Respiratory monitoring during mechanical ventilation

SYMPOSIUM: RESPIRATORY MEDICINE

Respiratory monitoring during mechanical ventilation

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.

Robinder G Khemani

Gas exchange

Robert D Bart III

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.

Christopher JL Newth

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, oedema, 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 circumstances, 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 improving 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.

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 oesophageal 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; plethysmography; respiratory-function tests; ventilation

paediatrics;

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 ventilation. Paramount to ensuring adequate support is close supervision of therapeutic interventions – through both invasive and non-invasive forms of respiratory monitoring. This discussion concentrates on common means of respiratory monitoring used

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:

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.

Minute ventilation ðV E Þ ¼ ½respiratory rate ðf Þ½tidal volume ðV T Þ; 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.

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

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.

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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.

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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 inexpensive, 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 medications, 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

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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 phasecharacterized 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.

(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):

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.

¯ 2 =PaCO2 , V D =V T ¼ ½PaCO2  ECO where E¯CO2 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 pneumotachograph 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 exhalation time or dead-space ventilation.10 Acute respiratory distress syndrome (ARDS) and other diseases affecting the lung parenchyma may cause markedly widened A–a carbon dioxide gradients (20–30 mm Hg) at the peak of the lung disease, and

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 respiratory rate and rhythm, dead space calculations, cardiac output, confirmation of endotracheal tube (ETT) placement, mechanical failure of the ventilator from kinking, displacement or obstruction 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

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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

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 capnography cannot be employed (e.g. high-frequency ventilation, nonintubated 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

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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.

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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 respiratory 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.

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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.

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Monitoring respiratory mechanics

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:

Ventilator management of respiratory failure needs to cater to the underlying disease pathology. Paramount to optimal management 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

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.

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Abdomen ABD paradoxical Figure 3 Respiratory plethysmography with the Respitrace. On the left-hand side, RC and ABD movements are plotted as a function of time, and the right-hand side graphically represents the phase angles and direction of the loop. Note in the usual situation where the diaphragm leads inspiration, as breathing moves from synchronous to asynchronous, the size of the phase angle loop widens, although preserving counterclockwise rotation. However, with diaphragm paralysis (paradoxical), the RC and ABD are exactly 180 degrees out of phase, with clockwise movement.

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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.

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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 longterm 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 ETT with 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.

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Restrictive lung disease Restrictive lung disease from pneumonia, ARDS, pleural effusions 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 endexpiratory lung volume resulting in alveolar collapse. Therefore, effective management of restrictive lung disease requires normalisation 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 derecruitment (below the lower inflection point), and overdistension (above the upper inflection point). End-expiratory lung volumes are maintained above the lower inflection point with positive end-expiratory pressure (PEEP). While recommendations 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

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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), represented 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.

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500 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.

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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 flowvolume loops should return towards normal (Figure 7).

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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.

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 appearance 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

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 obstruction affecting medium (asthma) or small (bronchiolitis) airways allows the development of air trapping. Here end-expiratory lung

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peak expiratory flow and a return of a flat or slightly convex shape to the decelerating limb of expiratory flow (Figure 8a).

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Large airway disease: a spontaneously breathing, non-intubated patient with extrathoracic obstruction (e.g. croup, laryngomalacia, 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.

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Clinical application in medium and small airway disease: when mechanically ventilating patients with significant obstructive airway disease, care must be taken to prevent dynamic hyperinflation and the creation of auto-PEEP. Whenever possible,

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–20 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.

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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.

gic states can be detected before disease progression, allowing for early interventions and prevention of worsening disease. ~

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 endexpiratory 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 autoPEEP) will help minimise respiratory muscle fatigue. Of course, the level of support should ultimately be determined by patient comfort and WOB.

REFERENCES 1 Dantzker DR, Brook CJ, Dehart P, et al. Ventilationperfusion distribution in the adult respiratory distress syndrome. Am Rev Respir Dis 1979; 120: 1039–52. 2 Hubble CL, Gentile MA, Tripp DS, et al. Deadspace to tidal volume ratio predicts successful extubation in infants and children. Crit Care Med 2000; 28: 2034–40. 3 Courtney SE, Weber KR, Breakie LA, et al. Capillary blood gases in the neonate. A reassessment and review of the literature. Am J Dis Child 1990; 144: 1287–88. 4 Schnapp LM, Cohen NH. Pulse oximetry: uses and abuses. Chest 1990; 98: 1244. 5 Barker SJ, Tremper KK, Hyatt J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1989; 70: 113. 6 Meliones J, Wilson BG, Cheifetz IM, et al. Respiratory monitoring. In: Rogers, et al. (eds): Textbook of pediatric intensive care. Baltimore: Williams and Wilkins, 1996. p. 338. 7 Sivan Y, Eldadah MK, Cheah TE, Newth CJ. Estimation of arterial carbon dioxide by end-tidal and transcutaneous PCO2 measurements in ventilated children. Pediatr Pulmonol 1992; 12: 153–7. 8 Martin L. Mechanical ventilation, respiratory monitoring, and the basics of pulmonary physiology. In: Tobias JD. (eds): Paediatric critical care: The essentials., Armonk, NY: Fugura Publishing Co, Inc, 1999. p. 57–105. 9 Krauss B, Deykin A, Lam A, et al. Capnogram shape in obstructive lung disease. Anesth Analg 2005; 100: 884–8. 10 Thompson JE, Jaffe MB. Capnographic waveforms in the mechanically ventilated patient. Respir Care 2005; 50: 100–9.

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. Moreover, with close monitoring, aberrations or changes in physiolo-

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11 Yaron M, Padyk P, Hutsinpiller M, Cairns CB. Utility of the expiratory capnogram in the assessment of bronchospasm. Ann Emerg Med 1996; 28: 403–7. 12 Epstein MF, Cohen AR, Feldman HA, Raemer DB. Estimation of PaCO2 by two non-invasive methods in the critically ill newborn infant. J Pediatr 1985; 106: 282. 13 Benditt J. Esophageal and gastric pressure measurements. Respir Care 2005; 50: 68–77. 14 Milic-Emili J. Measurements of pressures in respiratory physiology: techniques in the life sciences. Shannon: Elsevier Scientific, 1984. p. 1–22. 15 Agostoni E. Deformation of chest wall during breathing effort. J Appl Physiol 1966; 21: 1827–32. 16 Hammer J, Deakers TW, Newth CJ. Lissajous figure analysis in infants with thoracoabdominal asynchrony due to neuromuscular diseases. Am J Respir Crit Care Med 1994; 149: A36. 17 Willis BC, Graham AS, Wetzel RL, Newth CJ. Respiratory inductance plethysmography used to diagnose bilateral diaphragmatic paralysis. A case report. Pediatr Crit Care Med 2004; 5: 399–402. 18 Main E, Castle R, Stocks J, James I, Hatch D. The influence of endotracheal tube leak on the assessment of respiratory function in ventilated children. Intensive Care Med 2001; 27: 1788–97. 19 Newth CJ, Rachman B, Patel N, Hammer J. The use of cuffed versus uncuffed endotracheal tubes in pediatric intensive care J Pediatr 2004; 144: 333–7. 20 ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2004; 42: 1301–8. 21 Neve V, de la Roque ED, Leclerc F, et al. Ventilator-induced overdistension in children: dynamic versus low-flow inflation volumepressure curves. J Respir Crit Care Med 2000; 162: 139–47. 22 Fisher JB, Mammel MC, Coleman JM, et al. Identifying lung overdistention during mechanical ventilation by using volumepressure loops. Pediatr Pulmonol 1988; 5: 10–4.

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23 Smith TC. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction. J Appl Physiol 1988; 65: 1488–99. 24 Graham AS, Chandrashekharaiah G, Citak A, Wetzel RC, Newth CJL. Positive end-expiratory pressure and pressure support in peripheral airways obstruction. Intensive Care Med 2007; 33: 120–7. 25 Blanch L, Bernabe F, Lucangelo U. Measurement of air trapping, intrinsic positive end-expiratory pressure and dynamic hyperinflation in mechanically ventilated patients. Respir Care 2005; 50: 110–24.

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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

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