Hemodynamic alterations

Hemodynamic instability and shock, which is often unresponsive to volume loading and vasopressor agents, are prominent features of acute hypoadrenalism (adrenal crisis). Several mechanisms contribute to cardiovascular failure. Mineralocorticosteroid deficiency resulting in sodium and water loss and subsequent hypovolemia, which may be aggravated by vomiting and diarrhea, is the major pathogenetic factor.

However, glucocorticoids are also of prime importance in maintaining adequate cardiovascular function as shock may occur in glucocorticoid deficiency. Glucocorticoid deficiency is associated with reduced myocardial contractility which responds to corticosteroid treatment. Withdrawal of glucocorticosteroid treatment in patients with chronic hypoadrenalism results in a pronounced fall in lymphocyte b 2-adrenergic receptor density, which may reflect changes in cardiovascular b-receptors, and a reduced cAMP response to isoprenaline. This is associated with impaired left ventricular relaxation and diastolic filling which may contribute to cardiovascular failure in adrenal crisis. Patients with substituted chronic hypoadrenalism have significantly lowered levels of plasma epinephrine (with normal norepinephrine levels), indicating that high local adrenocortical glucocorticoid concentrations are necessary for normal epinephrine production via adrenal medullary enzyme induction. This may have implications for patients in adrenal crisis. Glucocorticoid deficiency is associated with a reduced peripheral vascular adrenergic tone, which may be due to a reduced sensitivity to pressor effects of angiotensin II and norepinephrine, decreased synthesis of renin substrate, and loss of glucocorticoid-induced inhibition of vasodilating prostaglandins. Such mechanisms may explain the hyperdynamic profile with a high cardiac output and a low peripheral vascular resistance observed in patients with hypoadrenalism after correction of hypovolemia.

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