Although oxygen is frequently administered to patients with obliterative pulmonary vascular disorders (OPVD) for diagnostic and therapeutic purposes, its hemodynamic effects in these patients have not been systematically evaluated. The response to administration of 50 to 70% oxygen was studied in 14 patients with pulmonary hypertension secondary to OPVD. Mean pulmonary artery pressure decreased (from 62 ± 5 to 57 ± 5 mm Hg, p < 0.01) after oxygen inhalation secondary to a decrease in cardiac index (1.9 ± 0.2 to 1.8 ± 0.2 liters/min/m2, p < 0.01), without changes in pulmonary arteriolar resistance. This decline in forward output appeared to result from a systemic vasoconstrictor effect of oxygen (change in systemic vascular resistance from 1,965 ± 275 to 2,297 ± 336 dynes s cm-5, p < 0.01), which decreased heart rate (from 93 ± 3 to 89 ± 2 beats/min, p < 0.01) by stimulation of baroreceptor reflexes and decreased stroke volume (from 22 ± 3 to 21 ± 2 ml/beat/m2, p < 0.05) by increasing impedance to left ventricular ejection. The decrease in left-sided cardiac output likely led to a decline in venous return to the right side of the heart and, consequently, to a decrease in right atrial and pulmonary arterial pressures. Accordingly, the percent decrease in mean pulmonary artery pressure varied linearly and directly with the percent increase in systemic vascular resistance (r = 0.84), but not with changes in pulmonary arteriolar resistance (r = 0.15). Hence, amelioration of the pulmonary hypertensive state after oxygen inhalation in patients with OPVD cannot be taken as evidence of an oxygen-responsive pulmonary vasculature, unless changes in cardiac output and pulmonary resistance are measured concomitantly. In addition, oxygen therapy may decrease cardiac output, which may limit its benefits in some patients with OPVD.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine