Heart failure


Congestive heart failure (CHF), also called congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood throughout the body. It is not to be confused with "cessation of heartbeat", which is known as asystole, or with cardiac arrest, which is the cessation of normal cardiac function with subsequent hemodynamic collapse leading to death. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure". Congestive heart failure is often undiagnosed due to a lack of an universally agreed definition and difficulties in diagnosis, particularly when the condition is considered "mild." Even with the best therapy, heart failure is associated with an annual mortality of 10%.[1]

Causes

Causes and contributing factors to congestive heart failure include the following (with specific reference to left (L) or right (R) sides):

Classification

There are many different ways to categorize heart failure, including:

Signs and Symptoms

Left Heart Failure: Symptoms of decompensated heart failure include dyspnea (shortness of breath) on exertion, orthopnea (dyspnea that increases upon lying down), fatigue and paroxysmal nocturnal dyspnea ("cardiac asthma", shortness of breath that occurs hours or minutes after lying down), nocturnal cough, confusion and memory impairment (in advanced stages), and diaphoresis and cool extremities at rest.

Signs of decompensated left heart failure include: Displaced apex beat (usually to left due to cardiomegaly), Pathologic S3 Gallop, S4, crackles at the lung bases due to pulmonary edema (fluid accumulation in the lungs), dullness to percussion and tactile fremitus of lower lung fields. Increased intensity of pulmonic component of 2nd heart sound.

Right Heart Failure: Symptoms and Signs include: Peripheral edema (fluid build-up in dependent portions of the body), ascites (fluid in the abdominal cavity), nocturia (due to increased venous return with leg elevation), Jugular venous distention, Epistaxis (due to an increase in venous pressure), Hepatomegaly, hepatojugular reflux, and right ventricular heave.

Individuals with heart failure are sensitive to small shifts in their intravascular volume status (the amount of fluid in their circulatory system). Increasing the volume in their circulatory system can cause symptoms and signs of decompensated heart failure, while decreasing the volume in the circulatory system can cause hypotension.

Chest X-rays (CXRs) are frequently used to aid in the diagnosis of CHF. Signs of CHF on CXR are[2]:

Diagnostic Lab Values

Treatment

The treatment of CHF focuses on treating the symptoms and signs of CHF and preventing the progression of disease. If there is a reversible cause of the heart failure (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, or hypertension), that should be addressed as well. Reversible cause treatments can include exercise, eating healthy foods, reduction in salty foods, and abstinence of smoking and drinking alcohol.

Non-pharmacological measures

Patients with CHF are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include (Smith et al., 2003):

Pharmacological management

There is a significant evidence–practice gap in the treatment of CHF; particularly the underuse of ACE inhibitors and β-blockers and aldosterone antagonists which have been shown to provide mortality benefit. (Jackson et al., 2005) Treatment of CHF aims to relieve symptoms, maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g. spironolactone). It should be noted that while intuitive, increasing heart function with some drugs, such as the positive inotrope Milrinone, leads to increased mortality[4][5].

Angiotensin-modulating agents

ACE inhibitor (ACE) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.[6][7] (NICE, 2003) ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy (also referred to as AT<sub>1</sub>-antagonists or angiotensin receptor blockers), particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy.[8][9]

Diuretics

Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure (Smith et al., 2003):

Beta blockers

Until recently, β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure. (NICE, 2003) As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, and extended-release metoprolol.

Positive inotropes

Digoxin, once used as first-line therapy, is now reserved for control of ventricular rhythm in patients with atrial fibrillation; or where adequate control is not achieved with ACEI plus loop diuretic. There is no evidence that positive inotropes reduce mortality in CHF.it is contraindicated in cardiac tamponade and restrictive cardiomyopathy

Alternative vasodilators

The combination of isosorbide dinitrate/hydralazine is the only vasodilator regimen, other than ACE inhibitors or angiotensin II receptor antagonists, with proven survival benefits. This combination appears to be particularly beneficial in CHF patients with an African American background, who respond less effectively to ACEI therapy.[10][11]

Aldosterone Receptor Antagonists

For patients with advanced HF (EF≤35-40%, NYHA III-IV) should be treated with aldosterone receptor antagonists in addition to standard treatment options (unless risk of contraindication. Results from the RALES and EPHESUS trials show that aldosterone receptor antagonists decrease mobidity and mortality in this patient group.[12]

Devices and surgery

Patients with NYHA class III or IV, left ventricular ejection fraction (LVEF) of 35% or less and a QRS interval of 120 ms or more may benefit from cardiac resynchronization therapy (CRT; pacing both the left and right ventricles), through implantation of an bi-ventricular pacemaker, or surgical remodelling of the heart. These treatment modalities may make the patient symptomatically better, improving quality of life and in some trials have been proven to reduce mortality.

The COMPANION trial demonstrated that CRT improved survival in individuals with NYHA class III or IV heart failure with a widened QRS complex on EKG.[13] The CARE-HF trial showed that patients receiving CRT and optimal medical therapy benefited from a 36% reduction in all cause mortality, and a reduction in cardiovascular-related hospitalization.[14]

Patients with NYHA class II, III or IV, and LVEF of 35% (without a QRS requirement) may also benefit from an implantable cardioverter-defibrillator (ICD), a device that is proven to reduce all cause mortality by 23% compared to placebo. This mortality benefit was observed in patients who were already optimally-managed on drug therapy.[15]

Another current treatment involves the use of left ventricular assist devices (LVADs). LVADs are battery-operated mechanical pump-type devices that are surgically implanted on the upper part of the abdomen. They take blood from the left ventricle and pump it through the aorta. LVADs are becoming more common and are often used by patients who have to wait for heart transplants.

The final option, if other measures have failed, is cardiac transplant surgery (heart transplant) or implantation of an artificial heart. A radical new type of surgery, which is largely untested and is still in its first stages of development, was invented by Brazilian doctor Randas Batista in 1994. It involves removal of a swath of the left ventricle, to make contractions more efficient and prevent backflow of blood into the left atrium through the bicuspid valve.

See also

Footnotes

External links

Citations