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# Norepinephrine
## Overview
Norepinephrine (Levophed) is a potent endogenous catecholamine and sympathomimetic amine that acts as a vasopressor. It primarily stimulates alpha-1 adrenergic receptors, causing peripheral vasoconstriction and an increase in blood pressure. It also has some beta-1 adrenergic activity, increasing heart rate and contractility.
## Primary Indications
* Severe hypotension and shock (e.g., septic shock, cardiogenic shock) refractory to fluid resuscitation.
## Adult Dosing
* **Initial Dose:** 0.01 to 0.02 mcg/kg/minute, administered via continuous IV infusion.
* **Titration:** Increase dose by 0.01 to 0.02 mcg/kg/minute increments every 5 to 15 minutes as needed to achieve target MAP (typically $\geq$ 65 mmHg).
* **Maximum Dose:** Doses up to 0.5 mcg/kg/minute may be required in severe cases.
## Pediatric Dosing
* **Initial Dose:** 0.05 to 0.1 mcg/kg/minute, administered via continuous IV infusion.
* **Titration:** Increase dose by 0.05 to 0.1 mcg/kg/minute increments every 5 to 15 minutes as needed.
* **Maximum Dose:** Doses up to 1 mcg/kg/minute have been used.
*Note: Dosing in both adults and pediatrics should be guided by institutional protocols and patient response.*
## Dose Adjustments
* No specific dose adjustments are recommended for renal or hepatic impairment, but close monitoring is essential due to potential altered pharmacokinetics.
## Contraindications
* Hypersensitivity to norepinephrine.
* Hypotension due to relative hypovolemia (vasopressors should not be the primary treatment for hypovolemia; fluid resuscitation is paramount).
* Use during cyclopropane or halogenated hydrocarbon anesthesia due to potential for severe arrhythmias.
## Adverse Effects
* **Cardiovascular:** Arrhythmias (ventricular and atrial), bradycardia, hypertension, peripheral ischemia, vasoconstriction, extravasation leading to tissue necrosis.
* **Central Nervous System:** Headache, anxiety, dizziness.
* **Metabolic:** Hyperglycemia, lactic acidosis.
* **Other:** Dyspnea, reduced blood flow to vital organs (kidneys, brain, heart) with prolonged or high-dose use.
## Key Drug Interactions
* **Monoamine Oxidase Inhibitors (MAOIs):** Potentiate hypertensive crisis. Avoid concurrent use; if unavoidable, use extreme caution and consider dose reduction. A washout period of 14 days is generally recommended after MAOI discontinuation.
* **Tricyclic Antidepressants (TCAs):** May potentiate the pressor response. Use with caution.
* **General Anesthetics (e.g., Halothane, Cyclopropane):** Increased risk of arrhythmias.
* **Alpha- and Beta-Adrenergic Blockers:** May interfere with the pressor effects or cause additive effects.
* **Ergot Alkaloids, Guanethidine, Methyldopa:** May potentiate the pressor effect.
* **Diuretics:** May enhance the pressor effect by increasing vascular reactivity.
## Monitoring
* **Hemodynamics:** Continuous ECG, arterial blood pressure (MAP), central venous pressure (CVP), cardiac output (if available).
* **Perfusion:** Urine output, peripheral pulses, skin temperature, mental status.
* **Metabolic:** Blood glucose, serum lactate.
* **Infusion Site:** Frequent checks for signs of extravasation.
## Clinical Pearls
* Norepinephrine should be administered via a central venous catheter to minimize the risk of extravasation and tissue necrosis.
* If extravasation occurs, discontinue the infusion immediately. If blood flow is compromised, consider infiltration with an alpha-adrenergic blocking agent such as phentolamine.
* Norepinephrine infusion should be tapered gradually to avoid sudden hypotension.
* Ensure adequate intravascular volume status before and during norepinephrine administration.
* Monitor for signs of limb ischemia, especially in patients with peripheral vascular disease.
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*This information is intended for healthcare professionals. It is essential to consult the most current prescribing information and institutional guidelines for definitive patient care decisions.*
