The decreased central blood volume caused by standing includes reduced atrial, ventricular, and pulmonary vessel volumes. These volume reductions unload the cardiopulmonary receptors and elicit a cardiopulmonary reflex. Reduced left ventricular end-diastolic volume decreases stroke volume and pulse pressure as well as cardiac output and mean arterial pressure, leading to decreased firing of aortic arch and carotid baroreceptors. The combined reduction in firing of cardiopulmonary receptors and baroreceptors results in a reflex decrease in parasympathetic nerve activity and an increase in sympathetic nerve activity to the heart.
When a person stands up, the heart rate generally increases by about 10 to 20 beats/min. The increased sympathetic nerve activity to the ventricular myocardium shifts the ventricle to a new function curve and, despite the lowered ventricular filling, stroke volume is decreased to only 50 to 60% of the recumbent value. In the absence of the compensatory increase in sympathetic nerve activity, stroke volume would fall much more. These cardiac adjustments maintain cardiac output at 60 to 80% of the recumbent value. An increase in sympathetic activity also causes arteriolar constriction and increased SVR. The effect of these compensatory changes in heart rate, ventricular con-
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