STUDIES OF PULMONARY HYPERTENSION. IX. THE EFFECTS OF INTRAVENOUS HEXAMETHONIUM ON PULMONARY CIRCULATION IN PATIENTS WITH MITRAL STENOSIS1

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Abstract
Hexamethonium bromide was given through a catheter into the pulmonary artery of 27 patients with mitral stenosis in doses sufficient to produce an initial depression of about 30 mm Hg in the systolic pressure in the brachial artery. Over the course of the following 0.5-1 hour, changes in cardiac output, heart rate, and stroke volume were insignificant. The pulmonary artery pressure declined significantly in over half the cases, the change being roughly proportional to the change in systemic artery pressure. The pulmonary "capillary" pressure also fell in more than 2/3 of observations. There was no consistent change in PAm-"PC"m gradient, although pulmonary vascular resistance fell in a few instances. The paradox of declining pulmonary "capillary" pressure with constant cardiac output is discussed. On hydraulic grounds it is unlikely that this could be explained solely by any vasoshifts of blood from pulmonary to peripheral reservoirs, although both may occur in addition. Changes in heart rate may play a small contributing role. Two other possible explanations are discussed: changes in left ventricular diastolic pressure, and increases in the transport of blood through intrapulmonary vascular shunts. The clinical importance of hexamethonium on the pressure in the pulmonary circuit is illustrated by 2 cases successfully treated for acute pulmonary edema developing in patients with mitral stenosis during cardiac catheterization.