Vasopressors I: Introduction

Few therapies are as strongly associated with the ICU setting as vasopressor medications. In most centers, you cannot administer continuous vasopressor infusions outside of a critical care environment, due the close monitoring they require.

A basic understanding of these drugs is bread and butter for the critical care clinician. Let’s discuss the fundamentals.


The simplest indication for vasopressors is hypotension.

Hypotension is not a diagnosis, nor is it a disease; it is simply a number. Patients do not die of hypotension; they die of shock, a syndrome of poor end-organ perfusion. The physiological derangement in this condition is inadequate blood flow, not inadequate blood pressure.

However, an adequate blood pressure is a prerequisite for flow, which is why we often treat it as a surrogate. It is possible to be in shock with a fairly normal blood pressure; it is also possible to be adequately perfused despite a low blood pressure. But these are sophisticated diagnoses to make, so in most cases we target a reasonable blood pressure—such as a MAP >65—and then follow other measures of perfusion, like urine output or serum lactate.

Of course, there are other treatments for both shock and hypotension, and pressors are not always the answer. If the shock is from a distributive mechanism, probably they are. But sometimes the patient needs preload instead—i.e. fluid—and sometimes they need cardiac support. Sometimes they need an entirely different therapy, such as relief of cardiac tamponade.

Shock is a big topic, and we will explore its subtleties another time. For now, let’s just talk about pressors.


There are numerous drugs often referred to as “pressors,” but some important distinctions can be made. Let’s draw a few lines to build the major categories.

A drug may or may not cause vasoconstriction—narrowing in diameter of the vasculature, primarily occurring at the arteriole level. (Some constriction on the venous side is also possible and may have therapeutic relevance, but is not as well understood and is probably not the active mechanism for most of the effect we see.) These are the agents that can most accurately be called vasopressors, or merely pressors.

Many of these drugs also have an effect on the heart. Generally, this is a stimulatory effect of supporting or augmenting cardiac output. When necessary, this can be divided into effects of positive inotropy (making the heart squeeze harder) and positive chronotropy (making the heart squeeze faster). On occasion it is even useful to discuss lusitropy (how fast the heart relaxes), dromotropy (how fast the heart’s electrical system conducts), or other changes, but in general, a drug will either stimulate or depress all of these pathways together. Thus, when these distinctions are not important, a drug whose primary effect is cardiac augmentation is often referred to simply as an inotrope.

Many drugs have both vascular and cardiac effects. We could therefore describe a combined category of inopressors (though this useful term is not universally understood), agents that cause both vasoconstriction and increased cardiac output. And finally, there is the distinct group of agents that support the heart, but dilate the vasculature, reducing cardiac afterload; these are inodilators, used primarily in cardiogenic shock.

Stepping back from the clinical effects, we can also consider which receptors are in play. The majority of pressors and inotropes make use of catecholamine (or adrenergic) receptors, binding either alpha (α in the Greek alphabet; for ease of typing we will transliterate the Greek characters here) or beta (β) receptors. Alpha usually means alpha-1, found predominantly in the vasculature and causing vasoconstriction when activated. Beta typically means the beta-1 receptors found in the heart, causing positive inotropy (and the other cardiac effects mentioned above), although most of our agents are fairly non-specific and will also bind beta-2 receptors in the lungs, yielding bronchodilation. The ligands for these receptors will be the catecholamine hormones, such as epinephrine. However, non-catecholamine-based pressors also appear in our armamentarium and bind to other classes of receptor.

Tune in for Part II, where we’ll talk about the two most frequently-used inopressors in most ICUs: norepinephrine and epinephrine.

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