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Pharmacological Management of Congestive Heart Failure Using Captopril and Its Therapeutic Implications (Drug Study ) - Research Paper Example

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This paper ventured to describe and critically examine the pharmacological management of congestive heart failure (CHF) using Captropril an angiotensin-converting enzyme (ACE) inhibitor class of anti-hypertensive drugs…
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Pharmacological Management of Congestive Heart Failure Using Captopril and Its Therapeutic Implications (Drug Study Paper)
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Pharmacological Management of Congestive Heart Failure Using Captopril and Its Therapeutic Implications (Drug Study )

Download file to see previous pages... The readings also showed that the pharmacological management of CHF may be typified into first line and second line agents. The first line agents consist mainly of ACE-I, diuretics and beta blockers, while the second line agents consists of digoxin and hydralazine-isosorbide dinitrate. Captropil belongs to the second line of pharmacological agents. Use of Captropil had been found to enhance cardiac performance, among others. However, ACE inhibitors like Captropil sometimes causes in amigo-edema, painful tongue ulcers, and alveoli is to name a few. The implications of these and the rest of the findings are discussed in the conclusion. Discussion Congestive heart failure Congestive heart failure (CHF) is defined as an inability of the heart in supplying normal oxygen and nutrient demands to the body. CHF can be caused by a number of diseases which: (1) weaken the cardiac muscle; (2) harden the cardiac muscle; and (3) increase tissue oxygen demand beyond the capacity of the heart. This condition occurs primarily on elderly patients (Kaufman et al., 2008). Congestive heart failure commonly results from a dysfunctional heart muscle or myocardial dysfunction. CHF may also result from changes in the structure and function of the heart medically termed as progressive cardiac remodeling (Medifocus, 2011). The heart muscle enables it to pump blood to facilitate metabolism for the various tissues of the body. When the heart muscles do not function normally, blood flow through the heart and the entire body proceeds slower than normal. This causes increased pressure in the heart. The body responds to the decrease in the heart’s pumping capacity by the so-called compensatory mechanisms so that cardiac function can be maintained, such as the renin-angiotensin-aldosterone system and the sympathetic nervous system (Medifocus, 2011).         The compensatory mechanisms can be activated for a period of months or years. During the time that these compensatory systems are functioning, no evident symptoms of heart failure are presented and the patient is regarded as asymptomatic (Medifocus, 2011). Heart disease classified as asymptomatic is one in which the patient does not experience undue fatigue, dyspnea, palpitations and chest pain during ordinary activities (Capezuti, Siegler, & Mezey, 2008).         It should, however, be made very clear at this point that the functioning of the aforementioned compensatory systems will cause further damage to the heart in the long run, and consequently affect the circulation of the blood in the body. Such damage is caused by the changes brought about by process of structural remodeling where the heart may enlarge, the cardiac walls may thicken or become thinner and further decrease in the pumping capacity of the heart. One or a combination of these changes further weakens the heart and causes the pumping to be less effective until the patient eventually develops symptomatic heart failure (Medifocus, 2011). How CHF manifests itself depends on the type of stress the heart is being subjected to, in addition to which ventricle is affected. For example, disease affecting the left ventricle causes pulmonary edema. Meanwhile, disease affecting the right ventricle is more likely to cause edema to the lower limbs and other parts of the body. Moreover, CHF can affect the flow of blood to other organs. For example, inadequate blood flow to ...Download file to see next pagesRead More
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