jet ventilation, 236 Trapping, 75 Trigger, external, 129 Tube
endobronchial, 182 double-lumen, 27
Tuffier, 12
Ultrasonic spirometer, 82
Vagal nerve activity, 23 Valve
electronic-magnetic, 129 pneumatic, 14, 15, 16, 31, 87, 275 rotating, 106 solenoid, 52, 72, 81, 84, 106,
133, 172, 241
Vasoconstriction, pulmonary, 178 Velocity, 51
axial, 155 gas, 24, 88 linear, 39, 42 oscillatory, 26
Ventilation alveolar, 27 digital, 173 forced diffusion, 55, 241 intermittent mandatory, 262 low-compressive volume-controlled,
16 one-lung, 31, 178 postoperative, 247 transtracheal, 314 volume-controlled, 16 volume cycled, 262
Vent:ilator fluidic, 30 low-compressive, 25 valveless, 140
Vesalius, 12
Vibration, 323 Viscosity, 41
kinematic, 49 Volume
calibrated tidal, 172 compressible, 13, 14
low, 93 compression, 276
Volume flow, 10 Volumeter, ultrasonic, 276 Volumetric pump, 200 Vortices, 41
Washout, 56 Washout of N2 , 150 Washout technique, 9 Waveshape, 79
jet pressure-flow, 71 rectangular, 74
329
Weaning, 34, 233, 235, 247, 249, 260, 262, 263
Zenkers diverticulum, 209