MANAGEMENT OF CHRONIC HEART FAILURE
The major steps in the management of patients with chronic heart failure are outlined in Table 13–3. The 2009 update to the ACC/ AHA 2005 guidelines suggests that treatment of patients at high risk (stages A and B) should be focused on control of hyperten-sion, hyperlipidemia, and diabetes, if present. Once symptoms and signs of failure are present, stage C has been entered, and active treatment of failure must be initiated.
SODIUM REMOVAL
Sodium removal—by dietary salt restriction and a diuretic—is the mainstay in management of symptomatic heart failure, especially if edema is present. In very mild failure a thiazide diuretic may be tried, but a loop agent such as furosemide is usually required. Sodium loss causes secondary loss of potassium, which is particu-larly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of an ACE inhibitor or a potassium-sparing diuretic such as spironolactone. Spironolactone or eplerenone should probably be considered in all patients with moderate or severe heart failure, since both appear to reduce both morbidity and mortality.
ACE INHIBITORS & ANGIOTENSIN RECEPTOR BLOCKERS
In patients with left ventricular dysfunction but no edema, an ACE inhibitor should be the first drug used. Several large studies have showed clearly that ACE inhibitors are superior to both pla-cebo and to vasodilators and must be considered, along with
VASODILATORS
Vasodilator drugs can be divided into selective arteriolar dilators, venous dilators, and drugs with nonselective vasodilating effects. The choice of agent should be based on the patient’s signs and symptoms and hemodynamic measurements. Thus, in patients with high filling pressures in whom the principal symptom is dyspnea, venous dilators such as long-acting nitrates will be most helpful in reducing filling pressures and the symptoms of pulmo-nary congestion. In patients in whom fatigue due to low left ven-tricular output is a primary symptom, an arteriolar dilator such as hydralazine may be helpful in increasing forward cardiac output.In most patients with severe chronic failure that responds poorly to other therapy, the problem usually involves both elevated filling pressures and reduced cardiac output. In these circumstances, dila-tion of both arterioles and veins is required. In a trial in African-American patients already receiving ACE inhibitors, addition of hydralazine and isosorbide dinitrate reduced mortality. As a result, a fixed combination of these two agents has been made available as isosorbide dinitrate/hydralazine (BiDil), and this is currently approved for use only in African Americans.
BETA BLOCKERS & ION CHANNEL BLOCKERS
Trials of ฮฒ-blocker therapy in patients with heart failure are based on the hypothesis that excessive tachycardia and adverse effects of high catecholamine levels on the heart contribute to the down-ward course of heart failure. The results clearly indicate that such therapy is beneficial if initiated cautiously at low doses, even though acutely blocking the supportive effects of catecholamines can worsen heart failure. Several months of therapy may be required before improvement is noted; this usually consists of a slight rise in ejection fraction, slower heart rate, and reduction in symptoms. As noted above, not all ฮฒ blockers have proved useful, but bisoprolol, carvedilol, metoprolol, and nebivolol have been shown to reduce mortality.
In contrast, the calcium-blocking drugs appear to have no role in the treatment of patients with heart failure. Their depressant effects on the heart may worsen heart failure. On the other hand, slowing of heart rate with ivabradine (an If blocker) appears to be of benefit.
Digitalis
Digoxin is indicated in patients with heart failure and atrial fibril-lation. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms.
The major steps in the management of patients with chronic heart failure are outlined in Table 13–3. The 2009 update to the ACC/ AHA 2005 guidelines suggests that treatment of patients at high risk (stages A and B) should be focused on control of hyperten-sion, hyperlipidemia, and diabetes, if present. Once symptoms and signs of failure are present, stage C has been entered, and active treatment of failure must be initiated.
SODIUM REMOVAL
Sodium removal—by dietary salt restriction and a diuretic—is the mainstay in management of symptomatic heart failure, especially if edema is present. In very mild failure a thiazide diuretic may be tried, but a loop agent such as furosemide is usually required. Sodium loss causes secondary loss of potassium, which is particu-larly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of an ACE inhibitor or a potassium-sparing diuretic such as spironolactone. Spironolactone or eplerenone should probably be considered in all patients with moderate or severe heart failure, since both appear to reduce both morbidity and mortality.
ACE INHIBITORS & ANGIOTENSIN RECEPTOR BLOCKERS
In patients with left ventricular dysfunction but no edema, an ACE inhibitor should be the first drug used. Several large studies have showed clearly that ACE inhibitors are superior to both pla-cebo and to vasodilators and must be considered, along with
VASODILATORS
Vasodilator drugs can be divided into selective arteriolar dilators, venous dilators, and drugs with nonselective vasodilating effects. The choice of agent should be based on the patient’s signs and symptoms and hemodynamic measurements. Thus, in patients with high filling pressures in whom the principal symptom is dyspnea, venous dilators such as long-acting nitrates will be most helpful in reducing filling pressures and the symptoms of pulmo-nary congestion. In patients in whom fatigue due to low left ven-tricular output is a primary symptom, an arteriolar dilator such as hydralazine may be helpful in increasing forward cardiac output.In most patients with severe chronic failure that responds poorly to other therapy, the problem usually involves both elevated filling pressures and reduced cardiac output. In these circumstances, dila-tion of both arterioles and veins is required. In a trial in African-American patients already receiving ACE inhibitors, addition of hydralazine and isosorbide dinitrate reduced mortality. As a result, a fixed combination of these two agents has been made available as isosorbide dinitrate/hydralazine (BiDil), and this is currently approved for use only in African Americans.
BETA BLOCKERS & ION CHANNEL BLOCKERS
Trials of ฮฒ-blocker therapy in patients with heart failure are based on the hypothesis that excessive tachycardia and adverse effects of high catecholamine levels on the heart contribute to the down-ward course of heart failure. The results clearly indicate that such therapy is beneficial if initiated cautiously at low doses, even though acutely blocking the supportive effects of catecholamines can worsen heart failure. Several months of therapy may be required before improvement is noted; this usually consists of a slight rise in ejection fraction, slower heart rate, and reduction in symptoms. As noted above, not all ฮฒ blockers have proved useful, but bisoprolol, carvedilol, metoprolol, and nebivolol have been shown to reduce mortality.
In contrast, the calcium-blocking drugs appear to have no role in the treatment of patients with heart failure. Their depressant effects on the heart may worsen heart failure. On the other hand, slowing of heart rate with ivabradine (an If blocker) appears to be of benefit.
Digitalis
Digoxin is indicated in patients with heart failure and atrial fibril-lation. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms.
