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Flashcards in Antiarrhythmic Drugs Deck (28):

What are the classes of anti-arrhythmic?

  • I - Sodium channel Blockers
    • Ia - Moderate phase 0 depression and slowed conduction (2+), prolong repolarization
    • Ib - Minimal phase 0 depression and slow conduction (0-1+); shorten repolarization
    • Ic - Marked phase 0 depression and slow conduction (4+); little effect on repolarization
  • II - Beta-Adrenergic Blockers
  • III - Potassium Channel Blockers (prolong repolarization)
  • IV - Calcium Channel Blockers


What is the mechanism of Class I drugs?

  • Act on fast response cells
  • Reduce membrane responsiveness
  • Increase threshold for AP firing Reducing Vmax (depress conduction velocity)
  • Prolong effective refractory period (ERP)


What is a Class 1A Drug? What are its direct effects? What are its indirect effects? What are its indications?


  • Direct: Increase AP threshold, ERP; Decrease Vmax
  • Indirect effects: Blocks K channels leading to early afterdepolarizations (EADs), vagolytic effect
  • Use: A-Flutter/fib, Prevention of V-Tach/Fib


What are Quinidne's side effects? Where is it metabolised? Can it be used with renal failure?

  • SE: GI effects - Diarrhea, cramps; Vagolytic in heart, P450 inhibition, Proarrythmic for other arrythmias, reduces renal clearance of digitalis
  • Liver metabolism
  • Tolerated in patients with renal failure


What is a Class 1B Drug? What are its direct effects? What are its SE? What are its indications?


  • Direct: Increase AP threshold; Decreases Vmax/Na channel activity at high HR, AP duration, ERP SE: Dizziness, seizures
  • Use: V-Tach, Digitalis inudced arrhythmias, Safe with long QT patinets


What is a Class 1C Drug? What are its direct effects? What is its major SE? What is its indication?


  • Direct: Increase AP threshold; decrease Vmax/conduction velocity; variable effects on ERP; Slow Na channel dissociation
  • SE: Pro-arrhythmic
  • Use: Life-threatening situations where supraventricular and ventricular arrhythmias are resistant to other drugs


What are some class II drugs and their specific kinetics? What is their mechanism? Which part of the action potential do they affect?

  • Drugs: Propranolol - Long acting, oral Esmolol - Short acting, IV
  • Mechanism: Competitive inhibitor of catecholamines for the beta-adrengergic receptors of cardiac cells
  • Affects phase 4 (diastolic) depolarization in the presence of catecholamines


What are the indications for beta-blockers? What are the major side effects?

  • All atrial arrhythmias, V-Tach/Fib when there are high levels of catecholamines
  • Most useful antiarrhythmic drugs due to safety and wide clinical applications
  • Safe for long QT syndrome patients because they do not prolong repolarization in ventricular tissues
  • Major side effects - Negative inotropic effect, heart block, bradycardia, bronchospasm


What are some class III drugs? What is the general mechanism? What is the most common target? What is the main common effect?

Amiodarone, Sotalol

  • Main mechanism: K+ Channel Block, prolongs AP repolarization; reverse use-dependence
  • Target: IKr (hERG channel)
  • Effect: Increased ERP


What are the channel actions of amiodarone? What are its effects? What are its indications? What are its major side effects?

  • Potent K+ channel blockers, modest Na+, Modest Ca2+, Modest Beta-blocker
  • Effect: Potent K+ channel blocker, Increased AP duration, ERP
  • Use: V-Tach/Fib, prevention of recurrent paroxysmal A-Fib/Flutter SE: Triggered arrhythmias (EADs), rarely Torsades de Pointes; Altered thyroid function/hypothyroidism, pulmonary fibrosis often irreversible


What are the actions of Sotalol? What are the indications of Sotalol? What is the most serious side effect?

  • Actions: Main: IKr block, Beta-blocking secondary actions
  • Uses: V-Tach/Fib. Supraventricular tach, A-Fib
  • Side effect: Triggered arrhythmias, Torsades de Pointes


What is this?

Q image thumb

Torsade de Pointes


What are some Class IV drugs and the family they belong to?
What is their primary mechanism?
What are the major effects?
What are the indications?

Diltiazem (Benzothiazepines), Verapamil (Phenylalkylamines)
Mechanism: Acts primarily on slow response cells (SA & AV node), dependent on Ca2+ influx for depolarization
Increase threshold for AP firing in nodal cells, nodal cell refractory period; depress conduction velocity in the SA and AV nodes
Uses: A-Tach (Paroxysmal supraventricular tachycardia); Rarely for V-Tach


Why are 1,4-DHPs not generally used for arrythmias?

They target vascular instead of cardiac cells; instead prescribed for treatment of angina to releieve arterial spasms


What are the major side effects of Ca2+ blockers?
Specific (Nifedipine, Verapamil, Diltiazem)

Common: Negative chronotropic effect - decreases SA node automaticity (bradycardia)
Negative inotropic effect - decreases Ca2+ influx during plateau of ventricular AP
Hypotension - Decreases Ca2+ influx into vascular smooth muscle cells

Peripheral edema (N-type mostly)
Constipation (V especially)
With digitalis to slow AV node leading to heart block (V&D)
Increase plasma digitalis levels by competiting for renal excretion (V&D)


What is the mechanism of adenosine?
What is the indication?

  • Mechanism: Very rapidly activates K+ channels to slow phase 4 depolarization at AV node  (Half-life of 10 seconds)
  • Blocks cAMP-enhanced Ca2+ channel activity in AV node
  • Use: Supraventricular Tachycardia - Slows AV conduction and heart rate


What is digoxin?
What is its mechanism?
What is its indication?

Digitalis Glycoside
Mech: Enhances vagal parasympathetic activity to slow conduction at the AV node
Use: A-Fib, Supraventricular Tachycardia to control ventricular response rate


What ECG pattern is this?

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Normal Sinus Rhythm


What ECG pattern is this?

Q image thumb

Sinus Tachycardia


What ECG pattern is this?

Q image thumb

Atrial Fibrilation


What ECG pattern is this?

Q image thumb

Ventricular Tachycardia


What ECG pattern is this?

Q image thumb

Ventricular Fibrillation


What ECG pattern is this?

Q image thumb

Ventricular Asystole (Flat line)


What are the three main mechanisms of arrhythmias?

Increased automaticity (Inappropriately excitable cells)
Triggered automaticity (Normal AP is interrupted or followed by an abnormal depolarization; afterdepolarizations)
Re-entry (Abnormal impulse conduction)


What changes can occur in increased automaticity?

Slope of phase 4 is increased
Threshold potential is more negative
Maximum diastolic potential (MDP) is more positive


What is Early Afterdepolarization (EAD)?
What exacerbates it?
What can it result in?

Depolarization that interrupts repolarization
Exacerbated by slow rate/long QT syndrome
Torsades de Pointes results


What is Delayed Afterdepolarization?
What exacerbates it?

Depolarization after repolarization
Exacerbated by fast rates, high intracellular Ca 2+, digitalis toxicity, catecholamines, ischemia


What is re-entry?
What causes functionally defined re-entry?
Where can anatomic re-entry occur?

Re-excitation of a localized region of tissue from the same impulse (Current goes backwards)
Functionally defined: Ischemia and hypoxia
Anatomic: AV node