Antiarrhythmics Flashcards
2 etiologies of arrhythmias
Abnormal impulse formation and alterations in impulse conduction
Most life threatening arrhythmias
Ventricular tachycardia
Class 1 antiarrhythmic drugs
Sodium channel blockers
Class 2 antiarrhythmic drugs
Beta blockers
Class 3 antiarrhythmic drugs
Potassium channel blockers
Class 4 antiarrhythmic drugs
Calcium channel blockers
Fast response fibers
Located in muscle–ventricle and atria
Phase 0 of AP in fast response fibers
Na channels open, rapid depolarization
Class 1 drugs can slow or block phase 0
Phase 1 of AP in fast response fibers
Na+ channels are inactivated
No effect of anti arrhythmic drugs
Phase 2 of AP in fast response fibers
Plateau phase due to L type Ca channels
Inward Ca balanced by outward K
Class III drugs prolong plateau by blocking K channels
Class IV drugs have little effect on this type of Ca channel
Phase 3 of AP in fast response fibers
Repolarization phase due to K leaving and Ca channels inactivated
Class III drugs prolong repolarization
Phase 4 of AP in fast response fibers
Return to resting membrane potential
Due to Na/K pump
Digoxin can be pro-arrhythmic through blockade of phase 4
Slow response fibers
SA and AV nodes
No participation of Na
Class 1 drug has no effect
What is solely responsible for AP in slow response fibers
Ca
Class IV drugs block phase 0
Prolonging action potential duration with antiarrhythmics
Prolongs refractoriness to pathologic stimuli and slows down rhythm