Chronic Heart Failure
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For most physicians, current recommendations about how to take care of patients with chronic heart failure (CHF) differ significantly from those they learned during training.
From new multi-drug regimens to a new interpretation of heart failure as being a chronic—not acute—illness, where prevention and early treatment are key, some of the latest thinking can be "counterintuitive" for many clinicians, explained Lee R. Goldberg, MD, MPH, assistant professor of medicine at the University of Pennsylvania, associate medical director of its heart failure and transplant program and co-author of ACP's PIER module on heart failure.
"We now know that you want to get two classes of drugs—ACE inhibitors and beta-blockers—started early, even in the absence of symptoms," he said. "Getting those medications on board at the earliest possible time—as soon as you discover that someone has heart dysfunction—can improve mortality, but can also prevent the symptoms of heart failure from developing" for a much longer period of time.
"In terms of using beta blockers, people literally have to be re-educated and become comfortable doing something they were taught wasn't the right thing to do," he said.
As a result, most physicians wait too long to start their heart failure patients on drugs, said Dr. Goldberg. They also fail to prescribe large enough doses, and they are too quick to pull patients off their medications. "Clinicians tend to underestimate the risk of the disease and the benefit of the drug," he said, "and to overestimate the risks of the drugs."
For instance, when surveyed, general internists often estimate that as many as 20%-50% of their heart failure patients have problems with beta-blockers, whereas clinical trials have found that those drugs cause problems for only 1%-2% of patients. "Obviously in the real world, there will be more problems, but not nearly as many as people think," Dr. Goldberg said.
And some of the side effects that clinicians are quick to blame on the drugs (fatigue in the case of beta-blockers and cough when it comes to ACE inhibitors) may in fact be due to something else.
"When patients complain of fatigue, clinicians tend to perceive the fatigue is due to the beta-blocker, but patients with heart disease have fatigue for many reasons. It could be the heart disease itself. It could be that they are depressed. It could be that they have sleep apnea, which is associated with heart failure and hypertension," Dr. Goldberg said. "Many internists will throw in the towel on the beta-blocker pretty quickly, rather than saying, 'the beta-blocker has mortality benefit, so let me look under every other stone possible before give up on the beta blocker.'"
The problem is less dire with ACE inhibitors in large part because there is a good pharmaceutical alternative—angiotensin-receptor blocker (ARBs). "They don't cause the cough, but they do have another side effect—high cost—which means that shifting some patients from an ACE inhibitor to an ARB may prompt patients who can't afford the new regimen to stop taking the drugs altogether, leaving them totally unprotected." Similarly, he said, internists are too quick, in general, to stop ACE inhibitors or ARBs just because a patient's creatinine rises slightly.
"We used to say that you push the dose of ACE inhibitor up as high as you could go and then add the beta-blocker," said Dr. Goldberg. Now there is pretty good data to argue just the opposite but it has taken a long time to re-educate doctors. The best combination, he said, is a low- to moderate-dose of ACE inhibitors and a maximally tolerated beta-blocker.
Evidence points to a basic strategy for most patients with asymptomatic to moderate heart failure, he said. That includes an ACE inhibitor, a beta-blocker, diuretics (if needed), and, if symptoms persist, digoxin.
According to the American Heart Association and American College of Cardiology, about 5 million Americans have CHF, more than 550,000 new cases are diagnosed each year, and 200,000 people die of the disease annually. More people are surviving acute myocardial infarction, but many eventually die of heart failure, resulting in a steady increase over the years in the heart-failure death rate.
The difficulty of treating heart failure, said Dr. Goldberg, is that the patient can feel fine from the time the heart dysfunction is first discovered to the end-stage disease period. "If you can stop the progression early," he said, "you can prevent them from getting to the point where they are very symptomatic."
This edition of ACP Observer Special Focus is designed to help optimize your ability to diagnose, treat and manage patients with heart failure.
Since aggressive risk factor control can reduce the subsequent development of heart failure, identify and treat the following diseases and disorders strongly associated with heart disease:
Hypertension. Control blood pressures that are greater than 140/90 mmHg in healthy adults or 130/80 mmHg in patients with additional cardiac risk factors.
Diabetes. Aggressively control blood pressure and lipids. Use ACE inhibitors or angiotensin-receptor blockers. (See the PIER module on Diabetes Mellitus, Type 2.)
Hyperlipidemia. Order aggressive lifestyle therapy (diet and exercise) and add drug therapy if necessary. (See the PIER module on Lipid Disorders.)
Hypothyroidism and hyperthyroidism. Treat patients according to guidelines and monitor thyroid home levels regularly. (See also PIER modules on Hypothyroidism and Hyperthyroidism.)
Supraventricular tachycardia and atrial fibrillation. Treat a sustained resting tachycardia to avoid the development of ventricular dysfunction. (See PIER modules on Atrial Fibrillation and Supraventricular Tachycardia.)
Coronary Artery Disease (CAD). For patients with known CAD, recommend aggressive lipid-lowering therapy with an HMG co-A reductase inhibitor, an ACE inhibitor, a beta-blocker and aspirin, unless contraindicated. (See the PIER modules on Chronic Stable Angina and CAD in Women.)
Advise patients to avoid alcohol, tobacco and illicit drugs, particularly cocaine.
Identify patients with heart murmurs, those at high risk for atherosclerosis and those with a family history of cardiomyopathy.
In patients with heart murmurs, first determine if a valve can be repaired or replaced or identify patients who may benefit from endocarditis prophylaxis by obtaining an echocardiogram in any patient with a diastolic, holosystolic or grade 3 or greater midsystolic heart murmur, or if there are symptoms of heart failure, MI, syncope, endocarditis or thromboembolism.
To learn if CAD could be the cause of LV dysfunction and CHF, use cardiac perfusion imaging at the time of exercise stress testing. When necessary, treat CAD with angioplasty and coronary artery bypass surgery.
Since CHF from dilated cardiomyopathy may be inherited in about half the cases, obtain a detailed family history from patients with a family history of unexplained heart failure, sudden cardiac death, progressive heart failure in young people or congenital heart disease. Also obtain family history of hemochromatosis, Wilson's disease, hypertrophic cardiomyopathy, autoimmune diseases and amyloidosis. Consider echocardiographic screening of asymptomatic family members. (See also the PIER modules on Hemochromatosis, Hypertrophic Cardiomyopathy, and Amyloidosis.)
A physical examination can detect the multiple physical signs of volume overload experienced by most CHF patients. Look for the following:
- Elevated jugular venous pressure
- Heart murmurs
- Gallops (S3 or S4)
- Pulmonary rales
- Peripheral edema
Electrocardiograms evaluate cardiac rhythm; discern a previous infarction; help identify left ventricular hypertrophy, arrhythmias and atrial or conduction abnormalities; sometimes pick up active ischemia; and can serve as a baseline of comparison with future studies.
Use echocardiography to define left ventricular function, the presence and extent of potentially reversible valvular disease and of regional wall-motion abnormalities, to differentiate between systolic and diastolic heart failure and to exclude primary or secondary pulmonary hypertension. (See also the PIER module on Pulmonary Hypertension.)
Formal exercise testing (or dipyridamole or adenosine testing in patients who cannot exercise) provides a qualitative measure of functional capacity. It also can provide evidence of myocardial ischemia and determine functional class in patients who are cardiac transplant candidates. Combine exercise stress testing with respiratory gas analysis to differentiate between cardiac and pulmonary limitations to exercise. (See also the PIER module on Cardiac Stress Testing.)
Peak oxygen consumption plus clinical determination of function are the most powerful predictors of survival and outcomes in patients with CHF. Use the New York Heart Association classification to determine functional capacity.
Consider electrophysiologic testing when patients with CHF experience syncope, sudden cardiac death or sustained ventricular arrhythmias especially if the cause of the CHF is ischemic cardiomyopathy. After more than three months of maximal medical therapy and, if indicated, revascularization, empiric ICD placement should be considered for all patients with persistent low ejection fraction < 35%. ICD should be placed only in the setting of an anticipated survival of greater than 18 months and a reasonable quality of life at baseline. Hospitalize patients with unexplained syncope or presyncope for monitoring to exclude a significant arrhythmia. Syncope in the setting of heart failure, regardless of its cause, is associated with an increase in sudden cardiac death.
Recommend cardiac catheterization and coronary angiography to CHF patients with potentially reversible coronary artery or valvular heart disease. Perform angiography in male patients over age 30 and female patients over age 40 or who have CAD risk factors to determine the presence and severity of CAD.
Consider cardiac catheterization for endomyocardial biopsy only in certain cases, such as when there is a suspicion of giant cell myocarditis. These patients should be managed at transplant centers or by experienced physicians.
Rule out occult thyroid disease with a serum TSH in all patients with new onset heart failure. Restore euthyroidism to improve cardiac function.
Since pulmonary disease symptoms may often mimic or exacerbate symptoms of heart failure, consider obtaining pulmonary function testing, chest x-ray and smoking history and performing cardiopulmonary exercise testing with respiratory gas exchange analysis to differentiate pulmonary and cardiac causes of dyspnea. When diagnostic uncertainty persists, obtain a B-type natriuretic peptide (BNP) assay and consider obtaining a pulmonary consultation. If there still is diagnostic uncertainty, request a cardiology consultation.
First, recommend diet and lifestyle modifications, particularly limiting salt and fluid intake (to 2g sodium and 2 quarts of fluid per day) and encouraging aerobic exercise tailored to the functional capacity of the patient. Advise obese patients to lose weight. Screen for and treat sleep apnea.
Many drugs can be used to treat heart failure. They fall into the following categories:
ACE inhibitors. Use in all CHF patients regardless of functional class, except where there is a history of angioedema. Start enalapril, captopril, lisinopril or ramipril at low doses and titrate up as tolerated by blood pressure, which can be as low as 80-90mg/Hg systolic as long as patients stay asymptomatic. Cough, worsening renal insufficiency or hyperkalemia are signs of intolerance to these drugs. Many patients with prior ACE intolerance will benefit from a rechallenge with ACE inhibitors.
Angiotensin-receptor blockers. Valsartan, losartan and candesartan are effective alternatives to ACE inhibitors, especially in patients who experience cough and other intolerable side effects of ACE inhibitors.
Beta-blockers. Start carvedilol, sustained release metoprolol or bisoprolol for all heart failure patients who are stable on ACE inhibitors or other vasodilators and not volume overloaded. Begin at the lowest dose and slowly titrate upward to the highest therapeutic dose tolerated as determined by bradycardia, hypotension or side effects. Although most patients' heart failure symptoms are alleviated by beta blockade, patients with less-severe heart failure can expect the greatest long-term benefit.
- Hydralazine combined with nitrates. Use this combination as an alternative to ACE inhibitors or ARBs in patients intolerant to both. Consider prescribing hydralazine plus nitrates in addition to standard therapy, including an ACE inhibitor or ARB in black patients with symptomatic heart failure
Aldosterone antagonists. Prescribe low doses of spironolactone in patients whose NYHA class II to IV symptoms persist despite ACE inhibitor and beta-blocker therapy. Keep an eye on serum potassium levels in these patients. A new, more selective aldosterone antagonist option is eplerenone for patients with intolerance to spironolactone.
Loop diuretics. To control volume overload, use furosemide, torsemide, bumetanide or ethacrynic acid. Refrain from using them alone to treat heart failure because they do not prevent the progression of the disease or maintain clinical stability over time. Monitor patients' renal function and electrolytes frequently.
Thiazide diuretics. For patients resistant to loop diuretics alone, augment with metolazone or chlorthalidone. Adding a second class of diuretic can work synergistically on diuresis and can be part of an effective "sliding" diuretic regimen.
Anticoagulants. Use aspirin or clopidogrel in all patients with CHF, and initiate anticoagulation with warfarin in patients with documented left ventricular clot, atrial fibrillation or prior embolic event. Full anticoagulation in patients with cardiomyopathy remains controversial.
Digitalis glycoside. Prescribe digoxin for patients with NYHA class II to IV heart failure symptoms despite ACE inhibitors, beta blockers and diuretics, and monitor levels shortly after starting and then periodically, especially if renal function is changing. Women should use digoxin cautiously. Use it only in patients experiencing symptoms.
Positive inotropic agents. For patients with low cardiac output unresponsive to traditional heart failure medications, use dobutamine or milrinone, given as continuous intravenous infusions, in a monitored inpatient setting or for palliation of end-stage patients. Consider invasive hemodynamic monitoring to guide therapy.
Although there are no randomized trials of the treatment for diastolic heart failure-a clinical syndrome characterized by the signs and symptoms of heart failure in the setting of a preserved ejection fraction and evidence of diastolic dysfunction-treat such patients by controlling volume status, heart rate and blood pressure. Use diuretics, beta-blockers, nitrates, ACE inhibitors and angiotensin-receptor blockers. Calcium-channel blockers may also have a role.
Hospitalization may be necessary if the patient fails to respond to outpatient management, particularly in the case of NYHA class IV CHF, severe fatigue or volume overload that is unresponsive to oral diuretics. Therapy guided by hemodynamics may be better than therapy guided only by clinical findings for patients with advanced heart failure. Hospitalization may also be necessary for patients with life-threatening ventricular arrhythmias or atrial arrhythmias that worsen CHF symptoms or cause hypotension. (See also the PIER module on Sudden Cardiac Death.)
Consult a cardiologist if a patient's symptoms worsen despite optimal medical therapy. A stress test with respiratory gas analysis, pulmonary artery catheterization, electrophysiologic study or coronary angiography may be required to determine the need for a biventricular pacemaker, left ventricular assist device, referral for cardiac transplantation or implantable cardioverter defibrillator (ICD).
Refer CHF patients younger than age 65 on maximal medical therapy—and without end-organ damage from diabetes or vascular disease, a malignancy, a previous stroke, active psychiatric illness and poor psychosocial support—to a cardiac transplantation program for evaluation.
PATIENT EDUCATION AND FOLLOW-UP
Teach patients about the importance of monitoring their daily weight, eating a low-sodium diet and limiting their fluid intake, participating in regular aerobic activity, understanding their medical regimen and recognizing the symptoms of worsening CHF.
Interdisciplinary teams of physicians and nurses working with patients are the best defense against heart failure hospital admissions. Tracking daily morning weight is a cornerstone to that care.
Given the complicated nature of many medical regimens, provide accurate medication lists and educate patients and family members about their proper use.
Encourage family members to learn CPR.
Schedule regular follow-up appointments where you:
- Assess and record volume status.
- Determine and track functional capacity, using the NYHA system.
- Record weight.
- Reinforce patient education.
- Counsel patients about drugs that may exacerbate heart failure or may be contraindicated, such as NSAIDs, COX-2 inhibitors, thiazolidinediones or metformin.
- Consult a cardiologist if status deteriorates despite maximal medical therapy.
- Obtain laboratory studies at least annually, including serum electrolytes and digoxin levels, tests necessary to assess renal function, and anemia evaluation.
- Monitor high-risk medications closely by following INR in patients on warfarin, liver enzymes and lipid levels in patients on HMG-CoA reductase inhibitors, thyroid function tests in patients on amiodarone or with thyroid disease, and drug levels in patients on digoxin or antiarrhythmics.
|This information comes from the PIER module "Chronic Heart Failure."|
The information included herein should never be used as a substitute for clinical judgment and does not represent an official position of ACP.
Stage A - At high risk of developing left ventricular dysfunction
Stage B - Asymptomatic left ventricular dysfunction without ever having had symptomatic heart failure
Stage C - Current or any history of symptomatic heart failure in the setting of left ventricular dysfunction
Stage D - Persistent symptoms at rest despite maximally tolerated medical and device therapies
Having patients walk for six minutes at every visit can be a good way to track the progression of their disability. It can help primary care physicians identify which patients with progressive heart failure may benefit from specialized care or cardiac transplantation.
Studies have found the following six-minute walk test to be a reasonable objective proxy for exercise stress testing:
- Ask patients to walk between two points separated by 60 feet in a straight line, back and forth, for six minutes.
- Allow patients to stop and rest or even sit if necessary. (Use two chairs at either end of the course.)
- Calculate the total distance walked in six minutes.
The American Thoracic Society's statement and guidelines for the test are online.
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