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# Norepinephrine
## Overview
Norepinephrine is a potent alpha-1 adrenergic agonist and a less potent beta-1 adrenergic agonist. It primarily causes vasoconstriction, leading to increased systemic vascular resistance and blood pressure. Beta-1 effects can increase heart rate and contractility, but are often overridden by reflex bradycardia due to increased blood pressure.
## Primary Indications
* Severe hypotension and shock (e.g., septic shock, cardiogenic shock) refractory to fluid resuscitation.
## Adult Dosing
* **Initiation:** Typically 0.01 to 0.05 mcg/kg/min IV.
* **Titration:** Increase dose by 0.01 to 0.05 mcg/kg/min every 5-10 minutes as needed to achieve target blood pressure.
* **Maximum:** Doses up to 0.5 mcg/kg/min may be required in severe cases, though doses exceeding 0.1 mcg/kg/min are associated with increased risks. Target mean arterial pressure (MAP) is often 65 mmHg or higher, but may vary based on patient condition and local protocol.
## Pediatric Dosing
* **Initiation:** 0.05 to 0.1 mcg/kg/min IV infusion.
* **Titration:** Titrate by 0.05 to 0.2 mcg/kg/min every 10-15 minutes as needed to maintain adequate blood pressure.
* **Maximum:** Doses up to 1 mcg/kg/min have been used, but higher doses are associated with increased risk. Target MAP is often 40-50 mmHg or higher, or systolic blood pressure >70 mmHg, but may vary based on patient condition and local protocol.
## Dose Adjustments
* No dose adjustments are typically needed for hepatic or renal impairment, as norepinephrine is rapidly metabolized. However, clinical response must be closely monitored.
## Contraindications
* Hypersensitivity to norepinephrine.
* Should not be used as the sole agent to correct hypotension due to hypovolemia.
## Adverse Effects
* **Common:** Hypertension, bradycardia, peripheral ischemia (due to vasoconstriction), arrhythmias, anxiety, headache, dizziness, extravasation leading to tissue necrosis.
* **Serious:** Myocardial infarction, stroke, severe hypertension, rupture of the aorta.
## Key Drug Interactions
* **MAO inhibitors and Tricyclic Antidepressants:** Potentiate hypertensive effects. Discontinue MAO inhibitors at least 14 days prior to norepinephrine initiation.
* **Beta-blockers:** Can unmask or potentiate alpha-adrenergic effects, leading to severe hypertension and reflex bradycardia.
* **Ergot alkaloids, Oxytocin:** May cause severe hypertension.
* **Anesthetics (e.g., cyclopropane, halothane):** May increase myocardial irritability and risk of arrhythmias.
## Monitoring
* Continuous electrocardiogram (ECG) and blood pressure monitoring.
* Urine output.
* Peripheral circulation (e.g., color, temperature, capillary refill).
* Central venous pressure (CVP) and/or pulmonary artery pressures if available and indicated.
* Assess 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, stop the infusion immediately and infiltrate the affected area with phentolamine.
* It should be used with caution in patients with severe peripheral vascular disease, diabetes mellitus, or hypertension.
* Regularly reassess the patient's fluid status and consider other vasopressors or inotropes based on the underlying cause of shock.
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*This information is intended for healthcare professionals and does not replace current prescribing information or clinical judgment. Always consult the official product monograph or relevant clinical guidelines for complete and up-to-date information before making any treatment decisions.*
