Physiological Response to Blood Loss

Physiological Response to Blood Loss (25% of Blood Volume)
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Physiological Response to Blood Loss (25% of Blood Volume)
Concerning the case of Johh, the body quickly feels a drop in blood pressure via its cardiopulmonary and arterial baroceptors and subsequently stimulates the sympathetic adrenergic system to activate the heart and constrict blood vessels. The sympathetic stimulation insignificantly affects the coronary blood vessels and brain and, therefore, these flows can gain from the vasoconstriction that happens in other organs that raise systemic vascular resistance and arterial pressure (Schiller, Howard & Convertino, 2017). Reduced organ blood circulation due to vasoconstriction and decreased arterial pressure results in systemic acidosis, which is felt by chemoreceptors. Furthermore, the chemoreceptor reflex then triggers the sympathetic adrenergic system and hence strengthening the baroreceptor reflex (D’Alessandro et al. 2015).
Next, the combined impacts of decreased arterial pressure and sympathetic stimulation result in the triggering of humoral compensatory responses. The adrenal glands sympathetic activation activates the catecholamines discharge into the blood, thereby strengthening the impacts of sympathetic stimulation on the vasculature and heart (Schiller, Howard & Convertino, 2017). The kidneys produce more renin after blood loss resulting in increased aldosterone and angiotensin II flowing levels. The activity results in vascular constriction, improved sympathetic activity, activation of vasopressin discharge, stimulation of thirst mechanisms, and increased water and sodium renal reabsorption to raise blood volume (D’Alessandro et al.

2015). The renal activity is especially significant in the long-term salvage from the loss of blood.
Finally, arterial hypotension, together with the precapillary resistance vessel constriction leads to a drop in capillary hydrostatic pressure. The tension usually stimulates fluid filtration from the blood via the capillary endothelium and into the interstitial area (Schiller, Howard & Convertino, 2017). The reduction of capillary hydrostatic tension is decreased, less fluid comes out of the capillaries, and the sufficiently low drop in pressure (due to the 25%/moderate to severe blood loss), the remaining fluid reabsorption can happen from the tissue interstitium into the capillary plasma (D’Alessandro et al. 2015). The reabsorbed fluid results in blood hemodilution and, therefore, red cell hematocrit drops in reaction to the fluid change. The response can result in about one liter per hour of fluid to be taken from interstitial areas into the plasma.

References
D’Alessandro, A., Moore, H. B., Moore, E. E., Wither, M., Nemkov, T., Gonzalez, E., & Banerjee, A. (2015). Early hemorrhage triggers metabolic responses that build up during prolonged shock. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 308(12), R1034-R1044.
Schiller, A. M., Howard, J. T., & Convertino, V. A. (2017). The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage. Experimental Biology and Medicine, 242(8), 874-883.