Congestive heart failure overview

Congestive Heart Failure Microchapters
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Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF
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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Congestive heart failure end-of-life considerations
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:

Because heart failure is a clinical syndrome that is the end result of multiple different heart diseases, the following measures are critical:

• Treat the underlying cardiac disease(s) such as:

Hypertension

Myocardial ischemia

Valvular heart disease

• Treat exacerbating conditions such as pneumonia, arrhythmia such as atrial fibrillation, hypokalemia.
• Restrict sodium intake to minimize volume overload.

Medications:

• Diuretics: 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. Given the risk of hypo or hyperkalemia, the blood level of electrolyes should be checked regularly.

• Angiotensin converting enzyme inhibitors (ACEI): Angiotensin converting enzyme inhibitors (ACEI) are widely used in cardiovascular diseases. 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 who can not tolerate cough are often switched to an angiotensin II receptor antagonist. Patients with bilateral renal artery stenosis or severe renal impairment are not appropriate for angiotensin converting enzyme inhibitor (ACEI).

• Angiotensin II receptor antagonist: These type of drugs can 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.

• Beta blockers: 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. Clinical trials have demonstrated that Bisoprolol, Carvedilol and sustained-release Metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure. Patients with asthma, severe conduction block or severe heart failure may not be appropriate candidates for beta blocker therapy.
• Digitalis: Digitalis can strengthen the contractility of the heart. However, the toxic levels of digitalis are only slightly higher than the therapeutic levels, and as a result, digoxin should be administered under the close supervision of a cardiologist or qualified health care professional.

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.