3. Antiarrhythmics Flashcards

1
Q

Class I Antiarrhythmics

A

Na channel blockers

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2
Q

Class IA Antiarrhythmics - Available Drugs

A
  • Quinidine
  • Procainamide
  • Disopyramide

“Double Quarter Pounder”

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3
Q

Class IA Antiarrhythmics - MOA

A

Anti-arrhythmic Local anesthetics

  • Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
    • Decrease slope of phase 0 depolarization (Na channel block)
    • Increase threshold for firing in abnormal pacemaker cells.
  • Increase AP duration
  • Increase effective refractory period
  • Increase QT interval
  • Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.

[Quinidine, Procainamide, Disopyramide]

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4
Q

Class IA Antiarrhythmics - Clinical Use

A
  • Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.

[Quinidine, Procainamide, Disopyramide]

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5
Q

Class IA Antiarrhythmics - Toxicities

A
  • Thrombocyopenia
  • Torsade de pointes due to increased QT
  • Procainamide can cause a reversible SLE-like syndrome
  • Quinidine can cause cinchonism
  • Hyperkalemia increases toxicities

[Quinidine, Procainamide, Disopyramide]

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6
Q

Class IB Antiarrhythmics - Available Drugs

A
  • Lidocaine
  • Mexiletine
  • Tocainide

“Lettuce, Mayo, Tomato”

  • Sometimes Phenytoin is included in this group
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7
Q

Class IB Antiarrhythmics - MOA

A

Anti-arrhythmic Local anesthetics

  • Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
    • Decrease slope of phase 0 depolarization (Na channel block)
    • Increase threshold for firing in abnormal pacemaker cells.
  • Decrease AP duration
  • Preferentially affect ischemic or depolarized Purkinje and ventricular tissue

[Lidocaine, Mexiletine, Tocainide]

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8
Q

Class IB Antiarrhythmics - Clinical Use

A
  • Ventricular arrhythmias, especially post MI
  • Digitalis-induced arrhythmias

[Lidocaine, Mexiletine, Tocainide]

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9
Q

Class IB Antiarrhythmics - Toxicities

A
  • Local anesthetic
  • CNS stimulation / depression
  • Cardiovascular depression
  • Hyperkalemia increases toxicities

[Lidocaine, Mexiletine, Tocainide]

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10
Q

Class IC Antiarrhythmics - Available Drugs

A
  • Flecainide
  • Propafenone
  • maybe encainide

“Fries Please”

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11
Q

Class IC Antiarrhythmics - MOA

A

Anti-arrhythmic Local anesthetics

  • Slow or block conduction, especially in depolarized cells –> depress tissues that are frequently depolarized –> state dependent.
    • Decrease slope of phase 0 depolarization (Na channel block)
    • Increase threshold for firing in abnormal pacemaker cells.
  • No effect on AP duration

[Flecainide, Propafenone]

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12
Q

Class IC Antiarrhythmics - Clinical Use

A
  • V-tachs that progress to V-fib
  • Intractable supraventricular tachycardia
  • Usually only used as a last resort for refractory tachyarrhythmias
  • For patients without structural abnormalities.

[Flecainide, Propafenone]

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13
Q

Class IC Antiarrhythmics - Toxicities

A
  • Proarrhythmic, especially post-MI
    • “IC’s are CI (contraindicated) post-MI”
  • Significantly prolongs refractory period in AV node
  • Hyperkalemia increases toxicities

[Flecainide, Propafenone]

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14
Q

Class II Antiarrhythmics - Available Drugs

A

Beta Blockers

  • Propranolol
  • Esmolol
  • Metoprolol
  • Atenolol
  • Timolol
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15
Q

Class II Antiarrhythmics - MOA

A
  • Decrease cAMP –> Decrease Ca currents
  • Suppress abnormal pacemakers by decreasing slope of phase 4.
  • AV node particularly sensitive - Increased PR interval
  • Esmolol very short acting

[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]

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16
Q

Class II Antiarrhythmics - Clinical Use

A
  • V-tach
  • Supraventricular tach.
  • Slow ventricular rate during atrial fib. and flutter.

[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]

17
Q

Class II Antiarrhythmics - Toxicities

A
  • Impotence
  • Asthma exacerbation
  • Bradycardia, AV block, CHF
  • Sedation, sleep alterations
  • May mask signs of hypoglycemia
  • Metoprolol can cause dyslipidemia
  • Treat overdose with glucagon –> increase cAMP independent of Beta receptor.

[Propranolol, Esmolol, Metoprolol, Atenolol, Timolol]

18
Q

Class III Antiarrhythmics - Available Drugs

A

K channel blockers

  • Ibutilide,
  • Sotalol,
  • Bretylium,
  • Amiodarone,
  • Dofetilide

“K IS BAD”

19
Q

Class III Antiarrhythmics - MOA

A

Block K channels

  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval - only used when other antiarrythmics fail.

[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]

20
Q

Class III Antiarrhythmics - Clinical Use

A

Used when other antiarrhythmics fail

[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]

21
Q

Class III Antiarrhythmics - Toxicities

A
Sotalol
 - Torsade de pointes, Excessive b-block
Ibutilide
 - Torsade
Bretylium
 - New arrhtyhmias, HTN
Amioderone
 - PULMONARY FIBROSIS
 - HEPATOTOXICITY
 - HYPO / HYPER thyroid (Amioderone is 40% iodine)
 - CHECK PFT's, LFT's, and TFT's
 - corneal deposits, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF
 - Has class I, II, III, and IV activity because it alters the lipid membrane.

[Ibutilide, Sotalol, Bretylium, Amioderone, Dofetilide]

22
Q

Class IV Antiarrhythmics - Available Drugs

A

Ca channel blockers (Non-dihydropyridines)

  • Verapamil
  • Diltiazem
23
Q

Class IV Antiarrhythmics - MOA

A

Block Ca channels

  • Decreased conduction velocity
  • Increased effective refractory period
  • Increased PR interval

[Verapamil, Diltiazem]

24
Q

Class IV Antiarrhythmics - Clinical Use

A

Prevention of nodal arrhythmias (ie Supraventricular tach.)

[Verapamil, Diltiazem]

25
Q

Class IV Antiarrhythmics - Toxicities

A
  • Constipation, flushing, edema
  • CHF, AV block, Sinus node depression

[Verapamil, Diltiazem]

26
Q

Other Drugs Used as Antiarrhythmics

A
  • Adenosine

- Mg2+

27
Q

Adenosine - MOA

A

Increase K flow out of cells

  • Hyperpolarize the cell and decrease intracellular Ca
  • Very short acting
  • Effects antagonized by Theophylline
28
Q

Adenosine - Clinical Use

A

DOC in diagnosing and abolishing supraventricular tach.

29
Q

Adenosine - Toxicities

A
  • Flushing, hypotension, chest pain
30
Q

Mg2+ - Clinical Use

A

Effective antiarrhythmic in Torsade de pointes and digoxin toxicity