β Scribed by Weygandt, Glenn R. ;Kopman, Ercument A. ;Ludbrook, Philip A.
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We and others have previously demonstrated a consistent significant decline In arterial oxygen tensbn (paol) after sublingual nitraglycerin In premedkated and unpremedicated patients both wlth and without coronary artery disease and/or obstructlve ventilatory disease. Thus, in our 19 patients, Pa02 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 occiusive pressure by 62% (5.3 mm Hg), and cardiac Index by 16% (0.37 litedmidm2) [P < 0.001 for each] after nitroglycerin. Prevbus experimental studies suggest that the mechanism for the reductbn of PaOa may be relief of hypoxk pulmonary vasoconstriction with an Increase in perfusbn to poorly ventilated or nonventilated regions of the iungs.To examine this possibllity, pulmonary vasodiiatatbn was precluded by administratbn of a pulmonary vasoconstrictor (phenyiephrine) simultaneously with nttroglycerin in nine patients with coronary artery disease. No significant change was observed in systemk or pulmonary arterial pressure, pulmonary arterial occlusive pressure. or systemic and pulmonary vascular resistance, and Paol dkl not decline. In ten other patients with coronary artery dlsease, the intrapulmonary right-to-left shunt fractbn was determined before and after sublingual nitroglycerin; only a minlmal increase in shunt fractbn of 1.4% was observed, quantitatively insuffkient to account for the observeddecline in P a , thus excluding a predominant effect of nitroglycerin on nonventilated alveoli as a cause of the hypoxemla. We conclude that the reductbn of P a 0 2 after nitroglycerin administratbn is attributable to pulmonary vasodiiatatbn with a relative increase in perfusbn of poorly ventilated lung unlts.
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