One of the very first responses observed in animal studies of acute hemorrhage is a fall in blood pressure that cannot be accounted for simply by the initial reduction in intravascular volume.1 It is likely that the fall in blood pressure is caused by a sudden reduction in systemic vascular resistance, although the mechanism has not been explained. The fall in blood pressure is sensed by both high-pressure baroreceptors in the carotid artery sinus and the aortic arch as well as low-pressure baroreceptors in the left atrium and pulmonary veins. Stimulation of these baroreceptors, in turn, causes disinhibition of the medullary vasomotor center, a subsequent decrease in vagal tone, and an increase in the secretion of norepinephrine (NE). Decreased vagal tone increases heart rate and cardiac output. NE increases heart rate and myocardial contractility, stimulates renin secretion, and causes intense vasoconstriction, especially of splanchnic and musculoskeletal blood vessels. Such vasoconstriction provides a functional reservoir that can be used to compensate for acute blood loss, since 20 to 30 percent of the circulating blood volume resides in the splanchnic bed.
Cardiac output typically falls during hemorrhage, due to a decrease in atrial filling or preload, despite increases in myocardial rate and contractility. It is commonly taught that afterload rises during acute hemorrhage in order to maintain blood pressure. In fact, there is little evidence to support this claim. It is more likely that, early in the course of hemorrhage, total systemic vascular resistance falls or remains at near-normal levels in order to facilitate flow to vital organs. There are, however, increases in regional resistance that cause redistribution of blood flow away from skin, muscle, and gut to favor the brain, heart, and kidneys.
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