1.5.6 The ventricular depolarisation process
1.5.6 The ventricular depolarisation process

The ventricular depolarisation process has been shown to be different in horses (designated along with other ungulates as category B mammals) compared with humans and small animals (category A mammals).

In category A mammals, the Purkinje network carries the impulse to the submyocardium and depolarisation then spreads out from the ends of the fibres, through the myocardium to the sub-epicardial layers, in a series of wavefronts. The initial overall direction of the wavefront is mainly from the left to the right side of the interventricular septum initially, followed by a wavefront which is substantially directed towards the left ventricular apex, and finally towards the cardiac base (Figure 1.14). Because the LV is normally the most substantial muscle mass, the sum of the electromotive force is primarily directed towards the left apex, resulting in a large R wave in lead II of Einthoven's triangle (the lead axis which is approximately parallel to the direction of the wavefront). The main cardiac vector is altered when there is considerable change in the relative proportions of the left and right ventricles. The average of the cardiac vector in the frontal plane is known as the mean electrical axis (MEA).

In category A mammals, increased LV muscle mass can cause a prolonged QRS duration because the wavefront takes longer to spread throughout the enlarged myocardium. In addition, the amplitude of the R wave in lead II is often increased in individuals with hypertrophy of the LV, as a result of the increased muscle mass. RV hypertrophy increases the contribution of the RV to the mean vector and may result in a right axis deviation. These changes are relatively specific for enlargeof the left or right ventricles but are comparatively insensitive. Even in category A mammals, radiography and echocardiography are usually more sensitive techniques for detecting hypertrophy, particularly LV hypertrophy.

In the horse the Purkinje fibres extend throughout the myocardium and venactivation takes place from multiple sites. The apical section of the WS is the first part of the myocardium to be depolarised. This depolarisation often spreads from the left to the right side of the septum, but can be in either direction. Vectors of local electrical activity may even point in both directions, resulting in a cancellation of electromotive forces reaching the body surface and therefore without any deflection on the ECG. The bulk of the ventricular myocardium depolarises shortly afterwards; however, no large wavefronts are formed because of the multiple sites from which activation occurs. Because the surface ECG represents the sum of the electromotive forces within the heart, the overall effect of the depolarisation of this tissue on the ECG is minimal. Most of the electrical activity seen at the body surface occurs as a result of the depolarisation of the basal part of the IVS and a small portion of the LV free-wall. The wave-front spreads towards the heart base so the vector is directed dorsally and cranially with respect to the body surface (Figure 1.14).

The range of MEA measured in normal horses is extremely wide an4 MEA is therefore of very limited clinical value in horses. In addition, the time taken for the ventricles to depolarise does not depend on the spread of a wavefront across them so QRS duration is not necessarily related to ventricular size. Thus, for all practical purposes, ECGs provide little or no information about heart size in horses, although they do give useful information about heart rate and rhythm.