Congestive Heart Failure - Research Paper Example

In case of congestive heart failure, there is an insufficient blood supply to the heart resulting in the intolerance for any kind of exertion and the individual witness shortness of breath. Chest-radiography and blood tests are performed to confirm the diagnosis. Such physiological hyperadrenergic condition cannot be retained for long and, therefore, restoration should be performed as soon as possible. Restoration is performed with changes in lifestyle, medication involving a blend of an angiotensin-converting-enzyme inhibitor and a gradual ?

-blocker titration. In certain cases, a device is also implanted or surgery is performed to relive the CHF cases. The condition is often found to generate susceptibility for pulmonary complications. Introduction Congestive heart failure, CHF, is a condition where heat is not able to meet the metabolic demands of the body due to low cardiac output. Congestive Heart Failure involves 2 different mechanisms which are attributed to decrease in the cardiac output. Those are: A. Systolic dysfunction – damage to myocardium, mitral stenosis. B. Diastolic dysfunction – decreased capacity of the ventricle to fill with blood, e.g. constructive pericarditis.

(Figueroa & Peters, 2006) Pathophysiology of CHF CHF can be of two types: low output failure which is due to weak contractions or low ejections of blood from ventricles, e.g. . E.g. if the left ventricle is not able to propel the blood to the aorta it leads to residual volume during each systole. This residual volume gradually builds up and dilates the left side of the heart resulting in backward failure theory due to poor contractions of the left side of the heart. The blood stagnates in the right auricle which is passed to pulmonary veins; subsequently, this back pressure or stagnation of blood is passed to the blood vessels of lungs, leading to an increase in the intrahydrostatic pressure in the pulmonary vessels resulting in transudation of fluid from intravascular to extra-vascular compartments, a condition known as pulmonary edema which is responsible for clinical features like dyspnea, hemoptysis, PND (Paraxosymal Nocturnal Dyspnea).

If the condition is left untreated, back pressure is transmitted to the right side of the heart because of existing pulmonary hypertension. As the pressure in the pulmonary artery increases, gradually it results in right-sided failure which is characterized by increased JVP (Jugular Venous Pulse); hepatomegaly, pedal edema, etc. There is a constant low cardiac output in the initial stages as per Starling's law, an increase in the myocardial muscle fiber length, and there is a compensatory tachycardia to meet the metabolic demands of the body.

If left untreated, there is a failure of this compensatory mechanism resulting in dilated inefficient heart. These compensatory mechanisms are also responsible for cardiac remodeling which is characterized by deposition of fibrous tissues in heart matrix and increased oxygen demand of myocardium. This is mostly due to an active renin-angiotensin system which is stimulated due to low blood supply to