Congestive heart failure

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Template:DiseaseDisorder infobox | }} 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 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".

Contents 1 Causes 2 Classification 3 Symptoms and signs 4 Treatment 4.1 Non-pharmacological measures 4.2 Pharmacological management 4.2.1 Angiotensin-modulating agents 4.2.2 Diuretics 4.2.3 Beta blockers 4.2.4 Positive inotropes 4.2.5 Alternative vasodilators 4.3 Devices and surgery 5 See also 6 External links 7 References 8 See also

Causes

Causes and contributing factors to congestive heart failure include: genetic family history of CHF, infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, and hypertension. 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.

Classification

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.

Symptoms and signs

Signs of decompensated heart failure include pulmonary edema (fluid accumulation in the lungs), 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.

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).

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<ref>Singh VN. Congestive Heart Failure. eMedicine.com. URL: http://www.emedicine.com/radio/topic189.htm. Accessed on April 14, 2006.</ref>:

• Vascular redistribution
• Peribronchial cuffing/interstitial edema
• Kerley B lines
• Consolidation of lower lung fields

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 reduction or 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):

• 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.

Pharmacological management

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 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.

Angiotensin-modulating agents

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 AT₁-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)

Diuretics

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):

• Loop diuretics (e.g. furosemide) – most commonly used class in CHF, usually for moderate CHF.
• Thiazide diuretics (e.g. hydrochlorothiazide) – useful for mild CHF.
• Potassium-sparing diuretics (e.g. amiloride) – used first-line use to correct hypokalaemia.
  • Spironolactone is used as add-on therapy to ACEI plus loop diuretic in severe CHF.
  • Eplerenone is specifically indicated for post-MI reduction of cardiovascular risk.

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.

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. (Exner et al., 2001; Taylor et al., 2004)

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. (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.

See also

• Cardiogenic shock
• Heart transplant

External links

• Congestive Heart Failure information from Seattle Children's Hospital Heart Center

References

• Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005;352(3):225-37. PMID 15659722
• Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004;350:2140-50. PMID 15152059
• Cleland JGF, Daubert J-C, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005;352(15):1539-49. PMID 15753115
• Donatelle RJ. Health: The basics, 6th edition. San Francisco: Pearson Education; 2005.
• Exner DV, Dries DL, Domanski MJ, Cohn JN. Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction. N Engl J Med 2001;344(18):1351-7. PMID 11333991
• Granger CB, McMurray JJ, Yusuf S, Held P, Michelson EL, Olofsson B, et al. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial. Lancet 2003;362(9386):772-6. PMID 13678870
• Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation 2005;112(12):e154-235. PMID 16160202.
• Jackson S, Bereznicki L, Peterson G. Under-use of ACE-inhibitor and β-blocker therapies in congestive cardiac failure. Australian Pharmacist 2005;24(12):936.
• Krum H, National Heart Foundation of Australia and Cardiac Society of Australia & New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel. Guidelines for management of patients with chronic heart failure in Australia. Med J Aust 2001;174(9):459-66. PMID 11386592
• National Institute for Clinical Excellence. Chronic heart failure: management of chronic heart failure in adults in primary and secondary care. Clinical Guideline 5. London: National Institute for Clinical Excellence; 2003 Jul. Available from: www.nice.org.uk/pdf/CG5NICEguideline.pdf
• Pfeffer MA, Swedberg K, Granger CB, Held P, McMurray JJ, Michelson EL, et al. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet 2003;362(9386):759-66. PMID 13678868
• Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
• Taylor AL, Ziesche S, Yancy C, Carson P, D'Agostino R Jr, Ferdinand K, et al. Combination of isosorbide dinitrate and hydralazine in blacks with heart failure. N Engl J Med 2004;351(20):2049-57. PMID 15533851

See also

• ACE inhibitor
• Isosorbide dinitrate/hydralazine
• Killip class
• Ventricular remodelingde:Herzinsuffizienz

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