Since the effect of prolonged exposure to high concentrations of oxygen on regional ventilation and perfusion has not been previously, a reproducible primate model of oxygen toxicity was developed to investigate the pathophysiologic changes that occur. Regional ventilation and perfusion were measured by 133Xe techniques in 10 baboons before and after 108 hours of continuous exposure to an inspired oxygen concentration of more than 90%. Arterial blood gases, shunt fraction (QS/QT), cardiac output, physiologic dead space (VD/VT), and pulmonary vascular resistance were also measured. Light and electron microscopic histology confirmed early pathologic changes of oxygen toxicity in every animal after exposure. PaO2 in room air decreased markedly after exposure from 90 +/- 4 to 46 +/- 5 mm Hg, and QS/QT rose to 30 +/- 2%. VD/VT, PaCO2, and pH were not altered by exposure to hyperoxia. Similarly, cardiac output and pulmonary vascular resistance remained unchanged. The distribution of regional ventilation and perfusion remained normal during and after prolonged high-oxygen exposure. Early oxygen toxicity was characterized by profound hypoxemia without regional ventilation-perfusion mismatch. Although impaired diffusion through a thickened alveolar membrane may be partially responsible for this hypoxemia, the markedly increased alveolar-arterial oxygen gradient when FIO2 = 1.0 indicates that shunting at the alveolar level (secondary to absorptive collapse or pulmonary edema) is a major cause of the hypoxemia.
Animals Hemodynamics