While this option lies outside the scope of clinical pharmacology, an important element in meeting the objectives of treatment (p. 515) is to recognise when further drug treatment is unlikely to improve symptoms or prognosis. It is the physician who must first consider the possibility of a surgical intervention, which increasingly may involve procedures short of transplantation itself, e.g. bypass grafting or stenting where stenosed vessels contribute to the cardiac failure. On occasion, it can help the patient to be made aware that failure of both the heart and the drugs is not necessarily the end of the road.
• Cardiac failure is present when the heart cannot provide all organs with the blood supply appropriate to demand.
• Stroke volume is regulated by preload, afterload and contractility.
• In chronic cardiac failure, diuretics and nitrates reduce preload and provide symptomatic relief without affecting outcome.
v ACE inhibitors reduce both preload and afterload and reduce morbidity and mortality by about one-third in all patients.
• P-adrenoceptor blockade, gradually introduced, has an effect equivalent to that of ACE inhibition in patients with moderate or severe heart failure (NYHA III
• Spironolactone, in low dose, adds further benefit.
• Digoxin improves myocardial contractility most effectively in the dilated, failing heart but also in the longer term, including in patients in sinus rhythm.
• The principal agents for treating acute left ventricular failure arc frusemide (furosemide). diamorphine and oxygen.
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