James S. Bower

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

We have examined the mechanisms of abnormal gas exchange in seven patients with chronic obliteration of the pulmonary vascular bed secondary to recurrent pulmonary emboli or idiopathic pulmonary hypertension. All of the patients had a widened alveolar-arterial oxygen gradient and four were significantly hypoxemic with arterial partial presssures of oxygen less than 80 torr. Using the technique of multiple inert gas elimination, we found that ventilation-perfusion (VA/Q) relationships were only minimally abnormal with a mean of 10% (range, 2--19%) of cardiac output perfusing abnormal units. These units consisted of shunt and units with VA/Q ratios less than 0.1. In addition, the dead space was found to be normal in each patient. There was no evidence for diffusion impairment, and the widened alveolar-arterial oxygen gradient was completely explained by VA/ inequality. Significant hypoxemia occurred only when VA/Q inequality was combined with a low mixed venous oxygen content.

Hemodynamic and gas exchange effects of intravenous diltiazem in patients with pulmonary hypertension

In studies of five patients treated with acute intravenous administration of diltiazem, hemodynamic improvement occurred in the four patients with precapillary pulmonary hypertension. This was manifested by modest declines in pulmonary arterial pressure and total pulmonary resistance at rest and during exercise. Unlike other vasodilators, diltiazem did not worsen pulmonary gas exchange or ventilation-perfusion distribution.