Sympathomimetic- Norepinephrine Flashcards Preview

Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso > Sympathomimetic- Norepinephrine > Flashcards

Flashcards in Sympathomimetic- Norepinephrine Deck (31)
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1
Q

NE receptors

A

a1 a2 b1

minimal b2 per flood

2
Q

what medication is the immediate precursor to EPI

A

NE

3
Q

NE activates beta 1 which increases what 3 things in the heart

A

HR, conduction, and contractility

4
Q

NE is a potent alpha 1 agonist - what are the effects

A

intense arterial and venous vasoconstriction in all vascular beds

5
Q

does NE vasoconstrict the coronary arteries

A

no

6
Q

NE causes greater increase in what 4 things related to BP compared to EPI

A

SVR, SBP, DBP & MAP

7
Q

NE heart rate change is minimal due to what

A

baroreceptor reflexes triggered by arterial vasoconstriction are counter acted by beta 1 mediated increases in HR

8
Q

EPI or NE has a greater chronotropic effect

A

EPI

9
Q

higher doses of NE- what effect predominates

A

vasoconstriction

10
Q

NE and EPI increases total peripheral vascular resistance more than which drug

A

dobutamine

11
Q

what are the NE metabolic effects

A

minimal

12
Q

what are the effects in the blood sugar with NE

A

hyperglycemia is unlikely

13
Q

IV NE has intense vasoconstriction of what body systems

A

skeletal muscle
liver
kidneys
skin vascular beds

14
Q

NE has peripheral vasoconstriction such that what condition is seen

A

metabolic acidosis

15
Q

continuous infusion of NE dose

A

2-16mcg/min

16
Q

why do we place NE in a 5% glucose solution

A

prevents oxidation of the drug

17
Q

chronic infusion or increase in circulation of NE may be associated with what three things

A

pheochromocytoma

precapillary vasoconstriction

loss of protein free fluid into the extracellular spcae

18
Q

what additional monitoring is needed with NE

A

hemodynamic monitoring

19
Q

what additional vascular access do we need with NE

A

CVL- due to risk of extravasation

20
Q

metabolism of NE

A

eliminated by REUPTAKE into the ADRENERGIC NERVE ENDINGS where it is stored for future release

  • only small amounts are metabolized
21
Q

NE is a first line agent to treat

A

refractory hypotension during severe sepsis

22
Q

after a CABG- why give NE

A

treat low systemic vascular resistance

23
Q

what is the primary use for NE

A

potent vasoconstrictor to increase PVR and MAP

24
Q

NE effects in splanchnic blood flow and UOP in severely hypotensive septic patients

A

increase in blood flow and urine output

25
Q

Why is NE used cautiously in patients with RV failure

A

alpha effects of…
increases PAWP
increases right partial pressure

26
Q

NE and increased peripheral resistance and increased after load will result in what

A

decreased CO and increase work of LV

27
Q

NE & hr

A

may cause tachycardia- more seen with EPI

28
Q

side effect of NE

A

organ ischemia

29
Q

NE and renal effects

A

renal arterial vasoconstriction may lead to oliguria and renal failure

30
Q

large doses of NE and adequate fluids volume resuscitation can do what to renal blood flow

A

increase perfusion pressure of renal blood flow

31
Q

how does NE augment stroke volume and CO

A

vasoconstriction and increase venous return due to decrease venous capacitance

(The measure of a BLOOD VESSEL’s ability to increase the volume of BLOOD it holds without a large increase in BLOOD PRESSURE. Thevascular capacitanceis equal to the change in volume divided by the change in pressure).