Heart failure occurs when the pumping capacity of the heart is compromised.
It is a condition which the heart has trouble pumping blood because it has become weak or stiff; thereby decreasing its ability to meet the demand of the body’s need for oxygen and nutrients. It is important to understand that the symptoms of heart failure may be due to systolic dysfunction emanating from the right or left side of the heart, or may occur with preserved systolic function with symptoms due to the abnormal diastolic function of the heart. Systolic failure happens when the heart is not contracting well, meaning the blood can’t get out of the heart so the blood can’t get in because there is still blood in the heart. In diastolic failure, the blood can’t come into the heart because the ventricle is too thick and as a result of that, if the blood can’t come into the heart there is no blood to pump out causing HF. Heart failure can manifest in many ways, depending on how far ventricular remodeling and dysfunction have advanced.
Heart failure may be discovered because of a known clinical syndrome such as MI or because decreased exercise tolerance, fluid retention, or admission to the critical care unit for an unrelated condition (https://www.clinicalkey.com/nursing/).American Heart Association (AHA) estimated that there were 5.1 million of people with HF in the United States in 2006 and 23 million people with HF worldwide (AHA,2013). Heart failure and LV dysfunction has a correlation with age.
The prevalence among men is 8 per 1,000 at age 50-59 years, increasing to 66 per 1,000 at ages 80-89 years. Similar values (8 and 79 per 1000) were noted in women. The prevalence in African-Americans is reported to be 25%higher than in whites (Vasan ; Wilson, 2018). It is estimated that by 2030, an additional 3 million people will be diagnosed with heart failure (http://www.clinicalkey.com/nursing/).
Acute vs chronicAcute and chronic heart failure can be determined depending on the rapid progression of the syndrome. The presence and the activation of compensatory mechanisms, and the presence or absence of fluid accumulation in the interstitial space. Acute heart failure has a sudden onset, with no compensatory mechanisms.
The patient may experience acute pulmonary edema, low cardiac output, or cardiogenic shock. The deterioration into acute heart failure can be precipitated by the onset of dysrhythmias, acute ischemia, sudden illness, or cessation of medications. This may necessitate admission to critical care unit, on the other hand, patients with chronic heart failure is an ongoing process, with symptoms that may be made tolerable by medication, diet, and a reduced activity level. Patients with chronic heart failure are hypervolemic, have sodium and water retention, and have structural heart chamber changes such as dilatation or hypertrophy. Hypertension is the primary precursor of heart failure in women, whereas CHD, specifically MI, is the primary cause of heart failure in men.
In right-sided heart failure, the right ventricle fails to pump blood effectively, and blood may back up into other areas of the body (Kumar, Abba, ; Aster, 2013). The right side of the heart has anineffective right ventricular contractile function. Patients with right heart failure leak fluid into the tissue and organs that deliver blood to the right heart through the vena cava. Usually, right ventricular failure is commonly caused by failure of the left side of the heart. The common manifestations of right ventricular failure are jugular venous distention, elevated central venous pressure, weakness, peripheral or sacral edema, hepatomegaly (enlarged liver), jaundice, and liver tenderness. Gastrointestinal symptoms also include poor appetite, anorexia, nausea, and an uncomfortable feeling of fullness.
Right-sided failure also can occur in patients with primary pulmonic or tricuspid valve disease, or congenital heart disease causing chronic volume and pressure overloads (Voelkel, 2006). Failure of the left ventricle to contract results in a low cardiac output state, leading to vasoconstriction of the arterial bed that increases systemic vascular resistance and creates congestion and edema in the pulmonary circulation and alveoli. When the left ventricle cannot pump blood to the body and fluid backs up and leaks into the lungs causing shortness of breath.
Clinical manifestations of left ventricular failure include decreased peripheral perfusion with weak or diminished pulses, cool, pale extremities, and in later stages, peripheral cyanosis.Over time, with the progression of the disease state, the fluid accumulation behind the dysfunctional left ventricle elevates pulmonary pressures, that contributes to pulmonary edema and congestion, and produces dysfunction of the right ventricle resulting in failure of the right side of the heart (Hughes, 2009). Risk factorsThere are several contributing factors that leads to heart failure. Risk of heart failure increases as person ages. It may also be a consequence of atherosclerotic heart disease or some health problems such as heart attack (myocardial infarction). Injured tissues, which is caused by heart attack, does not contract as well as the heart’s ability to pump blood is weakened.
High blood pressure (hypertension) causes heart muscle to work harder than normal. High blood pressure eventually causes the heart to become stiff and weak. Coronary artery disease (CAD) also causes buildup of cholesterol and fat (plagues) in the arteries of the heart.
Heart muscle disease (cardiomyopathy or myocarditis). Heart muscle disease is damage to the heart muscle from a variety of causes, such as drug or alcohol abuse, infections, or unknown causes. Abnormal heart valves, when the heart valves do not open and close properly, the heart muscle must pump harder to keep the blood flowing.
Lung disease will also be a contributing factor because if the lung is not working properly the heart must work harder. Heart failure is also more likely to develop in persons who are: overweight, male, smoker or chew tobacco, those who abuse alcohol or illegal drugs, have taken medicines that can damage the heart such as chemotherapy drugs, those who have diabetes thus damaging the tiny blood vessels that carry nutrients to the heart muscle, those with abnormal heart rhythms, thyroid problems and low blood counts (https://lms.elsevierperformancemanager.com/ContentArea/PatientEducation/getPatientEdu..
.) Possible consequences:Congestive heart failure is basically progressing if not detected and controlled. An important issue in congestive heart failure is the risk of patients ending up with heart rhythm disturbances (arrhythmia).
Deaths that occurred in individuals with heart failure, approximately 50% of which are related to progressive heart failure. Importantly, the other 50 % is thought to be related to serious arrhythmias. If left untreated, dysrhythmia, followed by pump failure is the leading cause of death in HF. Most patients have >5 comorbidities (especially CAD, chronic kidney disease, and diabetes).
Prevention StrategiesDevelopment of preventive strategies should be established so that emphasis on self-management among patients will be practiced. These may include heart failure education and other actions designed to sustain engagement of patients with their heart failure care. A developed process to provide to the patient and or caregiver should focus in the area of lifestyle modification such as diet, exercise, fluid regulation, smoking cessation, energy conservation and how to incorporate exercise into their daily lives, and weight maintenance.
Sodium causes an increase in fluid accumulation in the body’s tissues. In congestive heart failure, the tissues are mostly swollen because of the fluid buildup therefore, patients become very sensitive to small intake of sodium and water intake. Because of these underlying causes, patients are advised to reduce salt intake and to choose foods labeled ‘no added salt’ or ‘low salt ‘.
They should also be instructed to avoid processed foods, salty snacks, fast foods and adding salt during cooking. Referring the patient to a dietitian for support with dietary changes may be advisable (National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand,2012). Exercise is also beneficial in maintaining overall capacity, quality of life, and improves survival. Patients are taught to weigh themselves daily that any weight gain of 2-3 pounds over a couple of days should be reported to the doctor. Treatment ModalitiesThe treatment of heart failure is focused on improving hemodynamics, relieving symptoms and blocking the neurohormonal response to hopefully improve survival. The treatment’s goal is on how to have the heart beat more efficiently so it can meet the energy needs of the body.
Specific treatment depends upon underlying cause, medications like diuretics, are used initially in fluid overload and fluid restriction and decrease salt intake will be very helpful. ACE inhibitors and ARBs are medicines that also shown to increase survival by decreasing systemic resistance and favorable altering hormonal issues, that affects cardiac performance. Beta blockers are also used in systolic or diastolic HF by increasing cardiac output.
Digoxin is also helpful in increasing cardiac output and control symptoms. In end-stage congestive heart failure (NYHA stage IV) patients may require aggressive treatments including left ventricular assist devices (LVAD), an implanted pump that helps increase the heart’s ability to squeeze or even heart transplantation. Consideration can be made for patients over 70 years with few comorbid conditions.
If a defective heart valve is responsible for the cause of HF, heart valve repair ans surgery is also recommended.(Http://www.medicine.com/congestive_heart_failure_chf_overview/article.htm#what_is_congestive_heart _failure_chf).References:https://www.clinicalkey.com/nursing/).https://lms.elsevierperformancemanager.com/ContentArea/PatientEducation/getPatientEdu…) http://www.medicine.com/congestive_heart_failure_chf_overview/article.htm#what_is_congestive_heart _failure_chf).National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand, 2012)