2.2.1 Congestive heart failure
2.2.1 Congestive heart failure

The processes involved in the development of congestive heart failure (CHF) are complex and as yet are not fully understood. More detailed discussions of the processes involved are contained in some of the recommended reading. In summary, they involve peripheral vascular changes which take place in order to maintain delivery of blood to vital organs, sodium and water retention to increase blood volume, increased heart rate and ventricular hypertrophy (Table 2.1). The homeostatic mechanisms which control cardiac output and peripheral vascular tone, and therefore blood pressure, were described in detail in Chapter 1

Peripheral vascular changes

The changes which occur in heart failure are similar to those that are responsible for maintaining blood pressure. When cardiac output is reduced, peripheral arteriolar and venous constriction maintains blood pressure until output can be increased by other homeostatic mechanisms. In addition to autonomic changes, accumulation of local vasoactive compounds affects blood flow to some areas. If cardiac output is critically low, the periphery will be poorly perfused and cool extremities may be clinically detectable.

Sodium and water retention to increase blood volume

One of the principal responses to a fall in blood pressure is a complex interaction of numerous homeostatic mechanisms which increase sodium and water retention (see section 1.4.4). This results in an increase in blood volume and maintenance of preload. Changes in each of these mechanisms are exaggerated during the development of congestive heart failure (CHF).

CHF develops when volume retention becomes excessive and preload is inappropriately high. This occurs because the homeostatic mechanisms can increase blood volume to such a degree that the heart can no longer pump the required stroke volume, resulting in increased filling pressure. In addition, in severe disease, increased myocardial oxygen consumption makes the ventricles relatively stiff, further increasing filling pressure. The result is that blood dams back in the veins, capillary pressure rises and consequently fluid leaks out into the extracellular space. Oederna formation is one of the principal factors contributing to clinical signs of CHF.

Increased heart rate

One of the principal mechanisms of maintaining blood pressure in the face of decreased forward stroke volume is increased heart rate, mediated by increased sympathetic discharge and decreased parasympathetic tone. This may occur, for example when preload is reduced by haemorrhage. However, a raised heart rate reduces the duration of diastole and therefore limits the time for ventricular filling and for coronary artery flow and is very energy consuming. In the long-term the tachycardia itself can result in myocardial failure and CHF. In compensated CHF, homeostatic mechanisms compensate so that stroke volume is raised, distribution is efficient and heart rate may return to normal. An increased resting heart rate, in the absence of causes other than cardiac disease, is a strong indicator of the presence of significant heart disease.

Ventricular hypertrophy

Cardiac hypertrophy occurs in response to either pressure or volume overload Both of these processes increase myocardial wall tension in line with the law of Laplace (see section 1.4.6). Hypertrophy occurs in order to reduce tension.

Concentric hypertrophy is the response to pressure overload. The increase in wall thickness reduces wall tension; the stroke volume of the ventricle remains unchanged or falls. In horses, left ventricular (LV) pressure overload is very rare.

Eccentric hypertrophy is commonly found in horses, both as a normal phyresponse to exercise training and as a result of the volume overload in animals with valvular regurgitation. In eccentric hypertrophy, dilation of the chamber results in a proportional increase in stroke volume for the same reduction in myocyte length during contraction. However, the geometrical change which results in increased efficiency also causes an increase in wall tension which must be offset by a concomitant increase in wall thickness. The increased stroke volume gives greater cardiac reserve in athletically trained animals. In volume overload, eccentric hypertrophy occurs in order that a norcardiac output can be produced at a resting heart rate, without severe changes in peripheral blood supply, although it brings with it the problem of increased myocardial oxygen consumption. Eccentric hypertrophy is therefore one of the first changes which can be measured in horses with heart failure.