Hartfalen II: Fysiopathologie

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.