No abstract

In an attempt to objectively evaluate the status of the left ventricle in 32 patients with mitral stenosis, a modified form of supine leg exercise was done during simultaneous left and right heart catheterization. Besides measuring the usual hemodynamic parameters, a ratio of mitral valve flow (MVF) or diastolic left ventricular volume change (Δv/Δt) and the slope of the rise of left ventricular diastolic pressure (Δp/Δt) was calculated at rest and during exercise (Δv/Δp). The results of these measurements were compared with those obtained on nine patients with either innocent functional heart murmurs or hemodynamically insignificant stenotic valvular lesions. None of the nine control patients had left ventricular end-diastolic pressures (LVEDP) greater than 12 mm Hg either at rest or with exercise. Exercise also did not appreciably alter the Δv/Δp ratio. Among the patients with mitral stenosis eight patients had distinctly elevated (greater than 14 mm Hg) LVEDP with exercise and 19 patients, including the eight with abnormal LVEDP, decreased the Δv/Δp ratio with exercise. The difficulties and limitations associated with this type of study are discussed. However, there is a distinct possibility that these results are indicative of an abnormal left ventricle in some patients with mitral stenosis. It is further suggested that this abnormality may be related in some way to decreased left ventricular compliance. In addition, a close statistical correlation between Δv/Δp and cardiac output implicates this left ventricular abnormality as a possible etiological factor in the reduced cardiac output seen in many patients with mitral stenosis.

No abstract

The relationship between the effects of potassium and vagal stimulation on transmission through the atrioventricular transmission system was investigated. It was observed that infusion of isotonic potassium chloride alleviated atrioventricular block induced by vagal activity. This occurred at plasma potassium levels ranging from 4.8 to 6.9 mEq/liter. This antagonism does not appear to be mediated by catecholamine release since infusion of epinephrine (0.23 µg/min) did not relieve the block. At plasma levels higher than those capable of inhibiting vagal action, potassium enhances parasympathomimetic actions on A-V transmission and, at still higher levels, potassium is capable of inducing A-V block which is independent of the vagus.