QJM Advance Access originally published online on November 5, 2008
QJM 2009 102(4):235-241; doi:10.1093/qjmed/hcn147
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High output heart failure
From the 1Clinical Cardiology, National Heart and Lung Institute, Imperial College, Dovehouse Street, London SW3 6LY, UK and 2Cardiology Department, The Hillingdon Hospital, Pield Heath Road, Uxbridge, Middlesex, London UB8 3NN, UK
Address correspondence to P.A. Mehta, Clinical Cardiology, National Heart and Lung Institute, Imperial College, Dovehouse Street, London SW3 6LY, UK. email: p.mehta{at}imperial.ac.uk
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Abstract |
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The symptoms and signs of heart failure can occur in the setting of an increased cardiac output and has been termed ‘high output heart failure’. An elevated cardiac output with clinical heart failure is associated with several diseases including chronic anaemia, systemic arterio-venous fistulae, sepsis, hypercapnia and hyperthyroidism. The underlying primary physiological problem is of reduced systemic vascular resistance either due to arterio-venous shunting or peripheral vasodilatation. Both scenarios can lead to a fall in systemic arterial blood pressure and neurohormonal activation leading to overt clinical heart failure. In contrast to low output heart failure, clinical trial data in this area are lacking. The use of conventional therapies for heart failure, such as angiotensin converting enzyme inhibitors, angiotensin receptor blockers and certain β-blockers with vasodilatory properties, is likely to further reduce systemic vascular resistance resulting in deterioration. The condition, although uncommon, is often associated with a potentially correctable aetiology. In the absence of a remediable cause, therapeutic options are very limited but include dietary restriction of salt and water combined with judicious use of diuretics. Vasodilators and β-adrenoceptor positive inotropes are not recommended.