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Acute cardiac failure: definitions, investigation, and management 

Acute cardiac failure: definitions, investigation, and management

Acute cardiac failure: definitions, investigation, and management

Andrew L Clark

and John G. F Cleland

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date: 25 March 2017

Presentations of acute heart failure fall into three overlapping categories: (1) acute breathlessness and pulmonary oedema, (2) chronic fluid retention and peripheral oedema (anasarca), and (3) cardiogenic shock. Examination features include tachycardia, hypotension, a raised venous pressure, basal crackles, and peripheral oedema. Auscultation may reveal a third heart sound or features of precipitating valvular heart disease. Initial management focuses on confirming the diagnosis and identification of the immediate precipitant (e.g. arrhythmias, myocardial infarction, decompensating valvular heart disease). Initial investigations include a 12-lead electrocardiogram (ECG), chest radiograph, full blood count, biochemical screen, troponin and thyroid function. Brain natriuretic peptide (BNP) is useful in confirming the diagnosis where clinical features are present and a normal BNP is helpful in excluding the diagnosis. All patients should undergo echocardiographic assessment early in the course of a hospital admission to assess left ventricular function and to look for underlying valvular heart disease. In patients with acute pulmonary oedema investigation and management should proceed simultaneously. Intravenous loop diuretics and nitrates are commonly used therapies and may be combined with ventilatory support with oxygen and continuous positive airways ventilation. Mechanical support may be appropriate as a bridge to definitive therapy in potentially reversible causes. Inotropes are often used but without convincing evidence that they improve outcome. In patients with features are of peripheral oedema and low cardiac output, fluid retention (usually >5 litres) is the predominant feature. Management is principally with bed rest, loop diuretics (usually by intravenous infusion), and, where appropriate, aldosterone antagonists. Thiazide diuretics can be added in resistant cases. Prophylactic low molecular weight heparin should be prescribed. Careful monitoring of fluid balance with daily weights and daily electrolytes is essential. Angiotensin converting enzyme (ACE) inhibitors and subsequently β‎-blockade can be introduced once a satisfactory diuresis has been achieved. Management of cardiogenic shock is usually determined by the cause. Fluid status should be assessed and an adequate left ventricular filling pressure ensured by the administration of intravenous fluids where required (particularly in the case of right ventricular infarction). Revascularization is the mainstay of therapy in acute myocardial infarction. Circulatory support with intra-aortic balloon counter-pulsation (IABP), inotropic agents, ventricular assist devices (VADs), and extracorporeal membrane oxygenation should be considered for reversible causes (e.g. ventricular septal rupture, papillary muscle rupture, acute myocarditis and postpartum cardiomyopathy). Hospital admission with acute heart failure caries a poor prognosis with an average in-hospital mortality of 10–15% rising to up to 60% at 30 days in cases of cardiogenic shock.

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