The role of pacemaker activity in the electrocardiogram formation mechanism in terms of the active diastole theory

Abstract

A description of the electrocardiogram (ECG) signal formation mechanism taking into consideration the general bioelectric activity of pacemaker cells is formulated in terms of a biphase model of pulse hemodynamics (the active diastole theory) developed earlier. For this purpose, the pacemaker action potential is represented as a biphase oscillation. In the first (systolic) phase, a sodium ion flow spreads from pacemakers to myocardial cells; in the second (diastolic) phase, potassium ions flow from myocardial cells to pacemaker cells. The relationship between the pacemaker action potential as an effective alternating electromotive force, the transmembrane action potential (TAP) of myocardial cells as a voltage, and the ECG signal as an electric current measured between two points on the body is described. According to this relationship, the ECG signal is represented as a sum of the first time derivatives of the TAPs of atrial and ventricular myocardial cells, with the segment from the S wave to the end of the T wave inverted. This inversion is accounted for by the change in the direction of the cardiac dipole vector to the opposite one during the diastolic phase of the action potential of pacemaker cells. The mean rate of the decrease in the ventricular myocardial cell TAP is suggested as an estimate of the bioelectric activity of the diastolic process in the heart ventricles. This rate is determined as the ratio of the integral of the ECG over the T wave to the length of the T wave. The resolution of the myocardial cell TAP into the sodium, calcium, and potassium components, performed earlier, is revised with special emphasis on the pattern of changes in the potassium component.