The Pulmonary Physician in Critical Care C 7: Ventilator Induced Lung Injury T Whitehead, a S Slutsky

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The Pulmonary Physician in Critical Care C 7: Ventilator Induced Lung Injury T Whitehead, a S Slutsky 635 REVIEW SERIES Thorax: first published as 10.1136/thorax.57.7.635 on 1 July 2002. Downloaded from The pulmonary physician in critical care c 7: Ventilator induced lung injury T Whitehead, A S Slutsky ............................................................................................................................. Thorax 2002;57:635–642 The main risk factors for ventilator induced lung injury tube, although the principles are equally relevant are reviewed, together with the possible mechanisms to non-invasive or negative pressure ventilation. It has become clear that the degree of VILI is deter- and its clinical relevance. mined by the interaction of the ventilator settings .......................................................................... and patient related factors, particularly the condition of the ventilated lung. echanical ventilation has become an indispensable tool, facilitating general Ventilator determinants of VILI Manaesthesia and supporting life in the Airway pressure and lung distension critically ill. However, its application has adverse Conceptually, it seems obvious that inflation of effects including an increased risk of pneumonia, the lung will cause damage if airway pressures are impaired cardiac performance, and neuromusc- high enough. The important issues for the ular problems relating to sedation and muscle clinician have been (1) what levels of airway relaxants. Moreover, it has become clear that pressure are dangerous and (2) can they be applying pressure—whether positive or avoided in the mechanical ventilation of patients negative—to the lung can cause damage known with stiff lungs, as in ARDS? as ventilator induced lung injury (VILI). This The association between high airway pressure concept is not new. In his treatise on resuscitation and air leaks has long been recognised.45 How- of the apparently dead, John Fothergill in 1745 ever, this relationship does not necessarily imply suggested that mouth to mouth inflation of the causality as damaged, stiff lungs that require high victim’s lungs might be preferable to using a pair airway pressures for ventilation may be intrinsi- of bellows as “the lungs of one man may bear, without injury, as great a force as another man cally more prone to air leaks. Recent large studies can exert; which by the bellows cannot always be in patients with ARDS have, in fact, shown a poor http://thorax.bmj.com/ determin’d”.1 Although not specifically ad- correlation between airway pressure (or tidal vol- dressed, Forthergill’s admonition against the use ume) and the occurrence of air leaks, which 2 6–8 of the bellows probably related to gross air leaks occurred in 8–14% of the patients. However, produced by large pressures. This type of injury is these data should not be interpreted as demon- now called barotrauma and was the first widely strating that the degree of lung distension is recognised manifestation of VILI. The clinical and unimportant in the development of barotrauma. radiological manifestations of barotrauma in- In these studies airway pressures and tidal clude pneumothorax, pneumomediastinum, and volumes were lower than those used in the past surgical emphysema. when barotrauma rates as high as 39% were on September 28, 2021 by guest. Protected copyright. Later, evidence accumulated to suggest that reported in patients ventilated for acute respira- ventilation causes more subtle morphological and tory failure.9 functional changes and can excite an inflamma- More subtle lung damage was first unequivo- tory response within the lung. This type of injury cally shown by Webb and Tierney who ventilated was not recognised for many years as the pattern rats for 1 hour using different airway pressures of damage is often indistinguishable from that with and without positive end expiratory pressure seen in other forms of lung injury such as the (PEEP).10 Animals ventilated with a peak airway acute respiratory distress syndrome (ARDS), for pressure of 14 cm H O had no histological which mechanical ventilation is an indispensable 2 changes in the lung, while those ventilated with a treatment. Studies using animal models were pressure of 30 cm H O had mild perivascular necessary to define key aspects of VILI. Based on 2 oedema. In contrast, all rats ventilated at these, many clinicians in the 1990s began to 45 cm H O (without PEEP) developed severe adopt ventilatory strategies designed to minimise 2 lung injury, although the clinical importance of hypoxia and died before the end of the hour. Their VILI has only recently been established.2 lungs had marked perivascular and alveolar In this review we summarise the main risk fac- oedema. Similar findings have been observed in tors for VILI, its possible mechanisms and its other species, although there is considerable vari- See end of article for clinical relevance. Specific ventilation techniques ation in the susceptibility to VILI. Whereas in rats authors’ affiliations ventilation at high peak inspiratory pressure for ....................... for ARDS are addressed in a separate article in this series3 and will only be alluded to here for the just 2 minutes is sufficient to induce pulmonary Correspondence to: purpose of illustrating general principles. oedema, larger animals such as rabbits and sheep Dr A S Slutsky, St Michael’s require much longer periods of ventilation for Hospital, Toronto, Ontario, MAJOR DETERMINANTS OF VILI changes to be evident.11–13 This is clearly important Canada M5B 1W8; arthur.slutsky@utoronto.ca Most research into VILI is based on positive pres- when extrapolating data from animal studies to ....................... sure ventilation delivered via an endotracheal humans. www.thoraxjnl.com 636 Whitehead, Slutsky Pressure or volume? Although the term barotrauma is commonly used when Thorax: first published as 10.1136/thorax.57.7.635 on 1 July 2002. Downloaded from discussing VILI, the evidence indicates that the degree of lung inflation is a more important determinant of lung injury than Deflation airway pressure per se. This may be inferred from the observa- tion that trumpet players commonly achieve airway pressures UIP of 150 cm H2O without developing repetitive episodes of gross 14 Inflation air leakage. The relative contribution of pressure and volume Volume to lung injury was first studied by ventilating rats whose tidal excursion was limited by strapping the chest and abdomen.15 High airway pressure without a high tidal volume did not pro- duce lung injury. By contrast, animals ventilated without tho- FRC LIP racic restriction using high tidal volumes, achieved either with 0 0 high positive inspiratory pressure or negative pressure in an Pressure iron lung, developed severe injury. These results have been confirmed in other species.16 17 Figure 1 Pressure-volume curve derived from a patient with ARDS. FRC=functional residual capacity; LIP=lower inflection point; The term volutrauma is therefore more accurate than UIP=upper inflection point. Adapted from Matamis et al23 with per- barotrauma, although in practice the two are closely related. mission. The degree of alveolar distension is determined by the pressure gradient across the alveoli, approximated by the transpulmonary pressure, the difference between the static portion of the pressure-volume curve where the lung is most airway pressure (estimated clinically by the plateau airway compliant. The value of PEEP would be sufficient to prevent pressure) and the pleural pressure. Peak airway pressure is not derecruitment but not so great as to lead to overdistension. necessarily a reflection of alveolar pressure and is greatly High frequency oscillatory ventilation (HFOV) potentially influenced by the resistance to flow in the airways. Recent offers the ideal combination of minimum tidal volume while guidelines have therefore emphasised the importance of lim- maintaining maximal recruitment (the “open lung”), pro- iting plateau pressures and of being aware of factors that vided sufficient end expiratory lung volume is maintained.25 26 increase (or decrease) the degree of alveolar distension for a Although theoretically sound, the explanation of VILI given alveolar pressure.18 For example, conditions associated according to the pressure-volume curve is certainly a gross with increased chest wall compliance such as immaturity oversimplification. Recruitment is not complete at the LIP and increase lung distension, and hence damage, for a given continues at higher inflating pressures.27 28 Similarly, the UIP alveolar pressure. Conversely, chest wall compliance is does not necessarily reflect the onset of overdistension. commonly reduced by abdominal distension,19 which can Instead, it may represent the point at which recruitment is result in lower alveolar inflation, derecruitment, and hypoxae- complete and therefore compliance decreases. Furthermore, mia if the plateau pressure is inappropriately low. inflation may be expanding alveoli without necessarily over- distending them.28 In addition, it is difficult to show that Lung injury at low lung volumes recruitment-derecruitment actually occurs,29 and dynamic http://thorax.bmj.com/ There is evidence that lung damage may also be caused by ventilation may not follow the pattern of the static pressure- ventilation at low lung volume (meaning low absolute lung volume curve. Indeed, a recent study using saline lavaged rab- volume rather than low tidal volume). This has been well bits suggested that ventilation follows the deflation limb of defined in animal models, but the relevance to humans is not
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