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(Circulation. 1966;34:423.)
© 1966 American Heart Association, Inc.

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Kinetocardiogram, Phonocardiogram, and Arterial Pulse Waves During Acute Hemodynamic Changes

ROBERT C. DADDARIO M.D.¹ EDWARD D. FREIS M.D.¹

¹ From the Veterans Administration Hospital and the Department of Medicine, Georgetown University School of Medicine, Washington, District of Columbia.

The effects of drugs that produce known hemodynamic alterations were assessed on externally recorded pulse waves, heart sounds, and the relationship of these to each other and to the electrocardiogram.

The shape of the carotid pulse and the carotid-femoral pulse-wave transmission time difference showed changes that could be related to alterations in central arterial distensibility. The ratio of the second to the first positive inflection, and of the incisura to the first positive inflection of the carotid pulse wave, increased following use of drugs which raised mean arterial pressure and decreased after those which lowered blood pressure. The carotid-femoral transmission time difference decreased with vasopressor agents, increased with amyl nitrite and hexamethonium, and showed no consistent change after isoproterenol.

Left ventricular ejection time, measured from the carotid pulse, changed in relation to heart rate, increasing with cardiac slowing and decreasing when the rate accelerated. The ejection time index remained unchanged except for a slight increase following amyl nitrite and a decrease after hexamethonium.

Alterations in isovolumic contraction time approximately paralleled changes in diastolic pressure. The ratio of diastolic pressure to isovolumic contraction time provides an index of the rate of rise of left ventricular pressure. The quotient of diastolic pressure divided by isovolumic contraction time increased with adrenergic stimulation (isoproterenol) and decreased after ganglion blockade. It was not significantly changed by angiotensin II, methoxamine, or amyl nitrite.

The interval between the onset of QRS and the beginning of the first heart sound (Q-S₁), shortened considerably after isoproterenol and moderately following amyl nitrite. It increased after hexamethonium and remained essentially unchanged following angiotensin II or methoxamine. These results suggest that the Q-S₁ interval may reflect ventricular contractility in the absence of mitral valvular disease.

The amplitude of the first heart sound appeared to be a sensitive indicator of ventricular contractility increasing with isoproterenol and amyl nitrite, decreasing with hexamethonium and remaining unchanged following use of angiotensin II or methoxamine.