Norepinephrine is an a-receptor agonist that promotes widespread vasoconstriction. As a result of early reports of renal failure from norepinephrine, combined with a general decrease in enthusiasm for vasoconstrictor drugs, norepinephrine is no longer considered a first-line drug for the management of circulatory shock. In cases of hypotension refractory to dopamine, it can be added as a second agent.

There is some renewed interest in norepinephrine because of reports showing that there is less vasoconstriction and even improved organ perfusion in response to norepinephrine in patients with septic shock. However, it seems foolish to expect that a switch to norepinephrine will improve the clinical outcome in septic shock.


Norepinephrine produces a dose-dependent increase in systemic vascular resistance. Although the drug can stimulate cardiac b-receptors over a wide range, the cardiac output is increased only at low doses. Over the remainder of the therapeutic dose range, the inotropic response to norepinephrine is overshadowed by the vasoconstrictor response. At high dose rates, the cardiac output decreases in response to the vasoconstriction and increased afterload.


In cases of septic shock where the desired vasoconstriction is not achieved by a dopamine infusion norepinephrine can be added as a second drug.


One milligram of norepinephrine is added to a diluent volume of 250 mL (4 ug/mL). The infusion should be begun at 1 ug/min (15 microdrops/min) and titrated to the desired effect. The usual dose rate is 2 to 4 ug/min, with a range of 1 to 12 ug/min. The effective dose of norepinephrine can vary widely, and in clinical reports involving patients with septic shock, the effective norepinephrine dose has varied from 0.7 to 210 ug/min.


The administration of any vasoconstrictor agent carries a risk of hypoperfusion and ischemia involving any tissue bed or vital organ. For any condition that requires vasoconstrictor drugs to maintain a blood pressure, it may be difficult to distinguish adverse drug effects and adverse disease effects. Furthermore, if an adverse drug effect is identified or suspected, there may be little or no room for therapeutic manipulations.

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