pressure-support ventilation and diaphragm shortening in

www.aana.com/members/journal/ AANA Journal/August 2005/Vol. 73, No. 4 277

induced by the ventilator, the endotracheal tube, andsecretions.7-9 When PSV is used, the patient’s sponta-neous inspiration is augmented by delivering a presetpressure that is held constant throughout the inspira-tory cycle. The patient controls the rate and timing ofthe delivered pressure, thus controlling flow and tidalvolume (VT). Consequently, PSV decreases the overallWOB during weaning by supporting spontaneousinspiratory effort.10-14

Sanders et al15 found that invasive technology suchas endotracheal tubes and ventilator circuits increasethe WOB. They suggested that the increase in WOBwithout the use of PSV may delay weaning frommechanical ventilation, thus increasing the chance foriatrogenic infections, increased length of stay, andsubsequent rise in patient morbidity and healthcarecosts. Sanders et al15 reported that the WOB decreased38% to 64% with the application of 15 cm H2O of PSV.Other studies have shown that PSV decreases respira-tory rate,10,16 increases VT,10,16 reduces oxygen con-sumption,9,11 promotes recovery from diaphragmmuscle fatigue,1 and allows the diaphragm to rest,

Little is known about how pressure-support ventilationaffects diaphragm performance because there is no directmeasurement of diaphragm function in the clinical setting.An indicator of diaphragm performance or work is the prod-uct of diaphragm muscle shortening and intrathoracic pres-sure during inspiration.

We studied the effect of pressure-support ventilation ondiaphragm shortening, diaphragm work, and other car-diopulmonary parameters. In 15 anesthetized Sprague-Dawley male rats, pressure support was increased from 0 to10 cm H2O in 2 cm increments. Increasing pressure supportfrom 0 to 10 cm H2O resulted in respiratory rate decreasing25%, tidal volume increasing 148%, minute ventilationincreasing 91%, end-tidal carbon dioxide decreasing 5%,and cardiac output decreasing 30%. Progressively increas-

ing pressure support to 10 cm H2O was accompanied by

decreases in the end-inspiratory pressure without signifi-

cant increases in diaphragm shortening. Therefore, dia-

phragm work was decreased.

The lack of an increase in diaphragm shortening in the

presence of an increase in tidal volume indicated that there

was an augmentation of thoracic volume in the coronal

and/or horizontal axes instead of the cephalocaudal axes

throughout inspiration. These findings may be useful to

nurse anesthetists in the understanding of diaphragm work

when patients are being ventilated with pressure-support

ventilation.

Key words: Diaphragm shortening, pressure-support venti-

lation (PSV).

Pressure-support ventilation and diaphragmshortening in the rat modelCaryl Goodyear-Bruch, RN, PhD, CCRN Kansas City, Kansas

L. Rae Long, CRNA, MSKansas City, Missouri

Peggy Simon, RNC, MSNSpringfield, Missouri

Richard L. Clancy, PhDJanet D. Pierce, DSN, ARNP, CCRNKansas City, Kansas

Anesthesia providers are often confrontedwith patients who fail to meet extubationparameters after surgery. These patientsmay experience difficulty weaning frommechanical ventilation and may require

assistance with maintaining adequate tidal volumes.Diaphragm muscle fatigue is presently considered to beone of the causes of failure to wean from mechanicalventilation.1 It is estimated that 60% to 75% of the workof breathing (WOB) is performed by the diaphragmduring normal respiration.2 The overall WOB consistsof the following factors: (1) compliance work, the workrequired to overcome the elastic forces of the lung; (2)tissue-resistance work, the work required to overcomethe viscosity of the lung and thoracic cage; and (3) air-way resistance, the work required to overcome theresistance to the flow of air through the airways.3

In the 1980s, pressure-support ventilation (PSV)was introduced as an assist mode to augment ventila-tion in select spontaneously breathing patients.4-6

Pressure-support ventilation decreases dyspnea andincreases patient comfort by decreasing the resistance

278 AANA Journal/August 2005/Vol. 73, No. 4 www.aana.com/members/journal/

making weaning more comfortable and efficient.17-19

Investigators have suggested that PSV lowers respi-ratory oxygen consumption by decreasing the WOBmore than either synchronized intermittent mandatoryventilation5 or continuous positive airway pressure.6,20

The latest mode of ventilation designed to augment theweaning process is called proportional assist ventila-tion. Delaere et al4 demonstrated no difference in termsof WOB between PSV and proportional assist ventila-tion. Hart et al21 concluded that compared with pro-portional assist ventilation, PSV provided more patientcomfort and a greater decrease in respiratory work.

Presently, there are no direct clinical methods tomeasure changes in workload on the diaphragm duringPSV. Evaluation of decreased diaphragmatic workloadand respiratory muscle endurance can be accomplishedonly by indirect methods that do not distinguishbetween the performance of the diaphragm and otherrespiratory muscles.22

The purpose of this study was to examine theeffects of PSV on diaphragm work by using a minia-turized ultrasonic transducer to directly measurediaphragm shortening. In addition, cardiopulmonaryparameters associated with PSV were evaluated. Thisinformation will be useful for nurse anesthetists inunderstanding and using PSV to discontinue mechan-ical ventilation in surgery patients.

Materials and methodsA total of 15 Sprague-Dawley male rats were used forthis study. The weight of rats ranged from 310 to 450g with a mean weight of 400 g. The rats were main-tained at a reversed 12-hour light-dark cycle, withlights on at 8:00 PM and off at 8:00 AM. This study wasapproved by the University of Kansas Medical CenterInstitutional Animal Use and Care (Kansas City, Kan).

The rats were anesthetized with sodium pentobar-bital (65-80 mg/kg of body weight) administered viaintraperitoneal injection. Atropine (0.10 mg/kg ofbody weight) was administered intraperitoneally toreduce respiratory secretions. When a surgical planeof anesthesia was reached, assessed by the pinch testand corneal reflex test, the following procedures wereperformed:

The trachea was exposed and cannulated usingpolyethylene 240 tubing. Next, a catheter (4F) wasinserted in the oral cavity and advanced down theesophagus until the catheter tip was 1 to 2 cm abovethe diaphragm. The catheter was connected to a pres-sure transducer for continuous monitoring ofesophageal pressure, which served as a measure ofintrathoracic pressure (ITP).

A polyethylene (50) catheter was inserted into the

left femoral artery and advanced until the catheter tipwas in the descending aorta, approximately 1.5 cmbelow the renal arteries. The catheter was connected toa pressure transducer-recorder system for measuringsystolic, diastolic, and mean arterial pressures (MAPs)and heart rate. This catheter also was used for measur-ing arterial blood gases, including pH, arterial partialpressure of carbon dioxide (PaCO2), arterial partialpressure of oxygen, bicarbonate, and oxygen satura-tion (blood sample volume was 100 µL). A thermo-couple catheter was inserted in the left carotid arteryand advanced until the catheter was positioned in theaortic arch and connected to a cardiac output monitor.

A second polyethylene (50) catheter was insertedin the right jugular vein and the tip advanced into theright atrium for measuring central venous pressure(CVP). In addition, this catheter was used as the sitefor injecting saline (0.5 mL) for determination of car-diac output (CO) using the thermal dilution tech-nique. All catheter positions were verified by autopsyat the conclusion of the experiment.

The diaphragm was exposed via an abdominal mid-line incision. A miniaturized ultrasonic transducer formeasuring diaphragm shortening was attached to theinferior surface of the middle costal portion of the righthemidiaphragm. The abdominal incision was notclosed to allow assessment of sensor attachment duringthe experiment. The ultrasonic transducer was coupledto a Crystal Biotech Tracker (Crystal Biotech, North-borough, Mass). The instrument used conventionalultrasonic transmission-reflection principles to meas-ure the distance between the transducer and a point ofchange in medium density within the diaphragm. Theinstrument was adjusted to track sound waves reflectedfrom a reference plane 0.2 to 0.3 mm from the inferiorthoracic diaphragm surface, providing a continuous,dynamic measurement of diaphragm thickness. It wasassumed that the volume of the muscle cell does notchange during contraction and relaxation. Therefore,during contraction, muscle cell diameter increased indirect proportion to decreased muscle cell length. Con-sequently, the increase in diaphragm thickness duringinspiration is related directly to the overall extent ofdiaphragm shortening. Thus, during inspiration, themovement of the reference plane is directly propor-tional to the degree of diaphragm shortening. Theextent to which the reference plane moved was desig-nated as the percentage of fractional thickening (Figure1). Earlier studies supported the miniaturized ultra-sonic transducer as a device that measures diaphragmshortening with precision and accuracy during nor-moxia, hypoxia, and hypercapnia.13,23

Once the animal preparation was completed, the


rat was connected to a Siemens Servo 300 ventilatorset (Dräger Medical, Telford, Pa) as follows: PSV, 0 cmH2O; trigger sensitivity, 0; and end-expiratory pres-sure, 1 cm H2O. Pressure-support ventilation wasincreased sequentially by increments of 2 cm H2Oevery 2 minutes to 10 cm H2O and then sequentiallyreturned to 0 cm H2O. Waveform measurements ofarterial blood pressure, CVP, diaphragm shortening,ITP, end-tidal CO2 (PETCO2) and peak inspiratory pres-sure were obtained throughout the experiment via aCODAS computer data acquisition software package(DataQ Instruments, Inc, Akron, Ohio). Tidal volumeand respiratory rate (f) were measured during the last20 seconds of each 2-minute period. An analog signalfrom the Siemens ventilator to the computer wasestablished to provide an accurate and precise contin-uous measure of VT. Cardiac output and arterial bloodgases were measured following a 5-minute stabiliza-tion period at PSV 0 and 10 cm H2O.

Power analysis revealed that 15 animals wouldallow detection of an effect size of 0.15 with 80%power at a type I error rate of 5%. All measurements

were compared using the 1-way repeated-measuresanalysis of variance and the Tukey procedure for post-hoc multiple comparisons of group means (SPSS-pc;SPSS, Inc., Chicago, Ill).

ResultsVariables measured or calculated from the experimentincluded MAP, CVP, CO, systemic vascular resistance,peak inspiratory pressure, VT, f, minute ventilation(V̇E), PETCO2, ITP, and fractional thickening.

As shown in Figure 2, when PSV was increasedfrom 0 to 10 cm H2O, a significant decrease in COfrom 282 to 200 mL/min per kilogram occurred, F (1,14) = 13, P = .0060. In addition, an increase in CVPfrom –0.90 cm H2O to approximately –0.01 cm H2Owas observed, F (1, 14) = 5.75, P = .0310. IncreasingPSV from 0 to 10 cm H2O resulted in an insignificantdecrease in MAP, 107 to 98 mm Hg (P = .0740). Sys-temic vascular resistance increased 26%, which wasnot statistically significant (P = .0830).

Increasing PSV in increments of 2 cm H2O up to 10cm H2O resulted in progressive decreases in respira-tory rate (Figure 3). At a PSV of 10 cm H2O, the res-piratory rate was statistically significantly differentfrom baseline, F (1, 14) = 371.89, P = .0010. Minuteventilation increased significantly from 210 mL/minper kilogram at a PSV of 0 cm H2O to 400 mL/min perkilogram at a PSV of 10 cm H2O, F (1, 14) = 39.39, P= .0001. The V̇E increase accompanied by the decreasein respiratory rate associated with increasing PSVresulted in significant increases in VT from 2.7 mL ata PSV of 0 cm H2O to 6.7 mL at a PSV of 10 cm H2O,F (1,14) = 959.73, P < .0001. With the application ofPSV, there was a decrease in PETCO2 (from 38 to 32mm Hg); however, this decrease was not significant (P= .3300). End-inspiratory ITP became progressivelyless negative with each 2-cm H2O increase in PSV(Figure 4). At a PSV of 10 cm H2O, the end-inspira-tory ITP was significantly different from baseline, F(1, 14) = 139.13, P < .0010. End-expiratory ITPremained unchanged with incremental increases inPSV. There were no significant changes in fractionalthickening of the diaphragm among the PSV levels. Ata PSV of 0 cm H2O PSV, fractional thickening was24.38% and only increased to 26.63% at a PSV of 10cm H2O, which was not statistically significant, F(1,14) = 2.57, P = .1300 (Figure 5). However, theunchanged diaphragm shortening occurred in thepresence of progressive decreases in inspiratory ITP.

DiscussionAn index of the work of the diaphragm (WD) is the prod-uct of the difference between end-expiratory and end-

Figure 1. Illustrates the placement of the ultrasonicsensor on the right hemidiaphragm in relation to thecentral tendon muscle

As the muscle contracts, the diaphragm becomesthicker and, thus, shortens, which causes the increasein the amplitude of the signal. On relaxation of thediaphragm, the muscle is not as thick and the signalreturns to the baseline. During contraction of themuscle, the extent of the reference plane (r)movement is proportional to DS.

DS indicates diaphragm shortening; % FT, percentage of fractional thickening.


inspiratory ITP (DITP) times diaphragm shortening.

WD = DITP ¥ DS

By increasing PSV from 0 to 10 cm H2O, the DITP(see Figure 4) was decreased by 33%. Consequently,because diaphragm shortening was unchanged withincreasing PSV, there was an approximate 33%decrease in diaphragm work per breath. In addition,the decrease in the respiratory rate with increasing

PSV resulted in a further decrease in the WD perminute. Thus, the decrease in the WD decreased thediaphragm oxygen consumption and protected thediaphragm muscle from fatigue, which wouldenhance weaning from mechanical ventilation. Thissupports the theory of MacIntyre24 and MacIntyre etal25 that PSV is an energy-efficient form of reducingthe workload on the diaphragm.

Because PSV decreases the resistance from endotra-

Figure 3. Mean and SEM for minute ventilation and respiratory rate for various levels of pressure-supportventilation (PSV)

The “d” after numbers indicates decreasing the amount of PSV.

Figure 2. Effect of 0 and 10 cm H2O pressure-support ventilation (PSV) on cardiac output (CO) and centralvenous pressure (CVP)

KgBW indicates kilograms of body weight.


Figure 4. Mean and SEM for intrathoracic pressure (ITP) at the end of expiration and end of inspiration atvarious levels of pressure-support ventilation (PSV)

The letter “d” after numbers indicates decreasing the amount of PSV.

Figure 5. Mean and SEM for fractional thickening of the diaphragm at different levels of pressure-supportventilation (PSV)

The letter “d” after numbers indicates decreasing the amount of PSV.


cheal tubes and ventilatory circuitry, diaphragm short-ening should be enhanced with increasing PSV. WhenPSV levels increased, VT and V̇E increased, resulting inaugmentation of alveolar ventilation and, thus, areduction in PaCO2. The lower PaCO2 would decreasethe activity of the central nervous system respiratorycenters. If this resulted in a decrease in the duration ofinspiration, the degree of activation of the diaphragmmuscle would be reduced, and, thus, there would beless diaphragm shortening. Alternatively, the decreasein central nervous system respiratory center activitymay diminish the frequency of phrenic nerve actionpotentials. Therefore, there would be a reduction inthe magnitude of diaphragm activation. Either ofthese 2 mechanisms could account for the absence ofan increase in diaphragm shortening with a decreasingload (DITP). The possibility of decreased inspiratoryduration and/or phrenic nerve discharge frequency issupported by the observations of Uchiyama et al,14

who found that peak diaphragm electromyogram sig-nals were decreased with application of PSV.

During inspiration, the thorax is enlarged by a low-ering of the diaphragm due to contraction of its mus-cle fibers and by elevation and expansion of the thorax(ribs and sternum).26 Consequently, the chest expandsanteroposteriorly (coronal axis), transversely (hori-zontal axis), and vertically (median or cephalocaudalaxis). The finding that an increased VT with PSV with-out a change in diaphragm shortening indicated thatduring inspiration there was an augmentation of chestmovement in the coronal and horizontal axes.

A major hemodynamic effect associated with theapplication of PSV in this study was a 30% decrease inCO with a PSV of 10 cm H2O. This finding supportsthe work of Dries et al27 in cardiac surgery patients inwhich they observed a decrease in CO with higher lev-els of PSV. Putensen et al,28 in examining the effects ofspontaneous ventilation vs PSV on the ventilation-perfusion ratio, reported a significant decrease in COat high levels of PSV. Dries et al27 found that as PSVwas decreased, subsequent increases occurred in heartrate, MAP, and pulmonary capillary wedge pressure.Increasing ITP with application of PSV resulted in adecrease in right ventricular filling that caused CO todecrease. Consequently, PSV increased ITP, whichimpaired venous return and, hence, CO.

To summarize, PSV is a partial assist mode of ven-tilation that can be used by anesthesia providers toaugment spontaneously breathing patients who maynot meet extubation criteria following surgery. Thismode of ventilation is more comfortable for thepatient and improves patient-ventilator interac-tion.24,29 The results of this investigation demon-

strated there was a decrease in WD, although dia-phragm shortening remained significantly unchangedwith PSV. Thus, PSV, by decreasing diaphragm work,decreases diaphragm oxygen demand, which may pre-vent diaphragm fatigue, one of the main causes of fail-ure to wean from mechanical ventilation.

Monitoring V̇E, as a respiratory muscle load indica-tor,30 and monitoring saturation of arterial oxygen31,32

when weaning patients from mechanical ventilatorsare prudent clinical measures. By using PSV duringweaning to decrease the imposed WOB caused by theendotracheal tube and circuitry, VT is improved whilerespiratory rate decreases, thus improving V̇E Further-more, this study showed that the increase in VT and,thus, alveolar ventilation improved with the use ofPSV resulting in decreased PETCO2.

Further study of PSV compared with other modesof ventilation (such as volume support) is essential fordetermining the most effective method for discontin-uing patients from mechanical ventilation. Becausenew modes of mechanical ventilation are used in theclinical setting each year, anesthesia providers need tounderstand how the modes affect the respiratory mus-cles, in particular, the diaphragm, in order to provideoptimal patient care.

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AUTHORSCaryl Goodyear-Bruch, RN, PhD, CCRN, is an assistant professor,School of Allied Health, Nurse Anesthesia, University of Kansas Med-ical Center, Kansas City, Kan. Email: [email protected]

L. Rae Long, CRNA, MS, is a nurse anesthetist, North Kansas CityHospital, Kansas City, Mo.

Peggy Simon, RNC, MSN, is a psychiatrist nurse, Cox Health Sys-tems, Adult Psychiatric Unit I, Springfield, Mo.

Richard L. Clancy, PhD, is a consultant, School of Nursing, Univer-sity of Kansas Medical Center, Kansas City, Kan.

Janet D. Pierce, DSN, ARNP, CCRN, is an associate professor, Schoolof Nursing, University of Kansas Medical Center, Kansas City, Kan.

ACKNOWLEDGMENTFinancial support provided by National Institutes of Health, NationalInstitute of Nursing Research grant No. 5 KO7 NROOO59-02.

pressure-support ventilation and diaphragm shortening in

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