Heart Failure PDF

10/18/23, 3:00 AM Realizeit for Student Heart Failure Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac disorders so that the heart is unable to pump enough blood to meet the body’s metabolic demands or needs (American Heart Association [AHA], 2019a). The te...

10/18/23, 3:00 AM Realizeit for Student Heart Failure Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac disorders so that the heart is unable to pump enough blood to meet the body’s metabolic demands or needs (American Heart Association [AHA], 2019a). The term heart failure indicates myocardial disease in which impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) may cause pulmonary or systemic congestion. Some cases of HF are reversible, depending on the cause. Most often, HF is a heart failure. These episodes are characterized by increased symptoms of respiratory distress, decreased cardiac output (CO), and poor perfusion. These episodes are also associated with increased hospitalizations, increased health care costs, and decreased quality of life (Benjamin et al., 2019).chronic, progressive condition that is managed with lifestyle changes and medications to prevent episodes of acute decompensated Approximately six million people in the United States have HF, and 870,000 new cases are diagnosed each year (AHA, 2019a). As more people live longer with chronic heart diseases, HF has become an epidemic that challenges the country’s health care resources. HF is the most common reason for hospitalization of people older than 65 years and is the second most common reason for visits to a provider’s office. Emergency department (ED) visits and hospital readmissions for this disorder are very common, despite efforts to prevent rehospitalizations. Over 20% of patients discharged after treatment for HF are readmitted to the hospital within 30 days, and nearly 50% are readmitted to the hospital within 6 months (O’Connor, 2017). The estimated economic burden caused by HF in the United States is more than $30 billion annually in direct and indirect costs and is expected to continue to increase over time (CDC, 2017). HF is more prevalent among African Americans and Hispanics than among Caucasians. The risk for having HF increases with advancing age. For adults over 60 years of age, HF is more prevalent among men than women (Benjamin et al., 2019). As typical for other major cardiovascular diseases and disorders, cigarette smoking, obesity, poorly managed diabetes, and metabolic syndrome are all risks for HF (Benjamin et al., 2019). The onset of HF is typically a morbid consequence of another disease or disorder, including coronary artery disease (CAD), hypertension, cardiomyopathy, valvular disorders, and renal dysfunction with volume overload (McCance, Huether, Brashers, et al., 2019). Atherosclerosis of the coronary arteries is a primary cause of HF, and CAD is found in the majority of patients with HF. Ischemia causes myocardial dysfunction because it deprives heart cells of oxygen and causes cellular damage. Myocardial infarction (MI) causes focal heart muscle necrosis, the death of myocardial cells, and a loss of contractility; the extent of the infarction correlates with the severity of HF. Revascularization of the coronary artery by a percutaneous coronary intervention (PCI) or by coronary artery bypass surgery (coronary artery bypass graft [CABG]) may improve myocardial oxygenation and ventricular function and prevent more extensive myocardial necrosis that can lead to HF. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IYH%2fMiUZkmGn1VrFXwQeG%2fpUCxJZEI1Lebfhwo2Y… 1/5 10/18/23, 3:00 AM Realizeit for Student Systemic or pulmonary hypertension increases afterload (resistance to ejection), increasing the cardiac workload and leading to the hypertrophy of myocardial muscle fibers. This can be considered a compensatory mechanism because it initially increases contractility. However, sustained hypertension eventually leads to changes that impair the heart’s ability to fill properly during diastole, and the hypertrophied ventricles may dilate and fail (Norris, 2019; Yancy, Jessup, Bozkurt, et al., 2017). Cardiomyopathy is a disease of the myocardium. The various types of cardiomyopathy lead to HF and arrhythmias. Dilated cardiomyopathy (DCM), the most common type of cardiomyopathy, causes diffuse myocyte necrosis and fibrosis, and commonly leads to progressive HF (Norris, 2019). DCM can be idiopathic (unknown cause), or it can result from an inflammatory process, such as myocarditis, or from a cytotoxic agent, such as alcohol or certain antineoplastic drugs. Usually, HF due to cardiomyopathy is chronic and progressive. However, cardiomyopathy and HF may resolve following removal of the causative agent. Genetic testing may be recommended for idiopathic cardiomyopathy (van der Meer, Gaggin, & Dec, 2019). Valvular heart disease is also a cause of HF. The valves ensure that blood flows in one direction. With valvular dysfunction, it becomes increasingly difficult for blood to move forward, increasing pressure within the heart and increasing cardiac workload, leading to HF. Several systemic conditions, including progressive kidney failure, contribute to the development and severity of HF. Nearly 30% of patients with chronic HF also have chronic kidney disease (Benjamin et al., 2019). In addition, cardiac arrhythmias such as atrial fibrillation may either cause or result from HF; in both instances, the altered electrical stimulation impairs myocardial contraction and decreases the overall efficiency of myocardial function. Other factors, such as hypoxia, acidosis, and electrolyte abnormalities, can worsen myocardial function (Yancy et al., 2017). Pathophysiology Regardless of the etiology, the pathophysiology of HF results in similar changes and clinical manifestations. Significant myocardial dysfunction usually occurs before the patient experiences signs and symptoms of HF such as shortness of breath, edema, or fatigue. As HF develops, the body activates neurohormonal compensatory mechanisms. These mechanisms represent the body’s attempt to cope with the HF and are responsible for the signs and symptoms that develop (Norris, 2019). Understanding these mechanisms is important because the treatment for HF is aimed at correcting them and relieving symptoms. The most common type of HF is systolic HF, also called Heart Failure with reduced Ejection Fraction (HFrEF; see later discussion in Assessment and Diagnostic Findings). Systolic heart failure results in decreased blood ejected from the ventricle. The decreased blood flow is sensed by baroreceptors in the aortic and carotid bodies, and the sympathetic nervous system is then stimulated to release https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IYH%2fMiUZkmGn1VrFXwQeG%2fpUCxJZEI1Lebfhwo2Y… 2/5 10/18/23, 3:00 AM Realizeit for Student epinephrine and norepinephrine (Fig. 25-1). The purpose of this initial response is to increase heart rate and contractility and support the failing myocardium, but the continued response has multiple negative effects. Sympathetic stimulation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the kidneys. Renin converts the plasma protein angiotensinogen to angiotensin I, which then circulates to the lungs. Angiotensin-converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention by the renal tubules and an increase in blood volume. These mechanisms lead to the fluid volume overload commonly seen in HF. Angiotensin, aldosterone, and other neurohormones (e.g., endothelin) lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an increase in cardiac workload. A counterregulatory mechanism is attempted through the release of natriuretic peptides. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP; brain type) are released from the overdistended cardiac chambers. These substances promote vasodilation and diuresis. However, their effect is usually not strong enough to overcome the negative effects of the other mechanisms (Norris, 2019). As the heart’s workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricle (ventricular dilation). The heart compensates for the increased workload by increasing the thickness of the heart muscle (ventricular hypertrophy). Hypertrophy results in abnormal changes in the structure and function of myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones (e.g., angiotensin II), enlarged myocardial cells become dysfunctional and die early (a process called apoptosis), leaving the other, functional myocardial cells struggling to maintain CO. As cardiac cells die and the heart muscle becomes fibrotic, diastolic heart failure, also called Heart Failure with preserved Ejection Fraction (HFpEF) (see later discussion in Assessment and Diagnostic Findings), can develop, leading to further dysfunction. A stiff ventricle resists filling, and less blood in the ventricles causes a further decrease in CO. All of these compensatory mechanisms of HF have been referred to as the “vicious cycle of heart failure” because low CO leads to multiple mechanisms that make the heart work harder, worsening the HF. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IYH%2fMiUZkmGn1VrFXwQeG%2fpUCxJZEI1Lebfhwo2Y… 3/5 10/18/23, 3:00 AM Realizeit for Student https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IYH%2fMiUZkmGn1VrFXwQeG%2fpUCxJZEI1Lebfhwo2Y… 4/5 10/18/23, 3:00 AM Realizeit for Student https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IYH%2fMiUZkmGn1VrFXwQeG%2fpUCxJZEI1Lebfhwo2Y… 5/5