Question

describe the neutral and hormonal mechanism that work to maintain blood pressure after significant (hemorrhaging) blood loss associated with an injury

Answer 1

Hemorrhagic shock or hemorrhage is a clinical syndrome which results from decreased blood volume (blood loss), leading to reduced cardiac output. The volume of blood that is lost in the injury and the rate at which it is lost determines severity of hemorrhagic shock. Usually, blood loss of <15% of total blood volume does not significantly change arterial pressure. However, arterial and pulse pressures fall with 15 to 40% loss of blood. Life threatening situation arises with >40% blood loss.

The reduction in blood volume, caused during blood loss in an injury (acute) causes central venous pressure to drop, causing reduction in cardiac output and arterial pressure. Under such conditions, the body activates its numerous compensatory mechanisms in an effort to restore arterial pressure and blood volume back to normal. Few of these mechanisms are Baroreceptor reflexes, Chemoreceptor reflexes, Circulating vasoconstrictors, Renal reabsorption of sodium and water and Activation of thirst mechanisms.

The body senses fall in blood pressure through its arterial and cardiopulmonary baroreceptors. This happens as soon as the blood pressure starts dropping. As a measure, the sympathetic adrenergic system is activated to stimulate the heart and constrict blood vessels. A redistribution event occurs where cardiac output is channelized to brain and myocardium, which are critical for survival; at the expense of less important organs. The reduction in organ blood flow caused due to vasoconstriction and reduced pressure causes systemic acidosis. The chemoreceptors sense this change and a reflex action brings about activation of sympathetic adrenergic system that assists/ improves the baroreceptor reflex. When the mean arterial pressures fall below 50 mmHg, causing hypotension and the brain becomes ischemic, an intense sympathetic discharge is produced which helps in reinforcing other autonomic reflexes. The combined effects of neural mechanisms (hypotension and sympathetic activation), activates humoral compensatory mechanisms. Adrenal glands are stimulated to release catecholamines into blood stream to reinforce effects of sympathetic activation on the heart and vasculature. Also increased are the levels of angiotensin II and aldosterone, brought about by rise in kidney renin. The renal mechanism functions to constrict vessels, enhance sympathetic activity, stimulate the release of vasopressin, activate thirst mechanisms, increase kidney’s ability to reabsorb sodium and water, so as to increase blood volume. Hypotension and vascular constriction together account for fall in capillary hydrostatic pressure. This pressure is necessary for filtration of fluid from the blood, across capillary endothelium and further into interstitial space. As the pressure on capillary is reduced, less fluid leaves capillaries and on pressure drop to low levels in injuries, fluid can be reabsorbed from the tissue interstitium back into the capillary plasma. The reabsorbed fluid does not contain cells but has electrolytes and few proteins that can increase the blood plasma volume, causing hemodilution and associated reduction in red cell haematocrit.

In cases where compensatory mechanisms fail to work, the body has in store decompensatory mechanisms.