Inotropic agents

Norepinephrine

Brand names: Levophed

Usual dose: 0 to 50 mcg/min IV (adults). Doses larger than 50 mcg/min can be given but often have little incremental effect. Very large doses can lead to limb ischemia.

What it’s good for: norepinephrine is the go-to pressor and inotropic agent in many critical care units. It has strong alpha, beta-1, and beta-2 receptor activity. It has excellent vasoconstrictive effects and moderate inotropic and chronotropic effects. It should increase MAP (mean arterial pressure) and total peripheral vascular resistance. Despite its positive inotropic and chronotropic effects, depending on the patient it can have a net positive or net negative effect on cardiac output. Norepinephrine was compared to dopamine in the setting of acute shock in the SOAP-2 trial (2010). In that trial, there were no significant differences in mortality although dopamine was associated with more arrhythmias.

Dopamine

Brand names: Intropin

Usual dose: 1 to 8+ mcg/kg/minute (1 to 3 mcg/kg/minute for patients in renal failure, and 3 to 8 mcg/kg/minute for patients with heart failure)

What it’s good for: dopamine should be available in pre-mixed form in most crash carts. This makes it a go-to pressor in times of emergency. At lower doses it is a mild inotrope and does not affect MAP. At higher doses, dopamine has strong alpha and beta-1 receptor activity and has strong vasoconstrictive and chronotropic effects. Dopamine also increases total peripheral vascular resistance at higher doses.

Epinephrine

Brand names: Adrenaline

Usual dose: 0.01 to 0.10 mcg/kg/minute

What it’s good for: at low doses, epinephrine interacts with mainly beta-1 and beta-2 receptors. It causes mild vasodilation while providing inotropic and chronotropic effect. At higher doses, it causes strong vasoconstriction through its interactions with the alpha receptor, and increases MAP, cardiac output, and total peripheral vascular resistance.

Cardiac inotropic agents

The following two agents, milrinone and dobutamine, are inotropes that can also increase cardiac output. This makes them potentially useful in situations involving heart failure, even diastolic dysfunction in the case of milrinone.

Milrinone

Brand names: Primacor

Usual dose: 0.125 to 0.750 mcg/kg/minute

What it’s good for: milrinone is a phosphodiesterase inhibitor. It increases cardiac output while causing vasodilation and lowering total peripheral vascular resistance. It is a moderate inotrope and mild chronotrope.

Dobutamine

Brand names: Dobutrex

Usual dose: 2.5 to 15.0 mcg/kg/minute

What it’s good for: dobutamine main appeal is that it is an inotrope without being a chronotrope, and it increases cardiac output. However it causes vasodilation and mildly reduces total peripheral vascular resistance. It’s net effect on MAP can be positive or negative. It has strong beta-1 and beta-2 activity, and mild alpha activity.

Vasopressors

Vasopressin

Brand names: Pitressin, Vasostrict

Usual dose: 0.02 to 0.05 units/minute

What it’s good for: vasopressin causes vasoconstriction and increases MAP. It has no other consistent hemodynamic effects. Combining vasopressin with norepinephrine in early shock may reduce the risk of renal failure requiring dialysis.

Phenylephrine

Brand names: none known

Usual dose: highly variable, IV boluses of 100 mcg to 500 mcg every 10 minutes as needed, or IV infusion of 40 to 60 mcg/minute after an initial infusion of 100 to 180 mcg/min.

What it’s good for: in the operating room, phenylephrine is given in small doses to increase blood pressure. It has strong alpha receptor activity. It causes vasoconstriction moreso than vasopressin, increases MAP, and increases total peripheral vascular resistance. It has a neutral to negative effect on cardiac output.

Approach in the setting of shock

Inotropes

References

TJ Ellender, JC Skinner. The use of vasopressors and inotropes in the emergency medicine treatment of shock. Emergency Medicine Clinics of North America 26(3):749-771 (2008)

CB Overgaard, V Dzavik. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. Circulation 118:1047-1056 (2008)