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# Norepinephrine
## Overview
Norepinephrine is a vasopressor and inotropic agent that acts primarily on alpha-1 adrenergic receptors, causing vasoconstriction, and to a lesser extent on beta-1 adrenergic receptors, increasing cardiac output.
## Primary Indications
* Treatment of hypotension and shock, particularly septic shock and cardiogenic shock, unresponsive to fluid resuscitation.
## Adult Dosing
* **Initial Dose:** 0.01 to 0.02 mcg/kg/min IV.
* **Titration:** Titrate infusion rate upward by 0.005 to 0.01 mcg/kg/min every 5-15 minutes to achieve target mean arterial pressure (MAP), typically 65 mmHg or higher.
* **Maximum Dose:** Generally 0.1 to 0.3 mcg/kg/min IV, though higher doses may be used in refractory shock under expert guidance. Specific maximums can vary based on institutional protocol.
## Pediatric Dosing
* **Initial Dose:** 0.05 to 0.1 mcg/kg/min IV.
* **Titration:** Titrate infusion rate by 0.05 to 0.2 mcg/kg/min every 5-15 minutes to achieve target MAP (e.g., > 50 mmHg or age-based threshold).
* **Maximum Dose:** Generally 1 to 2 mcg/kg/min IV, but doses up to 10 mcg/kg/min have been used in specific circumstances. Dosing is highly protocol-dependent.
## Dose Adjustments
* No specific dose adjustments are typically required for renal or hepatic impairment, as norepinephrine is rapidly metabolized. However, close monitoring of response and potential for accumulation is crucial in patients with severe organ dysfunction.
## Contraindications
* Hypersensitivity to norepinephrine.
* Use with cyclopropane or halogenated hydrocarbon anesthetics (risk of severe hypertension and arrhythmias).
## Adverse Effects
* **Common:** Hypertension, reflex bradycardia, peripheral ischemia (due to vasoconstriction), headache, anxiety, tremor, extravasation leading to tissue necrosis.
* **Less Common:** Arrhythmias, decreased renal perfusion, decreased splanchnic perfusion.
## Key Drug Interactions
* **Anesthetics (volatile):** Increased risk of arrhythmias and hypertension.
* **MAO inhibitors & tricyclic antidepressants:** Potentiate pressor response, potentially causing hypertensive crisis. Discontinue MAOIs at least 14 days prior to starting norepinephrine.
* **Beta-blockers:** Can blunt the beta-1 effects of norepinephrine, leading to unopposed alpha-1 vasoconstriction and potentially worsening hypertension.
* **Alpha-blockers:** Can antagonize the vasoconstrictive effects of norepinephrine.
* **Oxytocic agents:** May cause severe persistent hypertension.
* **Ergot alkaloids:** Potentiate vasopressor effect.
## Monitoring
* Continuous hemodynamic monitoring: Heart rate, blood pressure (arterial line preferred), central venous pressure (if available), urine output.
* Assess for signs of adequate tissue perfusion (e.g., mental status, skin temperature, capillary refill).
* Monitor infusion site for signs of extravasation.
* Cardiac rhythm monitoring.
* Lactate levels.
## Clinical Pearls
* Norepinephrine is typically administered via a central venous catheter to minimize risk of extravasation and tissue damage.
* If extravasation occurs, stop the infusion and administer phentolamine locally as soon as possible.
* Titration is essential to achieve the desired hemodynamic effect while minimizing adverse events.
* In sepsis, norepinephrine is the first-line vasopressor after initial fluid resuscitation.
* The goal is not to normalize blood pressure but to restore adequate organ perfusion.
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**Disclaimer:** This information is intended for healthcare professionals. Always consult the official prescribing information and institutional guidelines for the most current and complete drug details before prescribing or administering any medication.
