Pressors and Inotropes


a1, b1, minimal b2


Only presser to show better outcome if started early in septic shock

More rapid and effective BP control with less tachycardia and arrythymia than dopamine

Vasopressin v1

0.04 units/min

may work independently from catecholamines by decreasing NO production

has the theoretical disadvantage of constricting coronaries and pulm vasculature. can cause MI in high doses in cardiac patients.

phenylephrine a1


slight decrease in HR, good for tachyarrhthymias

dopamine D, B1, B2, a1

2 – 20 mcg/kg/min

0.5 – 3 mcg/kg/min – Dopamine receptors in the renal, mesenteric, and cerebral circulations causes increases blood flow. In the kidneys in vitro, dopamine increases urinary sodium and water excretion that is independent of the changes in renal blood flow.

3-7.5 mcg/kg/min – Dopamine stimulates b-receptors in the heart and peripheral circulations, and this produces an increase in cardiac output.

>7.5 mcg/kg/min – Dopamine produces a dose-dependent activation of a-receptors in the systemic and pulmonary circulations. This results in progressive vasoconstriction

Decreases prolactin and possibly causes immunosuppressive effect. Tachycardia and arrhythmia potential. Increase in pulmonary shunting. Low dose dopamine effective in in vitro but no effect in RCTs. Median dose for restoring MAP is 15mcg/kg/min.

Epinephrine B1, B2, a1, a2


Dobutamine B1 > B2,minimal a1, a2


Increases CI by 12-61% in septic shock studies. Increases blood flow to gut and kidneys.

Tachycardia with arrhythmia potential. Can lower SVR and BP.

Milrinone increases cAMP to increase Ca influx

0.375 – 0.75 mcg/kg/min

Causes hypotension and has long half life.

Pulmonary vasodilator.

Isoproterenol B1 B2

0.01 – 0.2 mcg/kg/min

Increases HR, bronchodilation, and contractility. Can cause hypotension.

Use in atropine resistant bradycardia, heart block after cardiac surg, or b-blocker overdose.