Mechanism of nitroglycerin-induced hypoxemia.

We and others have previously demonstrated a consistent significant decline in arterial oxygen tension (PaO2) after sublingual nitroglycerin in premedicated and unpremedicated patients both with and without coronary artery disease and/or obstructive ventilatory disease. Thus, in our 19 patients, PaO2 fell by an average of 17% (12 mm Hg), mean systemic arterial pressure by 19% (17 mm Hg), pulmonary arterial pressure by 38% (6 mm Hg), pulmonary arterial occlusive pressure by 62% (5.3 mm Hg), and cardiac index by 16% (0.37 liter/min/m2) [P less than 0.001 for each] after nitroglycerin. Previous experimental studies suggest that the mechanism for the reduction of PaO2 may be relief of hypoxic pulmonary vasoconstriction with an increase in perfusion to poorly ventilated or nonventilated regions of the lungs. To examine this possibility, pulmonary vasodilatation was precluded by administration of a pulmonary vasoconstrictor (phenylephrine) simultaneously with nitroglycerin in nine patients with coronary artery disease. No significant change was observed in systemic or pulmonary arterial pressure, pulmonary arterial occlusive pressure, or systemic and pulmonary vascular resistance, and PaO2 did not decline. In ten other patients with coronary artery disease, the intrapulmonary right-to-left shunt fraction was determined before and after sublingual nitroglycerin; only a minimal increase in shunt fraction of 1.4% was observed, quantitatively insufficient to account for the observed decline in PaO2, thus excluding a predominant effect of nitroglycerin on nonventilated alveoli as a cause of the hypoxemia. We conclude that the reduction of PaO2 after nitroglycerin administration is attributable to pulmonary vasodilatation with a relative increase in perfusion of poorly ventilated lung units.