Heart failure is a complex disorder characterized by the heart's inability to pump blood to meet the body's demands effectively.

Its pathophysiology involves the interconnection of four systems.

Factors that affect myocardial functioning may decrease cardiac output.

This triggers compensatory cardiac remodeling, characterized by myocyte hypertrophy, increased fibroblast proliferation, and extracellular collagen deposition.

These processes can contribute to cardiac cell death through apoptosis or necrosis.

Age or disease-related vascular stiffness also disrupts endothelial function, altering hemodynamic mechanisms and increasing afterload.

The kidneys are crucial for maintaining the intravascular volume. Heart failure can dysregulate the sodium and water levels, stimulating autoregulatory and neurohumoral pathways.

These neurohumoral mechanisms activate the sympathetic nervous system and renin-angiotensin-aldosterone or the RAAS system to counteract cardiovascular impairments.

However, prolonged activation of these systems further increases cardiac workload and contributes to a vicious cycle of cardiac remodeling, worsening heart failure.