Systolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and contractility to support the weakened myocardium.
Prolonged sympathetic activation has several adverse effects. The sympathetic nervous system induces vasoconstriction in the skin, gastrointestinal tract, and kidneys. Reduced renal perfusion and sympathetic stimulation trigger the kidneys to release renin. Renin converts the plasma protein angiotensinogen into angiotensin I, which then travels to the lungs. Within the pulmonary blood vessels, angiotensin-converting enzyme (ACE) transforms angiotensin I into angiotensin II. Angiotensin II, a potent vasoconstrictor, raises blood pressure and afterload. Angiotensin II also has pro-inflammatory and pro-fibrotic effects, contributing to the progression of heart failure.
Angiotensin II prompts the adrenal cortex to release aldosterone, causing the renal tubules to retain fluid and sodium, which increases blood volume. These mechanisms lead to the fluid overload typical of heart failure. Angiotensin II, aldosterone, and other neurohormones, such as endothelin, elevate preload and afterload, increasing ventricular wall stress and cardiac workload.
The body attempts a counter-regulatory response by releasing natriuretic peptides. B-type natriuretic peptide, or BNP, and atrial natriuretic peptide, or ANP, are released from the distended cardiac chambers, promoting vasodilation and diuresis. However, their effects are typically insufficient to counteract the adverse effects of the other mechanisms. Additionally, ANP and BNP are essential biomarkers for diagnosing and monitoring heart failure.
As the heart's workload increases, myocardial contractility decreases, leading to higher end-diastolic blood volume in the ventricle. This condition stretches the myocardial fibers, causing ventricular dilation. In response to an increased workload, the heart's muscle thickens, a condition known as ventricular hypertrophy, leading to structural and functional alterations called ventricular remodeling.
Neurohormones like angiotensin II contribute to hypertrophy and fibrosis of the myocardial cells, burdening the remaining functional cells with maintaining cardiac output. The loss of cardiac cells and the development of fibrosis can lead to diastolic heart failure (also termed HFpEF heart failure with preserved ejection fraction), further impairing heart function. A stiff ventricle resists filling, further decreasing cardiac output.
These compensatory mechanisms create a "vicious cycle of heart failure," where low cardiac output triggers processes that increase the heart's workload, worsening the condition.
The pathophysiology of systolic heart failure begins with the left ventricle pumping a reduced volume of blood.
Baroreceptors in the aortic arch and carotid sinuses detect this decrease, triggering the sympathetic nervous system to release epinephrine and norepinephrine, which boost heart rate and contractility.
The sympathetic stimulation also causes vasoconstriction in the skin, gastrointestinal tract, and kidneys.
Reduced renal perfusion from low cardiac output and sympathetic activation triggers renin release.
Renin converts angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II by the angiotensin-converting enzyme in the lungs.
Angiotensin II increases blood pressure and afterload and stimulates aldosterone release, causing sodium and fluid retention.
Additionally, natriuretic peptides, released from overdistended cardiac chambers, promote vasodilation and diuresis but are often insufficient.
Eventually, the increased workload on the heart decreases myocardial contractility, leading to ventricular dilation, hypertrophy, remodeling, and early myocardial cell death, resulting in diastolic heart failure.
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