Session 1: Classification and Class I Antiarrhythmics Flashcards

Vaughan Williams Classification and Class I Antiarrhythmics

1
Q

What is contractility in cardiac cells?

A

Ability of cardiac cells to shorten and return to their original length in response to an electrical impulse.

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2
Q

Define automaticity in cardiac cells.

A

Ability of cardiac pacemaker cells to depolarize spontaneously.

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3
Q

What is excitability in the context of cardiac cells?

A

Ability of resting, polarized cardiac cells to depolarize in response to an electrical impulse.

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4
Q

What does conductivity refer to in cardiac cells?

A

Ability of all cardiac cells to conduct electrical impulses to adjacent cardiac cells.

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5
Q

What is the effect of Class I sodium channel blockers on phase 0?

A

They inhibit fast sodium channels and reduce the maximal rate of rise of phase 0.

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6
Q

List the subclasses of Class I antiarrhythmic drugs.

A
  • Class IA
  • Class IB
  • Class IC
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7
Q

What effect do Class IA antiarrhythmic drugs have on the action potential?

A

They moderately block sodium channels, raise threshold potential, widen action potential duration, decrease conduction velocity, prolong repolarization, and decrease automaticity.

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8
Q

What ECG changes are associated with Class IA antiarrhythmic drugs?

A

Increased QRS duration and increased QT interval.

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9
Q

What are the indications for Procainamide?

A
  • Life-threatening ventricular tachycardia with normal LV function
  • Atrial fibrillation with antegrade conduction over an accessory pathway.
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10
Q

What are some adverse effects of Procainamide?

A
  • Mild negative inotrope
  • Hypotension with IV dose
  • Torsades de Pointes (rare).
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11
Q

What is a major indication for Disopyramide?

A

Life-threatening ventricular arrhythmias.

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12
Q

What are the adverse effects of Disopyramide?

A
  • Marked negative inotropic effect
  • Toxicity in renal insufficiency
  • Ventricular arrhythmias; Torsades de Pointes.
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13
Q

What is Quinidine used for?

A

Effective against supraventricular and ventricular arrhythmias, particularly in re-entrant arrhythmias.

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14
Q

What ECG changes are associated with Quinidine?

A

Increased QT interval.

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15
Q

What are the indications for Lidocaine?

A
  • Suppression of serious ventricular arrhythmias
  • Acute management of VT.
  • Ventricular arrhythmias caused by digoxin toxicity.
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16
Q

What are the common adverse effects of Lidocaine?

A
  • CNS side effects (confusion, seizures)
  • Dose-related side effects with increasing infusion rate.
17
Q

What is Mexiletine’s primary indication?

A

Ventricular arrhythmias.

18
Q

What are the common side effects of Mexiletine?

A
  • New or worsened arrhythmias
  • CNS side effects (dizziness, tremor).
  • GI effects (indigestion, nausea).
19
Q

What is Phenytoin primarily used for?

A

Treating epilepsy.

20
Q

List some contraindications for IV Phenytoin.

A
  • 2nd or 3rd degree heart block
  • Sinus bradycardia.
21
Q

What effects do Class IC sodium channel blockers have?

A
  • Marked blockage of sodium channels
  • Marked depression of the upstroke of action potential.
  • Prolonged repolarization.
22
Q

What are the indications for Flecainide?

A
  • Paroxysmal supraventricular tachycardias
  • WPW arrhythmias
  • Paroxysmal atrial flutter or atrial fibrillation.
23
Q

What are the contraindications for Flecainide?

A
  • Structural heart disease
  • 2nd or 3rd degree AV block.
24
Q

What is Propafenone’s mechanism of action?

A

Marked blockage of sodium channels with potent membrane stabilizing activity.

25
What are some common cardiac conditions requiring medications?
* Angina * Acute myocardial infarction * Hypertension * Heart failure * Cardiac arrhythmias.
26
What are the first-line drugs for angina?
* Beta blockers * Calcium channel blockers if beta blockers are contraindicated.
27
What is the standard treatment for acute myocardial infarction?
* Beta Blocker * ACE Inhibitor/ARB * Lipid Lowering Agents.
28
How do sodium channel blockers decrease automaticity?
They decrease the slope of phase 4 spontaneous depolarization and raise the threshold potential of pacemaker cells.
29
How does prolonging the effective refractory period help treat atrial fibrillation?
It decreases re-entry, stopping disorganized depolarizations of the atria.