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Heart Failure: Difference between revisions
→Pathophysiology of heart failure
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Another relevant issue is afterload of the left ventricle influencing the output of the heart: as the afterload of the aortic pressure also influences the timing of closure of the aortic valve, a high aortic pressure will close the aortic valve early and will therefore diminish the output. Decreasing (theoretically diastolic, but more practically systolic) aortic pressure will increase the stroke volume by later closure of the aortic valves. (Figure 2) | Another relevant issue is afterload of the left ventricle influencing the output of the heart: as the afterload of the aortic pressure also influences the timing of closure of the aortic valve, a high aortic pressure will close the aortic valve early and will therefore diminish the output. Decreasing (theoretically diastolic, but more practically systolic) aortic pressure will increase the stroke volume by later closure of the aortic valves. (Figure 2) | ||
[[Image: | [[Image:pressure_volume_curve.svg|thumb|400px|''Figure 2 Effects of decreased afterload. Red arrows indicate aortic valve opening, which occurs later and at higher LV systolic pressure when the diastolic aortic pressure is higher. Blue arrows indicate closing of the aortic valve. Bidirectional arrows represent stroke volume. When aortic pressure is decreased, stroke volume increases as a result of a lower aortic pressure during closure of the aortic valve.]] | ||
Hormonal/ sympathetic system mechanisms (RAAS/ Sympathetic overstimulation) of heart failure are as important as the hemodynamic mechanisms of heart failure. | Hormonal/ sympathetic system mechanisms (RAAS/ Sympathetic overstimulation) of heart failure are as important as the hemodynamic mechanisms of heart failure. | ||
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A decreased cardiac output leads to diminished renal perfusion and release of hormones in the RAA-system: renin released in the circulation by the renal juxtoglomerular apparatus, which is stimulating the cleavage of angiotensinogen into angiotensins I and II during passage through the lungs. Angiotensin II stimulates vasoconstriction in the kidneys, and in other vascular systems, increasing blood pressure; the second effect of angiotensins is stimulating the release of aldosterone from the adrenals into the plasma, which retains sodium from the kidney tubules in the blood and thereby water. The RAA –system, which works as a compensatory mechanism for heart failure to increase blood pressure and blood volume, also stimulates hypertrophy of muscle cells and stimulates the formation of fibrosis, which in the long term are detrimental to heart failure. | A decreased cardiac output leads to diminished renal perfusion and release of hormones in the RAA-system: renin released in the circulation by the renal juxtoglomerular apparatus, which is stimulating the cleavage of angiotensinogen into angiotensins I and II during passage through the lungs. Angiotensin II stimulates vasoconstriction in the kidneys, and in other vascular systems, increasing blood pressure; the second effect of angiotensins is stimulating the release of aldosterone from the adrenals into the plasma, which retains sodium from the kidney tubules in the blood and thereby water. The RAA –system, which works as a compensatory mechanism for heart failure to increase blood pressure and blood volume, also stimulates hypertrophy of muscle cells and stimulates the formation of fibrosis, which in the long term are detrimental to heart failure. | ||
The other compensatory mechanism for heart failure, stimulation of the sympathetic nervous system, increases heart rate to increase cardiac output, which is a powerful compensatory mechanism. However, chronic stimulation of the sympathetic nerves to the heart, leading to higher heart rates, is toxic to the heart, by continuous release of norepinephrin to the myocyte. In addition, by their continued stimulation, the betareceptors for norepinephrin are downregulated in heart failure, which further diminishes the function and functional reserve of the heart. | The other compensatory mechanism for heart failure, stimulation of the sympathetic nervous system, increases heart rate to increase cardiac output, which is a powerful compensatory mechanism. However, chronic stimulation of the sympathetic nerves to the heart, leading to higher heart rates, is toxic to the heart, by continuous release of norepinephrin to the myocyte. In addition, by their continued stimulation, the betareceptors for norepinephrin are downregulated in heart failure, which further diminishes the function and functional reserve of the heart. | ||
===Management=== | ===Management=== | ||