Neurohumoral activation in HF

Depressed ventricular contractility, induced by the underlying cardiac disease, leads to neurohumoral activation (moving clockwise) that is initially adaptive in that it maintains blood pressure and tissue perfusion. Over the long term, however, the increase in outflow resistance (afterload) hastens the rate of myocardial deterioration and worsens ventricular performance. This leads to a vicious cycle of increasing release of norepinephrine, angiotensin II, and ADH that further increases afterload.