Congestive heart failure overview

Congestive Heart Failure Microchapters
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Chronic Pharmacotherapy in HFrEF Diuretics ACE Inhibitors Angiotensin receptor blockers Aldosterone Antagonists Beta Blockers Ca Channel Blockers Nitrates Hydralazine Positive Inotropics Anticoagulants Angiotensin Receptor-Neprilysin Inhibitor Antiarrhythmic Drugs Nutritional Supplements Hormonal Therapies Drugs to Avoid Drug Interactions Treatment of underlying causes Associated conditions
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Surgical Therapy: Biventricular Pacing or Cardiac Resynchronization Therapy (CRT) Implantation of Intracardiac Defibrillator Ultrafiltration Cardiac Surgery Left Ventricular Assist Devices (LVADs) Cardiac Transplantation
ACC/AHA Guideline Recommendations Initial and Serial Evaluation of the HF Patient Hospitalized Patient Patients With a Prior MI Sudden Cardiac Death Prevention Surgical/Percutaneous/Transcather Interventional Treatments of HF Patients at high risk for developing heart failure (Stage A) Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B) Patients with current or prior symptoms of heart failure (Stage C) Patients with refractory end-stage heart failure (Stage D) Coordinating Care for Patients With Chronic HF Quality Metrics/Performance Measures
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Specific Groups: Special Populations Patients who have concomitant disorders Obstructive Sleep Apnea in the Patient with CHF NSTEMI with Heart Failure and Cardiogenic Shock
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Heart failure is a complex syndrome whereby there is inadequate output of the heart to meet the metabolic demands of the body. Abnormal function of different anatomic parts of the heart cause heart failure including the pericardium, the myocardium, the endocardium, the heart valves and the great vessels. Symptoms of heart failure are due to a lack of both forward blood flow to the body, and backward flow into the lungs. Heart failure is a clinical syndrome characterized by symptoms of dyspnea, edema and fatigue and signs such as rales on physical examination.

Classification

Several classification schemes are used to characterize heart failure based on:

• The pathophysiology of heart failure (systolic vs diastolic; left vs right; low output vs high output)
• The chronicity of heart failure (acute vs chronic)
• The severity of heart failure (the NY Heart Association Class)
• The stage of congestive heart failure (AHA Class A,B,C,D)

Pathophysiology

Heart failure can result from an abnormality of any one of the anatomical structures of the heart; the pericardium, the myocardium, the endocardium, the valvular structures or the great vessels. Heart failure was once thought to be secondary to a depressed left ventricular ejection fraction. However, studies have shown that approximately 50% of patients who are diagnosed with heart failure have a normal ejection fraction (diastolic dysfunction). Patients may be broadly classified as having heart failure with depressed left ventricular ejection fraction (systolic dysfunction) or normal/preserved ejection fraction (diastolic dysfunction). Systolic and diastolic dysfunction commonly occur in conjunction with each other.

Epidemioogy and Demographics

Heart failure affects close to 5 million people in the United States of America and each year close to 500,000 new cases are diagnosed. Congestive heart failure is responsible for a significant portion of the healthcare budget, and more than 50% of patients seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days. In 2005 the prevalence among adults aged 20 and older in the United States was 5,300,000 (about 2,650,000 males, and 2,650,000 females).

Diagnosis

Symptoms

The classic symptoms of heart failure include dyspnea, fatigue, and fluid retention.

Other symptoms include:

• Ankle edema or swelling of the feet and legs
• Claudication or pain with walking
• Confusion and altered mentation
• Cool extremities or cold and clammy hands
• Cyanosis or bluish color to the skin
• Dizziness
• Dyspnea on ordinary exertion or greater shortness of breath with usual activities
• Fainting
• Fatigue
• Hemoptysis or frothy sputum
• Nocturia or urination during the night
• Nocturnal cough
• Orthopnea or sleeping on pillows
• Palpitations or extra heart beats
• Paroxysmal nocturnal dyspnea or awakening at night with shortness of breath
• Shortness of breath
• Syncope or passing out
• Weakness
• Wheezing or cardiac asthma

Treatment

General Measures in the Management of Heart Failure

• Treat the underlying cause of heart failure such as ischemic heart disease, hypertension, and valvular heart disease.
• Treat other non cardiac diseases that might contribute to the symptoms of heart failure such as diabetes and hyperthyroidism.
• Treat with a low salt diet
• Follow the patient's weight to check for fluid overload
• Treat with vaccines for influenza and pneumococcus

Diuresis: First Step in the Management of Heart Failure

The treatment of chronic heart failure often begins with the administration of diuretics, particularly if the patient has signs or symptoms of volume overload. While increased left ventricular volume increases contractility to a point, if the heart is filled beyond that point, its contractility diminishes (the patient "falls of the Staring curve"). Diuretics can reduce volume overload and reduce shortness of breath and edema. There are three kinds of diuretics, loop diuretics, thiazides and potassium-sparing diuretics. Diuretics rapidly improve the symptoms of heart failure (within hours to days). Diuretics reduce excess volume that accumulates with heart failure and decrease pulmonary edema that causes symptoms of dyspnea and orthopnea. Lasix 20 to 40 mg PO daily is a conventional starting dose, but in some patients, torsemide may be a better choice due to its more predictable absorption. Once a day dosing of a given diuretic is preferred to twice a day dosing at a lower dose. A rise in BUN and Cr may reflect a reduction in renal perfusion, and further diuresis should only be undertaken with careful monitoring of renal function. The patient should weigh themselves each morning at the same time on the same scale, and the diuretic dosing should be adjusted to maintain a constant weight. Given the risk of hypokalemia or hyperkalemia, the blood level of electrolyes should be checked regularly.

ACE Inhibition and Angiotensin Receptor Blockade: Second Step in the Management of Heart Failure

After diuretics are started or at the same time they are started, an ACE inhibitor can be initiated . This includes a large group of drugs, such as Enalapril (Vasotec/Renitec), Ramipril (Altace/Tritace/Ramace/Ramiwin), Quinapril (Accupril), Perindopril (Coversyl/Aceon), Lisinopril (Lisodur/Lopril/Novatec/Prinivil/Zestril) and Benazepril (Lotensin). They can improve symptoms and prognosis of heart failure in several ways including afterload reduction and favorable ventricular remodeling. Usual side effects include dry cough and angioedema. Patients with bilateral renal artery stenosis or severe renal impairment are not appropriate for angiotensin converting enzyme inhibitor (ACEI).

During or after the initiation of diuresis, one could start, for example, lisinopril 5 mg Q day. Every 1 - 2 weeks, the dose would be escalated to achieve a target dose of 15 to 20 mg Q day. An ACE inhibitor is initiated before a beta blocker because an ACE inhibitor achieves its hemodynamic effect more rapidly, and is less likely to cause a decline in hemodynamics. Although there is some data to suggest that aspirin blunts the hemodynamic effect of ACE inhibitors, there is no data to suggest that aspirin reduces the clinical efficacy of ACE inhibitors in heart failure patients. Aspirin should be administered to patients with ischemic heart disease, but not to patients without it.

If a patient cannot tolerate a an ACE inhibitor (develops a cough), then an Angiotensin II receptor blocker can be administered in its place. Angiotensin II receptor antagonists block the activation of angiotensin II AT1 receptors. Blockade of AT1 receptors directly causes vasodilation, reduces secretion of vasopressin, reduces production and secretion of aldosterone. Because angiotensin II receptor antagonists do not inhibit the breakdown of bradykinin or other kinins, and are thus only rarely associated with the persistent dry cough and/or angioedema that limit ACE inhibitor therapy. Commonly administered agents in the management of heart failure include Candesartan, Valsartan, Telmisartan, Losartan, Irbesartan, and Olmesartan. The effectiveness of switching to an ARB from and ACE inhibitor was demonstrated for candesartan in the CHARM Alternative trial .

In general, ARBs are as effective or slightly less effective than ACE inhibitors in the treatment of congestive heart failure. It is a class 2a recommendation to substitute an ARB as an alternative to ACE inhibitors if the patient is already taking an ARB for another indication.

The efficacy of adding an ARB to an ACE inhibitor was assessed in the CHARM Added trial. While there was a reduction in the composite primary endpoint in the study, there was no reduction in mortality. Furthermore, the VALIANT trial demonstrated that an ARB should not be added to an ACE inhibitor in the post MI setting. These results for ARBs are in contrast to the results of the EMPHASIS HF trial showed that the addition of eplerenone (an aldosterone antagonist) to ACE inhibition improved clinical outcomes including mortality among patients with class II or III heart failure with a reduced LVEF. Thus, based upon the mortality benefit observed in the EMPHASIS HF trial, an aldosterone antagonist rather than and ARB should be added to an ACE inhibitor in patients with NYHA class II heart failure and an LVEF < 30%, in the post-MI patient who has an LVEF < 40% who has heart failure symptoms or diabetes, and the patient with class III or IV heart failure who has an LVEF < 35%.

"Triple therapy", the combined use of an ACE inhibitor, an ARB and an aldosterone antagonist is a relative contraindication.

Beta blockers: Third Step in the Management of Heart Failure

Beta blockers reduce the heart rate which lowers the myocardial energy expenditure. They also prolong diastolic filling and lengthen the period of coronary perfusion. Beta blockers can also decrease the toxicity of catecholamines on the myocardium.

Once you have achieved a stable dose of a diuretic and an ACE inhibitor, then one of the three beta blockers that have been associated with improved survival (carvedilol, metoprolol succinate or bisoprolol) can be added and the dose titrated based upon the patient's tolerance. You should avoid beta-blockers with intrinsic sympathomimetic activity (pindolol or acebutolol). It should be noted that the 35% reduction in one year mortality observed in meta-analyses of beta-blockers in heart failure was when these drugs were added to ACE inhibitors. There are no direct comparisons of the various beta-blockers, but some data does suggest that carvedilol may improve LVEF more than the others, but it may not be as well tolerated due to its vasodilatory properties. If the patient has been over diuresed, they may not tolerate the addition of a beta blocker.

Relative contraindications to beta-blocker administration include the following:

• Asthma or bronchospasm
• Hypotension resulting in poor end organ perfusion or symptoms
• Bradycardia or heart block (first degree heart block with a PR interval > 0.24, second degree heart block, third degree heart block
• Peripheral arterial disease with limb ischemia at rest
• Moderate or greater peripheral edema
• Recent intravenous inotropic therapy

Given the potential for hemodynamic decompensation, the initiation of beta-blockers is best undertaken by an individual or center specializing in heart failure management. The patient should be aware of potential side effects, and should be aware that it may take one to three months for the beta-blockers to improve heart failure symptoms. Therapy is initiated with very low doses, and the dose of the beta-blocker should be doubled every two weeks until the target dose is achieved or symptoms prevent further dose escalation.

• Carvedilol: Initial dose 3.125 mg twice daily, target dose 25 to 50 mg twice daily
• Metoprolol succinate: Initial dose 12.5 mg daily, target dose 200 mg daily
• Bisoprolol: Initial dose 1.25 mg daily, target dose 5 to 10 mg daily

Weight gain or peripheral edema that is not responsive to diuresis may require a reduction in the dose of beta-blockers.

Aldosterone Antagonism: Fourth Step in the Management of Heart Failure

An aldosterone antagonist can be added to the regimen of 'select' patients. These selected patients include:

• Class II heart failure and a left ventricular ejection fraction (LVEF) < 30%
• Class III/IV heart failure and a LVEF <35%
• Post ST segment elevation MI and a LVEF < 40% who have either symptomatic heart failure or diabetes.
• The serum potassium must be under 5.0 meq/li and the glomerular filtration rate (GFR) should be > 30 cc per minute

A requirement for aldosterone antagonist is that the patient's renal function and potassium can be carefully monitored. Eplerenone has fewer endocrine side effects (1%) than spironolactone (10%), but is more costly. A reasonable strategy is to initiate therapy with spironolactone at a dose of 25 to 50 mg daily, and then switch to eplerenone at a dose of 25 to 50 mg daily if endocrine side effects develop.

Risk Factors for the Development of Hyperkalemia on an Aldosterone Antagonist

• Triple therapy with an ACE inhibitor and angiotensin II receptor blocker makes this combination a contraindication
• Higher doses of either an ACE inhibitor or an angiotensin receptor blocker (ARB)
• Hyperkalemia prior to initiation of spironolactone
• Comorbidities such as diabetes and chronic renal insufficiency
• Higher NYHA heart failure class
• Concomitant administration of beta blockers, nonsteroidal anti-inflammatory drugs (NSAIDs) or potassium supplements
• A daily dose of Spironolactone greater than 50 mg

The Combination of Hydralazine and a Nitrate: Fifth step in the Management of Heart Failure

The combination of hydralazine and a nitrate (particularly among black patients) can be added if the patient continues to have symptoms on a diuretic, ACE inhibitor (or ARB in the intolerant patient) and a beta blocker. The initial dose is isosorbide dinitrate 20 mg three times a day along with hydralazine 25 mg three times a day. The dose(s) can be increased every 2 to 4 weeks to a target dose of isosorbide dinitrate 40 mg three times a day and hydralazine 75 mg three times a day.

Digoxin: Sixth step in the Management of Heart Failure

Digitalis can strengthen the contractility of the heart and can also be useful to achieve rate control in patients with heart failure who also have atrial fibrillation. In the DIG trial, digoxin reduced the rate of re-hospitalization but did not improve mortality among all patients enrolled in the trial. However, in a retrospective analysis, mortality was reduced in male patients who had digoxin levels between 0.5 and 0.8 ng/mL and was increased in male patients with digoxin levels > 1.2 ng/ml. A similar trend was observed among women patients: there was a trend towards lower mortality at digoxin concentrations between 0.5 to 0.9 ng/ml, but significantly higher mortality at digoxin concentrations > 1.2 ng/ml.

Digoxin should not be used as primary therapy for congestive heart failure. The administration of digoxin is reasonable in patients with NYHA class II-IV heart failure symptoms who have an LVEF of < 40% despite treatment with diuretics, angiotensin-converting enzyme inhibitors, beta blockers, and an aldosterone antagonist. Small doses of 0.125 mg per day of digoxin are often effective in maintaining a serum digoxin level between 0.5 and 0.8 ng/ml.

Cardiac Resynchronization Therapy

Cardiac Resynchronization Therapy (CRT) is recommended in congestive heart failure patients with:

• Symptoms: NYHA Class II-IV
• QRS: A prolonged QRS interval > 0.12
• LVEF: A LVEF < 30% to 35%

Percutaneous Coronary Intervention (PCI):

Coronary artery disease (CAD) and impaired blood flow to the heart is one of the main causes of heart failure. Relieving the blockages in the coronary arteries can improve overall heart function, which may improve or resolve heart failure symptoms. The procedure is usually performed in a cardiac catherization laboratory. A catheter, a very small tube with a tiny deflated balloon on the end, is inserted through an incision in the groin area and then guided over a floppy wire to the section of the diseased artery. The balloon is then inflated to prop open the artery. The balloon is deflated and withdrawn once the artery has been fully opened. A stent may be placed during the procedure to keep the blood vessel open. Clinical trials have demonstrated that percutaneous coronary intervention (PCI) is a very effective and safe procedure to dilate blocked vessels and can improve a patient's symptoms if ischemia or lack of blood flow is the problem.

Left Ventricular Assist Device (LVAD):

A left ventricular assist device (LVAD) is a mechanical pump-type device that can help maintain the pumping ability of a failing heart. One type of LVAD has tubing that pulls blood from the left ventricle into a pump. The pump then ejects blood into the aorta. LVADs are typically used for weeks to months as a "bridge" to more definitive therapy such as a heart transplant rather than as a final or "destination" therapy.

Heart Transplantation

A Heart transplant may be the only effective treatment option for patients with severe, progressive heart failure that can not be helped by medications, dietary and lifestyle changes. During a heart transplant procedure, the surgeons connect the patient to a heart-lung machine, which takes over the functions of the heart and lungs. Then the surgeons remove the diseased heart and replace it with the donor heart. Finally, the major blood vessels are reconnected and the new heart is ready to work. The outlook for people with heart transplants is good during the first few years after the transplant. Over 85 percent of patients are alive more than a year after their heart transplant.