Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma
United States Department of Defense
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Loss of blood triggers a compensatory vasoconstriction and tachycardia, which permit a reduction of blood volume of 20-30% while maintaining the blood pressure at nearly normal levels. If hypovolemia results, and, if not corrected promptly, may cause death. Changes that are characteristic of the hypovolemic shock state are decreased cardiac filling pressures, decreased systemic arterial pressure, tachycardia, and increased systemic vascular resistance secondary to catecholamine release.
Liberation of histamine, serotonin, and prostaglandins, leukocytosis; the activation products of complement and coagulation systems; and neutrophils liberated form injured tissue all contribute to a local state of increased vascular permeability. This response can aggravate the intravascular volume deficit. The acute discharge of catecholamines form the sympathetic nervous system and the adrenal glands serves to maintain tissue perfusion in the face of acute intravascular volume loss.
The catecholamines exert an inotropic influence on the heart tending to increase cardiac output which is falling secondary to decreasing preload. Peripherally, there is a redistribution of blood flow, which is in part secondary to a graded autonomic innervation in the vascular beds of various organ systems. Blood flow to vital organs, such as the brain and heart, is maintained at the expense of decreasing flow to skin, muscle, renal, and enteric beds in a prioritized fashion. This response is regulated by the density of alpha receptors responding to the vasoconstrictive influence of circulating catecholamines and by that tissue's inherent local sympathetic nervous system innervation. Hence, we see a casualty with rapid, thready pulse, and pale cool skin, before development of hypotension. If this casualty is administered anesthetic agents that depress these compensatory autonomic responses in the hypovolemic patient, hypotension and shock may result.
Following these acute reflexes, which tend to maintain perfusion, a series of endocrine responses occurs, which serves to replenish the intravascular volume. As an initial response, vasopressin (ADH) is released from the posterior pituitary. ADH exerts a direct action on the renal collecting tubule to increase passive diffusion of water across the cell and back into the peritubular vessels. Under normal conditions, ADH is primarily regulated by hypothalamic osmoreceptors; however in the response to acute blood loss, volume stretch receptors, hypotholamic osmoreceptors, and a neural pain/stress response appear to play an important role. Subsequently, the release of aldosterone, mediated through the renin-angiotensin system, following stimulation of the juxtaglomerular apparatus of the kidney, acts to maintain extra-cellular fluid volume. Aldosterone, acting at the proximal renal tubular level, causes the reabsorption of sodium and the conservation of water.
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