1.4.6 Myocardial wall tension
1.4.6 Myocardial wall tension

Myocardial wall tension is another factor which has an important bearing on cardiac adaptation to physiological and pathological changes in loading condiWall tension is one of the components of afterload, and depends on the distension of the heart by preload. Tension is required to promote contractility via the Frank-Starling mechanism; however, increased tension increases myooxygen consumption.

The long-term response to volume overload is ventricular dilation. Initially, this is a result of changes in the length of sarcomeres. Later the myocytes themselves lengthen and the number of sarcomeres increases. The change in ventricular geometry allows a more efficient contraction and an increased stroke volume can be produced. There is no change in the efficiency of the myocardium until this compensation fails to meet demands and myocardial failure ensues, or if the dilation is sufficient to effect the efficiency of the AV valve apparatus.

A consequence of increased ventricular diameter is increased wall tension This relationship is described by the law of Laplace. In a simplified form, this states that wall tension is proportional to the radius of the chamber and the pressure within it, and inversely proportional to the wall thickness. The ventricles therefore respond to increased tension by increasing wall thickness. Pressure overload results in increased wall thickness with no change in the radius of the chamber (concentric hypertrophy) and is rare in the horse. If increased tension is due to volume overload, the ventricle responds (within limits) by increasing in radius without a change in wall thickness. This means that oxygen consumption will not increase unduly and is termed eccentric hypertrophy. The equation summarising the law of Laplace demonstrates this relationship (Figure 1.9). This process of hypertrophy is a normal, healthy response to increased load. In the horse, such loads are normally imposed by exercise training, or by increased preload related to a substantial regurgitant volume. Only at the point of myofailure does the wall thickness begin to decrease, resulting in increased tension and oxygen consumption.