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).
Patients presenting Symptoms: Gradual onset of dyspnea on exertion, fatigue, frequent dyspepsia with nausea and occasional epigastric pain, trouble breathing while lying on his back and, which is relieved by sitting up (orthopnea), an hypertension.
HCM happens when the heart muscle enlarges and thickens without an obvious cause. Usually the ventricles, the lower chambers of the heart, and septum thicken. The thickened areas create narrowing or blockages in the ventricles, making it harder for the heart to pump blood; however, in very few instances the heart actually contracts with much greater force causing an obstruction to the blood flow (CMUK, 2015). HCM also can cause stiffness of the ventricles, changes in the mitral valve, and cellular changes in the heart tissue.
In the valvular disease the regurgitation of blood back to the ventricles occurs when the valves fail to close tightly and this will result in ventricular overload and increased muscle stretching. This increases the heart muscles need for oxygen and energy resulting in the cardiac muscles to contract harder (Karch, 2013). The failure of the left ventricle to pump efficiently will lead to pulmonary vessel congestion and in severe cases, pulmonary edema whereas the inefficient pumping of right ventricle will lead to liver congestion and peripheral edema (edema of the legs and feet). The cardiovascular system works as a closed system and therefore, if one-sided failure left untreated, will eventually lead to failure of both sides (Karch, 2013). The American College of Cardiology (ACC)/ American Heart Association (AHA) has incorporated a classification system of heart failure that include four stages. This staging system (stage A to stage D) recognizes that there are established risk factors and structural abnormalities that are characteristics of the four stages of heart failure.
Cardiomyopathy is the deterioration of muscles within the heart which in turn causes the heart to become thick, rigid or enlarged; this physiological change causes decreased contractility and may lead to arrhythmias or heart failure (VanMeter and Hubert, 2013). In the case study, the client is a seven-year-old girl from Chetwynd who is recently diagnosed with dilated cardiomyopathy. When she was ten months old, she underwent a heart transplant for her hypoplastic left heart syndrome. Hypoplastic left heart syndrome is a complex and rare heart defect that is congenital, or present at birth, in which the left side of the heart is severely underdeveloped. The left ventricle is not functional and therefore the left side
Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further
A lot of people in this world are unknown to the heart disease called peripartum cardiomyopathy. This heart disease is a uncommon heart disease. It’s a heart failure that happens in some women in the last month of their pregnancy. With this heart disease the heart cannot pump enough blood to the body’s vital organs. Which then causes organ failure if not caught. PPCM is still being studied doctors still don’t know what exactly triggers the heart failure. They say it may be from autoimmunity, immune system micronutrient. In the beginning phase of PPCM it causes inflammation in the heart. The heart muscle cells start to become damaged. After the heart muscle is damaged scar tissue begins to form. Which makes it hard
Our patient Mr. P has been hospitalized for cardiomyopathy and congestive heart failure (CHF) symptoms. This paper will discuss the approach to care for the patient. In addition, it will recommend a treatment plan. Lastly, it will offer education and a teaching plan for both the patient and his wife to help cope with his condition.
Our case illustrates that TCM mimicks AMI. Although causality cannot be concluded if there is association. Takotsubo cardiomyopathy represents an estimated 1% to 2% of patients who present with an AMI, but low estimate may be because of under recognition. Advanced age and female are the most common known risk factors for developing TCM. The pathophysiology of TCM is unknown but it is believed to be caused by elevated cathecolamines secondary to acute somatic and emotional stressors.(6,7) Other associated risk factors includes intracranial events, severe infection, surgical trauma and respiratory diseases. Among the physical stressors known to be related with TCM are intracranial occasions, infection, surgical injury and respiratory disease.8 For our situation, the respiratory disease may have contributed to the development of TCM
Ryan Gillyard is a fifteen-year-old athlete boy who was passionate to play Division I college football. He was a “linebacker” and “running back” in football. He lived in Upper Darby and passed away on April 18, 2015.
Cardiomyocytes or cardiac muscle cells are vital for the heart function despite their numbers being considerably lower than other types of cells in cardiac tissue. The loss of cardiomyocytes and its insufficient regeneration is the major contributor in the pathogenesis of many cardiovascular diseases, including myocardial infarction, cardiac fibrosis and heart failure (Bergmann et al., 2009; Porrello et al., 2011b; Mollova et al., 2013). In fact, the injury induced adult myocardial tissue remodeling results from the lack of cardiomyocytes replenishment, while the neonatal and fetal myocardial tissues retain its contractile tissue from the proliferation of pre-existing cardiomyocytes after injury (Porrello et al., 2011b). This is mainly due
Arrhythmogenic right ventricular cardiomyopathy (ARVC) (1) is an inherited disease characterized by the progressive replacement of the myocardium by adipose and fibrous tissue (2) that predisposes to the development of ventricular tachycardia (VT) and to sudden cardiac death (SCD). This condition was described three decades ago, when fibro-fatty infiltration in the right ventricle was considered its pivotal indicator (3,4). It later became clear that the ARVC is mainly caused by mutations in the genes encoding for desmosomal proteins (1). This helped unveil that the disorder is often associated with biventricular manifestations (5) and the term "arrhythmogenic cardiomyopathy" has also been proposed (1). The unmet need in the management
Thanks for bringing up the idea of genetic counseling, because dominant and recessive genes are revealed and making the diagnosis will be much easier. As we know, hypertrophic obstructive cardiomyopathy is a common inherited cardiac disorder. The thickening of the septal wall decreases the outflow to the left ventricle wall. Increased heart rate and decrease intravascular volume leads to the obstruction of the left ventricular outflow. If the condition is not resolved ventricular dysrhythmias and sudden death may occur and this is commonly seem in more than 33% of young athletes (Huether & McCance, 2012). Individuals with such family history needs consistent health check up with the cardiologist. Good job.