Heart Failure Mechanisms And Compensatory

Heart failure is due to the inability of the heart to supply adequate cardiac output to the tissues. During systolic heart failure, the stroke volume is greatly reduced and the ventricular contraction is very weak. This leads to an increased amount of the end systolic ventricular volume. The ejection percentage therefore reduces from 65% to 20%. The initial compensatory mechanism of the heart kicks in. The genes in the cardiac myocytes that are responsible for hypertrophy are activated and their function is to thicken the ventricular wall and facilitate cardiac remodeling.

There is incomplete filling of the arteriolar system of the heart during systolic heart failure. There is a corresponding increase in the sympathetic neural system discharge, this increases the heart rate. The low blood pressure is detected in the kidney and renin is secreted. This causes vasoconstriction of the vessels and aldosterone hormone is secreted. Aldosterone hormone increases the reuptake of sodium ion and the osmolarity of blood, hence more water is selectively reabsorbed into the body in an attempt to increase the blood pressure in the body. When the initial response does not facilitate homeostasis in the body, the ventricles then dilate.


During diastolic heart failure, the ejection fraction of the heart is maintained as the elasticity of the myocardium is greatly reduced. This further reduces the filling during diastole. As a result of this, the stroke volume reduces and the cardiac output reduces. The blood pressure in the peripheral blood vessels decreases and when the kidney detects this it secretes both renin and aldosterone hormone to help raise the blood pressure by increasing the fluid amount. In the heart cardiac remodeling also takes place in both diastolic and systolic heart failure. Cardiac remodeling occurs when there is heart failure and the heart modifies itself in size, shape and function to respond to the failure. It is greatly influenced by neuro-humoral activation and production of cytokines, nitric oxide and oxidative substances. It occurs through concentric hypertrophy or eccentric hypertrophy. The former refers to an increase in the thickness of the left ventricular muscle while the latter refers to the dilation of the left ventricle.

During heart failure there is irreversible remodeling that takes place. There is a chronic overload that is disproportional to the heart. There is an increase in the oxidative chemicals and due to the mechanical stress, fibroblast produce interstitial collagen together with the smooth muscles. Fibrosis therefore occurs in the infracted and non-infracted muscle. The fibroblast and the collagen therefore replace the cardiomyocytes that are destroyed by necrosis and the stiffness of the heart increases. The contractility decreases and because there is no hypertrophy, ventricular dilation occurs. Ventricular dilation occurs as newly formed sacromeres are added in series to the existing. This is eccentric hypertrophy

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Concentric hypertrophy occurs when there is an increase in the afterload. There is a corresponding increase in the intra-ventricular pressure so as to be able to open the aortic valve during the ejection phase. Due to this intra-ventricular pressure there is an increase in myocardial wall stress. The systolic blood pressure increases and the intensity of isometric activity increases. The genes of the heart cells are activated and new sacromeres are synthesized and are added in parallel

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