Heart Suffufficiency: What Is Heart Insufficiency Or Heart Failure?

Heart failure may convey that the heart isn’t working anymore, but what it really means is that the heart isn’t pumping as well as it should be (REF). Heart failure is a chronic, progressive condition in which the heart muscle is unable to pump enough blood through to meet the body’s needs for blood and oxygen (REF). At first, the heart tries to make up for this by enlarging, developing more muscle mass, and pumping faster. As this happens, the blood vessels narrow to keep blood pressure up and the body diverts blood away from less important tissues and organs to maintain flow to the heart and brain (REF). Eventually, the body and heart cannot keep up and the patient begins to feel fatigue, breathing problems, weight gain with swelling in the feet, legs, ankles or stomach, and other symptoms that eventually leads to a hospital visit. The body’s coping mechanisms give us better understanding on why many are unaware of their condition until years after the heart declines (REF).

Congestive cardiac failure, also known as heart failure, occurs when the heart is weak and unable to sufficiently supply blood the body needs to function. Heart failure can often be successfully treated with

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).

Heart Failure is a progressive heart disease when the muscle of the heart is weakened so that it cannot pump blood as it should; the blood backs up into the blood vessels around the lungs and the other parts of the body (NHS Choice, 2015). In heart failure, the heart is not able to maintain a normal range cardiac output to meet the metabolic needs of the body (Kemp and Conte, 2012). Heart failure is a major worldwide public health problem, it is the end stage of heart disease and it could lead to high mortality. At present, heart failure is usually associated with old age, given the dramatic increase in the population of older people (ACCF/AHA, 2013). In the USA, there are about 5.7 million adults who have heart failure, about half of the people die within 5 years of diagnosis, and it costs the nation an estimated $30.7 billion each year (ACCF/AHA, 2013).

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).

Contractility is the pumping of the heart muscle. It is measured as the ejection fraction. Contractility directly influences stroke volume. Increased contractility will increase stroke volume with any amount of preload. Diseases that disrupt myocyte activity reduce contractility. Myocardial infarction is the most common. Others include, but are not limited to, cardiomyopathies, degenerative valve disease, and myocarditis (Francis & Tang, 2003). Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to neurohumoral , immune, and inflammatory changes and can cause ventricular remodeling. Ventricular remodeling occurs when the size, shape, and function of the affected chamber is distorted. Ventricular remodeling causes hypertrophy and dilation of the heart muscle and causes progressive myocyte contractile dysfunction over a period of time. When contractility is decreased, stroke

The diagnosis is made when an ejection fraction of less than 40% is found during an echocardiogram test. Patients with known systolic heart failure and current or prior symptoms are Stage C. Most common symptoms include, shortness of breath, fatigue and reduced ability to exercise. Stage D is patients with systolic heart failure and presence of advanced symptoms after receiving optimum medical care. Other risk factors for heart failure are some diabetes medications, sleep apnea, congenital heart defects, viruses, and irregular heartbeats. Heart Failure can be treated and managed but not cured. It is a chronic condition.

Diastolic dysfunction is a problem with the ventricle’s ability to relax and fill. Mixed systolic and diastolic dysfunction is a combination of the two defects (Williams and Hopper).

The reduced pumping can also lead to less blood being moved from the ventricle during systole. The left ventricle steadily fills with more and

Heart failure-is the main focus of this project and is when the pumping action of the heart cannot supply enough blood to the rest of the body as a result of damaged cardiac tissue in the heart specifically.

Heart failure is a condition in which the heart muscle becomes too weak to maintain an adequate cardiac output to meet the body’s

Common symptoms of Cardiomyopathy are dyspnea (breathlessness) and peripheral edema (swelling of the legs). It starts with the muscle becoming hard, thick, and engorged sometimes becoming replaced with scar tissue. As the muscle rigidifies, the heart weakens, is less bale to pump oxygen through the body, and starts to falter. Heart beat becomes irregular (called arrhythmias) and fluid can build up in lungs, ankles, feet, legs, or abdomen.

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

When the ventricles are contracting at a rate greater than one hundred beats per minute, the heart becomes inefficient. Blood cannot properly fill the ventricular chambers before it is forced out. This decreases the amount of oxygenated blood circulating through the body.

In a sweeping fashion, the right atrium contracts and forces the final volume of blood into the right ventricle. The left atrium contracts and contributes the final 20% of volume to the left ventricle.