Chapter 38

• Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are common causes of acute hypoxemic respiratory failure (AHRF).
• Both ALI and ARDS are characterized by hypoxemia that is resistant to oxygen therapy; this is due to widespread alveolar filling or collapse.
• Initial therapy for all patients with ALI and ARDS should be supplemental oxygen in the highest concentration available; failure to achieve 95% arterial saturation or greater confirms the presence of a large right-to-left shunt.
• Most patients with ALI and ARDS require early intubation because their hypoxemic respiratory failure is typically severe and may be prolonged.
• If a patient with severe hypoxemia as indicated by arterial blood gas analysis has a clear chest radiograph, consider a possible error (e.g., incorrect fractional inspired oxygen [Fio2] or arterial oxygen tension [Pao2]); in such situations, also consider the possibility of other types of right-to-left shunts (e.g., intracardiac shunts or pulmonary arteriovenous malformations) or the continued perfusion of an unventilated or poorly ventilated lung (e.g., due to acute mucous plugging of one main bronchus).
• The acute phase of ALI and ARDS is characterized by an exudative alveolar flooding due to pulmonary capillary leak and by extensive alveolar collapse due to loss of normal surfactant activity; while interventions directed at modulating inflammatory or other pathways of lung injury or restoring surfactant function hold theoretical promise, at present no specific pharmacologic therapy has been shown to improve outcomes; in this phase one provides mechanical ventilation and other supportive care while identifying and treating the precipitating cause or causes of ALI or ARDS.
• Ventilator management of patients with ALI and ARDS should use a strategy with low tidal volumes and limits to end-inspiratory pressure (i.e., plateau pressures [Pplat]), to reduce the risk of ventilator-induced lung injury (VILI); such a strategy gives higher priority to the goal of decreasing the risk of VILI by limiting end-inspiratory volume and pressure than the traditional goal of keeping arterial carbon dioxide tension (Pco2) and pH in the normal range.
• The target for oxygenation should be a Pao2 between 55 and 80 mm Hg (88% to 95% saturation); one should achieve this by adjusting Fio2 and positive end-expiratory pressure (PEEP) with the goal of decreasing Fio2 to 0.5 to 0.6 (or less), concentrations that are less concerning for pulmonary oxygen toxicity.
• In general, the ventilatory strategy should use a tidal volume of 6 mL/kg of predicted body weight (PBW) with a Pplat target that does not exceed 30 cm H2O; if Pplat exceeds 30 cm H2O with a 6 mL/kg PBW tidal volume, the latter should be decreased to 5 mL/kg PBW; if Pplat still exceeds 30 cm H2O, tidal volume should be further decreased to 4 mL/kg PBW.
• When changing to low tidal volume ventilation, one should increase the respiratory rate (RR) up to 35/min to maintain minute ventilation; the target ...

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