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# Norepinephrine
## Overview
Norepinephrine is a potent vasopressor that acts as an alpha-1 adrenergic agonist, causing vasoconstriction and increasing systemic vascular resistance. It also has beta-1 adrenergic activity, which can increase heart rate and contractility, though this effect is often blunted by reflex bradycardia.
## Primary Indications
* Severe hypotension and shock, particularly when unresponsive to fluid resuscitation.
* Cardiogenic shock.
* Septic shock.
## Adult Dosing
* **Initial dose:** 0.01 to 0.05 mcg/kg/min intravenously (IV).
* **Titration:** Increase dose in increments of 0.01 to 0.05 mcg/kg/min every 5-15 minutes as needed to achieve target blood pressure (e.g., mean arterial pressure [MAP] ≥ 65 mmHg).
* **Maximum dose:** Typically up to 0.5 mcg/kg/min IV, though higher doses may be used in refractory shock under expert guidance. Dosing is often guided by institutional protocols.
## Pediatric Dosing
* **Initial dose:** 0.05 to 0.1 mcg/kg/min IV.
* **Titration:** Increase dose in increments of 0.05 to 0.1 mcg/kg/min every 5-15 minutes.
* **Maximum dose:** Dosing varies significantly by indication and patient condition; refer to specific pediatric critical care guidelines or institutional protocols. Doses up to 1-2 mcg/kg/min have been reported.
## Dose Adjustments
No specific dose adjustments are routinely recommended for renal or hepatic impairment, as norepinephrine is rapidly metabolized. Dosing is primarily guided by hemodynamic response.
## Contraindications
* Hypersensitivity to norepinephrine.
* Severe uncontrolled hypertension.
* Use during general anesthesia with cyclopropane or halogenated hydrocarbons (risk of severe hypertension and arrhythmias).
## Adverse Effects
* **Cardiovascular:** Hypertension, reflex bradycardia, arrhythmias, peripheral ischemia, necrosis (especially with extravasation), decreased cardiac output (at very high doses).
* **Neurologic:** Headache, anxiety, tremor.
* **Other:** Hyperglycemia, dyspnea.
## Key Drug Interactions
* **Monoamine Oxidase Inhibitors (MAOIs) & Tricyclic Antidepressants (TCAs):** Potentiate pressor response; avoid or use with extreme caution and significantly reduced initial doses.
* **Beta-blockers:** May potentiate alpha-adrenergic effects, leading to severe hypertension.
* **Alpha-blockers:** May antagonize the vasoconstrictive effects.
* **Ergot alkaloids & Oxytocics:** May cause severe, prolonged hypertension.
* **Diuretics:** May potentiate hypotensive effects.
## Monitoring
* Continuous electrocardiogram (ECG) and invasive hemodynamic monitoring (e.g., arterial line).
* Central venous pressure (CVP) and pulmonary artery pressures (if available).
* Urine output.
* Peripheral perfusion (skin temperature, color, capillary refill).
* Lactate levels.
* Serum glucose.
## Clinical Pearls
* Administer via a central venous catheter to minimize risk of extravasation and tissue necrosis. If peripheral administration is unavoidable, use a large vein, monitor the site closely, and consider dilute solutions.
* If extravasation occurs, stop the infusion and infiltrate the area with phentolamine mesylate.
* Norepinephrine is a potent agent and requires continuous monitoring and titration.
* Taper infusions gradually to avoid rebound hypotension.
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*Please verify the current prescribing information for the most up-to-date and complete drug details.*
