Vasopressors Used in Shock/ICU

Vasopressor-dependent shock carries an average 28-day mortality of approximately 35% to

50%. Reduce the need for pressors by first prioritizing adequate fluid resuscitation. 

Alpha-1 Receptors Beta-1 Receptors Beta-2 Receptors

Vasoconstriction Cardioacceleration Vasodilation

Iris dilation Increased cardiac contractility Bronchodilation

Piloerection Lipolysis Increased glycolysis

Vasoconstrictor Agents

a)      Norepinephrine

i)       MOA: stimulates alpha-adrenergic receptors predominantly and beta-1 adrenergic

receptors causing increased contractility and heart rate as well as vasoconstriction;
increases BP

ii)      Dosing: Initial 0.05 to 0.15 mcg/kg/min and titrate to goal MAP (~65 mmHg); usual
dose range is 0.025 to 1 mcg/kg/min

iii)     ADRs: extravasation, tachycardia, peripheral vascular insufficiency

iv)     Clinical pearls: universal first line option for shock states (that persists after adequate
fluid replacement), administer infusions into a large vein, severe hypotension may occur
with abrupt discontinuation

b)      Epinephrine

i)       MOA: stimulates alpha, beta1, and beta2-adrenergic receptors resulting in relaxation of

smooth muscle of the bronchi, cardiac stimulation, and dilation of skeletal muscle
vasculature

Small doses can cause vasodilation via beta 2-vascular receptors; large doses may produce
constriction of skeletal and vascular smooth muscle

ii)      Dosing: 0.01 to 0.5 mcg/kg/min; titrate to goal MAP

iii)     ADRs: extravasation, tachyarrhythmias, pulmonary edema, renal blood vessel

constriction (decreased urinary output), may transiently increase BG levels, headache

iv) Clinical pearls: may be used as an adjunct therapy with norepinephrine; also used for
hypersensitivity reactions; central line preferred, sensitive to light (oxidation turns it pink
then brown)

c)      Phenylephrine

i)       MOA: potent, direct-acting alpha-adrenergic agonist with virtually no beta-adrenergic

activity; produces systemic arterial vasoconstriction

Increases in systemic vascular resistance (SVR) may result in dose-dependent increases in

systolic and diastolic blood pressure and reductions in heart rate and cardiac output (most
noticeable in patients with preexisting cardiac dysfunction)

ii)      Dosing: 0.5 to 6 mcg/kg/min; titrate to goal MAP

iii)     ADRs: rapid increase in BP can cause reflex bradycardia, reduced CO, peripheral
vascular insufficiency, acidosis, decreased renal and bowel perfusion
 iv)     Clinical pearls: use extreme caution in patients with heart failure; some dosage forms
may contain sodium benzoate which has been associated with potentially fatal “gasping
syndrome” in neonates

d)      Vasopressin

i)       MOA: stimulates a family of arginine vasopressin (AVP) receptors, oxytocin receptors,

and purinergic receptors

At therapeutic doses used for vasodilatory shock, stimulates the V1 receptor and increases
SVR and MAP; in response to these effects, a decrease in HR and CO may be seen

At pressor doses, also causes smooth muscle contraction in the GI tract by stimulating
muscular V1 receptors and release of prolactin and ACTH via V3 receptors

ii)      Dosing: Initial- 0.03 units/min. If the target blood pressure response is not achieved,
titrate up by 0.005 units/minute at 10 to 15-minute intervals (maximum dose: 0.1 units/min)

iii)     ADRs: reversible diabetes insipidus may occur following discontinuation, extravasation,
use with caution in patients with history of migraines, renal impairment, may cause “water
intoxication” and hyponatremia (drowsiness, headache, can lead to seizures/coma)

iv)     Clinical pearls: Doses >0.04 units/min are associated with coronary vasoconstriction
and peripheral necrosis; can cause coronary or bowel ischemia at high doses; vasopressin
increases factor VIII levels and may be useful in hemophiliacs

e)      Dopamine

i)       MOA: Dose-dependent effects

 Low doses (1-3 mcg/kg/min): mainly dopaminergic stimulating which dilates renal and cerebral
vasculature
 Intermediate doses (3-10 mcg/kg/min): beta-1 adrenergic receptor stimulation increases;
produces elevations in CO and MAP
 High doses (10-20 mcg/kg/min): alpha-1 adrenergic receptor stimulation increases along with
stimulation of endogenous norepinephrine causes increase in SVR

ii)      Dosing: 2 to 20 mcg/kg/min; titrate to goal MAP or end-organ perfusion

iii)     ADRs: contraindicated in uncorrected tachyarrhythmias and patients with

hypersensitivity to sulfites (commercial preparation contains sodium bisulfite);
extravasation, electrolyte imbalances (K and Mg), tissue necrosis/gangrene

iv)     Clinical pearls: the endogenous precursor to norepinephrine and epinephrine;

associated with increased risk of tachyarrhythmias and mortality compared to
norepinephrine, use with caution in patients taking MAO inhibitors (prolonged HTN)
Ionotropic Agents 

a)      Dobutamine

i)       MOA: stimulates myocardial beta1-adrenergic receptors primarily by the (+)

enantiomer and some alpha1 receptor agonism by the (-) enantiomer which results in
increased contractility and heart rate and stimulates both beta 2- and alpha1-receptors in the
vasculature

ii)      Dosing: Initial dose- 0.5 to 5 mcg/kg/min; titrate based on clinical endpoint (ex. BP, end-
organ perfusion); Usual dosing range- 2 to 20 mcg/kg/min; MAX dose: 20 to 40
mcg/kg/min

iii)     ADRs: ventricular arrhythmias, hypotensive or hypertensive (more common),

electrolyte imbalances, contraindicated in patients with hypersensitivity to sulfites (in some
formulations)

iv)     Clinical pearls:  produces a dose-dependent increase in HR, doses >20 mcg/kg/min not
recommended in heart failure and are considered salvage therapy (increased risk of death in
these patients), use with caution in patients taking MAO inhibitors (prolonged HTN)

c)      Milrinone

i)       MOA: selective phosphodiesterase inhibitor in cardiac and vascular tissue, resulting in

vasodilation and inotropic effects with little chronotropic activity

ii)      Dosing: 0.125 to 0.75 mcg/kg/min; titrate based on clinical end point (ex. end organ
perfusion)

iii)     ADRs: ventricular arrhythmias, hypotension, electrolyte imbalances, renal impairment

iv)     Clinical pearls: usually used in heart failure, does not produce tolerance like the
catecholamines
Pharmacotherapy Update on the Use of Vasopressors and Inotropes in the Intensive Care Unit. JC Jentzer, JC Coons, CB Link, M
Schmidhofer. Journal of Cardiovascular Pharmacology and Therapeutics. 2015, Vol. 20(3) 249-260. DOI: 10.1177/
1074248414559838