respiratory monitoring during mechanical ventilation

SYMPOSIUM: RESPIRATORY MEDICINE

Respiratory monitoringduring mechanicalventilation

Robinder G Khemani

Robert D Bart III

Christopher JL Newth

Abstract

Techniques to monitor the respiratory system during mechanical

ventilation have evolved significantly over the years. When integrated

with the physical examination, these tools aid the management of

respiratory disease, ultimately leading to safer and more effective care

for all mechanically ventilated children. This review will focus on readily

available methods of respiratory monitoring for children undergoing

mechanical ventilation. In particular, there will be a brief discussion on

gas exchange, capnography, respiratory plethysmography and oesopha-

geal manometry, as well as a more substantial discussion on

pressure–volume and flow–volume loops. Finally, we discuss using all

these tools to help determine optimal ventilator support for a variety of

pulmonary disease states.

Keywords capnography; manometry; mechanical; paediatrics;

plethysmography; respiratory-function tests; ventilation

Introduction

Respiratory failure is one of the most common reasons for

admission to paediatric intensive care units (PICUs), particularly

in the first 2 years of life. While patients are recovering from the

aetiology leading to respiratory collapse, intensivists are charged

with supporting the respiratory system with mechanical ventila-

tion. Paramount to ensuring adequate support is close super-

vision of therapeutic interventions – through both invasive and

non-invasive forms of respiratory monitoring. This discussion

concentrates on common means of respiratory monitoring used

Robinder G Khemani MD is at the Children’s Hospital Los Angeles,

Department of Anesthesiology and Critical Care, 4650 Sunset Blvd., Mail

stop 12, Los Angeles, CA 90027, USA.

Robert D Bart III MD is at the Children’s Hospital Los Angeles, Department

of Anesthesiology and Critical Care, 4650 Sunset Blvd., Mail stop 12, Los

Angeles, CA 90027, USA. Assistant Professor of Clinical Pediatrics,

University of Southern California, Keck School of Medicine.

Christopher J L Newth MB FRCPC FRACP is at the Children’s Hospital Los

Angeles, Department of Anesthesiology and Critical Care, 4650 Sunset

Blvd., Mail stop 12, Los Angeles, CA 90027, USA. Professor of Pediatrics,

University of Southern California, Keck School of Medicine.

PAEDIATRICS AND CHILD HEALTH 17:5 193

in intensive care units. In particular, it will focus on capnography,

work of breathing (WOB) measurements, and flow–volume and

pressure–volume loops. Additionally, substantial sections are

devoted to therapeutic interventions based on integrating

monitoring and the underlying disease state, particularly with

regards to optimising ventilator support.

Gas exchange

Regardless of the process leading children to require mechanical

ventilation, the paediatric intensivist must maintain gas exchange

to keep the body in a state of relative homeostasis. Inadequate

gas exchange manifests either as an inability to deliver adequate

oxygen or to eliminate carbon dioxide effectively.

Oxygenation

Manipulations of mechanical ventilator support for hypoxaemic

respiratory failure are targeted at maintaining oxygen delivery.

Fundamentally, two types of hypoxaemic respiratory failure exist.

Type I hypoxaemic respiratory failure results from ventilation–-

perfusion (V/Q) mismatch. In particular, it refers to areas of

intrapulmonary shunt generated from perfused alveoli that are

inadequately ventilated (due to atelectasis, consolidation, oede-

ma, etc.). Characteristic of this type of respiratory failure are large

differences between pAO2 (Alveolar oxygen tension) and pAO2

(arterial oxygen tension). This results in an increase in the

Alveolar–arterial (A–a) oxygen gradient. Under normal circum-

stances, this oxygen difference is less than 10 mm Hg. However,

with severe restrictive pulmonary disease, the A–a oxygen

gradient is often several hundred mm Hg.1 One goal of positive

pressure ventilation is to diminish intrapulmonary shunt by

recruiting atelectatic or consolidated lung units, thereby improv-

ing V/Q matching and reducing the A–a oxygen gradient.

Type II hypoxaemic respiratory failure is less common than

type I failure, and classically results from hypoventilation

without increase of the A–a oxygen gradient. For the most part,

pure Type II respiratory failure presents less of a challenge for

management as modest improvements in ventilation or small

increases in supplemental oxygen can often overcome the

hypoxaemia.

Ventilation

Positive pressure ventilation is commonly initiated for respiratory

failure that manifests by elevated PaCO2 (arterial carbon dioxide

tension), and is often associated with a disease causing an

increased A–a oxygen gradient. In the vast majority of cases this

results from insufficient alveolar minute ventilation, although in

rare cases, PaCO2 may rise from metabolic derangements and

increased production of CO2. The determinants of alveolar

minute ventilation are two-fold. Recall:

Minute ventilation ðVEÞ ¼ ½respiratory rate ðf Þ�½tidal volume ðVTÞ�;

where VT ¼ volume of dead space (VD)+alveolar volume (VA);

combining VE ¼ f(VD+VA), solving alveolar minute ventilation

(MVA) ¼ f[VT–VD].

VD is the volume within the respiratory system that does not

participate in gas exchange. In healthy individuals, this is made

up almost exclusively of anatomic dead space (oropharynx,

trachea, large conducting airways), with little contribution from

lung units. However, as pulmonary disease worsens, and V/Q

r 2007 Elsevier Ltd. All rights reserved.

2 (

mm

Hg

)

III

a’

a

70

60

50

40

30


mismatch ensues, dead space increases (this includes anatomic

dead space and lung units that are ventilated, but not perfused).

In normal individuals the dead space:tidal volume ratio (VD/VT)

is estimated to be 0.2–0.3. However, patients with significant lung

disease requiring positive pressure ventilation often have VD/VT

ratios exceeding 0.6.2 Therefore, elevated levels of PaCO2 can

come from three major mechanisms: increased CO2 production,

inadequate minute ventilation from low tidal volumes or

respiratory rates, or increases in dead space.

CO

Time (seconds)

I

II

IV20

10

0

0 2 4 6 108

Figure 1 Time-based normal capnograph (solid line) and capnograph of

obstructed airways (dotted line). (I) Contribution from anatomic dead

space- where CO2 content is near zero. (II) Mixture of dead space and

alveolar ventilation-abrupt rise in CO2. (III) CO2 plateau phase-

characterized by pure alveolar ventilation. (IV) Inspiration – a rapid fall

in CO2 (a & a’) End Tidal CO2. Note the upsloping of phase III from airway

disease.

Monitoring

Oxygenation

The gold standard for monitoring oxygenation is the arterial

blood gas (ABG). The ABG measures PaO2 directly from blood,

and uses values of temperature, pH, PaCO2 and PaO2 to calculate

the percent oxyhaemoglobin saturation. Only arterial samples

will suffice for estimations of PaO2. Capillary blood gases do not

reliably predict arterial PaO2.3 However, the advent of pulse

oximetry in the 1980s has provided an alternative for inexpen-

sive, accurate and continuous monitoring of arterial oxygen

saturation. Classic pulse oximeters are very accurate when

oxyhaemoglobin concentrations are greater than 60%. However,

they can underestimate oxygen saturation when perfusion to the

extremity where the probe is located is compromised, as is often

encountered with shock states, the use of vasoactive medica-

tions, peripheral oedema or peripheral vascular disease.4 Pulse

oximeters may also be inaccurate if other forms of haemoglobin

(i.e methaemoglobin or carboxyhaemoglobin) that absorb light at

similar wavelengths as oxyhaemoglobin or deoxyhaemoglobin

are present.5

Ventilation

Similar to PaO2 with oxygenation, the PaCO2, determined from an

ABG, best measures ventilation. Unlike PaO2, however, a free

flowing capillary sample adequately estimates PaCO2. Central

venous samples may accurately reflect pH, but peripheral venous

samples are inaccurate measures of systemic pH and PaCO2.3

However, short of repeated blood sampling, capnography and

transcutaneous CO2 detectors provide non-invasive alternatives

to monitor ventilation.

Capnography: capnography waveforms (either time or volume

based) provide a wealth of information. In addition to detecting

end-tidal CO2 (ETCO2), they provide information about respira-

tory rate and rhythm, dead space calculations, cardiac output,

confirmation of endotracheal tube (ETT) placement, mechanical

failure of the ventilator from kinking, displacement or obstruc-

tion of the ETT, patient–ventilator asynchrony and the presence

of obstructive airway disease.6

ETCO2 detectors are positioned at the adaptor end of the ETT,

and detect exhaled CO2 using an exhalation chamber, an infrared

light source and a detector. The module can be placed directly on

the end of the ETT or on the side via an aspirating catheter. The

absorption of CO2 is unique, and can be illustrated graphically as

a function of time or volume.

Time-based capnographs consist of four phases. Phases I–III

comprise exhalation, and Phase IV represents inhalation


(Figure 1). The level of CO2 detected during the plateau phase

gradually approaches the PaCO2 during normal physiologic

conditions, but never reaches it. The inflection point just prior

to inspiration is where ETCO2 is measured. Under normal

circumstances, without a significant ETT leak and during tidal

respiration, the ETCO2 estimates PaCO2 within 2–5 mmHg.7

An increased gradient between ETCO2 and PaCO2 signals

increased dead space, and may represent worsening underlying

disease, pulmonary vascular abnormalities, worsening cardiac

output or iatrogenic pulmonary overdistension. The capnogram

can be used to estimate the relative dead space:tidal volume ratio

(VD/VT):

VD=VT ¼ ½PaCO2 � ECO2�=PaCO2,

where ECO2 ¼ mean expired CO2, graphically represented as the

area under the curve of the time-based capnogram.8 This number

can be calculated using automated software with a pneumota-

chograph device, or crudely estimated from the difference

between ETCO2 and PaCO2. In reality, VD/VT ratios are more

easily calculated using volumetric capnograms (vide infra).

In addition to the numerical ETCO2 value, the graphic pattern

of a time-based capnogram can provide a clue to important

disease states and abnormalities. Obstructive airway disease

(Figure 1) shows a classic upslope of Phase III as restriction to

expiratory flow delays emptying of alveolar gas from the different

regions of the lung. In fact, the degree of upslope correlates well

with severity of airway obstruction.9 Rising baseline levels of CO2

on the capnogram may represent rebreathing of CO2 from

insufficient mechanical ventilatory support, inadequate exhala-

tion time or dead-space ventilation.10 Acute respiratory distress

syndrome (ARDS) and other diseases affecting the lung par-

enchyma may cause markedly widened A–a carbon dioxide

gradients (20–30 mm Hg) at the peak of the lung disease, and



subsequent narrowing occurs with disease resolution. Impaired

pulmonary blood flow from low cardiac output, pulmonary

embolus or severe elevations in pulmonary vascular resistance

may have low-amplitude capnogram tracings. The extreme

example of this is during cardiac arrest when lack of pulmonary

blood flow results in a very low ETCO2 value and a high PaCO2.

This combination immediately raises concern that the ETT is not

in the airway, but in reality the ETCO2 is low because there is no

pulmonary blood flow.

The volumetric capnogram traces CO2 concentration against

exhaled volume, and is particularly useful for performing dead

space calculations, determining optimal positive end-expiratory

pressure (PEEP), and titrating drug therapy for states of increased

airway resistance. It is composed of three phases (Figure 2a). In

addition, knowing the measured PaCO2 from an ABG allows easy

computation of VD/VT for each breath (Figure 2b). Just as with

the time-based capnogram, the slope of phases III will increase

with increased airway resistance from obstructive disease.11

FeC

O2

FeC

O2

Z

Y

X

Exhaled tidal volume

Art

erial P

CO

2

End-t

idal C

O2

Exhaled tidal volume

Phase IIPhase I Phase III

b

a

Figure 2 Volumetric capnogram (single breath) (a) Phase I represents

anatomic dead space. Phase II transition from early alveolar emptying,

and phase III the alveolar plateau with slowly rising CO2 from different

lung units; (b) explains the calculation of the VD/VT ratio when PaCO2 is

known. Here VD/VT ¼ (Y+Z)/(X+Y+Z), where X is the area of alveolar

ventilation, Z anatomic dead space, and Y imposed dead space from

poor perfusion or worsening lung disease.


While capnography is useful in the PICU, it has limitations.

First, it is designed for tidal breathing at relatively normal

respiratory rates; therefore, it is best when mechanically

ventilating at relatively slow rates. As such, spontaneously

breathing neonates and infants who normally have a rapid

shallow breathing pattern often lack the plateau phase on the

time-based capnogram. However, the numerical ETCO2 value is

accurate and predicts PaCO2. The tracing is also affected by large

air leaks around the ETT. In addition, care must be taken with

smaller diameter tubes not to kink the tube with the weight of the

end-tidal module. Even if there is a system error in the end-tidal

acquisition unit (such as a large leak around the ETT), the ETCO2

will always read lower than the PaCO2. Therefore, an elevation in

ETCO2 invariably means that the PaCO2 is at least as high, and

should be treated very seriously.

Transcutaneous CO2 monitoring: in situations where capnogra-

phy cannot be employed (e.g. high-frequency ventilation, non-

intubated patients), transcutaneous CO2 monitors (TCOM)

provide an alternative. The TCOM heats the skin, vasodilating

the capillary beds and increasing diffusion of CO2 across the skin.

The probe then detects the CO2 electrochemically. TCOMs are

generally accurate within 6–10 mmHg, and are particularly useful

to follow trends, especially in thinner patients and neonates.

Obesity, oedema, and hypoperfusion may make the TCOM less

accurate.12

Work of breathing measurements

In addition to normalising gas exchange, another goal of

mechanical ventilation is to support the patient while he/she is

recovering from the inciting event that led to respiratory failure.

To this end, minimising work of breathing (WOB) during

recovery by optimal selection of ventilator support allows the

patient the highest likelihood of weaning to extubation. This is

particularly useful for patients with obstructive airway disease.

Oesophageal manometry

Oesophageal manometry has long been used in animals and

adults to study the mechanics of breathing. An oesophageal

manometer can be used to subdivide measurements of respira-

tory system compliance into contributions from the chest wall

and those from the lung. Recall, respiratory system work is the

pressure applied to yield a change in volume of the system. In

reality, this work is comprised of elastic, resistive, inspiratory,

expiratory, lung and chest wall components.13 The most

significant and dynamic component of WOB is best estimated

by the change in pleural pressure needed to generate a change in

volume. An oesophageal manometer, placed correctly in the

lower third of the oesophagus, closely approximates pleural

pressure.14

Oesophageal manometry can monitor patient initiated work on

various levels of support. A good example of this is having a

spontaneously breathing patient on continuous positive airway

pressure (CPAP) and pressure support (PS) where optimal

ventilator support is titrated based on the patient’s WOB and

comfort. Modern ventilators increasingly have built-in software

to analyse WOB when paired with an oesophageal catheter.



Respiratory plethysmography

During normal tidal breathing, without significant pathology,

diaphragm contraction leads to inspiration followed quickly by

chest wall muscle activity. However, as respiratory pathology

develops, regardless of etiology, there is often an increasing

amount of thoraco-abdominal asynchrony (TAA), resulting from

worsening respiratory (initially intercostal) muscle fatigue. Such

TAA can be measured using respiratory plethysmography.

Elastic bands are placed around the rib cage (RC) and

abdomen (ABD). The output of these movements is then

downloaded to a computer program that displays characteristic

oscillatory patterns which approximate sine waves. The level of

synchrony between these two bands, the phase angle (Y), is then

calculated:

sin Y ¼ m=s,

where m is the length of the midpoint of the RC excursion and s is

the length depicting the ABD excursion.15

During normal breathing, the phase angle is less than 251

(mean 81), and creates a very tight, counterclockwise loop

(Figure 3).16 However, as TAA worsens, the loop opens and

widens, with larger phase angles. Additional information is

learned from the direction of rotation of the loop. If the RC leads

instead of the ABD, then the loop will take on a clockwise

rotation, commonly seen with bilateral diaphragm paralysis. If

one hemi-diaphragm or hemi-thorax is ineffective, the loop will

take on a ‘figure of 8’ appearance.17 As such, continuous phase

angle monitoring allows clinician’s to see the effect of medical

interventions (e.g. increased CPAP), monitor disease progression

(e.g. acute upper airway obstruction) and help wean patients

from mechanical ventilation.

Rib cage

Abdomen

Rib cage

Abdomen

Phase shift

Rib cage

Abdomen

Figure 3 Respiratory plethysmography with the Respitrace. On the left-hand

right-hand side graphically represents the phase angles and direction of the lo

breathing moves from synchronous to asynchronous, the size of the phase an

with diaphragm paralysis (paradoxical), the RC and ABD are exactly 180 deg


Monitoring respiratory mechanics

Ventilator management of respiratory failure needs to cater to the

underlying disease pathology. Paramount to optimal manage-

ment is not only initially selecting the correct mode and

ventilator settings for the underlying disease, but also monitoring

physiologic changes that occur from the disease state, or in

response to therapeutic interventions.

Flow–volume loops

Flow–volume loops are particularly useful in diagnosing the type

of respiratory disease present (restrictive versus obstructive). In

the case of lower airway obstruction they have a characteristic

shape, which may change in response to bronchodilators.

Moreover, in large airways (i.e. above the carina) they can help

identify the type of obstruction (fixed or variable) if obtained

while spontaneously breathing or if the ETT lies above the level

of obstruction.

For mechanically ventilated patients, loops vary depending on

the mode of ventilation selected. In volume ventilation, tidal

volume delivered is set with a constant inspiratory flow, and peak

and plateau airway pressures vary. In pressure ventilation,

inspiratory pressure delivered is set and volume varies; the flow

pattern is decelerating. In general, this decelerating flow pattern

yields lower peak inspiratory pressures than volume-limited

ventilation (Figure 4a).

It is necessary to understand the scales and axes when

interpreting flow–volume loops on ventilators and those

of usual pulmonary function testing. Classically, flow–volume

loops produced by spontaneously breathing patients are

inspiration negative and exhalation positive, moving

either clockwise or counterclockwise. However, with the display

RC

ABD synchronous

m/s = 0

φ = 0°

RC

ABD asynchronous

m/s = 0.71

φ = 45°m

s

RC

ABD paradoxical

m/s = 0

φ = 180°

side, RC and ABD movements are plotted as a function of time, and the

op. Note in the usual situation where the diaphragm leads inspiration, as

gle loop widens, although preserving counterclockwise rotation. However,

rees out of phase, with clockwise movement.


Flo

w (

L/m

in)

Tid

al vo

lum

e (

ml)

Pressure (cm H2O)

Volume control Pressure control

Exhalation

Inspiration

Inspiration

40

30

20

10

0500

500

400

300

200

100

0

–10

–20

–30

–40

400 300 200 100

0 40302010

Tidal volume (ml)

Flow-volume loop of normal lung

Pressure-volume loop of normal lung

Exhalation

b

a

Figure 4 Normal flow–volume (a) and pressure–volume (b) curves during

volume control and pressure control ventilation. (a) Flow–volume. By

convention, inspiration is on the bottom of the y-axis. As inspiration

ensues, (clockwise), volume gradually increases in a relatively constant

(volume control) or decelerating (pressure control) manner until end

inhalation. At inspiratory flow cessation, volume is exhaled passively

with a typical flat or slightly convex shape to the descending portion of

the expiratory flow limb. (b). Pressure-volume. Pressure rises to deliver a

preset volume (volume-limited) or pressure (pressure-limited), repre-

sented with counterclockwise rotation of the curve. Once inspiration is

terminated, pressure gradually returns to baseline as volume is exhaled.


on most mechanical ventilators the flow pattern is in

a clockwise direction and inspiration is on the positive

aspect of the y-axis, and exhalation on the negative. For the

purposes of this review all flow-volume loops are expressed in

the conventional way, with inspiration negative and exhalation

positive.


Pressure–volume loops

Pressure–volume loops are useful to help to determine optimal

lung recruitment, compliance and overdistension (Figure 4b).

Here, pressure is on the x-axis, and volume on the y-axis, a

reversal of classic nomenclature.

Special considerations

Precision of measurements

Before discussing characteristic patterns of various loops for

different disease states, it is necessary to discuss the accuracy and

reproducibility of these measurements. First, the presence of a

significant leak around the ETT will underestimate returned tidal

volumes and increase calculated resistance and compliance

values.18 This is easily overcome with a cuffed ETT. While there

is some reluctance by some of the critical care and anaesthesia

community to use cuffed ETTs for paediatric patients, good data

show that current low-pressure, high-volume cuffed tubes are no

different from uncuffed tubes in the incidence of acute or long-

term post-extubation complications.19 As with uncuffed ETTs,

cuffed tubes should be placed with an initial leak at less than

25 cm H2O.

Second, in order to obtain accurate flow–volume and

pressure–volume loops, as well as measurements of tidal volume,

it is important for measurements to occur as close to the tip of the

ETT as possible. While modern ventilator technology has

improved significantly, there are often large discrepancies (up

to 200%) between measurements taken at the tip of the ETTwith

a pneumotachograph and those recorded at the ventilator,

regardless of the software package in use. This is particularly

relevant with smaller patients, where the relatively compliant

ventilator tubing dead space volume may be greater than a small

patient’s tidal breath.

Restrictive lung disease

Restrictive lung disease from pneumonia, ARDS, pleural effu-

sions and similar entities constitutes the majority of ICU

admissions for respiratory failure. The hallmarks of restrictive

lung disease include decreased compliance, with end-expiratory

lung volumes that fall below normal functional residual capacity

(FRC). Moreover, alveolar closing pressures lie above end-

expiratory lung volume resulting in alveolar collapse. Therefore,

effective management of restrictive lung disease requires normal-

isation of end-expiratory lung volumes to a level closer to FRC.

The pressure–volume curve helps to this end.

The inspiratory limb of the pressure–volume curve of a patient

with restrictive lung disease (classically ARDS) has three main

segments, separated by upper and lower inflection points

(Figure 5). The goal is to maintain ventilation within the two

inflection points on the pressure–volume curve. This minimises

ventilator-induced injury from alveolar recruitment and de-

recruitment (below the lower inflection point), and overdisten-

sion (above the upper inflection point). End-expiratory lung

volumes are maintained above the lower inflection point with

positive end-expiratory pressure (PEEP). While recommenda-

tions differ, one strategy is to select a PEEP 2 cm H2O above the

lower inflection point, and attempt to stay in the zone of best

compliance by selecting a relatively conservative tidal volume

(6 ml/kg).20 If a low compliance zone is seen again on the


Tid

al vo

lum

e (

ml)

Zone of overdistension

Maximal compliance

Zone of under recruitment

Upper reflection point

Lower reflection point

500

400

300

200

100

0

0 10 20 30 60

ΔV

C = ΔV/ΔP

ΔP

5040

Pressure (cm H2O)

Figure 5 Pressure–volume loop in ARDS. Note the two inflection points

on the inspiratory limb of the pressure–volume loop. The first segment

shows relatively low compliance (manifest by the slope of the line on the

pressure–volume loop) with a flat appearance. This represents areas of

under recruitment. As recruitment improves and end-expiratory lung

volumes exceed the critical opening pressure of most alveoli,

compliance improves (lower inflection point). Compliance stays relatively

stable within this segment of ventilation, but may decrease again

towards the upper limit of a pressure control breath (upper inflection

point). This flattening of the curve represents relative overdistension. The

goal for mechanical ventilation is to keep tidal breaths between these

two inflection points, in the zone of maximal compliance.

Tid

al vo

lum

e (

ml)

Pressure (cm H2O)

500

400

300

200

100

0

0 10 20 30 40

Tid

al vo

lum

e (

ml)

500

400

300

200

100

0

0 10 20 30 40

Normal lung Low compliance lung

Pressure (cm H2O)

Normal lung Overdistended lung

b

a

Figure 6 Pressure–volume loops in states of low compliance. (a)

Pressure–volume loop of lungs with poor compliance. Note the lower

slope of the pressure–volume curve, and higher pressure needed to

generate less volume. (b) Pressure–volume curve of overdistended lungs

from excessive PEEP. Note the shift in end-expiratory lung volumes to the

right, and lower slope of the curve.


pressure–volume curve (beaking), then the pressure or volume

should be decreased to prevent overdistension. Less commonly,

overdistension from excessive PEEP may occur. This will not

manifest with the classic inflection points, but rather simply as a

pressure–volume curve that is shifted to the right with a smaller

slope (Figure 6). Other measures of overdistension derived from

mathematical examination of the pressure–volume curve21,22

have not been validated in the paediatric population.

In contrast to the pressure–volume curve, the flow–volume

loop for a patient with significant restrictive lung disease will

often have the same characteristic shape as a patient without

lung disease, but with smaller amplitude for a given flow.

Subsequent to changes in compliance through optimising PEEP

and improvements in the underlying disease, in concert with

conservative lung protective pressure-limited ventilation, the

amplitude of the flow�volume loops should return towards

normal (Figure 7).

Clinical entities causing obstructed airways

Medium and small airway disease: in contrast to restrictive lung

disease where disease pathology typically affects the alveoli,

obstructive disease affects airways. Significant airway obstruc-

tion affecting medium (asthma) or small (bronchiolitis) airways

allows the development of air trapping. Here end-expiratory lung


volumes reside above functional residual capacity, and airway

resistance is increased. The flow–volume loops are characteristic

of flow limitation on the expiratory limb. The flow–volume loop

therefore demonstrates lower peak expiratory flows, smaller tidal

volumes, as well as a hallmark ‘scooped-out’ or concave app-

earance to the descending limb of expiratory flow. Moreover, if

the obstruction is variable or reversible, the effect of a therapeutic

intervention (i.e. bronchodilator for an asthmatic) can be

followed. Here the flow–volume loop demonstrates improved


Flo

w (

L/m

in)

40

30

20

10

0500

–10

–20

–30

–40

400 300 200 100

Tidal volume (ml)

Figure 7 Flow–volume loop for restrictive lung disease. The shape of the

loop for a patient with significant restrictive disease like ARDS (solid line)

looks identical to the normal loop (dotted line), but with smaller volumes

and generally lower flows at each volume. However, there is no limitation

to flow.

Flo

w (

L/m

in)

40

30

50

20

10

0500

–10

–20

–30

–40

400 300 200 100

Flo

w (

L/m

in)

40

30

20

10

0500

–10

–20

–30

–40

400 300 200 100

Flo

w (

L/m

in)

40

30

20

10

0500

–10

400 300 200 100

Tidal volume (ml)

Tidal volume (ml)

Tidal volume (ml)

a

b

c

After response to

bronchodilator Normal

Diseased


peak expiratory flow and a return of a flat or slightly convex

shape to the decelerating limb of expiratory flow (Figure 8a).

Large airway disease: a spontaneously breathing, non-intubated

patient with extrathoracic obstruction (e.g. croup, laryngomala-

cia, tracheomalacia, vocal cord dysfunction, etc.) classically has

limitation of flow during inspiration. This flow limitation

manifests with a flattening of the inspiratory limb of the

flow–volume loop (Figure 8b). This can usually be overcome

by bypassing the obstruction with an ETT.

If the obstruction is not bypassed by the ETT and is in the

trachea distal to the tube (i.e. intrathoracic), the flow–volume

loop will show either flattening on exhalation (variable lesion

such as tracheomalacia) or flattening on both inspiration and

exhalation (fixed lesion) (Figure 8c). This latter situation is

commonly seen with foreign body aspiration, tracheal stenosis or

accidental kinking of an ETT.

Clinical application in medium and small airway disease:

when mechanically ventilating patients with significant obstruc-

tive airway disease, care must be taken to prevent dynamic

hyperinflation and the creation of auto-PEEP. Whenever possible,

–20

–30

–40

Figure 8 Various levels of obstruction and flow limitation. Normal loops

are dotted, diseased loops solid. (a) Variable intrathoracic obstruction,

from asthma. Note the diminished peak expiratory flow, smaller tidal

volumes, as well as the scooped out appearance of the decelerating limb

of expiratory flow. Note the increase in peak flow, and normalization of

the ‘scooped out’ shape after bronchodilator therapy. (b) Extrathoracic

obstruction, with predominance of flow limitation in inspiration. (c) Fixed

airway obstruction in a large airway, with limitation to flow throughout

inspiration and exhalation.

PAEDIATRICS AND CHILD HEALTH 17:5 199 r 2007 Elsevier Ltd. All rights reserved.

Time

V

Auto-PEEP

olume trapped

InspirationExhalation

Vo

lum

eP

ressu

reF

low

Figure 9 Obstructed medium and small airways with mechanical ventilation and progressive dynamic hyperinflation from insufficient expiratory time.

Note the failure of flow to return to zero (arrow) during exhalation on the flow versus time graph (top). The pressure-time graph (middle) displays

progressive air trapping and generation of auto-PEEP. The volume-time graph (bottom) displays a progressive rise in lung volumes as air is trapped with

each breath.


spontaneous breathing with CPAP and PS is preferable. This

allows patients the ability to set their own inspiratory:expiratory

ratio and CPAP is carefully applied to match the intrinsic level of

auto-PEEP that the patient has generated.23 This strategy can

minimise WOB, and PEEP can gradually be removed as the

airway obstruction improves.24 However, if such a strategy

cannot be employed and the patient is either paralysed or heavily

sedated, then care must be taken to allow sufficient expiratory

time to prevent further air trapping. This can be monitored by

examining the flow versus time curves, paying particular

attention to expiratory flow returning to zero before the initiation

of a subsequent breath. Evidence of dynamic hyperinflation may

be observed on the pressure or volume versus time curves, where

increased air trapping will manifest as gradual increases in end-

expiratory lung volumes and pressures (Figure 9).25 If total

ventilatory support is employed (no spontaneous breathing),

then extrinsic PEEP will worsen air trapping. However, if the

patient is completely spontaneously breathing, then the

application of extrinsic PEEP to match the patient’s

level of intrinsic or auto-PEEP (some advocate 80% of auto-

PEEP) will help minimise respiratory muscle fatigue. Of course,

the level of support should ultimately be determined by patient

comfort and WOB.

Conclusion

Firm understanding of respiratory monitoring tools is invaluable

for all physicians taking care of critically ill children. It allows for

titrating therapeutic interventions to the patient’s disease state,

and if used correctly can facilitate optimal respiratory support

and aid in eventual weaning to endotracheal extubation. More-

over, with close monitoring, aberrations or changes in physiolo-


gic states can be detected before disease progression, allowing for

early interventions and prevention of worsening disease. ~

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12 Epstein MF, Cohen AR, Feldman HA, Raemer DB. Estimation of PaCO2

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Practice points

� Capnography generally provides accurate estimates of arterial

CO2, in addition to helping detect obstructive airway disease,

the adequacy of pulmonary blood flow and increases in dead

space

� ETCO2 will always be lower than PaCO2, so elevations in ETCO2

should be taken seriously

� Oesophageal manometry and respiratory plethysmography are

useful surrogate objective measures of work of breathing

� Flow–volume loops are particularly useful for distinguishing

obstructive airway disease and restrictive lung disease on

mechanical ventilation

� With restrictive lung disease, pressure–volume loops help the

clinician optimise ventilator support, particularly with regard

to positive end-expiratory pressure, pressure support and

peak inspiratory pressure

� Pulse oximeter numbers lag the clinical situation by 15–20 s.

Values are not accurate unless the pulse rate determined by

the oximeter is the same as that determined from the bedside

monitor ECG recording

� Measurements of pulmonary function should occur as close to

the tip of the ETT as possible


respiratory monitoring during mechanical ventilation

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