Antiarrhythmic Agents Part 2 Flashcards

1
Q

Natural Catecholamines

A

Epinephrine
Norepinephrine
Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Synthetic Catecholamines

A

Isoproterenol

Dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Synthetic NonCatecholamines

A

Ephedrine

Phenylephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alpha Receptor Affinity

A

norepi>epi>iso

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Beta Receptor Affinity

A

Iso>epi>norepi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Alpha 1 Receptor Locations

A

post-synaptic
vasculature, heart, glands, and gut
activation causes vasoconstriction and relaxation at the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alpha 2 Receptor Locations

A

Presynaptic: peripheral vascular smooth muscle, coronaries, brain. Activation causes inhibition of norepi release and inhibition of SNS outflow leading to decreased BP, HR and inhibition of CNS activity.
Postsynaptic: coronaries and CNS. Activation causes constriction, sedation and analgesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Beta 1 Receptor Locations

A

myocardium, SA node, ventricular conduction system, coronaries, and kidney.
increases inotropy, chronotrophy, myocardial conduction velocity, coronary relaxation and renin release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Beta 2 Receptor Locations

A

vascular, bronchial, smooth muscle in the skin, myocardium, coronaries, kidneys and GI tract and uterine smooth muscle.
Vasodilation, bronchodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake (hypokalemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Use of CV agents in Anesthesia

A
  1. improve arterial BP
  2. improve myocardial contractility
  3. improve oxygenation through bronchodilation
  4. anaphylaxis treatment
  5. ACLS protocols
  6. Additive to L.A.
  7. sedation and analgesia (alpha2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alpha Adrenergic Receptors

A

GPCR
Ligands: NE, EPI, DOPA
Alpha 1: increases DAG + IP3, increased calcium leading to contraction
Alpha2: decreased camp leads to inhibition of Norepi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Beta Adrenergic Receptors

A

activation of adenyl cyclase, increased camp, increased kinase production and phosphorylation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Classes of Drugs to treat HTN: Sympathetic Nervous System

A

beta antagonists
alpha 1 antagonists
mixed alpha & beta antagonists
centrally acting alpha 2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classes of Drugs to treat HTN: RAAS

A

ACE-I
ARB
Diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Classes of Drugs to treat HTN: Endothelium derived mediator and/or ion channel modulators

A
direct vasodilators (nitro, hydralazine) 
calcium channel antagonists 
potassium channel opener
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When to Treat HTN

A

> 120/80 “lifestyle modifications”
<140/90 18-59 no comorbidities OR >60 with diabetes and/or CKD
<150/90 60 or older with no DM or kidney disease

17
Q

First Line Therapy HTN

A

Thiazide diuretic UNLESS compelling indication such as already showing organ decompensation
I.E. elevated BUN/Cr or cardiac hypertrophy

18
Q

Hypertensive Emergency

A

diastolic >120 with evidence of progressive end organ damage
Goal: decrease DBP to 100-105 within 24 hours (clonidine)

19
Q

Hypertensive Crisis

A

diastolic >120 with evidence of end organ FAILURE
Goal: decrease DBP to 100-105 ASAP
nitroprusside, nitroglycerin, labetalol, fenoldapam

20
Q

Alpha Antagonists

A

bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response

21
Q

Phenoxybenzamine

A

binds covalently, nonselective (less alpha 2)
less tachycardia with decreased SVR
PO med for preop BP control in pheochromocytoma
PRODRUG (1 hr onset, long acting 24 half time)

22
Q

Phentolamine

A

non selective, competitive alpha antagonist
reflex mediated and alpha2 associated increases in HR and CO
produce vasodilation and decrease in SVR

23
Q

Prazosin

A

selective alpha 1 competitive alpha antagonist
less likely to cause tachycardia
dilates arteries and veins
used preop for pheo patients, essential HTN with thiazides, decreasing afterload in HF, raynaud phenomenon

24
Q

Yohimibine

A

Competitive alpha antagonist
alpha 2 selective
increases release of NE from post-synaptic neuron (vasoconstriction)
used for orthostatic hypotension and impotence

25
Q

Alpha Antagonists for BPH

A

Terazosin & Tamsulosin
long acting selective alpha 1a
prostatic smooth muscle relaxation
orthostatic hypotension is biggest concern

26
Q

Alpha 1 Antagonism

A

decreases PVR and lowers BP

Postural hypotension d/t failure of venous vasoconstriction upon standing

27
Q

Alpha 2 Antagonism

A

increases NE release from nerve terminals results in tachycardia due to stimulation of beta receptors in heart

28
Q

Alpha 2 Antagonists Effects

A

blockade in prostate and bladder (muscle relaxation)
miosis
increased nasal congestion

29
Q

Phentolamine Dosing

A

30-70 mcg/kg intraop HTN emergencies, pheo or autonomic hyperreflexia
2.5mg to 5.0 mg for extravascular admin of sympathomimetic agents

30
Q

Beta Antagonists “Beta Blockers”

A

disallow sympathomimetics from provoking a beta response on the heart