Essay Example on Congestive Heart Failure: Causes & Effects of Heart Malfunction

Introduction: Understanding the Pathophysiology of Congestive Heart Failure

The heart is an essential organ in the body. It facilitates the pumping of blood across the body, which transports substances such as gases, nutrients, and electrolytes - the circulation of blood influences the body defense mechanism and nourishment of the body tissues. Heart failure can, therefore, lead to various health conditions. Congestive heart failure is one of the most prevalent cases reported on the heart malfunction. It is caused by various abnormalities such as loss of the functionality of the cardiac muscles, overload in pressure and volume of blood, and increased peripheral demands. Heart failure is characterized by abnormalities in the contractility, especially a reduction which leads to reduced cardiac output. Reduced cardiac output results in unmet peripheral demands. Pathophysiology of cardiac failure is characterized by reduced efficiency in the functioning of the heart muscles. The reduced functionality can be attributed to overloading or damage to the heart muscles. The conditions which cause heart failure include hypertension, amyloidosis, or myocardial infarction. These features lead to an increase in the heart's workload and therefore reduced efficiency in supplying blood to the various parts of the body. Myocardial infarction results from an insufficient supply of oxygen to the heart muscles and eventual death. Amyloidosis is presented by the deposition of the fat plaques in the cardiac muscles leads to the stiffening of the muscles and reduced cardiac output as well as the stroke volume.

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The Role of Cardiac Muscles and Abnormalities in Congestive Heart Failure

Dharmarajan and Rich (2017) contend that the pathophysiology of congestive heart failure is a vicious cycle that sets on from the weakening of the cardiac muscles. The damage to the heart muscles is caused by the clogging of the arteries that may arise from coronary heart disease. Congestive heart failure can also result from increased overload in the heart that is connected to long-term hypertension. The damage to the heart muscles leads to a decline in the blood pumped from each heat beat. This is referred to as stroke volume. A reduction in the stroke volume is characterized by subsequent reduction in the cardiac output, which the amount of blood that is pumped by the heart per minute. The decline in the stroke volume, as well as the cardiac output, calls for the implementation of mechanisms to restore normal functioning and maintain the regular rates. In this case, there is an increased heart rate, structural changes in the heart muscles, and adaptation of the kidney to enhance fluid retention.

Mechanisms to Restore Stroke Volume and Cardiac Output in Congestive Heart Failure

Stroke volume and cardiac output can be increased by increasing the heart rate. The increase in the heart rate exerts pressure on the arteries and therefore reduces the efficiency in the distribution of blood to the peripherals. The resultant impact of increased heart rate is fast pumping of the heart and the associated fast filling of the heart. Structural change changes occur in the walls of the heart, aimed at increasing the stroke volume as well as the cardiac output. The structural changes are presented in different forms, and therefore each has a unique impact on the functioning of the heart. One of the mechanisms adopted by the heart to increase the stroke volume is thinning of the ventricles, which is referred to as dilated cardiomyopathy (Ter Maaten, Valente, Damman, Hillege, Navis, & Voors,2016). Dilated cardiomyopathy is presented by the enlargement of the heart muscles to increase the stroke volume and the thinning of the ventricular walls. The thin ventricular muscles are weak to pump blood to meet the demands of the peripheral body tissues and organs. The thin muscles are weak and lack the ability to meet the required stroke volume and cardiac output. Failure to attain the body demands leads to attempts to restore the heart's pumping capacity.

Structural Changes in the Heart: Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy

The heart may also attempt to correct the decline in stroke volume by thickening of the ventricular muscles. The heart ventricles may thicken to increase the pumping capacity. This is referred to as hypertrophic cardiomyopathy. This situation leads to the thickening of the ventricular walls. The thickened ventricular walls become stiff and fail to attain the required stroke volume. The heart becomes rigid, and its physiological activity is impaired. The stiffening of the cardiac muscles reduces the efficiency of the pumping of blood, which witnessed in the impaired filling of the heart. Failure in the filling of the heart reduces the stroke volume along with the cardiac output.

The Role of the Kidney in Congestive Heart Failure: Fluid Retention and its Consequences

The kidney reacts to the declined rate of cardiac output. A decline in stroke volume leads to a significant deficiency in blood supply to peripheral organs and tissues (Masetic and Subasi, 2016). The kidney detects a decline in the blood content and tries to retain water. Therefore, it detects a drop in cardiac output and consequently initiates the release of renin. Renin causes the release of angiotensin hormone, which also triggers the release of the aldosterone hormone. Aldosterone hormone is imperative to the retention of water and electrolytes. In this case, retention of water and electrolytes is initiated, which leads to the volume overload in the heart muscles. According to Francis and Tang (2019), the action of renin-angiotensin II hormone and catecholamines induce the vasoconstriction of the glomerular arteriolar and therefore reduce the flow of the glomerular plasma flow. Increased levels of angiotensin II lead to decreased glomerular filtrate and, therefore, retention of salts and water. In the case of the failure on the left side of the heart, there is an accumulation of fluids in the lungs and, therefore, the name congestive. The congestion of blood in the lungs leads to the proliferation of blood in the underlying tissues and in the lungs leading to pulmonary edema. On the other hand, if the failure extends to the right side of the heart as it is usually the case, the drainage of the lower extremities and the brain is hampered, and therefore the peripheral parts of the body are affected. In this case, peripheral edema is experienced. Drainage of the head is significantly important, and therefore failure in drainage leads to the distention of the jugular vein.

Conclusion

In conclusion, the role played by the heart is crucial in the supply of essential substances across the body. This is, however, derailed by heart failure. Congestive heart failure is characterized by the accumulation of body fluids in different parts of the body due to the inability of the heart to effectively maintain a required stroke volume and cardiac output. A decline in cardiac output leads to an increase in heart rate to establish the required levels of stroke and cardiac output. The pathophysiology of congestive heart failure is, therefore, presented through the corrective mechanisms adopted by the heart to enhance the stroke volume and cardiac output. These mechanisms include increased heart rate, which results in a faster filling of the heart, impairing the pumping mechanism of the heart. The other approach adopted is the change in the structure of the heart to meet body requirements. This is presented through dilated cardiomyopathy and hypertrophic cardiomyopathy. The kidney also influences the manifestation of congestive heart failure through its sensitivity to declined cardiac output. The kidney senses and releases renin, which stimulates the release of angiotensin, which, on the other hand, triggers the release of the aldosterone hormone. Aldosterone hormone triggers the reabsorption of water and salts, leading to the accumulation of fluids. The accumulation of fluids is presented through pulmonary edema, distention of the jugular vein, and peripheral edema.

References

Francis, G. S., & Tang, W. W. (2019). Pathophysiology of congestive heart failure. Reviews in cardiovascular medicine, 4(S2), 14-20.

Ter Maaten, J. M., Valente, M. A., Damman, K., Hillege, H. L., Navis, G., & Voors, A. A. (2015). Diuretic response in acute heart failure-pathophysiology, evaluation, and therapy. Nature Reviews Cardiology, 12(3), 184.

Dharmarajan, K., & Rich, M. W. (2017). Epidemiology, pathophysiology, and prognosis of heart failure in older adults. Heart failure clinics, 13(3), 417-426.

Masetic, Z., & Subasi, A. (2016). Congestive heart failure detection using random forest classifier. Computer methods and programs in biomedicine, 130, 54-64.

Ziaeian, B., & Fonarow, G. C. (2016). Epidemiology and aetiology of heart failure. Nature Reviews Cardiology, 13(6), 368-378.