Pulmonary Gas Exchange Response to Oxygen Breathing in Acute Lung Injury

Abstract

The mechanisms and time course of the pulmonary gas exchange response to 100% O₂ breathing in acute respiratory failure needing mechanical ventilation were studied in eight patients with acute lung injury (ALI) (48 ± 18 yr [mean ± SD]) and in four patients (66 ± 2 yr) with chronic obstructive pulmonary disease (COPD). We postulated that, in patients with ALI while breathing 100% O₂, the primary mechanism of hypoxemia, i.e., increased intrapulmonary shunt, would further worsen (increase) as a result of reabsorption atelectasis. Respiratory and inert gases, and systemic and pulmonary hemodynamics were measured at maintenance fraction of inspired oxygen (Fi O₂ -m), at 30 and 60 min while breathing 100% O₂, and then at 30 min of resuming Fi O₂ -m. During 100% O₂ breathing, in patients with ALI, PaO₂ (by 207 and 204 mm Hg; p < 0.01 each), PaCO₂ (by 4 mm Hg each) (p < 0.05 each), and intrapulmonary shunt (from 16 ± 10% to 22 ± 11% and 23 ± 11%) (p < 0.05 each) increased respectively. By contrast, in patients with COPD, PaO₂ (by 387 and 393 mm Hg; p < 0.001 each), PaCO₂ (by 4 and 5 mm Hg) and the dispersion of pulmonary blood flow (log SDQ) (from 1.33 ± 0.10 to 1.60 ± 0.20 and 1.80 ± 0.30 [p < 0.05]) increased, respectively. In patients with ALI, the breathing of 100% O₂ deteriorates intrapulmonary shunt owing to collapse of unstable alveolar units with very low ventilation–perfusion (V˙ a/Q˙) ratios, as opposed to patients with COPD, in whom only the dispersion of the blood flow distribution is disturbed, suggesting release of hypoxic pulmonary vasoconstriction. Santos C, Ferrer M, Roca J, Torres A, Hernández C, Rodriguez-Roisin R. Pulmonary gas exchange response to oxygen breathing in acute lung injury.