Heart 1997;78:429-430 ( November )
Editorial
The origin of symptoms in chronic heart failure
| The first 150 words of the full text of this article appear below. |
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
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