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# Norepinephrine
## Overview
Norepinephrine is a potent catecholamine acting primarily on alpha-1 adrenergic receptors (vasoconstriction) and, to a lesser extent, beta-1 adrenergic receptors (inotropic effect). It is the first-line vasopressor for distributive (septic) shock.
## Primary Indications
* Acute hypotension (e.g., profound hypotension in septic, cardiogenic, or neurogenic shock)
* Adjunct in cardiac arrest (less common than epinephrine)
## Adult Dosing
* **Initial:** 0.05 to 0.1 mcg/kg/min (or 5–30 mcg/min).
* **Titration:** Titrate to clinical goal (usually MAP ≥ 65 mmHg) in increments of 0.05 mcg/kg/min every 2–5 minutes.
* **Maintenance Range:** Typically 0.01 to 3 mcg/kg/min; some refractory cases may require higher doses, though this increases risk of ischemia.
## Pediatric Dosing
* **Initial:** 0.05 to 0.1 mcg/kg/min.
* **Titration:** Titrate based on hemodynamic response.
* **Maximum:** Doses up to 2 mcg/kg/min have been used; clinical protocols vary significantly by institution.
## Dose Adjustments
* **Hepatic/Renal Impairment:** No specific dose adjustments established.
* **Refractory Shock:** If requirements exceed 0.5–1 mcg/kg/min, consider adding second-line agents (vasopressin or epinephrine) to minimize alpha-adrenergic toxicity.
## Contraindications
* Hypersensitivity to norepinephrine or sulfites.
* Hypotension due to uncorrected blood volume deficit (except as emergency support during fluid resuscitation).
* Mesenteric or peripheral vascular thrombosis.
## Adverse Effects
* **Cardiovascular:** Tachycardia, arrhythmias (atrial or ventricular), hypertension, bradycardia (reflex).
* **Extravasation:** Significant risk of tissue necrosis and sloughing due to intense vasoconstriction.
* **Metabolic:** Hyperglycemia, lactic acidosis.
* **Peripheral:** Digital ischemia, limb ischemia.
## Key Drug Interactions
* **MAO Inhibitors/Tricyclic Antidepressants:** May cause severe, prolonged hypertension.
* **Beta-blockers:** May cause unchecked alpha-mediated vasoconstriction and reflex bradycardia.
* **Anesthetics:** Halogenated hydrocarbons (e.g., halothane) may increase myocardial sensitivity to catecholamines, increasing arrhythmia risk.
## Monitoring
* **Continuous ECG:** Monitor for rate and rhythm disturbances.
* **Hemodynamics:** Arterial line recommended for precise BP monitoring and titration.
* **Perfusion:** Regular assessment of distal extremities for signs of ischemia.
* **Access site:** Monitoring for signs of extravasation (pallor, coldness, hardness at site).
* **MAP:** Target established by protocol (typically 65 mmHg).
## Clinical Pearls
* **Extravasation Management:** If extravasation occurs, stop the infusion immediately but do not remove the cannula initially; attempt to aspirate remaining drug. Administer **phentolamine** (5–10 mg in 10 mL saline) subcutaneously to the affected area promptly to counteract local vasoconstriction.
* **Administration:** Must be administered via a **central venous catheter** whenever possible to minimize necrosis risk. If peripheral administration is necessary, use the largest possible vein (proximal) and minimize duration.
* **Compatibility:** Highly compatible with most critical care infusions, but verify Y-site compatibility before co-administration.
* **Concentration:** Always verify dosing units (mcg/min vs. mcg/kg/min) to avoid significant medication errors.
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*Disclaimer: This information is for educational purposes and does not replace institutional clinical guidelines. Verify all doses and local protocols against current hospital formulary and prescribing information before administration.*
