Introduction
Background
Congestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump blood at the rate required by the metabolizing tissues or in which the heart can do so only with an elevation in filling pressure.
The heart's inability to pump a sufficient amount of blood to meet the needs of the body's tissues may be a result of insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanisms increase blood volume, as well as the cardiac filling pressure, heart rate, and cardiac muscle mass, to maintain the pumping function of the heart and to cause a redistribution of blood flow. Despite these compensatory mechanisms, the ability of the heart to contract and relax declines progressively, and heart failure (HF) worsens.
The clinical manifestations of HF vary enormously and depend on a variety of factors, including the age of the patient, the extent and rate at which cardiac performance becomes impaired, and which ventricle is initially involved in the disease process. A broad spectrum of severity of impairment of cardiac function is ordinarily included in the definition of HF. These impairments range from the mildest forms, which are manifest clinically only during stress, to the most advanced forms, in which cardiac pump function is unable to sustain life without external support.
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Pathophysiology
Clinical manifestations of HF
The clinical manifestations of heart failure arise as a consequence of inadequate cardiac output and/or the damming of blood behind 1 or both ventricles. The inability of cardiac muscle to shorten against a load alters the relationship between ventricular end-systolic pressure and volume so that end-systolic volume rises. The following sequence then occurs. At first, these mechanisms maintain cardiac output at a normal level:
- Ventricular end-diastolic volume and pressure increase.
- Volume and pressure increase in the atrium behind the failing ventricle.
- The atrium contracts more vigorously (a manifestation of the Starling law operating on the atrium).
- The pressure in the venous and capillary beds behind (upstream to) the failing ventricle rises.
- Transudation of fluid from the capillary bed into the interstitial space (pulmonary or systemic) increases.
Many of the symptoms characteristic of HF may be traced to this sequence of events and the resultant increase in fluid within the interstitial spaces of the lungs, liver, subcutaneous tissues, and serous cavities.
Right- versus left-sided HF
Implicit in the backward failure theory is the idea that fluid localizes behind the specific cardiac chamber that is initially affected. Thus, symptoms secondary to pulmonary congestion initially predominate in patients with left ventricular (LV) infarction, hypertension, or aortic or mitral valve disease; that is, they manifest left-sided HF. With time, however, fluid accumulation becomes generalized, and ankle edema, congestive hepatomegaly, ascites, and pleural effusion occur; therefore, the patients subsequently have right-sided HF as well.
Fluid retention in HF
Fluid retention in HF is caused in part by a reduction in the glomerular filtration rate and in part by activation of the renin-angiotensin-aldosterone system. Reduced cardiac output is associated with a decrease in the glomerular filtration rate and an increase in the elaboration of renin, which, through the activation of angiotensin, results in the release of aldosterone. The combination of impairment of hepatic function, owing to hepatic venous congestion, and a reduction in hepatic blood flow interferes with the metabolism of aldosterone, further raising its plasma concentration and augmenting the retention of sodium and water.
Cardiac output (and the glomerular filtration rate) may be normal in many patients with HF, particularly when they are at rest. However, during stress, such as occurs during physical exercise or fever, the cardiac output fails to rise normally, the glomerular filtration rate declines, and the renal mechanisms for salt and water retention described earlier come into play. In addition, ventricular filling pressure and therefore pressures in the atrium and systemic veins behind (upstream to) the ventricle may be normal at rest but rise abnormally during stress.
Acute versus chronic HF
The clinical manifestations of HF depend on the rate at which the syndrome develops. For example, when one suddenly develops a serious anatomic or functional abnormality of the heart, such as massive myocardial infarction (MI), rapid tachyarrhythmia, or rupture of a valve in association with endocarditis, a marked reduction in cardiac output occurs. This is associated with symptoms caused by inadequate organ perfusion and/or acute congestion of the venous bed behind the affected ventricle.
If the anatomic abnormality develops gradually, or if the patient survives the acute insult, a number of adaptive mechanisms become operational, especially cardiac remodeling and neurohormonal activation; these allow the patient to adjust to and tolerate not only the anatomic abnormality but also a reduction in cardiac output with less difficulty.
Low- versus high-output HF
Low cardiac output at rest or, in milder cases, during exertion and other stresses characterizes the HF that occurs with most forms of cardiovascular disease (eg, congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic conditions). Low-output HF is characterized by clinical evidence of systemic vasoconstriction; symptoms include cold, pale, and sometimes cyanotic extremities. In advanced forms of low-output failure, marked reduction in the stroke volume is reflected by a narrowing of the pulse pressure.
A variety of high–cardiac output states, including thyrotoxicosis, arteriovenous fistulas, beriberi, Paget disease of the bone, and anemia, may lead to HF as well. In high-output HF, the extremities are usually warm and flushed, and the pulse pressure is widened, or at least normal.
Systolic versus diastolic HF
HF may be caused by an abnormality in systolic function that leads to a defect in the expulsion of blood (eg, systolic HF) or by an abnormality in diastolic function that leads to a defect in ventricular filling (eg, diastolic HF). The former is the more familiar, classic HF associated with an impaired inotropic state. Less familiar, but perhaps just as important, is diastolic HF, in which the ability of the ventricles to accept blood is impaired. This may be the result of slowed or incomplete ventricular relaxation, which may be transient, as occurs in acute ischemia, or sustained, as in concentric myocardial hypertrophy or restrictive cardiomyopathy secondary to infiltrative conditions such as amyloidosis.
The principal clinical manifestations of systolic failure result from an inadequate cardiac output and secondary salt and water retention (forward HF), whereas the major consequences of diastolic failure relate to an elevation of the ventricular filling pressure and an elevation in venous pressure upstream of the ventricle, which cause pulmonary and/or systemic congestion (backward HF).
There are many examples of pure systolic HF and diastolic HF. An examples of the former is HF associated with acute massive MI or pulmonary embolism; an example of the latter is HF associated with hypertrophic or restrictive cardiomyopathy.
Community-based, epidemiologic studies have demonstrated that diastolic HF is more common than was previously thought; diastolic HF is particularly prevalent in elderly women with hypertension. However, in many patients, systolic and diastolic HF coexist. The most common form of HF, that caused by chronic coronary artery disease (CAD), is an example of combined systolic and diastolic failure. In this condition, systolic failure is caused by both the chronic loss of contracting myocardium secondary to prior MI and the acute loss of myocardial contractility induced by transient ischemia. Diastolic failure is caused by a reduction in compliance of the ventricle, caused by the replacing of normal, distensible myocardium with nondistensible fibrous scar tissue and by the acute reduction of diastolic distensibility during ischemia.
Classification of HF
Framingham criteria
In the Framingham classification system, the diagnosis of CHF requires that either 2 major criteria or 1 major and 2 minor criteria be present concurrently.1 Minor criteria are accepted only if they cannot be attributed to another medical condition.
The major criteria are the following:
- Paroxysmal nocturnal dyspnea
- Neck vein distention
- Rales
- Radiographic cardiomegaly
- Acute pulmonary edema
- S3 gallop
- Central venous pressure greater than 16 cm water
- Circulation time of 25 seconds
- Hepatojugular reflux
- Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
- Weight loss of 4.5 kg in 5 days in response to treatment
Minor criteria include the following:
- Bilateral ankle edema
- Nocturnal cough
- Dyspnea on ordinary exertion
- Hepatomegaly
- Pleural effusion
- A decrease in vital capacity by one third the maximal value recorded
- Tachycardia (rate of 120 bpm)
New York Heart Association functional classification
The New York Heart Association (NYHA) developed a classification of patients with heart disease on the basis of the relation between symptoms and the amount of effort required to provoke them. Although assigning numerical values to subjective findings have obvious limitations, this classification is nonetheless useful in comparing groups of patients, as well as comparing the condition of the same patient at different times. In addition, the NYHA class has proved to be a strong, independent predictor of survival in patients with chronic HF.
The severity of HF may be symptomatically classified according to the amount of effort needed to produce HF symptoms, as follows:
- Class I is no limitation. Ordinary physical activity does not cause undue fatigue, dyspnea, or palpitation. Patients have symptoms only at exertion levels similar to those of relatively healthy individuals.
- Class II is slight limitation of physical activity. Patients with class II disease are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or angina. Patients exhibit symptoms with ordinary exertion.
- Class III is marked limitation of physical activity. Although patients are comfortable at rest, less-than-ordinary activity leads to symptoms. Patients exhibit symptoms with minimal exertion.
- Class IV is the inability to carry perform any physical activity without discomfort. Symptoms of congestive failure are present even at rest. With any physical activity, increased discomfort is experienced.
Reports about the effects of drug treatment of HF often categorize patients' responses by NYHA class rather than by age. However, practitioners should be aware that, because of age-related changes in pharmacokinetics and pharmacodynamics, an 85-year-old patient with NYHA class IV HF may respond differently from a 50-year-old patient with equally severe disease.
Frequency
United States
Congestive heart failure is a common disorder. Approximately 4.6 million Americans are being treated for CHF, and 550,000 new cases are diagnosed each year. The prevalence of CHF increases dramatically with age, occurring in 1-2% of persons aged 50-59 years and in up to 10% of persons older than 75 years.
Approximately 80% of all HF admissions occur in patients older than 65 years. In fact, CHF is the leading hospital discharge diagnosis in individuals aged 65 years or older.
Despite a steady decline in the incidence of CAD and stroke, both the incidence and prevalence of CHF are on the rise. Between 1985 and 1995, the number of HF hospitalizations increased by 51%. Approximately, 870,000 hospital discharges of patients with HF occurred in 1996.
HF has a tremendous economic impact on the US healthcare system because of direct medical costs, disability, and loss of employment. Estimated treatment costs in 1994 were $38 billion, of which $23 billion were spent on hospitalizations. The cost of hospitalizations for HF is twice that for all forms of cancer and MI combined.
Mortality/Morbidity
In the US, approximately 45,000 deaths each year are primarily caused by congestive heart failure, and HF is listed as a contributing cause in 260,000 deaths. This trend may be partly the result of the aging of the population and partly the result of the improved survival of patients with cardiovascular disease.
Race
- The American Heart Association reports, "The annual rates per 1,000 population of new and recurrent CHF events for non-black men are 21.5 for ages 65-74, 43.3 for ages 75-84, and 73.1 for age 85 and older. For non-black women in the same age groups the rates are 11.2, 26.3 and 64.9, respectively. For black men the rates are 21.1, 52.0 and 66.7, and for black women the rates are 18.9, 33.5 and 48.4,respectively."2
- In 2001, the overall CHF-related mortality rate was 18.7%. Death rates were 19.6% for white males, 21.7% for black males, 18.1% for white females, and 18.8% for black females.2
Sex
According to the American Heart Association, 80% of men and 70% of women younger than 65 years 65 who have congestive heart failure will die within 8 years.2
- After CHF is diagnosed, survival is poorer in men than in women, but fewer than 15% of women survive more than 8-12 years.2
- In 2001, the overall CHF-related mortality rate was 18.7%. Death rates were 19.6% for white males, 21.7% for black males, 18.1% for white females, and 18.8% for black females.2
Age
- The prevalence of congestive heart failure increases dramatically with age, occurring in 1-2% of persons aged 50-59 years and in up to 10% of persons older than 75 years.
- Approximately 80% of all HF admissions occur in patients older than 65 years. In fact, CHF is the leading hospital discharge diagnosis in individuals aged 65 years or older.
Presentation
Symptoms and signs
Symptoms that suggest congestive heart failure include the following:
- Dyspnea on exertion
- Dyspnea at rest
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Fatigue
- Decreased exercise tolerance
- Unexplained cough, especially at night
- Acute confusional state, delirium
- Abdominal symptoms (nausea, abdominal pain or distention)
- Decreased food intake
- Decline in functional status
Signs that suggest CHF include the following:
- Tachycardia
- Third heart sound (S3)
- Increased jugular venous pressure
- Positive hepatojugular reflux
- Bilateral rales
- Peripheral edema not caused by venous insufficiency
- Laterally displaced apical impulse
- Weight gain
In cardiogenic cases, clinical findings include cold and clammy peripheral structures, resulting from low cardiac output. Jugular venous pressure is elevated, and a ventricular gallop (S3) is present. Lung examination reveals crackles.
In noncardiogenic cases, the periphery is usually warm as a result of a high-flow state. Jugular venous pressure is generally normal, the S3 gallop is absent, and the lungs are usually clear to auscultation.
Initial workup for reversible etiologies
The initial workup for reversible etiologies of HF include the following:
- Detailed assessment of the patient's cardiopulmonary history
- Physical examination
- Laboratory tests, including urinalysis and evaluations of the CBC count and electrolyte, thyroid stimulating hormone, blood urea nitrogen [BUN], and serum creatinine levels
- Chest radiography
- Electrocardiography
In cardiogenic cases, laboratory results show that the levels of cardiac enzymes, such as creatine phosphokinase (CPK and CPK-MB) and troponins, may be increased in the plasma. The edema fluid level is low in protein content (fluid-to–plasma protein <0.5). Intrapulmonary shunting is minimal. The pulmonary capillary wedge pressure (determined by pulmonary artery catheterization) is generally greater than 18 mm Hg.
In noncardiogenic cases, cardiac enzymes are usually normal. The ratio of edema fluid level to plasma protein level is greater than 0.5, and the pulmonary capillary wedge pressure is less than 18 mm Hg. Large intrapulmonary shunting is seen.
Etiologies
Reversible etiologies of HF include the following:
- Arrhythmia (eg, atrial fibrillation)
- Pulmonary embolism
- Accelerated or malignant hypertension
- Thyroid disease (hypothyroidism or hyperthyroidism)
- Valvular heart disease
- Unstable angina
- High output failure
- Renal failure
- Medication-induced problems
- High salt intake
- Severe anemia
Noncardiogenic etiologies of pulmonary edema include the following:
- Neurogenic causes (associated with sympathetic overactivity)
- Head trauma
- Seizures
- Subarachnoid hemorrhage
- Acute pulmonary embolism (associated with hypoxemia, pulmonary hypertension, and interventricular septal shift towards LV, reducing output)
- Massive pulmonary embolus
- Multiple small pulmonary emboli (associated with enhanced alveolar-capillary permeability)
- High altitude (ie, high-altitude pulmonary edema [HAPE])
- Rapid climb to greater than 8000 ft above sea level
- Abnormally increased hypoxic pulmonary vascular response
- Decreased clearance of endothelin-1, an immunogenic molecule associated with human leukocyte antigen (HLA)-DR6 and HLA-DQ4
- Open heart surgery
- Alteration of surfactant as a result of many hours of pulmonary collapse during operation
- Release of toxic agents (eg, thromboxane)
- Allergic reaction to fresh frozen plasma or protamine used during surgery
- Cardioversion
- Left atrial dysfunction
- Neurogenic causes
- Drugs
- Anesthetic
- Narcotic use (causing increased alveolar-capillary permeability)
- Heroin overdose
- Methadone
- Dextropropoxyphene
- Laryngospasm after anesthesia
- Hypoxia
- Hantavirus infection (seen in Asia)
- Hemorrhagic fever and kidney insufficiency
- Cytokines (Interferon-gamma and tumor necrosis factor produced by the action of T-cells on infected pulmonary vascular endothelium cause alveolar-capillary leakage.)
Differential diagnosis of CHF
The differential diagnosis of CHF (cardiogenic pulmonary edema) from noncardiogenic pulmonary edema includes cardiogenic and noncardiogenic conditions. Regarding the former, an acute cardiac event, such as acute MI, acute coronary syndrome, and tachyarrhythmias, may be identified. Regarding the latter, associated acute cardiac events are rarely identified. Other etiologies are often found.
Preferred Examination
Echocardiography
Echocardiography is the preferred examination. Two-dimensional and Doppler echocardiography may be used to determine systolic and diastolic LV performance, the cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. Echocardiography also may be used to identify clinically important valvular disease.
Radiography
In cardiogenic cases, radiographs may show cardiomegaly, pulmonary venous hypertension, and pleural effusions. Pulmonary venous hypertension (PVH) may be divided into 3 grades. In grade I PVH, an upright examination demonstrates redistribution of blood flow to the nondependent portions of the lungs and the upper lobes. In grade II PVH, there is evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, as well as interlobular septal thickening. In grade III PVH, perihilar and lower-lobe airspace filling is evident, with features typical of consolidation (eg, confluent opacities, air bronchogram and the inability to see pulmonary vessels in the area of abnormality). The airspace edema tends to spare the periphery in the mid and upper lung.
In noncardiogenic cases, cardiomegaly and pleural effusions are usually absent. The edema may be interstitial but is more often consolidative. No cephalization of flow is noted, though there may be shift of blood flow to less affected areas. The edema is diffuse and does not spare the periphery of the mid or upper lungs.
In cases of large, acute MI and infarction of the mitral valve, support apparatus may produce atypical patterns of pulmonary edema that may mimic noncardiogenic edema in patients who in fact have cardiogenic edema.
In cases that are clinically troublesome, multidetector-row gated CT scanning may provide excellent analysis of the heart and reveal the nature of the pulmonary edema.
Electrocardiography
In cardiogenic cases, the ECG may show evidence of MI or ischemia. In noncardiogenic cases, the ECG is usually normal.
Limitations of Techniques
Although echocardiography is simple and noninvasive, it proves to be inadequate in 8-10% of cases; in addition, the results are difficult to interpret in patients with lung disease.
Differential Diagnoses
Other Problems to Be Considered
CAD (angina or MI)
Chronic hypertension
Idiopathic dilated cardiomyopathy
Valvular heart disease (eg, mitral regurgitation, aortic stenosis)
Other cardiomyopathy (eg, sarcoidosis)
Arrhythmia (eg, atrial fibrillation)
Anemia
Fluid volume overload caused by noncardiac conditions
Thyroid disease (hypothyroidism or hyperthyroidism)
More on Congestive Heart Failure |
 Overview: Congestive Heart Failure |
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| Follow-up: Congestive Heart Failure |
| Multimedia: Congestive Heart Failure |
| References |
| Further Reading |
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References
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AHA. Heart disease and stroke statisticsâ€"2004 update. Accessed June 6, 2005. Dallas: American Heart Association;. 2004. [Full Text].
Saraiva RM, da Rocha Rde C, Martins AF, Duarte DM, Peixoto Rda S, de Castro SH, et al. Tissue Doppler imaging as a long-term prognostic index in left ventricular systolic dysfunction. Arq Bras Cardiol. Aug 2008;91(2):77-83. [Medline].
Keating GM, Goa KL. Nesiritide: a review of its use in acute decompensated heart failure. Drugs. 2003;63(1):47-70. [Medline].
Kukin ML. Beta-blockers in chronic heart failure: considerations for selecting anagent. Mayo Clin Proc. Nov 2002;77(11):1199-206. [Medline].
Mehra MR, Uber PA, Potluri S. Renin angiotensin aldosterone and adrenergic modulation in chronic heart failure: contemporary concepts. Am J Med Sci. Nov 2002;324(5):267-75. [Medline].
Davoodi S, Karimi A, Ahmadi SH, Marzban M, Movahhedi N, Abbasi K, et al. Coronary artery bypass grafting in patients with low ejection fraction: The effect of intra-aortic balloon pump insertion on early outcome. Indian J Med Sci. Aug 2008;62(8):314-22. [Medline].
Barlow JF. New rapid laboratory test for congestive heart failure B-type natriuretic peptide (BNP). S D J Med. Nov 2002;55(11):467. [Medline].
Bax JJ, Van der Wall EE, Schalij MJ. Cardiac resynchronization therapy for heart failure. N Engl J Med. Nov 28 2002;347(22):1803-4; author reply 1803-4. [Medline].
Cleland JG, Cohen-Solal A, Aguilar JC, et al. Management of heart failure in primary care (the IMPROVEMENT of Heart Failure Programme): an international survey. Lancet. Nov 23 2002;360(9346):1631-9. [Medline].
Flaker GC, Singh VN. Prevention of myocardial reinfarction. Recommendations based on results of drug trials. Postgrad Med. Nov 1 1993;94(6):94-8, 102-4. [Medline].
Gottlieb SS, Fisher ML. Cardiac resynchronization therapy for heart failure. N Engl J Med. Nov 28 2002;347(22):1803-4; author reply 1803-4. [Medline].
Hasegawa S, Yamamoto K, Sakata Y, Takeda Y, Kajimoto K, Kanai Y, et al. Effects of cardiac energy efficiency in diastolic heart failure: assessment with positron emission tomography with (11)c-acetate. Hypertens Res. Jun 2008;31(6):1157-62. [Medline].
Maddison R, Prapavessis H, Armstrong GP, Hill C. A Modeling Intervention in Heart Failure. Ann Behav Med. Aug 21 2008;[Medline].
Parker AB, Yusuf S, Naylor CD. The relevance of subgroup-specific treatment effects: the Studies Of Left Ventricular Dysfunction (SOLVD) revisited. Am Heart J. Dec 2002;144(6):941-7. [Medline].
Scardovi AB, De Maria R, Celestini A, Perna S, Coletta C, Feola M, et al. The additive prognostic value of the cardiopulmonary exercise test in elderly patients with heart failure. Clin Sci (Lond). Aug 12 2008;[Medline].
Singh VN. The role of gas analysis with exercise testing. Prim Care. Mar 2001;28(1):159-79, vii-viii. [Medline].
Tepper D. Frontiers in congestive heart failure: Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERICUS) study. Congest Heart Fail. Nov-Dec 2002;8(6):347-8.
Tkacova R, Stubna J, Tomori Z. Cardiovascular implications of sleep apnea in patients with congestive heart failure. Sb Lek. 2002;103(1):73-7. [Medline].
Further Reading
Chronic congestive heart failure. University of Texas Medical Branch Correctional Managed Care. 2000 Feb (revised 2003 Apr). 10 pages. NGC:003308
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).
American College of Cardiology Foundation. 1995 Nov 1 (revised 2005 Aug 16). 82 pages. NGC:004463
Heart failure.
American Medical Directors Association - Professional Association. 1996 (revised 2002; reviewed 2007). 18 pages. NGC:002529
Guidelines for the diagnosis and treatment of chronic heart failure (update 2005).
European Society of Cardiology - Medical Specialty Society. 2001 Sep (revised 2005). 45 pages. NGC:004345
Keywords
congestive heart failure, CHF, heart failure, HF, right-sided heart failure, left heart failure, systolic heart failure, diastolic heart failure, cardiomyopathy, chronic heart failure
