10.8:
Pathophysiology of Heart Failure
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.
10.8:
Pathophysiology of Heart Failure
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The pathophysiology of HF involves four major interrelated systems: the heart, vasculature, kidney, and neurohumoral regulatory circuits. Myocardial overload, hypertension, valvular defects, or genetic cardiomyopathies cause insufficient cardiac output, leading to compensatory cardiac myocyte hypertrophy, metabolic reprogramming, and altered gene expression.
Increased fibroblast proliferation and extracellular matrix deposition result in fibrosis, disrupting cardiomyocyte communication and causing cell death via apoptosis or necrosis. Vascular stiffness stems from impaired crosstalk between luminal endothelial and underlying smooth muscle cells, involving receptors that increase intracellular Ca2+ levels. Endothelial dysfunction disrupts the balance between vasodilating NO and vasoconstricting reactive oxygen species (ROS), increasing afterload. The kidney regulates Na+ and H2O levels, maintaining adequate GFR and diuresis through autoregulatory and neurohumoral mechanisms. If untreated, chronic activation of the sympathetic nervous system and RAAS leads to fatal cardiac tissue remodeling. Neurohumoral regulation creates a vicious cycle of vasoconstriction, increased afterload, volume overload, tachycardia, and positive inotropic actions. Common heart failure symptoms include tachycardia, decreased exercise tolerance, shortness of breath, maldigestion ascites, and peripheral and pulmonary edema. Heart failure ranges from Class I to IV. At the same time, the AHA and ACC extended this classification by adding stages A (preventable risk factors), B (asymptomatic stage requiring treatment), C (oscillations between symptoms in class II and III), and D (final stage requiring heart transplantation and left ventricular assist device implantation).