Chronic Heart Failure


Congestive Heart Failure

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Systolic Heart Failure

Related Conditions


Acute decompensated heart failure

1. Description of the problem

Chronic heart failure is common. Over 5 million people in the United States alone carry this diagnosis, and each year over 600,000 patients are newly diagnosed. At the same time, the morbidity and mortality associated with this disease process is staggering – there are over 1 million hospitalizations each year, nearly 300,000 annual deaths, and it is the largest Medicare expenditure.

Chronic heart failure can be caused by a number of clinical conditions – most commonly, it is the result of coronary artery disease. That being said, there are a number of non-ischemic etiologies, including myocarditis, hypertension, valvular disorders, genetic cardiomyopathies, drug and toxins, and connective tissue diseases, to name a few. In fact, nearly half of all patients with chronic heart failure have an idiopathic cardiomyopathy, in which a common etiology cannot be identified.

Patients can present with chronic heart failure in a variety of ways. Some patients will have absolutely no symptoms, and only have evidence of structural heart disease identified by screening study (e.g., echocardiography). Some patients experience mild symptoms exacerbated by conditions of increased myocardial demand; symptoms include dyspnea with exertion, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, and fatigue. Other patients will present in an acutely decompensated state, with or without hemodynamic stability, due to volume overload and/or low cardiac output.

Key management points

For most patients, a systematic evaluation using history, physical examination, and a number of ancillary studies will help to discern the etiology of their chronic heart failure. If coronary artery disease is considered to be the cause, careful consideration of the value of revascularization procedures for treatment should be considered.

Other important components of management include the use of diuretic therapy to achieve and maintain euvolemia, the application of neurohormonal (ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists) and sympathetic nervous system antagonist (beta blockers) therapies to promote myocardial recovery and reverse remodeling, cardiac resynchronization for patients with electrical ventricular dyssynchrony (widened QRS), and implantable cardioverter-defibrillator (ICD) implantation for patients with severely depressed ejection fractions at risk for sudden cardiac death.

2. Emergency Management

The management of chronic heart failure is rarely an emergency, unless the patient has had an acute decompensation. The goals of therapy in patients with chronic heart failure focus on the addition of neurohormonal antagonists (e.g., beta blockers, ACE inhibitors/angiotensin receptor blockers, aldosterone antagonists) to improve cardiac function, diuretic therapy to ensure euvolemia, ICDs for patients at high risk for sudden death, cardiac resynchronization therapy for patients with dyssynchrony, and pharmacologic (e.g., inotropes) or mechanical (e.g., ventricular assist device) circulatory support for patients with end-stage cardiomyopathy. Heart transplantation evaluation should also be considered for patients with advanced heart failure.

3. Diagnosis

Patients with chronic heart failure are most commonly evaluated with transthoracic echocardiography – this will confirm the presence of systolic dysfunction, will allow determination of an ejection fraction, and will help rule out evidence of other structural heart disease (e.g., valve stenosis or regurgitation, atrial or ventricular septal defect, congenital anomalies, etc.). When an etiology cannot be determined, and particularly when ischemic disease is a possibility, cardiac catheterization (or alternative diagnostic modality) should be considered to define the coronary artery anatomy and evaluate for the presence of obstructive coronary artery disease.

A careful history and physical examination is imperative for determining how compensated a patient is from a heart failure perspective, and also should provide important clues to the etiology of a patient’s cardiomyopathy.

Lab studies

Laboratory studies should complement the history, physical examination, and diagnostic imaging studies. Abnormalities in serum electrolytes, markers of renal function, and liver function tests can help identify patients who are decompensated and require more optimal pharmacologic therapy, including augmented diuresis.

Differential diagnosis

A number of disease entities can mimic a heart failure presentation. Some patients who present with dyspnea, orthopnea, peripheral edema, and other common heart failure symptoms, but who have a normal ejection fraction by imaging, may in fact have diastolic heart failure (i.e., heart failure with preserved ejection fraction). Other cardiopulmonary disorders that can present similarly include chronic thromboembolic disease, chronic angina/coronary artery disease, pulmonary hypertension, and other chronic lung conditions (e.g., interstitial lung disease, chronic obstructive lung disease).

Confirmatory tests

Transthoracic echocardiography can help identify patients with decreased contractile function. A proBNP or BNP may be elevated in patients with heart failure, particularly when they are acutely decompensated. When well compensated and euvolemic, the BNP or proBNP may not be increased. Additionally, proBNP and BNP levels tend to be lower in more obese individuals.

4. Specific Treatment

Diuretics: work to maintain euvolemia by increasing fluid excretion; these drugs improve symptoms, but do not decrease mortality, and in fact can be injurious to renal function. May include thiazide diuretics, loop diuretics. May be given orally, or by bolus dose IV or continuous IV infusion.

ACE Inhibitors:- block the conversion of angiotensin I to angiotensin II; decrease vasoconstriction, cardiomyocyte hypertrophy, aldosterone and vasopressin release; reduce hospitalizations and mortality

Angiotensin receptor blockers: block the effect of angiotensin II; have similar effects as the ACE inhibitors; reduce hospitalizations and mortality

Aldosterone antagonists: block the binding of aldosterone to its receptor; diminish sodium retention and cardiac fibrosis; reduce hospitalizations and mortality

Beta blockers: decrease arrhythmia, vasoconstriction, sodium retention, and renin release seen with activation of the sympathetic nervous system; reduce hospitalizations and mortality

Digoxin: inhibits Na+ export via the Na/K ATPase, promoting calcium retention and increased inotropy; reduces hospitalizations, but does not decrease mortality

Hydralazine and nitrates: improve overall survival in African Americans with moderate to severe heart failure symptoms who are already on optimal medical therapy

Drugs and dosages


Lasix: 20-80 mg initial dose; may use up to 600 mg/day; can be delivered orally or intravenously

Torsemide: 10-20 mg initial dose; may give up to 200 mg/day

Bumetanide:0.5-2 mg initial dose; may give up to 20 mg/day

Metolazone: 1-5 mg

Ace inhibitors

Captopril: starting dose 6.25-12.5 mg TID; target dose 50 mg TID; maximum dose 100 mg TID

Enalapril: starting dose 2.5 mg BID; target dose 10 mg BID; maximum dose 20 mg BID

Lisinopril: starting dose 2.5-5 mg DAILY; target dose 20 mg DAILY; maximum dose 40 mg DAILY

Ramipril: starting dose 1.25-2.5 mg DAILY; target dose 10 mg DAILY; maximum dose 10 mg BID

Beta blockers

Metoprolol succinate (Toprol XL): starting dose 12.5 mg DAILY; target dose 100-200 mg DAILY

Carvedilol: starting dose 3.125 mg BID; target dose 25 mg BID

Bisoprolol: starting dose 1.25 mg DAILY; target dose 10 mg DAILY

Angiotensis receptor blockers

Losartan: starting dose 25 mg DAILY; target dose 50 mg DAILY

Candesartan: starting dose 4 mg DAILY; target dose 32 mg DAILY

Valsartan: starting dose 80 mg DAILY; target dose 160 mg BID

Digoxin: target dose 0.125-0.25 mg DAILY (no loading dose)

Hydralazine: starting dose 25 mg TID; target dose 75 mg TID

Isosorbide dinitrate: starting dose 10 mg TID; target dose 4 0mg TID (should be used with hydralazine)

Aldosterone antagonists

Spironolactone: starting dose 12.5 mg DAILY; target dose 25 mg DAILY

Eplerenone: starting dose 25 mg DAILY; target dose 50 mg DAILY (used for post-MI patients with heart failure)

Refractory cases

For refractory cases, particularly those in whom diuresis has been challenging, consider increasing diuretic dose, changing to intravenous administration, delivering therapy as continuous intravenous infusion, or adding second diuretic agent.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

The goal of therapy is to achieve clinical euvolemia and to improve cardiac contractility. For some patients, the addition of evidence-based heart failure pharmacotherapies (as well as resynchronization mechanical therapy when indicated) can improve survival and return to the heart to its normal contractile state. For other patients, contractile dysfunction may remain, but symptoms are improved considerably. For others, their cardiomyopathy can progress, often necessitating consideration of advanced heart failure therapies including ICDs, ventricular assist devices, and cardiac transplantation.

Incorrect diagnosis

When a patient’s symptoms fail to improve with diuretic therapy, or when organ perfusion is impaired following the initiation of diuretics (with the development of acute renal failure, hypotension, etc.), an alternative diagnosis should be entertained.


All patients benefit by being followed in a dedicated heart failure clinic. Most of these clinics are multidisciplinary and provide important education and titration of evidence-based heart failure pharmacotherapies. Patients are usually followed very closely during both the initiation and titration of the medications outlined previously. Careful attention should be given to clinical decompensation and side effects when monitoring therapeutic response.


Heart failure is a complex clinical syndrome that results from the inability of the heart to meet the metabolic demands of the body. Patients with chronic heart failure have upregulation of both the neurohormonal as well as the sympathetic nervous systems. This activation leads to pathologic effects, including sodium retention, fluid retention, vasoconstriction, cardiac fibrosis, myocyte hypertrophy, and increased arrhythmogenesis.


Over 5 million people in the United States alone carry a diagnosis of chronic heart failure. The majority of patients will have cardiomyopathy due to obstructive coronary artery disease and as a sequela of prior myocardial infarction. Among those with initially unexplained heart failure, however, causes include idiopathic, connective tissue disease, valvular heart disease, peripartum cardiomyopathy, viral myocarditis, and toxin-induced cardiomyopathy, to name a few.


Heart failure is a progressive disease. The goals of initial, evidence-based pharmacologic therapies are to halt this pathologic progression and, in some cases, to reverse the myocardial injury. Patients with chronic heart failure have an increased risk of mortality, and many of the aforementioned medications will attenuate this effect. ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, and beta blockers all reduce hospitalizations and improve survival. In addition, for appropriate patients, ICDs significantly improve survival.

For patients who continue to have persistent contractile dysfunction and who require frequent hospitalizations for decompensated heart failure, mortality increases considerably. For those who progress to end-stage cardiomyopathy, advanced heart failure therapies are often required. Inotropic therapies (e.g., milrinone and dobutamine) improve symptoms but actually decrease survival. Consideration should also be given to the use of ventricular assist devices or cardiac transplantation in appropriate patients.

Special considerations for nursing and allied health professionals.


What's the evidence?

“AHA Statistical Update”. Circulation. vol. 119. 2009. pp. e21Newest statistics for patients with chronic heart failure.

Jessup, M, Brozena, S. NEJM. vol. 348. 2003. pp. 2007Guidelines for the management of patients with chronic heart failure.

Levy, W. Circulation. vol. 120. 2009. pp. 835-842. Guidelines for the use of ICDs in patients with chronic heart failure.