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(Circulation. 1966;34:833.)
© 1966 American Heart Association, Inc.

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Patterns of Brachial Arterial Blood Flow in Conscious Human Subjects with and without Cardiac Dysfunction

JAMES H. GAULT M.D.¹; JOHN ROSS JR. M.D.¹; DEAN T. MASON M.D.¹

¹ From the Cardiology Branch, National Heart Institute, Bethesda, Maryland.

The patterns of phasic and instantaneous mean brachial arterial blood flow at rest, and during various interventions, were studied in 35 conscious human subjects. Flow was measured with an electromagnetic flowmeter applied to the brachial artery (BA) prior to retrograde arterial catheterization of the left ventricle.

The patterns of phasic BA flow in six patients without left-heart disease were compared with those of patients having a variety of cardiac lesions. In three patients with aortic stenosis, a prolonged upslope and a delayed systolic flow peak were noted, while in five patients with severe aortic regurgitation, a progressive decline in flow occurred throughout diastole; retrograde diastolic flow occurred infrequently at end diastole, but was elicited in three patients by inflation of a wrist cuff. Among seven patients with idiopathic hypertrophic subaortic stenosis, those with large pressure gradients across the left ventricular outflow tract exhibited a bifid systolic brachial arterial flow pulse and an abnormal response in brachial arterial flow during the beat following a premature ventricular contraction. In patients with mitral stenosis, the flow pulse was normal, while in three patients with mitral regurgitation, the period during which systolic flow occurred was abbreviated.

Mean brachial arterial blood flow averaged 72.7 ml/min, and neither peak nor mean flow levels bore a relation to the cardiac lesion, the stroke volume, or the cardiac index. All patients exhibited spontaneous variations in resting brachial arterial flow. Usually the fluctuations were in phase with periodic fluctuations in mean arterial pressure, although in some patients periodic fluctuations in arterial pressure and brachial arterial flow occurred in opposite directions, and in other patients random flow changes were observed.

Contractions of the forearm muscles were found to cause striking mechanical limitation of instantaneous brachial arterial flow. During maximal contraction of the forearm muscles, actual cessation of flow occurred.

Prior to investigating the influence of reflex interventions on brachial arterial flow, studies were performed to determine whether or not local anesthesia and surgical exposure of the brachial artery altered resting flow in forearm bed or the reflex connections to the forearm. Plethysmographic determinations of the resting forearm blood flow, and of the response to a cold pressor test, before and after exposure of the brachial artery, indicated that resting flow was unchanged and that reflex activity was essentially intact. Carotid arterial compression in five patients resulted in a prompt increase in forearm vascular resistance (average 53.4%). The response to manual stimulation of the carotid sinus in four patients suggested that reflex forearm vasodilatation was rapidly induced. In six patients studied during the course of a 20-second Valsalva maneuver, marked reflex vasoconstriction occurred approximately 10 seconds after the onset of the maneuver.

The present technique has permitted the first description of the normal pattern of phasic brachial arterial flow in unanesthetized human subjects, as well as the alterations in phasic flow contour accompanying various cardiac lesions. In addition, it has allowed investigation of rapid, transient alterations in peripheral arterial blood flow not previously accessible to measurement.

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