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Pharmacology- Test 3 Material > 28- Anti-Arrhythmics > Flashcards

28- Anti-Arrhythmics Flashcards

1
Q

amiodarone (Cordarone)

A

K+ Channel Blocker

  • class III antiarrhythmic
  • prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
  • oral or IV
  • used for: atrial and ventricular arrhythmias
  • S/fx: bradycardia d/t B-blocking effects
  • less arrhythmogenic in patients with HF or post-MI (probably d/t pleotropic effects on other channels)
  • very lipid soluble so rapidly taken up into high fat tissues and take a long time before out of system
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2
Q

dofetilide (Tikosyn)

A

K+ Channel Blocker

  • oral class III antiarrhythmic started in hospital
  • prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
  • used for: atrial arrhythmias (relatively safe in HF)
  • S/fx: marked QT prolongation– torsades de pointes
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3
Q

ibutilide (Corvert)

A

K+ Channel Blocker

  • IV class III antiarrhythmic, in hospital
  • prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
  • used for: acute conversion of A-fib/flutter
  • S/fx: marked QT prolongation– torsades de pointes
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4
Q

sotalol (Betapace)

A

K+ Channel Blocker

  • class III antiarrhythmic
  • prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
  • oral, started in hospital d/t potential adverse effects
  • used for: atrial and ventricular arrhythmias
  • S/fx: bradycardia d/t B-blocking effects of L-isomer, marked QT prolongation– torsades de pointes
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5
Q

dronedarone (Multaq)

A

K+ Channel Blocker

  • oral class III antiarrhythmic
  • prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
  • used for: atrial and ventricular arrhythmias
  • lacks many of major s/fx of amiodarone but not as efficacious
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6
Q

diltiazem (Cardizem LA)

A

Ca++ Channel Blocker

  • oral or IV class IV antiarrhythmic
  • used for: re-entry SVT’s involving AV node, slows AV node conduction
  • S/fx: bradycardia, hypotension, negative inotrope
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7
Q

verapamil (Covera-HS)

A

Ca++ Channel Blocker

  • oral or IV class IV antiarrhythmic
  • more cardio-selective then dilt
  • used for: re-entry SVT’s involving AV node, slows AV node conduction
  • S/fx: bradycardia, hypotension, negative inotrope
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8
Q

delayed afterdepolarization (DAD)

A
  • occur after cell has completely repolarized
  • usually result from abnormal intracellular Ca handling that can occur from ischemia after MI or with digoxin use
  • both occur from Ca overload leading to spontaneous cyclic activation of Ca pumps and exchangers
  • DADs are more common in fast HR
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9
Q

early afterdepolarization (EAD)

A
  • occur before cell has completely repolarized
  • depolarization-dependent triggered activity
  • prolonged AP duration can cause EADs due to reactivation of VGCa channels before cell has fully repolarized which then triggers another AP through reactivation of VGCa channels
  • EADs can lead to run of spontaneous extrasystolic beats
  • can lead to torsades de pointes and are more common with slow heart rates, because AP duration correlates with HR
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10
Q

effective (absolute) refractory period

A
  • time from beginning of an action potential until cell is able to conduct another AP
  • stimulating cell during this period will not fire AP because few to no VGNa channels have reactivated
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11
Q

long QT syndrome

A
  • mutations in hERG or certain drugs make K+ channels less effective in opening which can prolong repolarization and prolong QT interval
  • this syndrome is predisposed to EADs, arrhythmias, and sudden cardiac death
  • FDA now requires that all drugs be tested for effects on hERG
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12
Q

reentry

A
  • abnormal impulse conduction that occurs due to:
    1. geometry for conduction loop
    2. unidirectional conduction block
    3. slow conduction (the effective refractory period must be less than propagation time around the loop)
  • if conduction too fast, will catch up to refractory period and transmission will cease
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13
Q

relative refractory period

A
  • time from end of effective refractory period until cell regains normal excitability
  • stimulating cell during this phase will produce weaker then normal APs until all VGNa channels have recovered
  • geometry can be anatomical or functional
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14
Q

state-dependent block

A
  • refers to how smart drugs, such as lido, only block channels when in activated or inactivated state
  • these drugs come off channel when channel is in resting state
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15
Q

supraventricular tachycardia

A
  • usually narrow complex QRS because it uses the normal His/Purkinje system to conduct implulse
  • can be atrial or nodal
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16
Q

torsades de pointes

A
  • common ventricular arrhythmia that occurs after EAD

- rotating ectopic folci causing ventricular depolarizations

17
Q

unidirectional block

A
  • tissue that allows impulse transmission in one direction but not the other
  • usually happens in ischemic tissue that results from MI
18
Q

use-dependent block

A

-refers to how smart drugs, such as lido, increases binding to channels that are activated more often as in tachycardia

19
Q

ventricular tachycardia

A

-usually wide complex because they originate in the ventricles and do not use His/Purkinje system to conduct impulse

20
Q

metoprolol

A

cardioselective beat-blocker

  • Class II antiarrhythmic
  • reduce AV conduction and slope of phase 4
  • PO or IV
  • Use: atrial arrhythmias,slow AV node conduction, prevent sudden cardiac death post-MI
  • S/E: bradycardia, negative inotropy
21
Q

atenolol

A

cardioselective beat-blocker

  • Class II antiarrhythmic
  • reduce AV conduction and slope of phase 4
  • PO or IV
  • Use: atrial arrhythmias,slow AV node conduction, prevent sudden cardiac death post-MI
  • S/E: bradycardia, negative inotropy
22
Q

esmolol

A

cardioselective beat-blocker

  • Class II antiarrhythmic
  • reduce AV conduction and slope of phase 4
  • IV
  • Use: atrial arrhythmias,slow AV node conduction
  • S/E: bradycardia, negative inotropy
  • metabolized by ester hydrolysis (very short t1/2)
23
Q

propranolol

A

Non-cardioselective beta-blocker (beta1 and beta2)

  • Class II antiarrhythmic
  • reduce AV conduction and slope of phase 4
  • PO or IV
  • Use: atrial arrhythmias,slow AV node conduction
  • S/E: bradycardia, negative inotropy, bronchoconstriction/bronchospasm
24
Q

digoxin

A

Cardiac glycoside

  • inhibits the Na/K ATPase leading to a decrease Na gradient and an inhibition in the NCX. This causes an increase in intracellular Ca leading to a stronger contraction and increases vagal tone on the heart (slows HR).
  • Inhibits ICa
  • Use: atrial arrhythmias (slows ventricullar response in AF/A flutter).
  • S/E: Arrhythmogenic in doses that produce inotropy.
25
Q

adenosine

A

Misc anti-arrhythmic

  • Acts on A-1 receptors and increases I-K while inhibiting I-Ca.
  • Uses: SVT; aid in Dx of AF/A Flutter
  • S/E: asystole (transient), AV node block
26
Q

procainamide

A

class 1A Na+ channel blocker

  • block K+ channels
  • prolong AP
  • unbind with medium kinetics
  • oral or IV
  • use- ventricular or recurrent atrial arrhythmia
  • side effects- lupus like effects, nausea
  • metabolite NAPA- prolongs QT predisposing patient to EADs and arrhythmia
27
Q

quinidine

A

class 1A Na+ channel blocker

  • block K+ channels
  • prolong AP
  • unbind with medium kinetics
  • oral or IV
  • use- ventricular or recurrent atrial arrhythmia
  • side effects- diarrhea
28
Q

disopryamide

A

class 1A Na+ channel blocker

  • block K+ channels
  • unbind with medium kinetics
  • oral
  • use- ventricular or recurrent atrial arrhythmia
  • side effects- negative inotrope (avoid in heart failure)
29
Q

lidocaine

A

class 1B Na+ channel blocker

  • IV
  • unbind with fast kinetics- shortens AP
  • use- acute ventricular arrhythmia
  • side effects- CNS toxicity
30
Q

mexiletine

A

class 1B Na+ channel blocker

  • oral
  • unbind with fast kinetics- shortens AP
  • use- chronic ventricular arrhythmia
  • side effects- CNS toxicity
31
Q

flecainide

A

class 1C Na+ channel blocker

  • oral
  • unbind with slow kinetics- no effect on AP
  • use- recurrent atrial arrhythmia
  • side effects- arrhythmogenic
  • avoid in patients with underlying structural heart disease or post-MI
32
Q

propafenone

A

class 1C Na+ channel blocker

  • oral
  • unbind with slow kinetics- no effect on AP
  • use- recurrent atrial arrhythmia
  • side effects- arrhythmogenic
  • avoid in patients with underlying structural heart disease of post MI

Pharmacology- Test 3 Material (10 decks)

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