Сердечная недостаточность II: Патофизиология

Baroreceptors in the aortic arch and carotid sinuses detect reduced blood pressure from decreased cardiac output. This triggers the sympathetic nervous system to release epinephrine and norepinephrine, which increase heart rate and contractility to support the weakened myocardium and restore blood pressure.

Low cardiac output and sympathetic activation cause vasoconstriction in the kidneys, reducing renal perfusion. This triggers renin release, which converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme in the lungs then converts angiotensin I to angiotensin II, a potent vasoconstrictor that raises blood pressure and afterload.

Angiotensin II stimulates the adrenal cortex to release aldosterone, which causes renal tubules to retain sodium and fluid. This increases blood volume and preload, contributing to the fluid overload characteristic of heart failure and further burdening the weakened heart muscle.

Natriuretic peptides like BNP and ANP are released from distended cardiac chambers to promote vasodilation and diuresis. However, their effects are typically insufficient to counteract the adverse effects of prolonged sympathetic activation, renin-angiotensin-aldosterone system activation, and other neurohormonal mechanisms driving heart failure.

As myocardial contractility decreases, end-diastolic blood volume increases, stretching myocardial fibers and causing ventricular dilation. The heart responds to increased workload by thickening its muscle, a process called ventricular hypertrophy. These structural changes constitute ventricular remodeling, which further impairs cardiac function.

Low cardiac output triggers compensatory mechanisms that increase the heart's workload, worsening the condition. Neurohormones like angiotensin II promote myocardial hypertrophy and fibrosis, causing cell death and loss of contractility. This cycle eventually leads to diastolic heart failure, where a stiff ventricle resists filling and decreases cardiac output.

Prolonged sympathetic activation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys, reducing perfusion to vital organs. This triggers renin release and activates the renin-angiotensin-aldosterone system, leading to increased blood pressure, fluid retention, and elevated preload and afterload that further stress the failing heart.