Case Study 2
Cardiomyopathy defines any disease of the heart muscle that hinders the heart’s ability in pumping blood with adequate force. It is classified as ischemic (caused by coronary artery disease) or nonischemic (Maron and Salberg, 2008). Examples include the follwoing;
- Dilated cardiomyopathy is a limitation in the heart’s walls that makes them to expand out, compromising the efficiency and raising the risk of arrhythmias, congestive heart failure and the formation of blood clots.
- Hypertrophic cardiomyopathy: This is an overgrowth of heart muscle that compromises the flow of blood through the heart.
- Restrictive cardiomyopathy defined as loss of elasticity of the heart walls. This hinders the heart from effectively filling with blood prior to contracting (Maron and Salberg, 2008).
In order to evaluate Mr. P for cardiomyopathy, I will first examine him. If necessary, I may ask him to be tested in one or more of the following tests: cardiac catheterization, electrocardiogram (ECG or EKG), pressure-volume loop analysis, echocardiogram, X-ray or biopsy (MacRae, 2010).
An electrocardiogram, records the heart’s electrical activity while at rest to establish abnormal heart rhythms. To evaluate pressures in the heart, I may perform an outpatient process called a cardiac catheterization. In this test, a thin plastic tube is inserted through a blood vessel until it reaches the heart. A dye is then injected into the blood vessels and X-rays taken to assess the heart’s structure as well as function. Simultaneously, I may do a pressure-volume loop analysis (Maron and Salberg, 2008). This test measures the amount of blood flow the heart puts out during each beat. The results will help me pinpoint the kind of cardiomyopathy Mr. P has. Performing an X-ray will help me see if the heart is enlarged, biopsy helps determine the extent of disease.
Possible courses of treatment:
According to Maron and Salberg (2008), cardiomyopathy is difficult to diagnose early, it is hardly ever treated in its commencement stage. I recommend a treatment goal to relieve any complicating factors, put symptoms under control, and stop the progression of the disease.
A medication should be administered to decrease heart muscle exertion, regulate the heartbeat improve the heart’s pumping ability and ease symptoms. A change in lifestyle changes is encouraged too, this includes avoiding strenuous physical activity, losing weight abstaining from alcohol, and minimizing the amount of salt intake in the diet. In case the heart muscle has been badly destroyed and the patient’s condition does not get better with medications as well as change in lifestyle, a heart transplant may be performed (Maron and Salberg, 2008).
A 2-g sodium diet is regularly recommended. This diet is unpalatable for some patients, while a 3-g sodium diet could a more reasonable aim for patients with gentle to modest heart failure. This can be attained by keeping off salty foods and by avoiding the adding of salt to foods after cooking. If patients need large doses of diuretics to avert fluid retention, intake of sodium has to be more sternly restricted, which calls for the careful reading of food labels (Starling 1998).
As a patient is guided in a program of heart failure management, there should be clear assessment of a complex clinical stability. The instability degree controls decisions concerning further medical therapy, like drugs, transfer back to a heart failure specialty plan, as well as consideration of protocols in transplantation or investigation. Additionally, the elements of both psychosocial and physiological stability control the allocation of precious personnel time for more education, recurrent telephone calls, as well as home visits (Maron and Salberg, 2008).
The teaching plan
An important position to start teaching is a plain, comprehensible, and easy clarification of the pathophysiology of heart failure. Scores of patients misunderstand the expression “heart failure” and suppose that it implies that the heart has permanently failed, hence death. The term should be carefully explained, with an emphasis that it is a decline in the hold back pumping power of the heart (Maron and Salberg, 2008).
The patient should be made to understand that it could limit their ability to perform some forceful activities. For many patients, flow at rest as well as during normal activities of everyday living is at normal levels (Maron and Salberg, 2008). It is important to clarify between expected signs of heart failure and signs of worsening failure. Patients should be given instruction to notify their healthcare giver immediately when at the occurrence signs of worsening failure to put off unnecessary complications or hospitalizations (Maron and Salberg, 2008).
References
MacRae, C. (2010). Genetics of Cardiomyopathy and Heart Failure: An issue of Heart Failure Clinics. London: Elsevier Health Sciences
Maron, J. B. and Salberg, L. (2008). Hypertropic Cardiomyopathy: For Patients, their Families and Interested Physicians. New York: John Wiley and Sons.
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