('''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 in the face of heart disease. 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 a universally agreed definition and difficulties in diagnosis, particularly when the condition is considered "mild".
Causes and contributing factors to congestive heart failure include (with specific reference to left (L) or right (R) sides):
- Genetic family history of CHF
- Ischaemic heart disease/Myocardial infarction (coronary artery disease)
- Infection
- Alcohol ingestion
- Anemia
- Thyrotoxicosis ( Hyperthyroidism )
- Arrhythmia
- Hypertension (L)
- Coarctation of the aorta (L)
- Aortic stenosis/regurgitation (L)
- Mitral regurgitation (L)
- Pulmonary stenosis/Pulmonary hypertension/Pulmonary embolism all leading to Cor Pulmonale (R)
- Mitral valve disease (R)
The usual heart irritants can make CHF deadly: arterial
Plaque , stress, smoking, old age, lack of exercise, overworked heart, and obesity. In genetic family history of CHF, the cause is a weak heart having thinner muscle walls than usual, and often weakened further by one or more of the above heart irritants. Arterial plaque (caused by eating fatty or greasy foods) lines the inside of the arteries and heart, increasing blood pressure and tiring the heart. In obesity cases, the heart is squashed by fat surrounding it, giving it too little room to beat. The result is irregular heart beats causing inefficient blood pumping and a tired heart.
There are many different ways to categorize heart failure, including:
- the side of the heart involved, (left heart failure versus right heart failure)
- whether the abnormality is due to contraction or relaxation of the heart ( Systolic heart failure vs. Diastolic heart failure)
- whether the abnormality is due to low cardiac output or low systemic vascular resistance (low-output heart failure vs. high-output heart failure)
The
NYHA Functional Class is a commonly used way to gauge the progression of CHF in a particular patient. This classification is used to determine how much CHF limits their lifestyle, and does not apply to a particular decompensated episode. Depending on symptoms, patients may move in either direction on the NYHA scale.
- Class I: No symptoms at any level of exertion
- Class II: Symptoms with heavy exertion
- Class III: Symptoms with light exertion
- Class IV: Symptoms with no exertion
Heart failure stages from the ACC/AHA guidelines represent a newer classification that complements the NYHA classification.
- Stage A: At risk for developing heart failure without evidence of cardiac dysfunction
- Stage B: Evidence of cardiac dysfunction without symptoms
- Stage C: Evidence of cardiac dysfunction with symptoms
- Stage D: Symptoms of heart failure despite maximal therapy
An important feature of the staging classification is that patients can only progress in one direction: from Stage A to D. This is meant to reflect the progressive nature of heart failure.
Signs of decompensated heart failure include
Pulmonary Edema (fluid accumulation in the lungs),
Ascites (fluid in the abdominal cavity),
Peripheral Edema (fluid build-up in dependent portions of the body). Other physical examination findings include
Rales heard on chest
Auscultation , an enlarged or
Pulsatile Liver , and
Jugular Venous Distension . Reduced function in other organs can occur because they are not receiving enough blood. The patient may experience other organ conditions years before CHF is diagnosed.
Symptom s 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).
Individuals with heart failure are sensitive to small shifts in their 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-ray s (CXRs) are frequently used to aid in the diagnosis of CHF.
Sign s of CHF on CXR areSingh VN. Congestive Heart Failure. eMedicine.com. URL:
http://www.emedicine.com/radio/topic189.htm . Accessed on April 14, 2006.:
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 reduction or abstinence of smoking and drinking alcohol.
Patients with CHF are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include (Smith et al., 2003):
- Moderate physical activity, when symptoms are mild or moderate; or bed rest when symptoms are severe.
- Weight reduction – through physical activity and dietary modification, as Obesity is a risk factor for heart failure and Ventricular Hypertrophy .
- Sodium restriction – excessive Sodium intake may precipitate or exacerbate heart failure, thus a "no added salt" diet (60–100 mmol total daily intake) is recommended for patients with CHF. More severe restrictions may be required in severe CHF.
- Fluid restriction – patients with CHF have a diminished ability to excrete free water load. They are also at an increased risk of Hyponatremia due to the combination of decreased sodium intake and diuretic therapy. Generally water intake should be limited to 1.5 L daily or less in patients with Hyponatremia , though fluid restriction may be beneficial regardless in symptomatic reduction.
It has been noted that there is a significant evidence–practice gap in the treatment of CHF, particularly the underuse of ACE inhibitors and β-blockers. (Jackson et al., 2005) Treatment of CHF aims to relieve symptoms, maintain a agents,
Vasodilator agents, positive
Inotrope s,
ACE Inhibitor s,
Beta Blocker s, and
Aldosterone Antagonist s (e.g.
Spironolactone ).
ACE Inhibitor (ACEI) therapy is recommended for ''all'' patients with systolic heart failure, irrespective of symptomatic severity or blood pressure. (Krum et al., 2001; NICE, 2003; Hunt et al., 2005) ACE inhibitors improve symptoms, decrease mortality and reduce
Ventricular Hypertrophy .
Angiotensin II Receptor Antagonist therapy (also referred to as AT
1-antagonists or angiotensin receptor blockers), particularly using
Candesartan , is an acceptable alternative if the patient is unable to tolerate ACEI therapy. (Granger et al., 2003; Pfeffer et al., 2003)
Diuretic therapy is indicated for the relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure (Smith et al., 2003):
Until recently, ,
Carvedilol , and extended-release
Metoprolol .
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.
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. (Exner et al., 2001; Taylor et al., 2004)
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 Ventricle s), 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 . (Bristow et al., 2004) 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. (Cleland et al., 2005)
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. (Bardy et al., 2005)
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 .
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