Oscillatory afterpotentials

Electrocardiographic record showing digitalis-induced bigeminy. The complexes marked NSR are normal sinus rhythm beats an inverted T wave and depressed ST segment are present. The complexes marked PVB are premature ventricular beats and are the electrocardiographic manifestations of depolarizations evoked by delayed oscillatory afterpotentials as shown in Figure 13-5. 

The oscillatory afterpotentials seen post-repolarization give the first clue that the drug is quinidine. Quinidine blocks sodium channels, which is consistent with the blunting of the amplitude or phase 0, and also potassium channels, which is consistent with the lengthening of phase 2 and the decrease in the slope of phase 3. The drug is thus identified as quinidine, a class la antiarrhythmic. 

Glycosides increase intracellular sodium and also extracellular potassium by inhibitory actions on sodium potassium ATPase. Thus, with chronic therapy, because intracellular sodium is increased, phase 0 may be blunted slightly. The increase in extracellular potassium results in a decrease in the rate of repolarization and thus a decrease in the slope of phase 3 of the action potential, and a skewed appearance. This results in a longer time for the membrane to repolarize and, accordingly, an increase in the effective refractory period. Because the objective of the drug is to increase the influx of calcium, the faster influx of calcium results in a shortened phase 2, because a shorter time is required for the membrane to reach the equilibrium potential for calcium. Finally, phase 4 is elevated and increased in slope, due to the alterations in sodium and potassium concentration. This, with chronic therapy, and particularly as toxicity is approached, results in delayed oscillatory afterpotentials (see Figure). 

Describe the generation of oscillatory afterpotentials by cardiac glycosides. 

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