As for cardiac arrhythmias, these are
• To reduce morbidity
• To reduce mortality.
There is some tension between these two objectives in that the action of diuretic and vasodilator drugs, which temporarily improve symptoms, can jeopardise survival. There is a further tension between the needs of treating the features oí forwards failure, or low output, and backwards failure, or the congestive features. The principal symptom of a low cardiac output, fatigue, is difficult to quantify, and patients have tended to have their treatment tailored more to the consequences of venous congestion.
Acute or chronic failure of the heart may result from disease of the myocardium itself, mainly ischaemic, or an excessive load imposed on it by arterial hypertension, valvular disease or an arteriovenous shunt. The management of cardiac failure requires both the relief of any treatable underlying or aggravating cause, and therapy directed at the failure itself.
The distinction between the capacity of the myocardium to pump blood and the load against which the heart must work is useful in therapy. The failing myocardium is so strongly stimulated to
12 NYHA Class 1 = minimal dyspnoea (except after moderate exercise)
Class 2 = dyspnoea while walking on the flat Class 3 = dyspnoea on getting in/out of bed Class 4 = dyspnoea lying in bed.
contract by increased sympathetic drive that therapeutic efforts to induce it to function yet more vigorously are in themselves alone unlikely to be of benefit. Despite numerous attempts over recent years, digoxin remains the only inotropic drug suitable for chronic oral use. By contrast, agents that reduce preload or afterload are very effective, especially where the left ventricular volume is raised (less predictably so for failure of the right ventricle). The main hazard of their use is a drastic fall in cardiac output in those occasional patients whose output is dependent on a high left ventricular filling pressure, e.g. who are volume depleted by diuretic use or those with severe mitral stenosis.
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