MECHANISM OF THE ARTERIAL PRESSURE RESPONSE TO THE VALSALVA TEST: THE BASIS FOR ITS USE AS AN INDICATOR OF THE INTACTNESS OF THE SYMPATHETIC OUTFLOW

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Abstract
Pressure changes in various parts of the circulatory system, resulting from a 30-sec. elevation of intrapul-monic pressure, form characteristic and consistent patterns. The arterial pressure response has 6 components, of which the poststimulus overshoot, or rise of blood pressure above the prestimulus level, is the main subject of this paper. This overshoot is the result of reflex sympathetic activity engendered by the hypotension present in the carotid sinuses during the period that venous return is impaired. (The extent of participation by the aortic receptors was undetd.) Removal or diminution of carotid sinus activity diminishes or abolishes the overshoot. Partial or complete blockade of reflex sympathetic activity either by tetraethylammonium chloride or by graded, segmental, spinal anesthesia diminishes the overshoot in direct proportion to the extent of the blockade. Vagal activity inhibits the overshoot to a variable degree. The presence of an excess of circulating epinephrine diminishes and may abolish the overshoot. The overshoot of right ventricular systolic pressure is influenced by the presence or absence of carotid sinus activity, much as is the overshoot of systemic arterial pressure. The standardization of any clinical test designed to use the degree of overshoot as a quantitative estimate of sympathetic activity should take into consideration the factors of medication, vagal activity, cold, apprehension, carotid sinus sensitivity and the presence of circulating epinephrine, as well as the patient''s blood volume.