Systolic Heart Failure
Ms. Boehmer has systolic heart failure. She has reported symptoms of dyspnea with exertions, orthopnea (evidenced by “sleeps on two pillows” at night), fatigue (evidenced by “she often feels tired”) and edema (evidenced by “reports that ankles are often swollen in the evening”) alterations in urination (evidenced by “nocturia X 2 and reports she sometimes has a strong urge to void and does not always make it to the toilet in time”). Physical examinations demonstrate S3 gallop. Cardiomegaly is present and cardiac output is decreased (evidenced by Echo result “mildly enlarged left atrium, ejection fraction 35%”). Other evidence includes a history of coronary artery disease and hypertension. (Brashers, 2012b). Diastolic heart failure is also
known as heart failure with normal ejection fraction. It can occur alone or along with systolic heart failure. Pulmonary congestion is often present in women with diastolic heart failure. It is often associated with decrease compliance of the left ventricle and abnormal diastolic relaxation that lead to increase in left ventricular end-diastolic pressure. The increased pressure leads to increased pulmonary circulation, and result in pulmonary edema. The primary causes of diastolic heart failure are hypertension-induced myocardial hypertrophy, and myocardial ischemia-induced ventricular remodeling. Calcium from cytosol are not being actively pumped due to hypertrophy and ischemia, which leads to impaired relaxation. Other causes of diastolic heart failure are aortic valvar disease, mitral valve disease, pericardial disease and cardiomyopathies. Diabetes is a major risk factor. The activation of RAAS and SNS are similar to the systolic heart failure (Brashers, 2012b). Systolic heart failure is primarily caused by myocardial infarction. Other causes may include myocarditis and cardiomyopathies. The interaction of hemodynamic, neurohumoral and inflammatory process steadily cause the myocardial function to decline. Pathologically, the myocyte structure and function of heart muscle changes occur slowly with the apoptosis of cells, deposition of fibrin, and remodeling of the myocardium. Contractility and the cardiac output are significantly affected. Symptoms can worsen over time, due to increased preload, increased afterload and decreased contractility (Brashers, 2012b).
known as heart failure with normal ejection fraction. It can occur alone or along with systolic heart failure. Pulmonary congestion is often present in women with diastolic heart failure. It is often associated with decrease compliance of the left ventricle and abnormal diastolic relaxation that lead to increase in left ventricular end-diastolic pressure. The increased pressure leads to increased pulmonary circulation, and result in pulmonary edema. The primary causes of diastolic heart failure are hypertension-induced myocardial hypertrophy, and myocardial ischemia-induced ventricular remodeling. Calcium from cytosol are not being actively pumped due to hypertrophy and ischemia, which leads to impaired relaxation. Other causes of diastolic heart failure are aortic valvar disease, mitral valve disease, pericardial disease and cardiomyopathies. Diabetes is a major risk factor. The activation of RAAS and SNS are similar to the systolic heart failure (Brashers, 2012b). Systolic heart failure is primarily caused by myocardial infarction. Other causes may include myocarditis and cardiomyopathies. The interaction of hemodynamic, neurohumoral and inflammatory process steadily cause the myocardial function to decline. Pathologically, the myocyte structure and function of heart muscle changes occur slowly with the apoptosis of cells, deposition of fibrin, and remodeling of the myocardium. Contractility and the cardiac output are significantly affected. Symptoms can worsen over time, due to increased preload, increased afterload and decreased contractility (Brashers, 2012b).