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Left heart failure (congestive heart failure) has two types, systolic heart failure (HFrEF) and diastolic heart failure (HFpEF). In systolic heart failure there is a reduced ejection fraction of < 40 % and the heart can not adequately perfuse vital tissues. Contractility of the heart is decreased by a MI or other disease that contributes to ventricular remodeling which results in dilation of the myocardium and cause myocyte contractile dysfunction. The dilation of the myocardium then leads to an increase in preload which causes stretching of the myocardium even more that causing dysfunction of the sarcomeres and decreased contractility. Hypertension can cause increased afterload which causes hypertrophy of the myocardium (myocyte death, fibrosis, inflammation) and collagen deposits. Systolic heart failure is also characterized by alterations in catecholamines, RAAS, Arginine vasopressin, natriuretic peptides, inflammatory cytokines, myocyte calcium transport, and insulin resistance and diabetes. he goals of management of systolic heart failure is to prevent worsening of decreasing contractility, increasing preload, and increasing afterload. Oxygen, nitrates, and morphine are used with the acute onset of heart failure due to an MI. Diuretics, ACE inhibitors, beta-blockers, intraaortic balloon pumps, left ventricular assist devices, and coronary bypass surgery are all interventions that can be taken to help manage left heart failure.
In diastolic heart failure there is preserved ejection fraction, that results in pulmonary congestion even with a normal stroke volume and cardiac output. The main causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia with resultant ventricular remodeling. The ventricular changes are caused by decreased compliance of the left ventricle due to changes in the myocardial structure from alterations in collagen and titin. It is also caused by abnormal diastolic relaxation due to changes in calcium transport, which leads to an increase in left atrial pressure resulting in pulmonary edema. Management of diastolic heart failure is aimed at improving ventricular relaxation and prolonging diastolic filling times to reduce diastolic pressure (McCance & Huether, 2019). Interventions used to manage diastolic heart failure are physical training such as aerobic and weight training, nitrates, beta-blockers, ACE inhibitors, and ARBs. There are still ongoing treatment trials but there has been little improvement in prognosis.
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.
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G-N: Discuss the pathophysiology of diastolic and systolic failure in left-heart failure and the nursing actions applicable to the care of patients with each type.
Folate is a vitamin that is essential for the synthesis of RNA and DNA. Impaired DNA synthesis secondary to folate deficiency results in megaloblastic cells with clumped nuclear chromatin. Anemia may result from the apoptosis of erythroblasts in the late stages of erythropoiesis. (McCance & Huether, 2019). A folate deficiency leads to the risk of cancer, specifically colorectal, as well as atherosclerosis. The symptoms associated with this condition are painful ulcerations of the buccal mucosa, cheilosis (fissures and scales in the corners of your mouth and on your lips), stomatitis (inflammation of the tongue, watery diarrhea, flatulence, and dysphagia. Unlike thiamine deficiency, there are no neurological symptoms present.
The mechanisms underlying the cause of folate deficiency remain unknown; however, inflammatory conditions of the gastrointestinal tract that are undiagnosed may play a role, such as Crohn’s disease and ulcerative colitis. Additional causes would be an increased need by the body of folate, decreased intake of folate by the individual, or impaired utilization. To evaluate a patient for folate deficiency, serum folate levels would have to be obtained along with documented symptoms that correlate with the deficiency. The treatment recommended is a daily dose of l mg of folic acid; however, if the individual is an alcoholic, the amount required would be 5mg/day. The dosage increase in alcoholics is due to how folate is absorbed.Once it is absorbed in our system, it is circulated in the liver; however, if the patient is an alcoholic, the absorption is affected by alcohol inhibiting how it would generally be metabolized by the liver—in turn, leading to depletion of the folate that is stored. If an individual is pregnant, the dosage ranges from 0.1-0.4 mg a day as a prophylactic measure to prevent a possible neural tubal defect in the fetus. Overall, with the inclusion of meals, the daily requirement is 50-200 mcg a day. Typically, once a person with folate deficiency anemia has taken their supplements for one to two weeks, the symptoms should resolve. Once the folate anemia has been corrected, taking supplements of folate long-term is unnecessary. However, that is only true if the patient can maintain an appropriate dietary intake.
McCance, K.L., & Heuther, S.E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). Elsevier.
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A-F: Select one of the anemias discussed in CH 29, preferably one that you are least familiar. Discuss the pathophysiology of the selected anemia, diagnosis, treatment options and nursing care.
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