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PDA2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

Describe the SA/AV node action potential

A

-phase 0= depolarization, Ca2+ influx/entry
-phase 3= repolarization, K+ efflux
-phase 4= pacemaker potential/spontaneous gradual depolarization, opening of special Na+ channels, inward Na+ entry (If-funny, slow Na+ channel)

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2
Q

What characteristics of phase 4 of AV/SA node indicates automaticity?

A

positive slope

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3
Q

What are the proposed mechanisms of tachyarrhythmias?

A

-enhanced/abnormal automaticity of SA node (further increase in phase 4 slope)
-conduction re-entry at AV, “dog chasing it’s tail”
-enhanced automaticity due to diastolic “leaky” channel of myocytes/purkinje cells (increased phase 4 slope)

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4
Q

Describe Phase 0 of Myocyte and Purkinje action potential

A

depolarization, use fast voltage gated Na+ channels

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5
Q

Explain propagation of action potential along cardiac cells through gap junctions

A

gap junctions are important for intercellular communication (Na+ movement) and spread of depolarization from one cell to another by fast voltage gated Na+ channels allowing rapid depolarization

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6
Q

What are the 3 stages of voltage gated Na+ channels?

A

-resting
-activated
-inactivated

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7
Q

What is the difference between myocyte and purkinje ion movement?

A

only purkinje have phase 1, transient K+ channels open and K+ efflux returns

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8
Q

What are the results of increase phase 4 slope?

A
  1. mechanical stretch of cardiac muscle cells
  2. hypokalemia/hypocalcemia
  3. beta stimulation
  4. hypoxia/ischemia
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9
Q

What is the mechanism for hypokalemia/hypocalcemia when there is increased phase 4 slope?

A

decreased outward leak of K+

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10
Q

What are the causes of Delayed after-depolarizations (DAD) aka intracellular Ca2+ overload?

A

myocardial ischemia, adrenergic stress, and Digoxin (digitalis toxicity)

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11
Q

What are the causes of Early after-depolarization (EAD) aka inward movement of Na+ or Ca2+ during phase 3?

A

phase 3 prolongation due to slowed repolarization, long QT interval, slow rate

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12
Q

What are the therapeutic treatment options for Delayed after-depolarization (DAD)?

A

-Ca2+ channel blockers
-Na+ channel blockers
-beta blockers

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13
Q

What are the therapeutic treatment options for Early after-depolarization (EAD)?

A

-Ca2+ channel blockers
-beta blockers

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14
Q

What drugs can treat conduction re-entry arrhythmias?

A

-Na+ blockers
-K+ channel blockers
-amiodarone

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15
Q

Describe Class 1 Na+ channel blockers

A

use/state/frequency- dependent fast Na+ channel blockers, channels that are used more frequently (activated) or are more inactivated state are more susceptible to block

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16
Q

What is the goal physiology of using Type 1 Na+ channel blockers?

A

stabilize membrane, depress 0 phase

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17
Q

What is the MOA of Class 1A Na+ channel blockers?

A

block fast Na+ channels (OPEN, ACTIVE Na+ CHANNELS) with moderate potency to decrease phase 0 upstroke velocity (decrease conduction velocity) and prolongs effective refractory period (ERP)

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18
Q

What is the MOA of the adverse effect of QT prolongation and Torsades de pointes in Class 1A Na+ channel blockers?

A

may also block K+ channels= reducing the K+ current which is responsible for repolarization of the membrane which can increases the effective refractory period
-> increased action potential duration= QT prolongation
-> QT prolongation= torsades de pointes

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19
Q

What effects do Type 1A Na+ channel blockers have on automaticity?

A

-little effect on SA node
-suppress automaticity of purkinje fibers by reducing the slope of phase 4 depolarization

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20
Q

What are the uses of Type 1A Na+ channel blockers?

A

NOT FIRST LINE, but due to MOA could treat DAD and conduction re-entry arrhythmias

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21
Q

What is the use of Quinidine?

A

Class 1A Na+ channel blocker, 2nd or 3rd line agent!
used for re-entry arrhythmias, paroxysmal supraventricular tachycardia (PSVT) and ventricular tachycardia (VTs)- slows conduction and prolongs the effective refractory period, and Afib

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22
Q

What is a unique MOA of Quinidine in class 1A antiarrhythmics?

A

anticholinergic (vagolytic) effects

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23
Q

What are the adverse effects of Quinidine?

A

-slows cardiac conduction= prolonged QRS duration, or SA/AV node disturbances
-Proarrhythmic effects= torsades de pointes due to prolonged QT interval
-CNS toxicity= cinchonism (tinnitus, hearing loss), confusion, vision disturbances, delirium, psychosis

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24
Q

What drug class does Procainamide belong to?

A

Class 1A Na+ channel blockers

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25
Q

What are the effects of Procainamides metabolites?

A

procainamide -> N actyl procainamide (NAPA)
has different effects than parent compound, K+ channel blocker (class 3 activity) and prolongs action potential duration (APD) of ventricular and purkinje fibers which is responsible for the SE of QT prolongation and torsade de pointes

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26
Q

What are the adverse effects of Procainamide?

A

-chronic therapy= systemic lupus like syndrome
-NAPA (metabolite) may cause QT prolongation and torsades de pointes

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27
Q

What is the MOA of Class 1B Na+ channel blockers?

A

block Na+ channels in OPEN and INACTIVATED conformation (rapid binding/unbinding) preferable targeting abnormal tissue (depolarized, arrhythmogenic tissue= no effect on healthy tissue) making ischemic cardiac myocytes the preferred target due to more open and inactive Na+ channels
slightly decreases APD

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28
Q

Class 1B Na+ channel blockers have no effect on QT interval- WHY?

A

no K+ channel block

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29
Q

What drug class is Lidocaine?

A

Class 1B Na+ channel blocker

30
Q

What is the use of Lidocaine?

A

ventricular arrhythmias (VT or VF) in emergent situations, high degree of effectiveness seen with acute MI
not suitable for supraventricular arrhythmias

31
Q

What are the adverse effects of Lidocaine?

A

-negative inotropic effect
-bradycardia, SA node depression, and His-purkinje block

32
Q

What drug class is Mexiletine?

A

Class 1B Na+ channel blocker

33
Q

What are the uses of Mexiletine?

A

-oral treatment for symptomatic ventricular tachyarrhythmias (VT)
-prophylaxis of ventricular arrhythmias
-long QT syndrome
-children with congenital heart disease and ventricular arrhythmias

34
Q

What are the adverse effects of Mexiletine?

A

severe bradycardia and abnormal SAQ node recovery in patients with sinus node disease
- N/V, tremor, dizziness, and confusion (dose related)

35
Q

What is the MOA of Class 1C Na+ channel blockers?

A

potent Na+ channel blockers (OPEN CHANNELS, slow binding/unbinding) and decreases rate of phase 0 upstroke on ventricular, atrial, and purkinje cells with little to no effect on APD

36
Q

What drug class is Flecainide?

A

Class 1C Na+ channel blocker

37
Q

What are the side effects of Flecainide?

A

-proarrhythmic (convert AFib -> atrial flutter)
-negative inotropic effects (worsen HF episodes)
-increased mortality or non fatal cardiac arrest

38
Q

What drug class is Propafenone?

A

Class 1C Na+ channel blocker

39
Q

What are the adverse effects of Propafenone?

A

weak beta antagonist= prolongs QRS
-proarrhythmic (less common than Flecainide)
-cardiovascular effects= AV block, sinus depression, worsening HF
-metallic taste

40
Q

What is the MOA of Class 2 beta blockers?

A

affects primarily SA and AV node through beta receptor blockade which decreases rate of spontaneous phase 4 depolarization= decrease automaticity, prolongs repolarization= increases effective refractory period= decreases incidence of re-entry, decrease automaticity of SA and AV conduction, and blocks sympathetic effects on the heart

41
Q

What are the uses of Class 2 beta blockers?

A

ventricular and supraventricular tachyarrhythmias precipitated by sympathetic stimulation

42
Q

What are the adverse effects of Class 2 beta blockers?

A

-cardiovascular events= excessive neg inotropic effects, heart block, bradycardia, AV block, hypotension
-impotence
-CNS= insomnia and depression
-smooth muscle spasms= bronchospasms (caution in asthma or COPD)

43
Q

What drug class is Propranolol?

A

class 2 beta blocker

44
Q

What is the 1/2 life of Propranolol?

A

2-6h

45
Q

What are the uses of Propranolol?

A

-prophylaxis of paroxysmal supraventricular tachycardia (PSVT)
- ventricular tachycardia (VT)
-management of pheochromocytoma (catecholamine producing tumor)
-short term treatment of tachycardia and arrhythmias due to thyrotoxicosis (hyperthyroidism)

46
Q

Which generation of beta blocker is most cardioselective?

A

2nd gen

47
Q

What drug is a 2nd gen beta blocker?

A

metoprolol

48
Q

What is the use of Esmolol?

A

emergency situations due to short 1/2 life (biphasic= 3-4 minutes, 15 minutes)

49
Q

What is the MOA of Class 3 antiarrhythmics?

A

-inhibit repolarization by inhibiting K+ channels involved in repolarization= increase absolute refractory period
-significantly prolong action potential duration (APD)
-little effect on phase 0 depolarization

50
Q

What is the MOA of Sotalol?

A

has beta adrenergic blocking activity as well as K+ block which prolongs action potential duration (APD), increased refractory period of atria and ventricles, and inhibits conduction in accessory pathways

51
Q

What are the indicated uses of Sotalol?

A

-treatment of life threatening ventricular arrhythmias
-maintenance of sinus rhythm in pt with AFib

52
Q

What are the adverse effects of Sotalol?

A

-QT PROLONGATION -> torsades de pointes
-beta blocker SE

53
Q

What are the monitoring parameters for Sotalol?

A

ECG for 72h

54
Q

What is the MOA off Amiodarone?

A

-blocks K+ channels= prolongs APD
-blocks inactive Na+ channels
-blocks beta adrenergic receptors(weakly)
-blocks Ca2+ channels(weakly)

55
Q

What are the uses of Amiodarone?

A

-wide range of uses in atrial and ventricular arrhythmias (drug with MOST EFFICACY)
-ventricular tachyarrhythmias
-supraventricular arrhythmias
-AFib

56
Q

What is the 1/2 life of Amiodarone?

A

50-60 days

57
Q

What are the adverse effects of Amiodarone?

A

-cardiovascular: decreased AV or SA node function (bradycardia, heart block), decreased cardiac contractility, hypotension
-highest incidence of torsades de pointes
-pneumonitis leading to pulmonary fibrosis
-hyper OR hypo-thyroidism
-elevated liver enzymes
-peripheral neuropathy, headache, ataxia, tremors
-corneal microdeposits (100% of pt will experience this after 6 months therapy)
-testicular dysfunction
-skin discoloration

58
Q

Describe how Amiodarone can cause hypothyroidism

A

inhibits T4 to T3 conversion (2-4% of population)

59
Q

Describe how Amiodarone can cause hyperthyroidism

A

excess iodine induces thyroid hormone synthesis

60
Q

What is the MOA of Dronedarone?

A

primarily K+ channel blocker but also very similar to Amiodarone

61
Q

How does Dronedarone compare to Amiodarone?

A

-less potent
-shorter t1/2 life (24h)
-less SE, but cardiovascular, elevated liver enzymes, and neurological SE still remain (to lesser extent)

62
Q

What is the MOA of Dofetilide?

A

K+ channel block= prolonged action potential (APD)

63
Q

What is the indication of Dofetilide?

A

AFib

64
Q

What are the adverse effects of Dofetilide?

A

QT interval prolongation= torsades de pointes
monitor ECG for 72h

65
Q

What are the indications of Ibutilide furamate?

A

AFib

66
Q

What are the adverse effects of Ibutilide furamate?

A

Qt prolongation= torsade de pointes
monitor ECG for 8h, short 1/2 life (IV prep)

67
Q

What classes of antiarrhythmic drugs prolong the QT interval?

A

class 1A and 3

68
Q

What are the class 4 antiarrhythmics?

A

calcium channel blockers (non-DHPs)

69
Q

What is the MOA of Class 4 Calcium Channel Blockers (Non-DHP)?

A

-blocks both active and inactive L-type Ca2+ channels
-slows action potential of SA and AV node= slows diastolic depolarization
-depresses automaticity of SA and conduction of AV
-prolongs refractory period at AV node

70
Q

What are the uses of Class 4 calcium channel blockers?

A

-rate control in AFib
-paroxysmal supraventricular tachycardia (PSVT)
-EAD and DAD

71
Q

What are the adverse effects of Class 4 calcium channel blockers?

A

-arrhythmias
-AV block
-bradyarrhythmia
-HF exacerbation
-gingival hyperplasia
-hypotension
-peripheral edema
-syncope

PDA2 (13 decks)

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