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Heart Failure: Difference between revisions
→Pathophysiology of heart failure
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HF is caused by a loss of cardiac pump function which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship determines that by loading the heart (increasing its filling or its pressure) the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart doesn’t pump out enough volume, and in the first phase of disease compensates for the loss of contractility. It takes more energy from the heart to work at increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of myocytes and dilatation by increasing myocyte length and matrix changes), which in the long term leads to a further loss in function. The result is further increased loading pressures in the heart and by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded, to leak water to the lungs. That is the actual restriction towards further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water. | HF is caused by a loss of cardiac pump function which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship determines that by loading the heart (increasing its filling or its pressure) the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart doesn’t pump out enough volume, and in the first phase of disease compensates for the loss of contractility. It takes more energy from the heart to work at increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of myocytes and dilatation by increasing myocyte length and matrix changes), which in the long term leads to a further loss in function. The result is further increased loading pressures in the heart and by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded, to leak water to the lungs. That is the actual restriction towards further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water. | ||
[[Image: | [[Image:frank_starling.svg|thumb|right|400px|Figure 1 Frank-Starling curve]] | ||
Hemodynamic explanations (the heart as a pump) use the concept of preload (filling) and afterload (workload of the heart, which is wall tension and arterial pressure or vascular resistance). In this way, the progression of left sided heart failure towards right sided heart failure is explained as follows: prolonged left ventricular failure increases pressures in the left atrium (preload), which in time leads to a subsequent increased resistance in the pulmonary vascular system (which is the afterload of the right ventricle) and eventually may also lead to right ventricular failure. | Hemodynamic explanations (the heart as a pump) use the concept of preload (filling) and afterload (workload of the heart, which is wall tension and arterial pressure or vascular resistance). In this way, the progression of left sided heart failure towards right sided heart failure is explained as follows: prolonged left ventricular failure increases pressures in the left atrium (preload), which in time leads to a subsequent increased resistance in the pulmonary vascular system (which is the afterload of the right ventricle) and eventually may also lead to right ventricular failure. | ||