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Use of vasopressors and inotropes

INTRODUCTION

Vasopressors are a powerful class of drugs that induce vasoconstriction and thereby elevate mean arterial pressure (MAP). Vasopressors differ from inotropes, which increase cardiac contractility; however, many drugs have both vasopressor and inotropic effects. Although many vasopressors have been used since the 1940s, few controlled clinical trials have directly compared these agents or documented improved outcomes due to their use [1]. Thus, the manner in which these agents are commonly used largely reflects expert opinion, animal data, and the use of surrogate end points such as tissue oxygenation as a proxy for decreased morbidity and mortality.

Basic adrenergic receptor physiology and the principles, complications, and controversies surrounding use of vasopressors and inotropes for treatment of shock are presented here. Issues related to the differential diagnosis of shock and the use of vasopressors in patients with septic shock are discussed separately. (See "Shock in adults: Types, presentation, and diagnostic approach" and "Evaluation and management of severe sepsis and septic shock in adults".)

RECEPTOR PHYSIOLOGY

The main categories of adrenergic receptors relevant to vasopressor activity are the alpha-1, beta-1, and beta-2 adrenergic receptors, as well as the dopamine receptors [2,3].

Alpha adrenergic — Activation of alpha-1 adrenergic receptors, located in vascular walls, induces significant vasoconstriction. Alpha-1 adrenergic receptors are also present in the heart and can increase the duration of contraction without increased chronotropy. However, clinical significance of this phenomenon is unclear [4].

Beta adrenergic — Beta-1 adrenergic receptors are most common in the heart, and mediate increases in inotropy and chronotropy with minimal vasoconstriction. Stimulation of beta-2 adrenergic receptors in blood vessels induces vasodilation.

                                    

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Literature review current through: Mar 2014. | This topic last updated: Mar 21, 2013.
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