neurohormonal changes in heart failure and relation to treatment
The neurohormonal mechanism role in progression of heart failure is an important topic in USMLE. Here is a simplified explanation.
The presence of heart failure leads to decrease tissue perfusion by definition, decreasing renal perfusion activates renin angiotensin axis resulting in salt and water retension, increased blood pressure (partly by increasing total peripheral resistance) and increased sympathetic output among other effects. High sympathetic output also increases renin release, an effect mediated by B1 receptors, and we have a viscious circle. The high sympathetic and renin angiotensin activity first compensate for heart failure by increasing cardiac output through increasing peripheral resistance, myocardial contractility and heart rate but eventually trigers myocyte hypertrophy, apoptosis and focal necrosis differentially. This is called remodelling especially after MI, and it is responsible for cardiac decompensation.
Any drug that cuts the viscious circle at any part delays the progression of heart failure. These include B1 blockers, ACE inhibitors, ATII receptor blockers and spironolactone.
It is worth mentioning that B blockers work by another well known mechanism that brings immediate relief in angina patients by delaying A-V conduction on the expense of diastole (becomes longer) which gives the heart more time to relax (decrease oxygen consumption), get blood suply(most blood supply to the heart is in diastole) and fill with blood (increase EDV and stroke volume).