A popular view of how the syndrome of chronic heart failure (CHF) develops is that initial myocardial damage causes a low output state and fluid retention; the fluid retention results in breathlessness as fluid “leaks” into the lungs, and the low output state results in fatigue due to failure of muscle perfusion. This model of CHF gives a central role to the baroreceptors; reduced cardiac performance results in baroreceptor activation and subsequent sympathetic activation and fluid retention in an attempt to maintain tissue perfusion pressure. The resultant vasoconstriction in turn leads to further demands on the failing myocardium, completing the vicious circle of CHF. This might be termed the “wet lung” hypothesis.

This theory has been added to in recent times by the emerging concept of heart failure as a multisystem neuroendocrine disease1; the principal focus is that the reduction in cardiac output leads to intense stimulation of the renin-angiotensin-aldosterone system leading to fluid retention and vasoconstriction secondary to the action of angiotensin II. Much of the interest in these hypotheses is driven by the potential for therapeutic modulation. This has perhaps diverted our attention from the more basic question of the factors responsible for the symptoms of CHF. One of our principal aims must be the reduction of the distressing sensations of breathlessness and fatigue that result in greater impairment of quality of life than caused by any other chronic medical condition.

A number of observations suggests that this model may be inaccurate. Baroreceptors appear to be inactivated in both animal models and human heart failure, suggesting that some other factor is responsible for sympathetic activation.2 There is little evidence in favour of central haemodynamics as predictors …