Question:

A 26-year-old man is being evaluated in the intensive care unit 24 hours after he was admitted with acute respiratory distress syndrome due to opioid overdose and aspiration of gastric contents. The patient is intubated, sedated, and receiving mechanical ventilation. The patient had anesthesia-induced hypotension after intubation, but has been hemodynamically stable after receiving 4 L of normal saline. Temperature is 38.1 C (100.6 F), blood pressure is 118/78 mm Hg, pulse is 96/min, respirations are 20/min, and oxygen saturation is 92%. The patient is receiving low tidal volume ventilation at 8 mL/kg ideal body weight, FiO₂ is 50%, and positive end-expiratory pressure is 12 cm H₂O. The patient-ventilator interaction is synchronous. Arterial blood gas analysis demonstrates pH 7.31, PaCO₂ 50, and PaO₂ 64. Chest x-ray shows patchy bilateral opacities consistent with pulmonary edema. Echocardiography shows normal left ventricular function. Which of the following interventions would be most helpful to promote recovery of the patient's respiratory failure?

Avoiding a positive fluid balance to reduce pulmonary edema

Increasing tidal volume to avoid "permissive" hypercapnia

Raising FiO₂ to keep oxygen saturation ≥96%

Maximizing airway pressure to hyperinflate the lung

Providing continuous sedation to maintain deep coma

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Explanation:

Acute respiratory distress syndrome: management & prognosis
Mechanical ventilation	Lung protection: limit alveolar distending volume (V_T 6 mL/kg) & pressure (Pplat ≤30 cm H₂O) Ventilation: tolerate permissive hypercapnia (ie, ↑ PaCO₂ & ↓ pH acceptable) to avoid excessive V_T Oxygenation: set lowest feasible FiO₂ (goal SpO₂ 92%-96%) to avoid O₂ toxicity
Supportive care	Treat underlying etiology: source control (eg, sepsis) Prevent iatrogenic harm: negative fluid balance, timely extubation (eg, minimize sedation) ± Corticosteroids: select patients with moderate-to-severe early ARDS
Prognosis	Mortality rate: 40% in hospital, death mostly due to multiorgan failure Morbidity rate: 50% with chronic cognitive impairment & physical debility, 25% with chronic pulmonary dysfunction (restriction & ↓ DLCO)
ARDS = acute respiratory distress syndrome; DLCO = diffusion capacity of lung for carbon monoxide; Pplat = plateau pressure; SpO₂ = oxygen saturation as measured by pulse oximetry; V_T = tidal volume.

This patient has acute respiratory distress syndrome (ARDS) due to aspiration pneumonitis. The hallmark of ARDS is neutrophilic lung inflammation with increased vascular permeability, leading to pulmonary edema in the absence of cardiac failure or volume overload. However, once ARDS is established, excessive intravascular volume serves only to exacerbate fluid escape, leading to worsened pulmonary edema and delayed recovery.

Fluid balance refers to the net sum of all fluid intake and output from the time of admission. Patients with ARDS often have an initial positive fluid balance (eg, volume resuscitation for sepsis, blood transfusion for trauma). During hospitalization, a conservative fluid strategy aimed at achieving a neutral or negative fluid balance accelerates recovery from ARDS, with a trend toward improved survival rate ("dry lungs = happy lungs").

This goal is accomplished by:

Minimizing intake: avoiding unnecessary fluid boluses, concentrating intravenous drips
Promoting removal: diuretics, renal replacement therapy

Patients with refractory hypotension (eg, septic shock) should be assessed for fluid-responsiveness prior to blind volume loading (eg, via passive leg raise to simulate a fluid bolus). Vasopressors (eg, norepinephrine) may be required to support hemodynamics to permit volume removal.

(Choices B and D) Lung inflation is determined by the set tidal volume and positive end-expiratory pressure (PEEP), which can be set on the mechanical ventilator. Low tidal volume ventilation (LTVV) (≤6 mL/kg) protects the lungs by limiting alveolar overdistension to mitigate further injury. LTVV often causes mild hypercapnic respiratory acidosis, as seen in this patient. This "permissive" hypercapnia is well-tolerated and correlated with improved survival. PEEP opens the lung by propping open collapsed alveoli (decreasing atelectasis); however, this must be balanced with the risk of overinflating alveoli that are already open. Therefore, tidal volume and PEEP must be carefully selected to optimize (rather than maximize) lung inflation while avoiding overdistension.

(Choice C) The ideal oxygen saturation range in ARDS, validated through clinical trials, is 92%-96%, corresponding to PaO₂ of 60-90 mm Hg. This avoids overt hypoxemia or hyperoxia (oxidative stress can aggravate lung injury).

(Choice E) Deep sedation may be required to promote patient-ventilator synchrony (ie, matching patient respiratory efforts to the mechanical ventilator breaths), which decreases oxygen consumption and self-inflicted barotrauma. However, excessive sedation increases the risk of delirium, deconditioning, and prolonged intubation. Sedation should be routinely tapered off (ie, daily sedation holiday) as soon as feasible to promote wakefulness and eventual extubation.

Educational objective:
A negative fluid balance decreases the formation of pulmonary edema and accelerates recovery from acute respiratory distress syndrome.