A B S T R A C T We have examined the mechanisiis of abnormal gas exchange in seven patients with chroniic obliteration of the pulmonary vascular bed secondary to recurrent pulmonary emboli or idiopathic pulmonary hypertension. All ofthe patients had a widened alveolararterial oxygen gradient and four were significantly hypoxemic with arterial partial pressures of oxygen <80 torr. Using the technique of multiple inert gas elimination, we found that ventilation-perfusion (VA/Q) relationships were only minimally abnormlal w\ith a imiean of 10% (range, 2-19%) of cardiac output perfusing abnormal units. These units consisted of shunt ancd units with VA/0 ratios <0.1. In addition, the dead space was found to be normal in each patient. There was no evidence for diffusion impairment, and the widenied alveolar-arterial oxygen gradient was completely explained by VA/Q inequality. Significanit hypoxemila occurred only when VA/Q inequality was combined with a low mixed venous oxygen content.

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Hypoxemia usually accompanies acute pulmonary embolism in humans, but its mechanism remains poorly understood. We studied 2 patients with acute, massive pulmonary embolism (APE) documented by pulmonary angiography. Both patients had a markedly increased alveolar-arterial oxygen difference (AaPO2). The technique of multiple inert gas elimination was used to determine the distribution of ventilation-perfusion ratios (VA/Q). An increase in VA/Q inequality was found in both patients, but this increased inequality was caused entirely by an increase in the ventilation of lung units with high VA/Q ratio. No blood flow was found perfusing lung units with a VA/Q ratio of less than 1.0. Both patients, however, had a large amount of blood flow (20 and 39% of the cardiac output) perfusing unventilated lung units (shunt), and the percent of minute ventilation to unperfused lung units as well as the VD/VT determined from the Bohr equation were increased. We conclude that in these 2 patients with APE, VA/Q inequality did not play a major role in their hypoxemia and that the widened AaPO2 is explained by the large shunts that were found.

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We have studied the influence of pulmonary vascular tone on ventilation-perfusion relationships in subjects with chronic obliterative pulmonary vascular disease. We administered oxygen, isoproterenol, or nitroprusside on 15 occasions in 7 subjects and observed a fall in pulmonary vascular resistance of greater than 15% in 8 of these 15 trials. When pulmonary vascular resistance was reduced, there was an increase in the perfusion of lung units with low ventilation-perfusion ratios (VA/Q) and/or shunt as determined by the multiple inert gas technique. The pattern of increased VA/Q inequality was independent of the specific agent used. In only one instance in which pulmonary vascular resistance was not reduced did drug administration lead to a worsening of VA/Q relationships. The detrimental effect of the increased perfusion of low VA/Q units on arterial oxygenation was frequently attenuated by an increased mixed venous oxygen content due to an increase in total cardiac output. We conclude that pulmonary vascular tone contributes to the maintenance of VA/Q matching in subjects with obstruction of the pulmonary vascular bed.