Shock Syndromes I

agents used to treat septic shock will be discussed in section VII, Sepsis.

Vasoactive agents can be broadly differentiated to (1) vasopressors, (2) inotropes, or (3) vasodilators.

Vasoactive agents may have several of these properties.

longer fluid responsive) or in the setting of severe hypotension while fluids are being administered. In

addition, if a patient is severely hypotensive, vasopressors may be initiated together with additional

fluid administration, even if a patient is still fluid responsive, to ensure adequate end-organ perfusion.

Because there are no definitive criteria for when vasopressors should be initiated in relationship to fluid

administration, bedside clinicians must often make a patient-specific assessment and decision.

Vasopressor agents primarily exert pharmacologic benefit by augmenting SVR. Some vasopressors

may also increase CO. Table 4 highlights the receptor pharmacology of the various agents.

Once the decision to start a vasoactive agent is made, a vasoactive agent or inotrope is largely

selected on the basis of the agent that best achieves the desired pharmacodynamic effect(s) (e.g.,

increase in SVR or increase in CO). In most shock syndromes, limited literature exists to guide

optimal vasoactive agent selection.

Catecholamine vasopressors primarily increase blood pressure by increasing SVR through their

actions on α1-receptors. Differing α1, β1, and β2 activity leads to differing pharmacodynamic effects

between agents, as outlined in Table 4.

Vasopressin increases SVR through V1R activity in smooth muscles resulting in vasoconstriction.

Activity at V2R receptors lead to antidiuretic hormone effects in the kidney. Selective sparing

of V1R in some vascular beds or V2R-mediated vasodilation leads to decreased vasoconstrictive

effects of vasopressin in the coronary, cerebral, and pulmonary circulation.

vascular smooth muscle contraction. Activation of AT-R1 receptors also stimulates the release of

norepinephrine, vasopressin, adrenocorticotropic hormone (ACTH), and aldosterone. Activation of

AT-R2 receptors can counterbalance the vasoconstrictive effects of AT-R1 in some vascular beds.

Some clinicians use an initial intravenous push/bolus of vasopressors (“push dose pressors”) in

patients with hypotension that is either severe or expected to be short in duration (e.g., medication-

associated hypotension in the setting of endotracheal intubation). Common doses include

phenylephrine 100–200 mcg and norepinephrine 1–2 mcg, each given every 2–3 minutes. The

efficacy and safety is unclear because few studies have evaluated this approach.