Anti-arrhythmics Flashcards

1
Q

use of anti-arrhythmics

A

restricted to dangerous/symptomatic arrhythmias –> Vtach, rapid afib

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2
Q

Class I/II MOA

A

block Na, K channel

myocyte AP

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3
Q

Class II/IV

A

slow sinus and AV node conduction

pacemaker AP

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4
Q

Class I MOA

A
  • some block Na –> prolong QRS
  • some block K –> prolong Qt
  • use dependence (effective @ fast HR)
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5
Q

use dependence

A
  • Class I (IC*)
  • bind best in open/inactivated state
  • (depress tissue that is freq depolarized –> tachycardia)
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6
Q

Class Ia drugs

A

quinidine
procanimide
disopyramide

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7
Q

Class Ia MOA

A
  • block Na (phase 0) (inc QRS)

- some block K (inc QT)

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8
Q

Class Ia AE

A

TDP (prolong QT)

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9
Q

quinidine

A
  • Ia
  • oral
  • dec recurrence rate of afib

AE: inc mortality, Cinchonism

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10
Q

procanimide

A
  • Ia
  • IV
  • slow conduction in accessory path (WPW), arrhythmias (bypass tracts)

AE: drug-induced lupus

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11
Q

Class Ib drugs

A

lidocaine

mexiletine

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12
Q

Class Ib MOA

A
  • least effect on AP of CI
  • slight dec AP
  • RAPID unbind (effective in tachy)
  • bind depolarized tissue (ischemia) (B=Best post MI)

AE: CNS stim (tremor, agitation)

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13
Q

lidocaine

A
  • Ib

- terminates arrhythmias by turning unidirectional block –> bidirectional block

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14
Q

mexiletine

A
  • Ib

- oral version of lidocaine

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15
Q

Class Ic drugs

A

flecainide

propafenone

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16
Q

Class Ic MOA

A
  • block open Na, very SLOW unbinding (PROLONGED QRS!!!!!!!!!)
  • use in struc NORM heart
  • dec afib recurrence

AE: proarrhythmic, cardiac arrest, cox at high HR

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17
Q

structurally normal heart

A

IC

18
Q

use post-MI

A

IB

B=Best post-MI

19
Q

Class III drugs

A

amiodarone
ibutilide
dofetilide
sotalol

AIDS

20
Q

Class III MOA

A
  • block K+ –> delay repolarization, prolong QT/AP/ERP in cardiomyocytes
    use: afib, a flutter, vtach

AE: torsades

21
Q

most adverse effects of any of the anti-arrhythmics

A

amiodarone

22
Q

amiodarone MOA

A

-CIII, but I/II/IV effects
-blocks K+, Qt
(lowest torsades incidence)

-use: afib, Vtach

-LIPOPHILIC and LONG half life…
AE: liver/lung accumulation, hypER/hypOthyroidism,
inc LFTs, skin sensitivity to sun, blue/gray man, normal deposits, DEATH BY PULMONARY FIBROSIS

23
Q

monitor these labs when rx amiodarone

A

CXR
PFTs
TFTs
LFTs

24
Q

sotalol

A

CIII

25
Q

dofetilide

A

CIII

26
Q

sotalol

dofetilide

A
  • block K+ (inc QT)
  • REVERSE use-dependence

AE: torsades, tox @ slow HR

27
Q

REVERSE use-dependence

A
  • bind best at resting state
  • tox @ slow HR
  • CIII
28
Q

Ibutilide

A
  • CIII
  • IV
  • use: chemical cardioversion

AE: torsades

29
Q

class II antiarrhymics MOA

A

beta blockers
main effects @ pacemaker cells of SA/AV node

  • dec slope of phase 4 (funny current, Na) –> slows HR
  • prolong phase 3 (repolariz) –> slows conduction in AV node
  • -> prolonged PR

AE: type I AV block, wenkebach (mobitz I)

use: afib, prevent SCD in systolic HF (dec EF pts) –> DEC MORTALITY

30
Q

Class II drugs

A
metoprolol
propanolol
esmolol
atenolol
timolol
carvedilol
31
Q

Class IV drugs

A

verapamil
diltiazem

(non-dihydropyridine CCBs)

32
Q

class II AE

A

AE: type I AV block, wenkebach (mobitz I)

  • impotence
  • COPD exacerbation and asthma
  • CVS effects (bradycardia, AV block, HF)
  • Mask signs of hypOglycemia
33
Q

Class IV MOA

A
  • block phase 0 of pacemaker AP
  • slow HR
  • slow AV conduction

use: afib (control ventric. rate) (SVTs)

AE: type I AV block, wenkebach (mobitz I)

34
Q

adenosine

A

“breaks AVNRT”
-inc K out (HYPERpolarize)
-dec Ca out
^dec AV node conduction

  • short half life
    use: dx/terminate certain forms of SVT
AE: flushing/hypotension (vasodilator)
CP
dyspnea
doom
bronchospasm
35
Q

Mg

A
  • blocks Ca influx (avoids early after depolarizations)

use: acute management of torsades AND digoxin toxicity

36
Q

atropine

A
  • muscarinic r. antagonist
  • parasympathetic block

use: bradycardia (*esp via AV block)

37
Q

ivabradine

A
  • selective inhibit of funny Na chan, prolong phase 4, dec SA node firing
  • negative chronotropic effect w/o isotropy
  • reduces cardiac O2 req

use: chronic stable angina in pt who can’t take beta blockers, chronic HF w/ reduced EF

AE: luminous phenomena/visual brightness, HTN, bradycardia

38
Q

metoprolol

A

B1 selective

39
Q

propranolol

A

B1 and 2 (non-selective)

40
Q

carvedilol

A

B1 and 2 (non-selective)