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(Circulation. 2008;118:1047-1056.)
© 2008 American Heart Association, Inc.

Contemporary Reviews in Cardiovascular Medicine

Inotropes and Vasopressors

Review of Physiology and Clinical Use in Cardiovascular Disease

Christopher B. Overgaard, MD; Vladimír Davík, MD

From the Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Correspondence to Dr Vladimír Davík, Division of Cardiology, Toronto General Hospital, 200 Elizabeth St, EN6-246, Toronto, Ontario, Canada M5G 2C4. E-mail vlad.dzavik@uhn.on.ca

Key Words: drugs • heart failure • inotropic agents • shock • vasopressin

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Inotropic and vasopressor agents have increasingly become a therapeutic cornerstone for the management of several important cardiovascular syndromes. In broad terms, these substances have excitatory and inhibitory actions on the heart and vascular smooth muscle, as well as important metabolic, central nervous system, and presynaptic autonomic nervous system effects. They are generally administered with the assumption that short- to medium-term clinical recovery will be facilitated by enhancement of cardiac output (CO) or vascular tone that has been severely compromised by often life-threatening clinical conditions. The clinical efficacy of these agents has been investigated largely through examination of their impact on hemodynamic end points, and clinical practice has been driven in part by expert opinion, extrapolation from animal studies, and physician preference. Our aim is to review the mechanisms of action of common inotropes and vasopressors and to examine the contemporary evidence for their use in important cardiac conditions.

	Cardiovascular Effects of Common Inotropes and Vasopressors

 
Catecholamines
Since the initial discovery of epinephrine, the principal active substance from the adrenal gland,¹ the pharmacology and physiology of a large group of endogenous and synthetic catecholamines or "sympathomimetics" have been characterized.² Catecholamines mediate their cardiovascular actions predominantly through ₁, β₁, β₂, and dopaminergic receptors, the density and proportion of which modulate the physiological responses of inotropes and pressors in individual tissues. β₁-Adrenergic receptor stimulation results in enhanced myocardial contractility through Ca²⁺-mediated facilitation of the actin-myosin complex binding with troponin C and enhanced chronicity through Ca²⁺ channel activation (Figure 1). β₂-Adrenergic receptor stimulation on vascular . . . [Full Text of this Article]