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# Norepinephrine
## Overview
Norepinephrine is a potent vasopressor and inotropic agent that acts on alpha- and beta-adrenergic receptors. It increases systemic vascular resistance and myocardial contractility, leading to an increase in blood pressure.
## Primary Indications
* Severe hypotension requiring vasopressor support, particularly in septic shock and cardiogenic shock.
* Cardiac arrest (as an adjunct to ACLS).
## Adult Dosing
* **Hypotension:** Typically initiated at 0.01 to 0.05 mcg/kg/min and titrated to achieve target MAP (often $\ge$ 65 mmHg). Usual maintenance doses range from 0.01 to 0.3 mcg/kg/min. Higher doses may be required in severe cases.
* **Cardiac Arrest:** 1 mg IV push every 3-5 minutes as needed.
## Pediatric Dosing
* **Hypotension:** Typically initiated at 0.05 to 0.1 mcg/kg/min and titrated to achieve target MAP. Usual maintenance doses range from 0.05 to 2 mcg/kg/min.
* **Cardiac Arrest:** 0.01 mg/kg IV/IO (10 mcg/kg), maximum 1 mg. Repeat every 3-5 minutes.
Dosing for both adults and pediatrics, especially for hypotension, is highly individualized and often guided by local protocols and institutional guidelines.
## Dose Adjustments
No specific dose adjustments for renal or hepatic impairment are established, but careful titration is essential given potential alterations in drug metabolism and excretion.
## Contraindications
* Hypersensitivity to norepinephrine.
* Severe peripheral or mesenteric vascular thrombosis (risk of exacerbating ischemia).
* Use during general anesthesia with cyclopropane or halogenated hydrocarbon anesthetics (risk of severe hypertension and arrhythmias).
## Adverse Effects
Common: Hypertension, bradycardia (reflex), peripheral ischemia, tissue necrosis (extravasation), headache, anxiety, tremor, dizziness. Less common: Arrhythmias, reduced blood flow to vital organs.
## Key Drug Interactions
* **Monoamine Oxidase Inhibitors (MAOIs) and Tricyclic Antidepressants (TCAs):** Potentiate hypertensive effects; may require significantly reduced initial doses or avoidance.
* **Beta-blockers:** May potentiate alpha-agonist effects, leading to unopposed alpha-stimulation and severe hypertension.
* **Alpha-blockers:** May decrease pressor effects.
* **Oxytocics:** Can cause severe persistent hypertension.
* **Ergot alkaloids, Guanethidine, Methyldopa:** May potentiate pressor effects.
## Monitoring
* Continuous blood pressure monitoring (arterial line preferred).
* Heart rate and rhythm.
* Urine output.
* Peripheral perfusion (skin temperature, color, capillary refill).
* Central venous pressure (if available and relevant).
* Assess for signs of extravasation.
## Clinical Pearls
* Administer via a central venous catheter to minimize the risk of extravasation and tissue necrosis. If peripheral IV administration is necessary, use a large vein, dilute significantly, and monitor closely.
* Have phentolamine or another alpha-adrenergic blocker readily available to treat extravasation and resultant tissue ischemia.
* Titrate to the lowest effective dose to achieve target MAP and organ perfusion, avoiding excessive hypertension.
* Norepinephrine infusion should not be stopped abruptly; taper gradually.
* In septic shock, norepinephrine is generally the first-line vasopressor.
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*Disclaimer: This information is intended for healthcare professionals. Always verify the most current prescribing information and consult relevant clinical guidelines and institutional protocols before use.*
