Abstract

The prevalence of heart failure (HF) is rapidly increasing due to the ageing of the population and improved survival rates in heart disease patients. Morbidity and mortality rates are high; more than one third of patients die within two years of the onset of clinical symptoms. This complex clinical syndrome emerges due to the inability of the heart to produce enough cardiac output at normal filling pressure, to meet the body's metabolic demands.Investigation and management of the condition directly relates to whether HF is a result of systolic or diastolic dysfunction. Left ventricular (LV) systolic HF is caused by contractile failure of the myocardium. This results in intravascular and interstitial volume overload and inadequate tissue perfusion. Reduced tissue perfusion stimulates compensatory mechanisms which are responsible for many of the clinical manifestations, and which actually perpetuate the condition.Reduced contractility of the failing heart increases left atrial (LA) pressure, resulting in backflow of blood into the pulmonary circulation. Raised capillary hydrostatic pressure causes transudation of fluid into pulmonary interstitial spaces and then into the alveoli; pulmonary oedema. Acute pulmonary oedema (APO) is a frequent cause of sudden death in HF.Increased pulmonary pressure can also impair the functioning of the right ventricle (RV), reducing venous return and thus causing congestion of organs, ascites and generalised body oedema. Hypertension can result.Nursing management in the Emergency Department (ED) aims at relieving hypoxia, reducing myocardial oxygen demand (MVO2) and reducing fluid overload. Current therapy is largely supportive. HF with associated APO constitutes a medical emergency requiring prompt intervention.Much has been learned about the pathophysiology of HF over the past two decades. Unfortunately, little impact has been made thus far to reduce its prevalence in society and to lower mortality rates.

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