Drug and Electrolyte Effects


Many drugs that are used and many electrolyte abnormalities affect the ECG. The most common drugs are the antiarrhythmic medications. The common drugs that affect the ECG and the common electrolyte abnormalities are covered below.

Pharmacologic Agents - Antiarrhythmic Drugs

The antiarrhythmic drugs are classified into five categories based on the various channels and the cardiac tissue they affect. Knowledge of the action potential, the channels involved in the action potential and the effects of the individual classes of antiarrhythmic drugs can be used to understand the effects the drugs have on the surface ECG.

Action Potential

The action potential of ventricular muscle will be used as an example as it is the tissue, which is responsible for the generation of the QRS complex. There are five phases to the action potential numbered 0 to 4.

Phase 0 is depolarization and is what is referred to when the electrical impulse is discussed. It involves the large influx of sodium through the rapid sodium channels causing the rapid change in the transmembrane potential and an electrical spike. This electrical spike causes the rapid sodium channels in adjacent cells to open and results in the propagation of the action potential. The faster the electrical spike occurs; the faster the wave of propagation. Depolarization of the ventricle corresponds to the QRS complex on the ECG.

Phases 1 through 3 represent repolarization. The time from the beginning of Phase 1 to the end of Phase 3 corresponds to the refractory period of the cell. Phase 4 is the time period before the next depolarization. After phase 3, the transmembrane potential is more negative than what is required to stimulate the next depolarization. During phase 4, there is a gradual influx of positive charges until the threshold for depolarization is reached.

Antiarrhythmic Drug Classification


Class I

Bind to sodium channels
Class Ia
procainamide, disopyramide, quinidine
Class Ib
lidocaine, phenytoin, tocainide, mexilitine
Class Ic
flecainide, encainide, propafenone, moricizine
Class II
Class III
Affect potassium channels, amiodarone, bretylium, ibutilide, sotalol, N-acetylprocainamide
Class IV
Calcium channel blockers
Class V
Digitalis agents

The Class I drugs are subdivided based on which sodium channels they affect.

  Class Ia Class Ib Class Ic Class III  


Electrolyte Abnormalities


There are many ECG changes that occur with hyperkalemia and these changes follow each other in a progression as the hyperkalemia worsens. The initial change is the appearance of symmetrical, thin, peaked T waves. The peaked T waves are followed by the development of PR interval prolongation and subsequent ST segment depression. At higher potassium levels, the QRS complex will begin to widen and the P waves may become absent. At high potassium levels, the atrial tissue becomes paralyzed and a P wave does not appear on the surface ECG. There is still sinus node activity and conduction to the AV node occurs through specialized intra-nodal tissue and is referred to as sino-ventricular conduction. The entire QRS complex continues to lengthen on the ECG and a sine wave appearance develops with eventual ventricular fibrillation.


Hypokalemia also has a progression on the surface ECG. The most classic and initial change is ST segment depression associated with a decrease in amplitude of the T wave. This decrease in amplitude is associated with an increase in amplitude of the U wave and the U wave may actually become higher than the T wave. As potassium levels lower, the P wave may become wider and the PR interval may prolong. The QRS complex may eventually widen with further ST segment depression and T wave inversion.


The effect of calcium on the surface ECG can be explained by its effect on the action potential within the myocyte. The role of calcium is most prominent in phase 2 of the action potential and corresponds to the ST segment on the surface ECG. As the action potential shortens, the ST segment shortens and vice versa. When hypercalcemia is present, the duration of phase 2 is lessened and therefore the ST segment is shortened resulting in the characteristic short QT interval of hypercalcemia. In some cases, there is apparently no ST segment and the T wave comes immediately off of the S wave.


The opposite effects of hypercalcemia occur with hypocalcemia. Namely, the QT interval lengthens and is due to the prolongation of the ST segment. The prolonged ST segment is due to the lengthening of phase 2 in the action potential.

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