Pulmonary gas exchange response to oxygen breathing in acute lung injury

The mechanisms and time course of the pulmonary gas exchange response to 100% O-2 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% O-2, 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 (Fl(O2)-m), at 30 and 60 min while breathing 100% O-2 and then at 30 min of resuming Fl(O2)-m. During 100% O-2 breathing, in patients with ALI, Pa,, (by 207 and 204 mm Hg; p < 0.01 each), Pa-CO2 (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, Pa-O2 (by 387 and 393 mm Hg; p < 0.001 each), Pa-CO2 (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% O-2 deteriorates intrapulmonary shunt owing to collapse of unstable alveolar units with very low ventilation-perfusion (VA/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.