Treatment of the Failing Heart

Treatment of heart failure is directed to correction of the two major problems associated with failure: venous congestion and reduced cardiac output. Systemic venous congestion can cause renal and liver damage as well as discomfort. The threat of pulmonary edema from pulmonary congestion has already been discussed. Diuretics and reduced salt intake can reduce the accumulated blood volume and venous congestion even though these treatments may actually lower the filling pressure of the heart and thus the stroke volume. One of the oldest cardiac drugs is digitalis, which increases the contractility of the heart by causing the muscle cells to accumulate SR calcium (see Chapter 11). Increasing contractility with digitalis increases the cardiac output and lowers the venous pressure. Digitalis in the absence of a diuretic will often cause a brisk diuresis, as the kidney detects the rising cardiac output. Although digitalis and other cardiac stimulants can improve the exercise tolerance in patients with mild failure, they have had little effect on prolonging their lives. Furthermore, in advanced failure these treatments have little beneficial effect.

Recently, beta-adrenergic receptor blockers have been tried in these patients with some success. The actual cause of the improvement is not entirely known but is in part related to reduced heart rate, which improves cardiac filling. Some of the benefit may also derive from increased diastolic compliance of the ventricles. Because of the chronically elevated sympathetic tone in these patients and the constant stimulation, the beta-receptors of the heart are downregulated, which blunts the effect of norepinephrine in the ventricle. It is thought that in the presence of low-dose beta blockade the receptors will again proliferate. Beta-receptors will then only be stimulated under conditions of elevated physical activity when enough norepinephrine is released to competitively overcome the beta-blocker. Although contractility at rest may be somewhat depressed, the reserve of the heart is actually increased.

Currently, the most promising treatment for heart failure is the use of angiotensin converting enzyme (ACE) inhibitors. ACE inhibitors not only lower the blood pressure and increase cardiac output but also interfere with the detrimental remodeling that occurs in the stressed heart. The important role that angiotensin II plays in the cellular changes that occur in hypertrophy and failure is only beginning to be understood.

Normal heart

Eccentric hypertrophy

FIGURE 3 Transverse section of three ventricles, one normal and two hypertrophied. Chronic pressure overload causes a remodeling of the heart, called concentric hypertrophy, in which the heart has a thick wall and small lumen. Chronic volume overload leads to eccentric hypertrophy, in which the diameter of the lumen is increased along with the muscle mass.

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