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Ventilatory Management of ALI/ARDS J J Cordingley, B F Keogh

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Ventilatory Management of ALI/ARDS J J Cordingley, B F Keogh 729 REVIEW SERIES Thorax: first published as 10.1136/thorax.57.8.729 on 1 August 2002. Downloaded from The pulmonary physician in critical care c 8: Ventilatory management of ALI/ARDS J J Cordingley, B F Keogh ............................................................................................................................. Thorax 2002;57:729–734 Current data relating to ventilation in ARDS are system (lung + chest wall) in a ventilated patient reviewed. Recent studies suggest that reduced mortality is calculated by dividing the tidal volume (Vt) by end inspiratory plateau pressure (Pplat) minus may be achieved by using a strategy which aims at end expiratory pressure + intrinsic PEEP preventing overdistension of lungs. (PEEPi). As the pathology of ARDS is heterogene- .......................................................................... ous, calculating static compliance does not provide information about regional variations in lung recruitment and varies according to lung he ventilatory management of patients with volume. Much attention has therefore focused on acute lung injury (ALI) and acute respiratory analysis of the pressure-volume (PV) curve. Tdistress syndrome (ARDS) has evolved in The static PV curve of the respiratory system conjunction with advances in understanding of can be obtained by inserting pauses during an the underlying pathophysiology. In particular, inflation-deflation cycle. A number of different evidence that mechanical ventilation has an methods have been described including the use of influence on lung injury and patient outcome has 1 a large syringe (super-syringe), or holding a emerged over the past three decades. The present understanding of optimal ventilatory manage- mechanical ventilator at end inspiration of ment is outlined and other methods of respiratory varying tidal volumes. The principles and meth- support are reviewed. ods of PV curve measurement have recently been reviewed.10 PATHOPHYSIOLOGY The PV curves thus obtained are sigmoidal and The pathophysiology of ARDS has been reviewed have an inspiratory limb that usually includes a by Bellingan in an earlier article in this series.2 point above which the curve becomes steeper (fig 4 However, it is useful to highlight important 1). Identification of the lower inflection point by features relevant to ventilatory management, in clinicians using PV curves is subject to large vari- 11 particular the anatomical distribution of pulmo- ability, but is improved by curve fitting. In some http://thorax.bmj.com/ nary pathology and the potential for ventilator patients the lower inflection point may be absent. induced lung injury. At higher lung volumes the curve becomes flatter The original description of ARDS included the again (upper inflection point), above which presence of bilateral infiltrates on the chest further increases in pressure cause little increase radiograph.3 Since the 1980s considerable re- in volume. Currently, ventilators used routinely in search has been undertaken using computerised intensive care units do not have automated func- tomographic (CT) scanning which has shown tions to obtain a static PV curve. Moreover, the that parenchymal consolidation, far from being static PV curve only provides information about 4 evenly distributed, is concentrated in dependent accessible lung and also includes chest wall com- on October 1, 2021 by guest. Protected copyright. lung regions leaving non-dependent lung rela- pliance. Separating the lung and chest wall com- tively spared. This pathological distribution of ponents requires the use of oesophageal pressure aerated lung lying over areas of dense consolida- measurement.12 tion has led to comparisons with ventilation of a Despite these limitations, many advances in 4 much smaller or “baby lung” and has important clinical management in patients with ALI/ARDS implications for ventilatory management. Thus, have been based on consideration of static PV the application of normal physiological tidal curves. More recently it has been proposed that volumes can lead to overdistension of the small analysis of the inspiratory pressure-time curve volume of normally aerated lung, while failing to under conditions of constant flow can provide recruit consolidated dependent regions. 13 useful information about lung recruitment. Ventilator induced lung injury5 can occur by several mechanisms: oxygen toxicity from the use 6 VENTILATORY STRATEGIES IN ARDS of high FiO2, overdistension of the lung causing 7 The goals of ventilating patients with ALI/ARDS See end of article for barotrauma and further inflammation, injurious authors’ affiliations cyclical opening and closing of alveoli from venti- should be to maintain adequate gas exchange and ....................... lation at low lung volumes,8 and by increasing avoid ventilator induced lung injury. systemic levels of inflammatory cytokines.9 Correspondence to: Maintenance of adequate gas exchange Dr B F Keogh, Department Ventilatory strategies must therefore be tai- of Anaesthesia and lored to minimise the risk of inducing or exacer- Oxygen Intensive Care, Royal bating further lung injury. High concentrations of inspired oxygen should be Brompton Hospital, Sydney avoided to limit the risk of direct cellular toxicity Street, London SW3 6NP, RESPIRATORY MECHANICS and to avoid reabsorption atelectasis. Arterial UK; b.keogh@ rbh.nthames.nhs.uk Decreased lung compliance is a prominent feature oxygen saturation (SaO2) is used as a target in ....................... of ARDS. The static compliance of the respiratory preference to arterial oxygen tension (PaO2)in www.thoraxjnl.com 730 Cordingley, Keogh required to the ventilator circuit and settings to prevent inad- vertent and potentially dangerous increases in intrinsic PEEP, Thorax: first published as 10.1136/thorax.57.8.729 on 1 August 2002. Downloaded from Vt, and peak airway pressure. In adult patients with ARDS, managed using pressure con- Upper inflection point trol ventilation, the introduction of continuous tracheal gas Expiration insufflation allowed a decrease in inspiratory pressure of Volume Inspiration 5cmH2O without increasing arterial carbon dioxide tension 21 (PaCO2). Tracheal gas insufflation may therefore be useful Lower inflection point when permissive hypercapnia is contraindicated. However, managing the appropriate ventilator settings and adjustment Pressure is complicated, with real potential for iatrogenic injury. In practice, PaCO2 is allowed to rise during lung protective Figure 1 Schematic representation of a static pressure-volume volume and pressure limited ventilation. PaCO2 levels of 2–3 curve of the respiratory system from a patient with ARDS. Note the times normal seem to be well tolerated for prolonged periods. lower and upper inflection points of the inspiratory limb. Renal compensation for respiratory acidosis occurs over several days. Many clinicians infuse sodium bicarbonate recognition of the fact that oxygen delivery is the important slowly if arterial pH falls below 7.20. determinant of tissue oxygenation. SaO2 values of around 90% are commonly accepted but oxygen delivery decreases quickly Avoidance of ventilator induced lung injury below 88% because of the shape of the oxyhaemoglobin disso- Traditional mechanical ventilation (as applied during routine general anaesthesia) involves tidal volumes that are relatively ciation curve. However, if a higher SaO2 can only be obtained by increasing airway pressure to levels that result in haemody- large (10–15 ml/kg) in order to reduce atelectasis. PEEP levels are adjusted to maintain oxygenation but high levels are gen- namic compromise, lower SaO2 may have to be accepted. There is no clinical evidence to support the use of specific erally avoided to prevent cardiovascular instability related to increased intrathoracic pressure. Present understanding of FiO2 thresholds, but it is common clinical practice to decrease ventilator induced lung injury suggests that traditional FiO2 below 0.6 as quickly as possible. Oxygenation can be improved by increased alveolar recruit- mechanical ventilation, using high tidal volumes and low ment through the application of higher airway pressure PEEP,is likely to enhance lung injury in patients with ARDS. provided that ventilation-perfusion (V/Q) matching is not Five randomised studies of “lung protective” ventilation in adversely affected by the haemodynamic consequences of ARDS have recently been published, four of which investi- increased intrathoracic pressure. Lung recruitment is usually gated limitation of tidal volume to prevent injury from over- obtained by applying extrinsic PEEP, increasing the inspirat- distension (table 1). ory:expiratory (I:E) ratio, or by specific recruitment manoeu- In these studies the protective ventilatory strategy was vres (discussed below). directed at preventing lung overdistension and was not designed to look at differences in ventilation at low lung vol- Carbon dioxide umes. Only the largest study (ARDSNet)1 showed an Limiting tidal volume and peak pressure to reduce ventilator advantage of such a protective strategy. The ARDSNet study induced lung injury may cause hypercapnia. Strategies used to had the largest difference in Vt and Pplat between the groups, http://thorax.bmj.com/ manage hypercapnia have included increasing tidal volume the highest power, and was the only study to correct respira- and airway pressure, or increasing CO2 removal with tory acidosis (table 2). techniques such as tracheal gas insufflation or extracorporeal Others studies have
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