Dilated Cardiomyopathy (DCM)

The prevalence of congestive heart failure is on the increase both in the United States and all over the world, and it is the leading cause of hospitalization in the elderly population. Congestive heart failure is a progressive disease generally seen in the elderly, which if not properly managed, can lead to repeated hospital admissions or death. Heart failure means that the heart muscle is weakened. A weakened heart muscle may not be strong enough to pump an adequate amount of blood out of its chambers. To compensate for its diminished pumping capacity, the heart may enlarge. Commonly, the heart's pumping inefficiency causes a buildup of blood in the

Heart failure can be attributed to either right sided, left or both. Left-sided heart failure is of two types, systolic failure and diastolic failure. Systolic failure is the when the left ventricle loses its ability to contract normally. The heart cannot pump with enough force to push enough blood into circulation. Diastolic failure is when the left ventricle loses its ability to relax normally. Which results in the heart not being able to fill with blood during the resting period. Both result in a decrease in cardiac output. (AHA, 2012). A decrease in the cardiac output into the systemic circulation causes blood to accumulate in the left ventricle, left atrium, and pulmonary circulation. This increase

Approximately, 1 of every 500 people is affected with hypertrophic cardiomyopathy, it is important for patients to understand the dynamics of the disease as it could potentially be life threatening. In most cases, the patients quality of life is not affected, but a few will experience symptoms that cause significant discomfort or undetected complications that could lead to sudden cardiac death. With that in mind, it would be beneficial to recognize what it is, specific causes, the steps of diagnoses, and the options for treatment.

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

Heart failure affects nearly 6 million Americans. It is the leading cause of hospitalization in people older than 65. Roughly 550,000 people are diagnosed with heart failure each year (Emory Healthcare, 2014). Heart failure is a pathologic state where the heart cannot pump enough blood to meet the demand of the body’s metabolic needs or when the ventricle’s ability to fill is impaired. It is not a disease, but rather a complex clinical syndrome. The symptoms of heart failure come from pulmonary vascular congestion and inadequate perfusion of the systemic circulation. Individuals experience orthopnea,

Primary treatments include antibiotic therapy, Fluid resuscitation, and crystalloid. Potential treatments depending on patient status include vasopressors and steroids, ventilator, renal dialysis, blood transfusion, and surgery.

Congestive heart hailure, also known as CHF or heart failure, affects the lives of 5 million Americans each year with 550,000 new cases diagnosed yearly. (Emory healthcare, 2013) CHF is a medical condition in which the heart has become weak and cannot pump enough blood to meet the need for oxygen rich blood required by the vital organs of the body, less blood is pumped out of the heart to the organs and tissues in the body and pressure in the heart increases, it does not mean the heart has stopped working. (Murphy, 2013) Once the heart has become weakened by conditions such as hypertension, abnormal heart

Varying patients may present to their clinician or the emergency department for treatment with heart failure. It is important to understand that there is more than one type of heart failure; primarily the focus is placed on diastolic heart failure and systolic heart failure. Depending upon the cause of heart failure and what areas are affected dictates the treatment plan needed. While there are similarities with both kinds of heart failure, there are also differences that can help the clinician distinguish the diagnosis needed to fit the patient. Once a diagnosis is made the clinician can move forward in determining if the patient is at risk for use of diuretics and then look towards prescribing ACEIs, ARBs, and beta-blockers.

Treatments include changes in your lifestyle such as reducing sodium, avoiding alcohol, and increasing exercise, taking medication for blood pressure, and possible surgery or carried cauterization. Patients can also take medications such as beta-blockers, digitalis, diuretics, as well as others. Beta-blockers can prevent death in some patients, digitalis slows the rhythm of the heart while increasing the patients heart beat, and diuretics will reduce the amount of fluids retained in the body. In certain cases pacemakers can be recommended or if medications are unsuccessful on their own, a patient may receive a heart pump. As a worst case scenario, a patient may require a heart

Defects and problems with vital organs can be remedied through installing a pacemaker, surgery to repair septal defects, abdominal surgeries to correct obstructions/damaging anatomical issues in the thoracic and abdominal area. Abdominal obstructions are serious and if not monitored and treated are life threatening. However not all patients need extreme medical procedure, like surgery, because of the complications that come with dextrocardia. In many cases antibiotics are prescribed to boost or maintain the immune system because of the increased probability of respiratory illness as a result of asplenia and respiratory malformations. On average people with dextrocardia contract infections more often but overall dextrocardia, even in complicated cases, is manageable with the right care, information and medical

Nonsurgical treatment usually involves medications such as diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), nitrates, digitalis, potassium, aspirin, calcium channel blockers, blood thinners, and beta blockers. Some surgical treatments include pacemakers, implantable cardioverter defibrillators (ICDs), intra-aortic balloon pump, ventricular assist devices (VADs), an implantable artificial heart, angioplasty and coronary bypass surgery, heart-valve surgery, heart transplantation, and myocardial replacement therapy. Some alternative medicines include antioxidants, homocysteine metabolism, magnesium, taurine, carnitine, essential fatty acids, diet, herbs, acupuncture, massage, biofeedback, and

Stem cells have made significant promise to help people understand and treat a broad range of injuries, diseases, and other health-related issues. This type of treatment has saved the lives of many people with leukemia and can also be used for tissue grafts to treat conditions with the skin, bone and surface of the eye ("Nine Things to Know about Stem Cell Treatments"). Dilated cardiomyopathy (DMC) is a disease characterized by expansion of the left ventricular chamber and it is usually associated with systolic dysfunction. The presentations of the condition include heart failure, myocardial infarction, and arrhythmia and as a refractory life-threatening condition which can cause heart failure, transplantation remains the ultimate therapy for

The major causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia-induced ventricular transformation (coronary artery disease). Hypertrophy and ischemia cause a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation. Some of the other causes are aortic valvular disease and cardiomyopathies. Diabetes can also lead to diastolic heart failure (Huether and McCune 2012). Other risk factors for this disease are chronic kidney disease, obstructive sleep apnea, and older age. There are two types of the heart failure: systolic heart failure and diastolic heart failure. In systolic heart failure, the left ventricle has difficulty contracting and ejecting blood into the circulation, which causes reduced left ventricular fraction. On the other hand, diastolic heart failure has a slow and delayed relaxation and increased chamber rigidity, which then causes inadequate filling of blood and

The term “ventricular remodelling” includes a complex of anatomic, functional, cellular, and molecular changes in the myocardium in response to the injury Markers of cardiac remodelling are hemodynamic and echocardiographic changes which correlate with cardiac impairment (Cohn et al., 2000; Kubanek et al., 2013). In HF animal models, the process of left ventricular (LV) remodelling begins rapidly, and continues to progress; LV are a greater cardiac chamber dilation, a greater increase in systolic and diastolic volume index and a progressive decline in the ejection fraction (EF) (Eaton et al., 1981; Korup et al., 1997; Cohn et al., 2000; Kubanek et al., 2013).