Anti-arrhythmic drugs Flashcards

1
Q

What is the major cardiovascular danger of anti-arrhythmic drugs (especially class III agents)?

A

Anti-arrythmic drugs (especially class III agents) can significantly prolong repolarization (QT) and therefore can result in Torsade de Pointe as a form of Proarrhythmia.

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2
Q

What is the only anti-arrythmic that has been shown to improve mortality in the post infarct patient?

A

Beta blocker

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3
Q

What is the preferred therapy for high risk arrhythmia patients (low EF <35% or sustained VT/VF)?

A

Implantable Cardioverter Defibrillator

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4
Q

What are class I anti-arrhythmic drug agents?

A

Class I => are Na channel blockers

  • Class Ia => moderate Na channel blocker (prolongs conduction and repolarization) and increases effective refractory period
  • Class Ib => weak Na channel blocker and decreases effective refractory period
  • Class Ic => strong Na channel blocker and maintains effective refractory period
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5
Q

What are some examples of Class Ia anti-arrhythmic drugs?

A

Quinidine

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6
Q

What are some examples of Class Ib anti-arrhythmic drugs?

A

Lidocaine

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7
Q

What are some examples of Class Ic anti-arrhythmic drugs?

A

Flecainide

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8
Q

What are class II anti-arrhythmic drug agents?

A

Class II => Beta Blockers

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9
Q

How do class III anti-arrhythmic drug agents act?

A

Class III => K channel blockers that delay depolarization

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10
Q

Why is Ibutilide a pseudo class III anti-arrhythmic drug?

A

Ibutilide causes a slow inward Na current that also delays depolarization

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11
Q

What are examples of class III anti-arrhythmic drug agents?

A

Sotalol, Dofetilide, Amiodarone, Dronedarone

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12
Q

How do class IV anti-arrhythmic drug agents act?

A

Act primarily on slow response cells (SA & AV node), which are dependent on Ca2+ influx for Phase 0 of the action potential.

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13
Q

What are 3 examples of class IV anti-arrhythmic drug agents?

A

Diltiazem

Verapamil

Adenosine

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14
Q

How does adenosine work to prevent arrhythmia?

A
  • Blocks A1 receptor
  • Prolongs AV conduction by causing cell hyperpolarization and reduces catacholamine stimulation
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15
Q

What drugs are used to treat SVT?

A

Adenosine

Beta blockers

Calcium Channel Blockers

Digoxin

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16
Q

What steps are taken if the routine SVT drugs do not work?

A
  • IV: Ibutilide, Quinidine, Procainamide, Amiodarone
  • PO: Quinidine, Procainamide, Amiodarone, Disopyramide, Flecainide, Propafenone, Sotalol, Dofetilide, Dronedarone
  • DC cardioversion
  • Ablation => now generally replaced traditional anti-arrhythmic therapy
17
Q

When does ablation NOT work better than “traditional” anti-arrhythmic therapy?

A

Atrial fibrillation

18
Q

Which drugs improve survival chances after MI?

A

Beta blocker (Class II) => propanolol

*Amiodarone (Class III) appears to increase the probability of survival but actually increases cumulative risk => pro-arrhythmia

19
Q

Which drug classes can cause Torsades from Early Afterdepolarization (EAD)?

A

Class III (K+ blockers)

Class Ia (Na + blockers)

20
Q

How do class Ic anti-arrhythmic drugs cause incessant monomorphic VT?

A

REMEMBER => Type 1C (Na+ blockers) delay conduction

-Slowing of conduction in limb 1 allows limb 2 to recover by the time the retrograde wavefront arrives at 2; thus facilitating reentry

21
Q

What drugs should be used in acute VT?

A

IV Lidocaine or Amiodarone till definitive therapy can be instituted

22
Q

Which drugs should be used in sustained VT?

A

Amiodarone

Sotalol

*However, ICDs are superior

23
Q

What is the most effective treatment strategy for reducing mortality in a patient with a low ejection fraction, and sustained ventricular tachycardia or cardiac arrest?

A

Empiric ICD