Heart failure

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Heart failure
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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 through 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 a 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] It is the leading cause of hospitalization in people older than 65.[2]

Signs and symptoms

Symptoms

The symptoms depend largely on the side of the heart which is failing predominantly. If both sides are functioning inadequately, symptoms and signs from both categories may be present.

Given that the left side of the heart pumps blood from the lungs to the organs, failure to do so leads to congestion of the lung veins and symptoms that reflect this, as well as reduced supply of blood to the tissues. The predominant respiratory symptom is shortness of breath on exertion (dyspnea, dyspnée d'effort) - or in severe cases at rest - and easy fatigueability. Orthopnea is increasing breathlessness on reclining, measured in the number of pillows required to lie comfortably. Paroxysmal nocturnal dyspnea is a nighttime attack of severe breathlessness, usually several hours after going to sleep. Poor circulation to the body leads to dizziness, confusion and diaphoresis and cool extremities at rest.

The right side of the heart pumps blood returned from the tissues to the lungs to exchange CO2 for O2. Hence, failure of the right side leads to congestion of peripheral tissues. This may lead to peripheral edema or anasarca and nocturia (frequent nighttime urination when the fluid from the legs is returned to the bloodstream). In more severe cases, ascites (fluid accumulation in the abdominal cavity) and hepatomegaly (painful enlargement of the liver) may develop.

Heart failure may decompensate easily; this may occur as the result of any intercurrent illness (such as pneumonia), but specifically myocardial infarction (a heart attack), anaemia, hyperthyroidism or arrhythmias. These place additional strain on the heart muscle, which may cause symptoms to rapidly worsen. Excessive fluid or salt intake (including intravenous fluids for unrelated indications), and medication that causes fluid retention (such as NSAIDs and thiazolidinediones), may also precipitate decompensation.

Signs

In examining a patient with possible heart failure, a health professional would look for particular signs. General signs indicating heart failure are a laterally displaced apex beat (as the heart is enlarged) and a gallop rhythm (additional heart sounds) in case of decompensation. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

Predominant left-sided clinical signs are pulmonary edema (abnormal lung sounds due to fluid accumulation), evidence for pleural effusions (fluid collection in the pleural cavity), and cyanosis (due to poor absorption of oxygen by fluid-filled lungs).

Right-sided signs are peripheral edema, ascites and hepatomegaly, an increased jugular venous pressure and hepatojugular reflux and parasternal heave.

Diagnosis

Imaging

Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy.

Chest X-rays are frequently used to aid in the diagnosis of CHF. In the compensated patient, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema.

Electrophysiology

An electrocardiogram (ECG/EKG) is used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block).

Blood tests

Blood tests routinely performed include electrolytes (sodium, potassium), measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. A specific test for heart failure is B-type natriuretic peptide (BNP), which is found to be elevated in heart failure. BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

Angiography

Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery.

Monitoring

Various measures are often used to assess the progress of patients being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts).

Diagnostic criteria

No system of diagnostic criteria has been agreed as the gold standard for heart failure. Commonly used systems are the "Framingham criteria"[3] (derived from the Framingham Heart Study), the "Boston criteria",[4] the "Duke criteria",[5] and (in the setting of acute myocardial infarction) the "Killip class".[6]

Functional classification is generally done by the New York Heart Association Functional Classification.[7] This score documents severity of symptoms, and can be used to assess response to treatment. While its use is widespead, the NYHA score is not very reproducible and doesn't reliably predict the walking distance or exercise tolerance on formal testing.[8] The classes (I-IV) are:

  • Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities.
  • Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion.
  • Class III: marked limitation of any activity; the patient is comfortable only at rest.
  • Class IV: any physical activity brings on discomfort and symptoms occur at rest.

In its 2001 guidelines, the American College of Cardiology/American Heart Association working group introduced four stages of heart failure:[9]

  • Stage A: a high risk HF in the future but no structural heart disorder;
  • Stage B: a structural heart disorder but no symptoms at any stage;
  • Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment;
  • Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

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 dysfunction vs. diastolic dysfunction)
  • whether the abnormality is due to low cardiac output or high systemic vascular resistance (low-output heart failure vs. high-output heart failure)
  • the degree of functional impairment conferred by the abnormality (as in the NYHA functional classification)

Causes

Causes and contributing factors to congestive heart failure include the following:[9]

Causes of heart failure
Left-sided: hypertension (high blood pressure), aortic and mitral valve disease, aortic coarctation Right-sided: pulmonary hypertension (e.g. due to chronic lung disease), pulmonary or tricuspid valve disease
May affect both sides: Ischemic heart disease (due to insufficient vascular supply, usually as a result of coronary artery disease); this may be chronic or due to acute myocardial infarction (a heart attack), chronic arrhythmias (e.g. atrial fibrillation), cardiomyopathy of any cause, cardiac fibrosis, chronic severe anemia, thyroid disease (hyperthyroidism and hypothyroidism)

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:[10]

  • 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.
  • Monitor weight - Weight gain of more than 2 pounds is associated with admission to the hospital for heart failure[11]
  • 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

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.[12] 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.[13][14]

Angiotensin-modulating agents

ACE inhibitor (ACE) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.[15][9][16] 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.[17][18]

Diuretics

Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure:[10]

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.[16] 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 an ACEI, a beta blocker and a loop diuretic.[16] There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions.[19] It is contraindicated in cardiac tamponade and restrictive cardiomyopathy.

The inotropic agent dobutamine is advised only in the short-term use of acutely decompensated heart failure, and has no other uses.[16]

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.[20][21]

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.[22] 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.[23]

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.[24]

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. [1]

Palliative care and hospice

The growing number of patients with Stage D heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines.

Prognosis

Among several clinical prediction rules for prognosing acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.[25] Easy methods for identifying low risk patients are:

  • ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications.
  • BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or less breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications.

References

  1. ^ Stefan Neubauer (2007). "The failing heart — an engine out of fuel". N Engl J Med. 356 (11): 1140–51. PMID 17360992.
  2. ^ Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ, Horwitz RI (2000). "Predictors of readmission among elderly survivors of admission with heart failure". Am. Heart J. 139 (1 Pt 1): 72–7. PMID 10618565.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ McKee PA, Castelli WP, McNamara PM, Kannel WB (1971). "The natural history of congestive heart failure: the Framingham study". N. Engl. J. Med. 285 (26): 1441–6. PMID 5122894.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Carlson KJ, Lee DC, Goroll AH, Leahy M, Johnson RA (1985). "An analysis of physicians' reasons for prescribing long-term digitalis therapy in outpatients". Journal of chronic diseases. 38 (9): 733–9. PMID 4030999.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Harlan WR, oberman A, Grimm R, Rosati RA (1977). "Chronic congestive heart failure in coronary artery disease: clinical criteria". Ann. Intern. Med. 86 (2): 133–8. PMID 835934.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Killip T, Kimball JT (1967). "Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients". Am. J. Cardiol. 20 (4): 457–64. PMID 6059183.
  7. ^ Criteria Committee, New York Heart Association. Diseases of the heart and blood vessels. Nomenclature and criteria for diagnosis, 6th ed. Boston: Little, Brown and co, 1964;114.
  8. ^ Raphael C, Briscoe C, Davies J; et al. (2007). "Limitations of the New York Heart Association functional classification system and self-reported walking distances in chronic heart failure". Heart. 93 (4): 476–82. doi:10.1136/hrt.2006.089656. PMID 17005715. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  9. ^ a b c 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ a b Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
  11. ^ Chaudhry SI; et al. (2007). "Patterns of Weight Change Preceding Hospitalization for Heart Failure". Circulation. doi:10.1161/CIRCULATIONAHA.107.690768. {{cite journal}}: Explicit use of et al. in: |author= (help)
  12. ^ 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.
  13. ^ Packer M (1989). "Effect of phosphodiesterase inhibitors on survival of patients with chronic congestive heart failure". Am. J. Cardiol. 63 (2): 41A–45A. PMID 2642629.
  14. ^ Packer M, Carver JR, Rodeheffer RJ; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  15. ^ 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.
  16. ^ a b c d 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
  17. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Haji SA, Movahed A (2000). "Update on digoxin therapy in congestive heart failure". American family physician. 62 (2): 409–16. PMID 10929703.
  20. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Auble TE, Hsieh M, McCausland JB, Yealy DM (2007). "Comparison of four clinical prediction rules for estimating risk in heart failure". Annals of emergency medicine. 50 (2): 127–35, 135.e1-2. doi:10.1016/j.annemergmed.2007.02.017. PMID 17449141.{{cite journal}}: CS1 maint: multiple names: authors list (link)

See also

External links

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