Home | | Anesthesiology | Adrenergic Agonists: Norepinephrine

Chapter: Clinical Anesthesiology: Clinical Pharmacology: Adrenergic Agonists & Antagonists

Adrenergic Agonists: Norepinephrine

Direct α1-stimulation with little β2-activity induces intense vasoconstriction of arterial and venous vessels.

NOREPINEPHRINE

Clinical Considerations

Direct α1-stimulation with little β2-activity induces intense vasoconstriction of arterial and venous vessels. Increased myocardial contractility from β1-effects, along with peripheral vasoconstriction,contributes to a rise in arterial blood pressure. Both systolic and diastolic pressures usually rise, but increased afterload and reflex bradycardia prevent any elevation in cardiac output. Decreased renal and splanchnic blood flow and increased myocar-dial oxygen requirements limit the outcome benefits of norepinephrine in the management of refrac-tory shock. Norepinephrine has been used with an α-blocker (eg, phentolamine) in an attempt to take advantage of its β-activity without the pro-found vasoconstriction caused by its α-stimulation. Extravasation of norepinephrine at the site of intra-venous administration can cause tissue necrosis.

Dosing & Packaging

Norepinephrine is administered as a bolus (0.1 mcg/ kg) or usually as a continuous infusion due to its short half-life at a rate of 2–20 mcg/min. Ampules contain 4 mg of norepinephrine in 4 mL of solution.

Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail
Clinical Anesthesiology: Clinical Pharmacology: Adrenergic Agonists & Antagonists : Adrenergic Agonists: Norepinephrine |


Privacy Policy, Terms and Conditions, DMCA Policy and Compliant

Copyright © 2018-2023 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.