Analysis Of The Pathophysiological Framework Of Dilated Cardiomyopathy

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

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).

Young children who have hypertrophic cardiomyopathy tend to have no symptoms of their condition until

Although these interventions may improve immediate survival in the short term, only coronary artery revascularization and cardiac transplantation have been shown to improve long-term survival.” (DeMarco & Chatterjee, 1993)

One of the rarest of congenital cardiac defects is Hypoplastic Left Heart Syndrome, HLHS. This syndrome is described as a collection of anomalies affecting the left heart and connecting structures. Due to advancements in surgical intervention mortality rates in neonates with Hypoplastic Left Heart Syndrome have decreased. Management of these patients requires a symphony of multidisciplinary teams including fetal and pediatric cardiologist, cardiac surgeons, neonatologist, pulmonologist, nutritionist and family counselors. Options currently comprise of heart transplant, three-staged palliative surgery and comfort care. There may be co-morbidities present which further complicate treatment, but with surgical intervention the

In cardiomyopathy the heart muscle becomes enlarged, thick or rigid, and in rare cases the muscle tissue can be replaced with scar tissue. As this disease worsens, the heart becomes weaker and unable to pump blood normally through the body and maintain a normal electrical rhythm. This can lead to heart failure or irregular heartbeats. The weakening of the heart also can lead to other problems such as heart valve problems. Cardiomyopathy can be acquired or inherited. It can affect people of all ages. There are various types of cardiomyopathy includes, hypertrophic, dilated, restrictive cardiomyopathy, Arrhythmogenic right ventricular dysplasia and unclassified cardiomyopathy. Some people with cardiomyopathy will never have any signs and symptoms. But in some people the signs and symptoms will develop in the early stages of the disease. As cardiomyopathy worsens and the heart weakens, signs and symptoms of heart failure usually occur. The signs and symptoms of cardiomyopathy includes, shortness of breath or trouble breathing, especially with physical exertion, fatigue, swelling in the ankles, feet, legs, abdomen, and veins in the neck. Other signs and symptoms may include dizziness, light-headedness, fainting during physical activity, irregular heartbeats, chest pain, especially after physical exertion or heavy meals, and heart murmurs. The treatment of cardiomyopathy include lifestyle changes, medicines, surgery, implanted devices to correct arrhythmias (National Heart, Lung, and Blood Institute,

Cardiomyopathy is a disease of the heart muscle. It is where the ventricular structure is impaired. The heart muscle

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

Robert H, et al (2005) describes the word hypoplastic as the state of an organ that has become stunted in its growth. Hypoplastic left heart syndrome occurs when parts of the left side of the heart are significant undeveloped including the left ventricular cavity and mass. The condition is present at birth. Usually, babies with hypoplastic left heart syndrome the mitral valve is not formed, the aortic valve is not formed and the ascending portion of the aorta is underdeveloped or is too small. Often, babies with hypoplastic left heart syndrome have an atrial septal defect.

Dilated Cardiomyopathy (DCM) is a type of heart disease in which the chambers of the heart increase in size and the muscle walls thin; the relative thinness of the heart’s walls, compared to the dilated size of the heart, leads to a weakened ability to pump blood to the rest of the body (3). DCM affects one out of 2500 people each year (4) and is one of the leading causes of heart failure in young adults (5). Diagnosis of this disease is difficult because its symptoms are not severe or debilitating, and diagnosis – taking a biopsy of the heart – is often invasive and risky (2); not as many people are being diagnosed with it as the number of those who have it. This limited sample size inhibits the study of

Diagnosed with Congestive cardiomyopathy implies that the patient’s heart muscle has been debilitated by ailment and cannot sufficiently pump blood through the heart, which can lead to heart failure (“Columbia University Medical Center”, 2016). In this case study, the current situation of a male patient Mr. P., who is 76 years old, and frequently hospitalized with CHF is given. The purpose of this paper is to describe an approach to care with treatment plan recommendation, provide education to both the patient and his family, and a teaching plan.

A little girl by the name of Jaelyn was born with congenital heart disease (CHD). Jaelyn’s parents learned about her condition called Ebstein’s Anomaly during a fetal echocardiogram when her mother was only 30 weeks pregnant. The doctors and nurses at Cardinal Glennon Children’s Hospital monitored Jaelyn in-utero to watch for hydrops (heart failure) and other indications her heart disease was affecting her growth. Jaelyn went into heart failure just five weeks later when her mother was only 35 weeks pregnant. She was given a 5% chance of survival due to the severity of her defect. The family was also told Jaelyn would not survive past her first birthday; she turns five in March. When Jaelyn was born, her entire family was afraid she wouldn’t survive the delivery, but thankfully, Jaelyn’s story is a true miracle. When the doctors see Jaelyn during routine checkups and physician visits, they can’t believe she has Ebstein’s Anomaly because for how far she has come and how healthy she looks. Sadly, not every child with congenital heart disease gets the miracle Jaelyn has been given. Congenital heart disease has many causes that impact the child and

Hypertrophic Cardiomyopathy is a genetic disorder that causes progressive abnormal thickening of the heart (1). This thickening of the muscle of the heart may be minor, slowly progressing or severe producing sudden death. People with Hypertrophic Cardiomyopathy have a large thick heart muscle, and as a result decreases the cavity size of the heart. This means the heart holds and pumps less blood. It also can make it harder for the heart to relax and fill with blood. (2) It is an obstruction to the flow of blood as it is pumped out of the heart. Once the muscle is too large, it’s function decreases and the heart starts to quiver in

Dr. Volk had several different heart issues that resulted in his eventual heart transplant. One of the issues was called dilated cardiomyopathy, or the enlargement of chambers of the heart that typically starts with the enlargement of the left ventricle (American Heart Association, 2016). When a heart is enlarged too much the cardiac muscles can’t work as efficiently resulting in weaker contractions. Since his left ventricle was enlarged he was unable to pump a sufficient amount of blood to his body (American Heart Association, 2016). This resulted in Dr. Volk’s body not getting sufficient oxygen or nutrients. When blood enters a normal sized heart the cardiac muscles are stretched to an ideal length based on the length-tension relationship