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Flashcards in Norepinephrine (NE) Deck (32):
1

What is the trade name for NE?

Levophed

2

What is the formal drug classification of NE?

NE is a direct acting catecholamine and adrenergic agonist

3

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!!!!!)

4

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

5

What is the MOA of NE?

NE binds to alpha and Beta-1 receptors and has DIRECT acting effects in a dose related manner;

6

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.

7

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!

8

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

9

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

10

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

11

What is the onset of IV NE?

RAPID

12

What is the DOA of NE?

limited

13

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

14

Where is monoamine oxidase (MAO) present, and how does it work?

present in the Liver, Kidneys, and GI tract, which catalyzes oxidative deamination

15

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

16

What is the urine metabolite of NE, and how much is normally excreted in a 24hr period?

Vanillylmandelic acid; 2-4mg in a 24hr period

17

What is the elimination route of NE?

25% of circulating NE is extracted during a single passage through lungs in normal resting ppl

18

What is the e 1/2 life for NE?

2.5 minutes

19

What are the side effects of NE usually the result of?

intense vasoconstriction; ischemic injury results from potent vasoconstrictor action and tissue hypoxia

20

What can happen/signs and symptoms from overdose of NE?

Severe HTN with violent headache, photophobia, stabbing retrosternal chest pain, pallor, intense sweating, and vomiting

21

What are the CV side effects of NE?

-sudden increase in SVR causes reflex baroreceptor mediated bradycardia despite active Beta stimulation

22

When should NE be used cautiously?

-in the management of cardiogenic shock due to vasoconstriction that increases the pressure work of the LV and has an adverse effect of the oxygen economy of the ischemic pump
-also further vasoconstriction and end organ ischemia in a syndrome in which intense constriction may already have occurred

23

What are the contraindications to NE?

-should not be given to patients who are Hypotensive from blood volume deficits except in emergency situations where cardiac and cerebral perfusion is necessary until blood volume has been replaced
-should not be used in patients with mesenteric or peripheral vascular thrombosis due to risk of increasing ischemia and extending area of infarction

24

When NE is given with either ____________ or ____________, it can significantly induce cardiac arrhythmias such as Vtach or Vfib

Cyclopropane and Halothane anesthetics

25

What drugs if taken with NE can produce severe, prolonged HTN or HTN crisis?

MAOIs or
Antidepressants of the triptyline or imipramine types

26

What can happen if NE and beta-blockers are administered together?

Beta-blockers can increase the hypertensive effect, thus avoid concurrent use

27

What can happen if NE and cocaine are administered together?

Cocaine can induce malignant arrhythmias

28

What drugs if given with NE can increase pressor response? (hint: 4)

Methyldopa
Guanethidine
TCAs
Reserpine

29

What is the standard concentration of NE?

4mg/250mL; 16mcg/mL

30

What is the dosage of NE?

0.01-0.1 mcg/kg/min OR
4-16 mcg/min IV

31

What is something to consider when administering Intravascular NE?

Should be given through a CENTRALLY placed IV to avoid tissue necrosis from extravasation

32

If extravasation of NE occurs, what should you do?

infiltrate the area immediately with 10-15mL of saline solution containing 5mg-10mg of PHENTOLAMINE (an adrenergic blocking agent) with a hypodermic needle. This will prevent sloughing and necrosis of the area