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140 Antiarrhythmic Drug Therapy Flashcards

1
Q

Mechanisms/Classifications of Bradyarrhythmias

A
  1. Diminished automaticity
  2. Block
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2
Q

Mechanisms of Tachyarrhythmias

A
  1. Enhanced automaticity
    1. Increased phase 4 depol
    2. Make threshold more negative
  2. Renentry
  3. Triggered activity
    1. Early after depols
      1. •During Phase 2, 3 of AP
  • Ca2+ current Dependent
  • Occurs in setting of prolonged APD (prolonged QT interval)
    1. Delayed afterdepols
      1. During Phase 4 of AP

Associated with high Ca2+ (eg digoxin toxicity)

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3
Q

Supraventricular tachyarrhythmias list

A

oSinus Tachycardia

oAtrial Premature Beats

oParoxysmal Supraventricular Tachycardia

(aka Supraventricular Tachycardia aka SVT)

oAtrioventricular Nodal Reentrant Tachycardia (AVNRT)

oAtrioventricular Reentrant Tachycardia (AVRT)

oEctopic Atrial Tachycardia

oAtrial Flutter

oAtrial Fibrillation

oMultifocal Atrial Tachycardia

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4
Q

Ventricular tachyarrhythmias list

A
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5
Q

AV Nodal Reentrant Tachycardia (AVNRT)

A
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6
Q

Atrioventricular Reentrant Tachycardia (AVRT)

A
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7
Q

Atrial Flutter

A
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8
Q

Atrial Fibrillation

A
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9
Q

Ventricular Tachycardia

A
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10
Q

Polymorphic Ventricular Tachycardia

A
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11
Q

Ventricular Fibrillation

A
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12
Q

Treating Enhanced Automaticity (theory)

A
  1. •Make maximum diastolic potential more negative
  2. •Reduce slope of phase 4 depolarization
  3. •Make the threshold potential more positive
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13
Q

Treating Reentry (theory)

A

Disrupt the Balance

  • e.g. slow the “slow conduction” even more so it blocks
  • supress premature beats which often set up slow conduction
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14
Q

Treating Triggered Activity (theory)

A
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15
Q

Rate Control vs. Rhythm Control in Atrial Fibrillation

A
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16
Q

Vaughan-Williams Classification

A
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17
Q

Na+-Channel Blockers Mechanism

A
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18
Q

Na+-Channel Blockers: Effect on Phase 0

Na+-Channel Blockers: Effect on Action Potential Duration

A
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19
Q

Procainamide

A

Class 1A

•Drug-induced Lupus: arthralgia, pleuritis, pericarditis with PO (not clinically available)

•Torsades de Pointes:

N-acetylprocainamide a first pass

metabolite with strong K+ channel

activity

20
Q

Quinidine

A

Class 1A

•Additional vagolytic effects

–eg urinary retention, constipation, blurred vision, dry mouth

•Cinchonism: CNS toxicity – tinnitus, psychosis

•Torsades de Pointes: K+ blocking activity

21
Q

Disopyramide

A

Class 1A

  • Additional stronger vagolytic effects
  • Additional negative inotropic effects

•Antimuscarinic: urinary retention, constipation, blurred vision, dry mouth

•Torsades de Pointes: K+ blocking activity

22
Q

Lidocaine

A

Class 1B

•CNS Toxicity:

confusion, delerium, grand mal seizures

good for post MI

23
Q

Mexelitine

A

Class 1B

•CNS Toxicity:

confusion, delerium, grand mal seizures

24
Q

Flecainide

A

Class 1C

  • Potent negative inotropic effects
  • Propafenone: beta-blocking effects
  • Slows conduction (because of potent Na+ blocking)

•Contraindicated in LV systolic dysfunction and heart block

25
Q

Propafenone

A

Class 1C

  • Potent negative inotropic effects
  • Propafenone: beta-blocking effects
  • Slows conduction (because of potent Na+ blocking)
  • Contraindicated in LV systolic dysfunction and heart block
26
Q

β-Blockers Mechanism

Side effects

A
  • Hypotension
  • Bradycardia
  • Depression, Bronchospasm, Cognitive Impairment, Sexual Dysfunction
27
Q

Esmolol

A

Beta blocker, Class 2

  • Hypotension
  • Bradycardia
  • Depression, Bronchospasm, Cognitive Impairment, Sexual Dysfunction

GIven IV

28
Q

Metoprolol

A

Beta blocker, Class 2

  • Hypotension
  • Bradycardia
  • Depression, Bronchospasm, Cognitive Impairment, Sexual Dysfunction

GIven PO

Side effect: oClass II (eg Metoprolol) – Depression, Bronchospasm, Cognitive Impairment, Sexual Dysfunction

29
Q

K+-Channel Blockers Mechanism

30
Q

Amiodarone

31
Q

Sotalol

A

Class 3 antiarrhythmic, K+ blocker

  • B-blocking effects
  • PO
  • •Prolong QT-interval à Torsades de Pointes
  • should be avoided in renal failure.
32
Q

Dofetilide

A

Class 3 Antiarrhthmic, K+ blocker

  • PO
  • requires renal dose adjustment
  • •Prolong QT-interval à Torsades de Pointes
33
Q

Ibutilide

A

Class 3 antiarrhtymic, K+ channel blocker

  • IV
  • •Prolong QT-interval à Torsades de Pointes
34
Q

Ca2+-Channel Blockers Mechanism

35
Q

Verapamil

36
Q

Diltiazem

A

Side Effect: oClass IV (eg Diltiazem) – Constipation, Peripheral Edema

37
Q

Adenosine

A

non classified antiarrythmic

  • Transient Elective Heart Block
  • Treatment of AVNRT, AVRT
    • – reentrant rhythms that depend on the AV node
  • Diagnosis of Supraventricular Tachyarrhythmias
    • –gets rid of QRS complexes
    • –see underlying Atrial Fibrillation or Atrial Flutter
38
Q

Digoxin

A

Unclassified antiarrythmic drug

  • Narrow Therapeutic Window
  • Toxicity: nausea, diarrhea, yellow vision
  • Proarrhythmic Effects:

–almost anything

•Treatment of severe toxicity:

anti-digoxin Fab fragments

Side effect: nausea, diarrhea, yellow vision

39
Q

Tx Disrupting AVNRT, AVRT

A
  • Acute: Adenosine – rapidly acting
  • Chronic: Beta Blockers, Calcium Channel Blockers, perhaps Digoxin
40
Q

Tx AFib, AFlutter: Rate Control

A

•Beta Blockers (Class II)

–slows conduction through AV node

•Calcium Channel Blockers (Class IV)

–slows conduction through AV node

•Digoxin

–slows conduction through the AV node

41
Q

Tx AFib, AFlutter: Rhythm Control

A

•Class Ic Agents: Flecainide, Propafenone

–Probably Interferes with Reentry by slowing conduction

•Class III Agents: Amiodarone, Sotalol, Dofetilide, Ibutilide

–Probably Interferes with Reentry by prolonging repolarization

•Class Ia Agents

–obsolete for this indication

42
Q

Tx Suppress VT and Symptomatic PVCs

A

•Class II Agents : beta-blockers

–Can slow conduction in sick tissue

•Class III Agents : Sotalol and Amiodarone

–Interferes with Reentry by prolonging repolarization

•Class Ib Agents

–Interferes with Reentry by slowing conduction

•Class Ia Agents

–almost obsolete for this indication

–Procainamide occasionally used in ischemic VT

–Disopyramide occasionally used in Hypertrophic Cardiomyopathy (negative inotropic effects)

43
Q

Tx

Suppress VT and Symptomatic PVCs

Special Case: In setting of Myocardial Infarction

A

•Class II Agents : beta-blockers

–Can slow conduction in sick tissue

  • Class III Agent: Amiodarone
  • Class Ib Agents

–Interferes with Reentry by slowing conduction

•Class Ia Agents

–almost obsolete for this indication

–Procainamide occasionally used in ischemic VT

–Disopyramide occasionally used in Hypertrophic Cardiomyopathy (negative inotropic effects)

44
Q

Tx

Suppress VT and Symptomatic PVCs

Special Case: Treatment of Torsades de Pointes

A
  • Magnesium
  • Phenytoin
  • Isoproterenol
  • Overdrive Pacing
  • Shock
45
Q

Pacemaker cells APs (vagus, b-adrenergic, SA node)

46
Q

Wolff-Parkinson-White

A
  • oWolff-Parkinson-White pattern
    • oECG finding only of a delta wave
  • oWolff-Parkinson-White syndrome
    • oECG finding of a delta wave
    • oECG evidence also of arrhythmia using accessory pathway
      • oAVRT – orthodromic vs. antidromic
      • oYou could also have Atrial Fibrillation, Atrial Flutter, or even AVNRT
47
Q

Tx AVRT

Cardiovascular (39 decks)

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