Direct α1-stimulation with little β2-activity induces intense vasoconstriction of arterial and venous vessels. Increased myocardial contractility from β1-effects, along with peripheral vasoconstriction,contributes to a rise in arterial blood pressure. Both systolic and diastolic pressures usually rise, but increased afterload and reflex bradycardia prevent any elevation in cardiac output. Decreased renal and splanchnic blood flow and increased myocar-dial oxygen requirements limit the outcome benefits of norepinephrine in the management of refrac-tory shock. Norepinephrine has been used with an α-blocker (eg, phentolamine) in an attempt to take advantage of its β-activity without the pro-found vasoconstriction caused by its α-stimulation. Extravasation of norepinephrine at the site of intra-venous administration can cause tissue necrosis.
Norepinephrine is administered as a bolus (0.1 mcg/ kg) or usually as a continuous infusion due to its short half-life at a rate of 2–20 mcg/min. Ampules contain 4 mg of norepinephrine in 4 mL of solution.