Treatment of heart failure

Treatment of CHF

Treatment of heart failure is aimed at the reduction of morbidity and mortality, including the prevention of acute cardiac decompensation and cardiac remodelling, and the relief of the main symptoms of fatigue, oedema, dyspnoea, and congestion. These goals can be achieved by increasing cardiac output and decreasing ventricular pressure. Hence, the workload of the heart must be diminished and sympathetic activation, RAAS activation, and inotropy of the heart must be inhibited. In addition to pharmacological agents, behavioural modifications such as diet (decreased fluid and salt intake) and exercise (when tolerated) should be attempted. Drugs in the therapy of heart failure include: ACE inhibitors: the basis of maintenance therapy: indicated for all classes of heart failure. They improve symptoms and prolong survival by decreasing preload, afterload and counteracting remodelling. Diuretics: loop diuretics and/or thiazides are used often for symptomatic treatment.

Whereas spironolactone (an aldosterone receptor antagonist) is used in the treatment of the late stages of heart failure. Beta blockers: decrease the neurohumoral response and are used (if not contraindicated) with all stable patients with left ventricular dysfunction. Angiotensin II receptor antagonists: indicated for all classes of heart failure when ACE-inhibitors are not tolerated. Cardiac glycosides (digoxin): are used when there is insufficient response to standard therapy, or in cases of atrial fibrillation and a high ventricular response. This positive inotrope improves cardiac output. Therapeutic regimen: No or little complaints: ACE-inhibitor, diuretic, and beta-blocker. Progressive complaints: addition of a diuretic, preferably spironolacton and/or digoxin. Serious complaints: addition of nitrates and hydralazine. The Frank-Starling curve shows the consequences of congestive heart failure and treatment with different drugs. In heart failure, the cardiac output is reduced and the set-point falls with concomitant symptoms. Compensatory mechanisms increase the end-diastolic pressure and improve cardiac output. This development, however, can induce backward failure symptoms.


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