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Vasopressor and Inotropic Agents

Vasopressor and inotropic agents are the drugs used to support the failing circulation in critically ill patients. Vasopressors raise blood pressure mainly by increasing vascular tone, while inotropes augment the force of cardiac contraction; many agents act on more than one pathway, and the choice among them is shaped by the underlying type of shock.

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Definition

Vasopressors are agents that raise arterial pressure chiefly by increasing systemic vascular tone, while inotropes are agents that increase the contractile force of the heart; both classes are used to restore perfusion in circulatory failure, and several agents have mixed actions.

Scope

The entry covers the pharmacological classes used in circulatory support — catecholamine and non-catecholamine vasopressors and inotropic drugs — the receptor mechanisms through which they act, and the major trials comparing them in shock. It is a reference description of these drug classes and their evidence base, not a guide to drug selection, dosing, or titration.

Core questions

  • How do vasopressors differ from inotropes in their hemodynamic effects?
  • Through what receptors and pathways do the main agents act?
  • What does trial evidence show about choosing among vasoactive agents in shock?

Key concepts

  • Vasopressors versus inotropes
  • Adrenergic receptor activity
  • Catecholamines (norepinephrine, epinephrine, dopamine)
  • Non-catecholamine vasopressors (vasopressin, angiotensin II)
  • Inotropic agents (dobutamine, milrinone, levosimendan)
  • Agent choice by shock type

Mechanisms

Most vasoactive agents act on adrenergic receptors: stimulation of alpha-1 receptors on vascular smooth muscle increases vascular tone and arterial pressure, while stimulation of beta-1 receptors on the myocardium increases the force and rate of contraction. Norepinephrine acts predominantly as a vasopressor with some inotropic effect; epinephrine and dopamine engage a broader range of receptors; dobutamine acts mainly as a beta-agonist inotrope. Non-adrenergic agents add complementary mechanisms — vasopressin acts on V1 receptors and angiotensin II on the renin-angiotensin system to restore tone in vasodilatory shock, while milrinone and levosimendan augment contractility through pathways independent of adrenergic receptors. Matching the agent's profile to the dominant derangement — low tone versus low output — is central to its rationale.

Clinical relevance

These drug classes organize how circulatory support is conceptualized in critical care, and the trials comparing them inform the evidence clinicians appraise. This entry describes the agents and their evidence base as a reference; it does not provide drug selection, dosing, titration, or any individualized treatment instruction.

Epidemiology

Vasoactive drugs are among the most frequently administered medications in intensive care, with norepinephrine widely used as a first-line vasopressor in many forms of shock. Patterns of use have shifted with trial evidence, for example away from dopamine as a default agent.

Evidence & guidelines

Randomized trials have compared specific agents — dopamine versus norepinephrine (De Backer et al., 2010), vasopressin versus norepinephrine (Russell et al., 2008), angiotensin II in vasodilatory shock (Khanna et al., 2017), and levosimendan versus dobutamine (Mebazaa et al., 2007). The Surviving Sepsis Campaign guidelines (Evans et al., 2021) integrate much of this evidence into recommendations for vasoactive therapy in septic shock.

History

Adrenergic agents have been used to support the circulation since the mid-twentieth century, but the comparative evidence base matured in the 2000s and 2010s as randomized trials tested specific agents against one another. These trials, together with the introduction of non-catecholamine vasopressors such as vasopressin and angiotensin II, refined how agents are matched to the type of shock.

Debates

Which vasopressor should be first-line in shock?
Comparative trials, such as dopamine versus norepinephrine, informed a shift toward norepinephrine as a default vasopressor in many settings, while the roles of vasopressin and angiotensin II as adjuncts in vasodilatory shock remain subjects of ongoing study.

Key figures

  • Daniel De Backer
  • James A. Russell
  • Alexandre Mebazaa

Related topics

Seminal works

  • debacker-2010
  • russell-2008-vasst
  • mebazaa-2007-survive

Frequently asked questions

What is the difference between a vasopressor and an inotrope?
A vasopressor raises blood pressure mainly by increasing the tone of blood vessels, while an inotrope increases the strength of the heart's contraction; some drugs have both effects to differing degrees.
Why does the choice of vasoactive agent depend on the type of shock?
Because different forms of shock derange different parts of the circulation — vasodilation calls for restoring tone, while low cardiac output calls for augmenting contraction — agents are matched to the dominant problem.

Methods for this concept

Related concepts