20.2
Hartfalen II: Fysiopathologie
Systolisch hartfalen en compenserende mechanismen
Systolisch hartfalen (ook wel HFrEF genoemd, Heart Failure with Reduced Ejection Fraction) is de mee…
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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Q1: What triggers the sympathetic nervous system response in systolic heart failure?
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.
Q2: How does reduced renal perfusion activate the renin-angiotensin-aldosterone system?
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.
Q3: What role does aldosterone play in fluid overload during heart failure?
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.
Q4: Why are natriuretic peptides insufficient to counteract heart failure progression?
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.
Q5: How does increased cardiac workload lead to ventricular dilation and hypertrophy?
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.
Q6: What is the vicious cycle of heart failure and how does it progress?
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.
Q7: What adverse effects result from prolonged sympathetic nervous system activation?
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.