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# Norepinephrine
## Overview
Norepinephrine is a potent vasopressor and inotrope that acts primarily on alpha-1 adrenergic receptors, causing vasoconstriction and increasing systemic vascular resistance. It also has some beta-1 adrenergic receptor activity, leading to increased myocardial contractility.
## Primary Indications
* Severe hypotension and shock, particularly septic shock and cardiogenic shock.
* To maintain adequate blood pressure during resuscitation efforts.
## Adult Dosing
* **Initiation:** Typically started as a continuous infusion at 0.01 to 0.05 mcg/kg/min.
* **Titration:** Titrated upward based on patient's hemodynamic response (e.g., mean arterial pressure [MAP] goal, typically >65 mmHg). Doses can range from 0.01 to 2 mcg/kg/min.
* **Maximum:** Doses up to 1 mcg/kg/min have been used, but higher doses increase the risk of adverse effects. Some protocols may allow for higher doses up to 10 mcg/kg/min for refractory shock, but this requires very close monitoring.
## Pediatric Dosing
* **Initiation:** Typically started as a continuous infusion at 0.05 to 0.1 mcg/kg/min.
* **Titration:** Titrated based on hemodynamic response, typically targeting MAP > gestational age + 2 years or >50 mmHg in older children. Doses can range from 0.05 to 1 mcg/kg/min.
* **Maximum:** Doses up to 2 mcg/kg/min may be used in refractory shock.
## Dose Adjustments
* No dose adjustment is typically needed for renal or hepatic impairment. However, careful monitoring is essential due to altered pharmacokinetics and pharmacodynamics.
## Contraindications
* Hypersensitivity to norepinephrine.
* Severe uncorrected hypotension secondary to volume deficit.
## Adverse Effects
* **Cardiovascular:** Arrhythmias (tachycardia, bradycardia, ventricular arrhythmias), hypertension, peripheral ischemia/vasoconstriction, angina, decreased cardiac output (at higher doses).
* **Local:** Extravasation can cause severe tissue necrosis and sloughing.
* **Other:** Headache, anxiety, dizziness, tremor, respiratory distress.
## Key Drug Interactions
* **Monoamine Oxidase Inhibitors (MAOIs) & Tricyclic Antidepressants (TCAs):** Potentiate the pressor effects of norepinephrine, leading to hypertensive crisis. Discontinue MAOIs at least 14 days prior to starting norepinephrine.
* **Alpha and Beta Blockers:** May antagonize or potentiate effects depending on receptor selectivity.
* **Ergot Alkaloids:** Can potentiate vasopressor effects.
* **Anesthetic Agents:** May increase the risk of arrhythmias.
## Monitoring
* **Hemodynamics:** Continuous arterial blood pressure monitoring is essential. Monitor heart rate, cardiac rhythm, central venous pressure (CVP), and pulmonary artery pressures if available.
* **Perfusion:** Monitor peripheral circulation (skin temperature, color, capillary refill), urine output, and mental status.
* **Infusion Site:** Frequent checks for signs of extravasation.
* **Electrolytes:** Monitor periodically, especially potassium.
## Clinical Pearls
* **Extravasation Management:** If extravasation occurs, immediately stop the infusion and aspirate any remaining drug. Infiltrate the affected area with phentolamine (an alpha-adrenergic blocker) diluted in saline.
* **Correct Volume Deficit First:** Norepinephrine is most effective when adequate intravascular volume is restored. Administer volume resuscitation before or concurrently with norepinephrine.
* **Central Line Preferred:** Due to risk of extravasation and tissue necrosis, administration via a large-bore central venous catheter is preferred.
* **Continuous Infusion:** Administered as a continuous infusion and must not be stopped abruptly. Taper gradually to avoid rebound hypotension.
* **Light Sensitivity:** Protect solutions from light.
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*This information is intended for healthcare professionals. Always consult the most current prescribing information and institutional protocols for definitive guidance.*
