The three compensatory pathways and remodeling form a closed loop. An initial injury — an infarct, chronic hypertension, a regurgitant valve — reduces stroke volume. Reduced stroke volume lowers effective arterial filling, which triggers sympathetic activation and RAAS, and raises filling pressures, which the failing ventricle tries to use as preload reserve. Sympathetic drive raises rate and contractility and constricts arterioles, raising afterload. RAAS raises preload through sodium and water retention and raises afterload through angiotensin II vasoconstriction. Both loads, plus the direct trophic effects of norepinephrine and angiotensin II, drive hypertrophy, dilation, and fibrosis. The remodeled ventricle has lower contractile efficiency and higher wall stress, so stroke volume falls further. That lower stroke volume is exactly the signal that re-activates sympathetic and RAAS pathways, and the cycle repeats with a lower output each time.
The loop is self-reinforcing because the sensors cannot distinguish a failing pump from a volume-depleted circulation. Baroreceptors and the juxtaglomerular apparatus read low effective volume and respond as they would to hemorrhage — retain salt and water, constrict, increase rate. In hemorrhage that restores output. In heart failure it adds load to a ventricle that cannot use it. This is why the same mechanisms that are life-saving acutely become the disease chronically, and why interrupting the loop, rather than simply supporting the pump, is the therapeutic logic.