Define circulatory shock. Explain how this condition may be caused by hypovolemia and discuss the compensatory mechanisms that occur during hypovolemia shock.

Outline:

·        Results of hypovolemia

·        Compensatory mechanism:

- baroreceptors: sympathetic stimulation

- circulation

- kidneys: actions of angiotensin II, ADH and aldosterone

Essay:

            Circulatory shock describes a generalized inadequacy of blood flow (tissue perfusion) throughout the entire body as a result of inadequate cardiac output. The cardiac output may be inadequate because the amount of fluid in the vascular system is inadequate to fill it (hypovolemic shock). Alternatively, it may be inadequate because the size of the vascular system is increased by vasodilation even though the blood volume is normal. Shock may also be caused by myocardial abnormalities (cardiogenic shock), and by inadequate cardiac output as a result of obstruction of blood flow in the lungs or heart (obstructive shock).

            Hypovolemic shock is characterized by hypotension; a rapid, thready pulse; a cold, pale, clammy skin; intense thirst; rapid respiration and restlessness or torpor. It is caused by hemorrhage as a result of trauma, severe burns leading to loss of plasma, dehydration, diarrhea or renal failure. All these can cause a drastic decrease in the circulating blood volume such that it is insufficient to perfuse the tissues. The decline in blood volume declines venous return, and cardiac output falls.

            When blood volume is reduced and venous return is decreased, the arterial baroreceptors are stretched to a lesser degree, and sympathetic output is increased. The vasoconstriction is generalized, sparing the vessels of the heart and brain. Vasoconstriction is most marked in the skin, where it accounts for the coolness and pallor, and in the kidneys and viscera. The widespread venoconstriction increase venous return and helps maintain pressure of the heart while the intense vasoconstriction in the splanchnic area shifts blood from the visceral reservoir into the systemic circulation. Blood is also shifted out of the subcutaneous and pulmonary veins. Contraction of the spleen discharges more ‘stored’ blood into the circulation. When arterial pressure falls below 50 mmHg, the central nervous system ischemic response is activated, which elicits an even more powerful sympathetic stimulation throughout the body. All these mechanisms serve to increase the mean filling pressure of the systemic circulation in an attempt to increase blood flow to the underperfused tissues.

            In the kidneys, the reduced renal blood flow and sympathetic stimulation leads to increased renin production and release by the juxtaglomerular cells. Renin cleaves angiotensinogen to angiotensin I which is converted to the active hormone angiotensin II by the angiotensin-converting enzyme. Angiotensin II is a potent vasoconstrictor itself and it acts on the renal tubules to increase NaCI reabsorption. It stimulates the synthesis and release of ADH by the posterior pituitary. ADH increases the permeability of the collecting ducts to water by insertion of water channels in the apical membrane and this helps the body to conserve water and hence body volume. Angiotensin causes thirst by an action on the subfornical organ and ingestion of fluids helps restore the ECF volume. The increases in circulating angiotensin II and ACTH levels increase aldosterone secretion. Aldosterone causes the retention of sodium, which helps reexpand the blood volume.

            If the hypovolemia is moderate, the circulating plasma volume is usually restored in 12-72 hours by these compensatory mechanisms.