Norepinephrine (NE) Flashcards
Please note that the drug card information is for Educational Use ONLY, and the source is from Carrie Bowman's glossary of drug cards permitted by use of Georgetown NAP students. No permission is given to use these cards for anything other than as a study resource for our program.
What is the trade name for NE?
Levophed
What is the formal drug classification of NE?
NE is a direct acting catecholamine and adrenergic agonist
What receptors does NE work on? Does NE have a preference for receptors?
Alpha and Beta-1»»Beta-2 (technically we believe it does NOT work at beta-2!!!!!)
What are the clinical uses of NE?
- NE is a potent vasoconstrictor generally used for patients with adequate cardiac output but low SVR in acute hypotensive episodes
- Preserves cerebral and coronary blood flow during hypotensive emergencies and is an adjunct in the treatment of cardiac arrest and profound hypotension
- one of the most useful drugs when intense activity is needed with reduced vascular tone states with or without cardiogenic shock, including separation from cardiopulmonary bypass or situations when other vasopressors fail to maintain a steady hemodynamic state
- also been shown to improve renal and splanchnic blood flow by increasing pressure provided the patient is volume resuscitated
What is the MOA of NE?
NE binds to alpha and Beta-1 receptors and has DIRECT acting effects in a dose related manner;
In general, what are the effects of NE in low doses?
- NE produces increased CO (inotropy and chronotropy) and BP
- once bound to a receptor, NE activates a specific class of G proteins. The G protein activates an effector protein such as the enzyme adenylate cyclase. Stimulation of thie enzyme causes increased production of cAMP.
What are the effects of NE in higher doses? What happens to coronary artery perfusion, and why?
- NE reduces flow because of alpha arteriolar constriction superseding the Beta-1 effects; the end result is unopposed alpha receptor stimulation and a decrease in vital organ flow
- coronary artery perfusion may be increased due to the increase in diastolic pressure!
Is NE a peripheral or central vasoconstrictor? What does this cause?
NE is a PERIPHERAL vasoconstrictor and causes a marked increase in peripheral vascular resistance and MAP
What does an increase in cAMP cause if the alpha-1 receptor is stimulated?
In alpha-1 receptors, cAMP will stimulate inward flux of calcium and facilitate the release of bound intracellular calcium causing vasoconstriction
What does an increase in cAMP cause if the Beta-1 receptor is stimulated?
In Beta-1 receptors, cAMP stimulates an influx of calcium, increasing cytoplasmic calcium concentrations. this enhances the intensity of actin and myosin interaction increasing myocardial contractility
What is the onset of IV NE?
RAPID
What is the DOA of NE?
limited
How is NE metabolized?
- It is inactivated by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) or both in the Blood, Liver, and Kidneys.
- NE that has undergone uptake will be metabolized in the cytoplasm by MAO and the excess NE that escapes uptake is metabolized by COMT
Where is monoamine oxidase (MAO) present, and how does it work?
present in the Liver, Kidneys, and GI tract, which catalyzes oxidative deamination
How does catechol-O-methyltransferase (COMT) work?
methylates the hydroxyl groups of catecholamines. Once methylated, the resulting metabolites are conjugated with glucuronic acid and normetanephrine
