Congestive heart disease - Symptoms, Diagnosis, Treatments, Cure & Causes

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Heart failure - From Wikipedia, the free encyclopedia

Heart failure

Classification & external resources ICD-10 I50.0

ICD-9 428.0

DiseasesDB 16209

MedlinePlus 000158

eMedicine med/3552

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]

Contents

1 Causes

2 Classification

3 Signs and Symptoms

4 Diagnostic Lab Values

5 Treatment

5.1 Non-pharmacological measures

5.2 Pharmacological management

5.2.1 Angiotensin-modulating agents

5.2.2 Diuretics

5.2.3 Beta blockers

5.2.4 Positive inotropes

5.2.5 Alternative vasodilators

5.2.6 Aldosterone Receptor Antagonists

5.3 Devices and surgery

6 See also

7 References

8 Footnotes

Causes

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

Genetic family history of CHF

Ischemic heart disease/Myocardial infarction (coronary artery disease)

Thyrotoxicosis (hyperthyroidism)

Anemia

Arrhythmia

Hypertension

Cardiac fibrosis

Coarctation of the aorta (L)

Aortic stenosis/regurgitation (L)

Mitral regurgitation (L)

Pulmonary stenosis/Pulmonary hypertension/Pulmonary embolism

Mitral valve disease (L)

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 lines the inside of the arteries that supply the heart and the rest of the body, meaning less blood gets to the heart itself, as well as the heart having to work harder to push blood through the thinner systemic arteries. 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)

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]:

Vascular redistribution

Peribronchial cuffing/interstitial edema (bat-shaped)

Kerley B lines

Consolidation of lower lung fields

Cardiomegaly

Diagnostic Lab Values

B-type natriuretic peptide, (BNP) is found to be elevated in people suffering from CHF. Measurement of BNP along with with other clinical information can be used to differentiate between causes of dyspnea due to congestive heart failure (CHF) from that of other causes of dyspnea.

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):

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.

Certain drugs can exacerbate HF and should be avoided: antiarrhythmic agents (with some exceptions); calcium channel blockers and first generation dihydropyridine; non-steroidal anti-inflammatory drugs, coxibs, and corticosteroids; and tricyclic antidepressants and lithium.[3]

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 a 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 AT1-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):

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.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.

See also

Cardiogenic shock

Heart transplant

Ventricular Restoration: The Dor Procedure

ACE inhibitor

Isosorbide dinitrate/hydralazine

Killip class

Ventricular remodeling

B-type natriuretic peptide

References

^ Stefan Neubauer (2007). "The failing heart — an engine out of fuel". N Engl J Med 356 (11): 1140-51. PMID 17360992.

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

^ Erik B Friedrich MD & Michael Böhm MD (2006). Treatment of Chronic Heart Failire.

^ Packer M, Department of Medicine, Mount Sinai School of Medicine, City University of New York. (1989). "Effect of phosphodiesterase inhibitors on survival of patients with chronic congestive heart failure.". Am J Cardiol 63 (2): 41A-45A. PMID 2642629.

^ Packer M, Carver JR, Rodeheffer RJ, Ivanhoe RJ, DiBianco R, Zeldis SM, Hendrix GH, Bommer WJ, Elkayam U, Kukin ML, et al., Department of Medicine, Mount Sinai School of Medicine, City University of New York. (1991). "Effect of oral milrinone on mortality in severe chronic heart failure. The PROMISE Study Research Group.". N Engl J Med 325 (21): 1468-75. PMID 1944425.

^ Krum H, National Heart Foundation of Australia and Cardiac Society of Australia & New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel. (2001). "Guidelines for management of patients with chronic heart failure in Australia.". Med J Aust 174 (9): 459-66. PMID 11386592.

^ Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, Jessup M, Konstam MA, Mancini DM, Michl K, Oates JA, Rahko PS, Silver MA, Stevenson LW, Yancy CW, Antman EM, Smith SC Jr, Adams CD, Anderson JL, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B; American College of Cardiology; American Heart Association Task Force on Practice Guidelines; American College of Chest Physicians; International Society for Heart and Lung Transplantation; Heart Rhythm Society. (2005). "ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult". Circulation 112 (12): e154-235. PMID 16160202.

^ Granger CB, McMurray JJ, Yusuf S, Held P, Michelson EL, Olofsson B, Ostergren J, Pfeffer MA, Swedberg K; CHARM Investigators and Committees. (2003). "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 362 (9386): 772-6. PMID 13678870.

^ Pfeffer MA, Swedberg K, Granger CB, Held P, McMurray JJ, Michelson EL, Olofsson B, Ostergren J, Yusuf S, Pocock S; CHARM Investigators and Committees. (2003). "Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme.". Lancet 362 (9386): 759-66. PMID 13678868.

^ Exner DV, Dries DL, Domanski MJ, Cohn JN (2001). "Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction.". N Engl J Med. 344 (18): 1351-7. PMID 11333991.

^ Taylor AL, Ziesche S, Yancy C, Carson P, D'Agostino R Jr, Ferdinand K, Taylor M, Adams K, Sabolinski M, Worcel M, Cohn JN; African-American Heart Failure Trial Investigators. (2004). "Combination of isosorbide dinitrate and hydralazine in blacks with heart failure.". N Engl J Med 351 (20): 2049-57. PMID 15533851.

^ Erik B Friedrich MD & Michael Böhm MD (2006). Treatment of Chronic Heart Failire.

^ Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, Carson P, DiCarlo L, DeMets D, White BG, DeVries DW, Feldman AM; Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. (2004). "Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure". N Engl J Med 350 (21): 2140-50. PMID 15152059.

^ Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L; Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. (2005). "The effect of cardiac resynchronization on morbidity and mortality in heart failure". N Engl J Med 352 (15): 1539-49. PMID 15753115.

^ Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH; Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. (2005). "Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure.". N Engl J Med 352 (3): 225-37. PMID 15659722.

Footnotes

Donatelle RJ. Health: The basics, 6th edition. San Francisco: Pearson Education; 2005.

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.

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

Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513

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