You are in: eMedicine Specialties > Radiology > CHEST Congestive Heart FailureArticle Last Updated: Sep 16, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 13
  Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine Vibhuti N Singh is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association Editors: Jeffrey A Miller, MD, Associate Professor of Clinical Radiology, University of Medicine and Dentistry of New Jersey; Associate Chief of Service, Department of Radiology, Veterans Affairs of New Jersey Health Care System; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; John D Newell, Jr, MD, FACR, FCCP, FASER, Co-Director of Thoracic Imaging, UCDHSC; Director of Lung Imaging Center, Professor of Radiology and Professor of Medicine, Department of Radiology, University of Colorado Health Sciences Center, National Jewish Medical and Research Center; Univ. Colorado Hospital; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Kavita Garg, MD, Professor, Department of Radiology, University of Colorado Health Sciences Center Author and Editor Disclosure Synonyms and related 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 INTRODUCTIONSection 2 of 13
  BackgroundCongestive 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. PathophysiologyClinical manifestations of HFThe 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:
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 HFFramingham 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:
Minor criteria include the following:
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:
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. FrequencyUnited StatesCongestive 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/MorbidityIn 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
SexAccording 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
Age
Clinical DetailsSymptoms and signs Symptoms that suggest congestive heart failure include the following:
Signs that suggest CHF include the following:
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:
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:
Noncardiogenic etiologies of pulmonary edema include the following:
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 ExaminationEchocardiography 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 TechniquesAlthough 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. DIFFERENTIALSSection 3 of 13
Other Problems To Be ConsideredCAD (angina or MI) RADIOGRAPHSection 4 of 13
FindingsTwo principal features of the chest radiograph are useful in the evaluation of patients with congestive heart failure: (1) the size and shape of the cardiac silhouette, and (2) edema at the lung bases (see Image 1). The size and shape of the cardiac silhouette provide important information concerning the precise nature of the underlying heart disease. Both the cardiothoracic ratio and the heart volume, as determined on plain film, are relatively specific but insensitive indicators of increased LV end-diastolic volume. There is a weak inverse correlation between the cardiothoracic ratio and LV ejection fraction (LVEF) in patients with HF; the relationship is not clinically useful in the individual patient. In the presence of normal pulmonary capillary and venous pressures, the lung bases are better perfused than the apices when the patient is in the erect position, and the vessels supplying the lower lobes are significantly larger than those supplying the upper lobes. With elevation of left atrial and pulmonary capillary pressures, interstitial and perivascular edema develops; such edema is most prominent at the lung bases because hydrostatic pressure is greater there. When pulmonary capillary pressure is slightly elevated (13-17 mm Hg), the resultant compression of pulmonary vessels in the lower lobes causes equalization in the size of the vessels at the apices and bases (early grade I PVH). With greater pressure elevation (18-23 mm Hg), actual pulmonary vascular redistribution into nondependent portions of the lung occurs (ie, with the patient in an upright patient, there is further constriction of the vessels that lead to the lower lobes, and there is dilatation of the vessels that lead to the upper lobes). When pulmonary capillary pressures exceed 20-25 mm Hg, interstitial pulmonary edema occurs (grade II PVH). With grade II PVH, there is evidence of interstitial edema, with ill-defined vessels and peribronchial cuffing, as well as interlobular septal thickening. The interlobular septal thickening is referred to as Kerley B lines. Early blunting of the lateral and posterior costophrenic angles may occur; such blunting indicates the presence of pleural fluid. When pulmonary capillary pressure exceeds 25 mm Hg, images may show large pleural effusions and grade III PVH, with consolidative alveolar edema in a perihilar and lower-lobe distribution. With elevation of the systemic venous pressure, the azygos vein, brachiocephalic veins, and superior vena cava may become enlarged. In patients with chronic LV failure, higher pulmonary capillary pressures may be accommodated with fewer clinical and radiologic signs, presumably because of enhanced lymphatic drainage. In a study of 22 patients with advanced HF who were referred for cardiac transplant evaluation and whose pulmonary capillary wedge pressure measurements were 25 mm Hg or greater, 68% had no or minimal pulmonary congestion, as shown on chest radiographs. In summary, the typical findings of CHF on the plain radiograph are cardiomegaly; grade I, II, or III PVH; and increased central systemic venous volume, with enlargement of the mediastinal veins (including the azygous vein) and pleural effusions. Degree of ConfidenceThe degree of confidence is low. The weak negative correlation between the cardiothoracic ratio and the ejection fraction does not permit accurate determination of systolic function in the absence of radiographic evidence of PVH or pleural effusions in individual patients with HF. For this reason, a chest radiograph may not be very useful for determining the type of LV dysfunction. During the treatment phase of CHF, chest radiographic findings often lag behind clinical improvement. False Positives/NegativesFalse-negative findings are frequent. CT SCANSection 5 of 13
FindingsCT of the heart is usually not required in the routine diagnosis and management of congestive heart failure. Multichannel CT scanning is useful in delineating congenital and valvular abnormalities; however, both echocardiography and MRI may provide similar information without exposing the patient to ionizing radiation. Degree of ConfidenceThe degree of confidence is moderate. False Positives/NegativesThe rates of false-positive and false-negative findings are low. MRISection 6 of 13
FindingsMRI is infrequently used in the workup of patients with congestive heart failure. Its main use involves delineation of congenital cardiac abnormalities and assessment valvular heart disease; it is also used in patients with other conditions. With the widespread acceptance of echocardiography, MRI is used only infrequently. Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesThe rates of false-positive and false-negative findings are low. ULTRASOUNDSection 7 of 13
FindingsTwo-dimensional echocardiography is recommended as an initial part of the evaluation of patients with known or suspected congestive heart failure. Ventricular function may be evaluated, and both primary and secondary valvular abnormalities may be accurately assessed (see Image 2).3 Doppler echocardiography may play a valuable role in determining diastolic function and in establishing the diagnosis of diastolic HF. HF in association with normal systolic function but abnormal diastolic relaxation affects 30-40% of patients presenting with CHF. Because the therapy for this condition is distinctly different from that for systolic dysfunction, establishing the appropriate etiology and diagnosis is essential. The combination of 2-dimensional echocardiography and Doppler echocardiography is effective for this purpose. Two-dimensional and Doppler echocardiography may be used to determine systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. Echocardiography may also be used to identify clinically important valvular disease. Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesThe rates of false-positive and false-negative findings are low. NUCLEAR MEDICINESection 8 of 13
FindingsECG-gated myocardial perfusion imaging The high photon flux of compounds labeled with technetium TC 99m makes it feasible to acquire myocardial perfusion images in an ECG-gated mode. ECG-gated myocardial perfusion images may be displayed as an endless-loop cine on the computer screen. ECG-gated single-photon emission CT (SPECT) images allow for assessment of global LVEF, regional wall motion, and regional wall thickening. Regardless of whether the injection of radiopharmaceutical was performed during peak stress or at rest, because the acquisition is performed at rest, ECG-gated SPECT images reveal resting global function and wall motion and resting wall thickening in areas with defects of exercise-induced myocardial perfusion. On ECG-gated SPECT images, regional wall thickening may be quantified as a percentage of wall thickening in comparison to end-diastole. Commercially available and validated software packages are available for the automatic calculation of resting global LVEF, LV volume, and regional wall thickening from ECG-gated SPECT sections. In general, LVEF from gated SPECT agrees well with resting LVEF, as determined with other modalities. Quality assurance is important. Determinations of LVEF with gated SPECT may be less accurate, even invalidated, in the presence of an irregular heart rate, low count density, intense extracardiac radiotracer uptake adjacent to the LV, or a small LV. Combined interpretation of perfusion and function on ECG-gated images substantially increases the confidence of interpretation. Taillefer and associates reported that the interpretation of stress and rest end-diastolic section, rather than summed ungated sections, may enhance the overall sensitivity for the detection of mild CAD. ECG-gated images are useful for recognizing artifactual defects caused by attenuation (breast and diaphragm) and thus are useful in the quality control of SPECT imaging. ECG-gated SPECT imaging is presently considered the state of the art of radionuclide myocardial perfusion imaging. Assessment of myocardial viability For patients with angina, known CAD, previous infarction, and LV dysfunction, a reliable method for assessing the presence, extent, and location of viable myocardium is of considerable clinical importance. It is well established that global or regional ischemic LV dysfunction is not always an irreversible condition. Approximately 25-40% of patients may experience improvement in function after adequate revascularization. Two important practical issues need to be addressed in the evaluation of patients with presumed ischemic dysfunction: (1) One should consider assessment of the relative regional myocardial uptake of thallium Tl 201 (often after rest reinjection), 99mTc-sestamibi, or 99mTc-tetrofosmin (often after rest administration of nitroglycerin). When the resting uptake of radiotracer is greater than 50% of normal, one may expect recovery of function after revascularization. (2) One should consider assessment of the presence of demonstrable ischemia (eg, partially reversible defect) in a myocardial segment with decreased uptake, even if the resting uptake is less than 50%. Equilibrium radionuclide angiocardiography Equilibrium radionuclide angiocardiography (ERNA) uses ECG events to define the temporal relationship between the acquisition of nuclear data and the volumetric components of the cardiac cycle. Sampling is performed repetitively over several hundred heartbeats, with physiologic segregation of nuclear data in accordance with their occurrence within the cardiac cycle. Data are quantified and displayed in an endless-loop, cinegraphic format for additional qualitative visual interpretation and analysis. Equilibrium blood-pool labeling is achieved by use of 99mTc. The intravascular label is affixed to the patient's own red blood cells by use of an in vitro or modified in vitro technique. Unlabeled stannous pyrophosphate is used to facilitate this reaction. Conventional Anger scintillation cameras are used for these studies. Data are analyzed by use of a computer, generally with some operator interaction. Analysis may be obtained in either the frame or list mode. Radionuclide data are collected and segregated temporally. The process generally requires 3-10 minutes for completion of each view. Following data acquisition, data from the several hundred individual beats are summed, processed, and displayed as a single representative cardiac cycle. Data from the left anterior oblique (LAO) view are also used for qualitative analysis of global LV function. On this view, overlap of the 2 ventricles is minimal. In a count-based approach, LVEF and other indices of filling and ejection are calculated from the LV radioactivity preset at various points throughout the cardiac cycle. Right ventricular function is best evaluated by first-pass techniques. The LAO view provides qualitative information concerning contraction of the septal, inferoapical, and lateral walls. The anterior view provides data concerning regional motion of the anterior and apical segments. The left lateral or left posterior oblique view provides optimal qualitative information concerning contraction of the inferior wall and posterobasal segment. Ventricular aneurysm may be best assessed in the lateral views as well. Each segment is generally graded on a 5-point scale, with specific numerical grades assigned for dyskinesis, akinesis, mild and severe hypokinesis, and normal function. ERNA may easily be combined with additional physiologic stress testing or provocation, which may be in the form of either physiologic stress, such as exercise; pharmacological stress, with the use of positive inotropic agents such as dobutamine or isoproterenol; or psychological stress. Degree of ConfidenceThe degree of confidence is moderately high. False Positives/NegativesFalse-positive and false-negative findings are infrequent. ANGIOGRAPHYSection 9 of 13
FindingsCardiac catheterization and coronary angiography have a useful role in patients with congestive heart failure, those with valvular heart disease, and those with congenial heart disease, as well as patients with other conditions. For patients with CHF, cardiac catheterization and coronary angiography are clearly indicated in the following situations:
For these patients, the procedures are frequently indicated when systolic dysfunction of unexplained cause is present on noninvasive testing or when normal systolic function with episodic HF suggests ischemically mediated LV dysfunction. In patients with valvular heart disease, cardiac catheterization and coronary angiography are clearly indicated in the following situations:
In patients with congenital heart disease, cardiac catheterization and coronary angiography are clearly indicated in the following situations:
For these patients, the procedures are frequently indicated before corrective open heart surgery for congenital heart disease in an adult whose risk profile is associated with an increased risk of coexisting CAD. In patients with other conditions, cardiac catheterization and coronary angiography are clearly indicated in the following situations:
For these patients, the procedures are frequently indicated in the following situations:
Degree of ConfidenceThe degree of confidence is moderately high. False Positives/NegativesThe rates of false-positive and false-negative findings are low. INTERVENTIONSection 10 of 13
General medical treatmentThe chronic underlying cardiac condition should be treated first. If treatment is acceptable to the patient or advocate, and after treatment has been initiated for reversible causes of HF, the next step is to address the consequences of the patient's failing heart. Specific pharmacotherapy is based on the presence or absence of fluid volume overload and the nature of the ventricular dysfunction. Nonpharmacologic approaches that should be considered for all patients with HF include psychosocial and spiritual support, a diet without added salt, and alcohol abstinence. Moderate restriction of calories and saturated fat may be helpful if obesity is present. Dietary restrictions should be ordered with care on an individual basis, by taking into account considerations of quality of life. No convincing evidence confirms that vitamin C and flavonoids are helpful in congestive heart failure, and evidence only suggests that vitamin E, coenzyme Q, and thiamine are helpful. If edema is present, consideration should be given to restricting the patient's fluid intake to less than 2 L/d. Patients with HF who develop bacterial or viral respiratory infections may decompensate; for this reason, all patients with HF should be offered pneumococcal vaccine and annual influenza vaccinations.4, 5, 6 Specific medical treatmentsTreatment of fluid overload Volume overload, if present, should be treated. Retention of salt and water causes fluid volume overload. Patients with fluid volume overload may have orthopnea, paroxysmal nocturnal dyspnea, sleep disturbance, peripheral edema, rales, and PVH on chest radiographs. For patients with fluid volume overload, a loop diuretic should be started immediately. Diuretics improve symptoms and quality of life but do not necessarily prolong life. However, in patients with severe HF, all available loop diuretics have altered pharmacodynamics, and their effectiveness is diminished. These agents also have profound effects on electrolyte balance and renal function. Consideration should be given to initiating loop diuretic therapy with oral furosemide, 20-40 mg once daily. Goals of titration should include maintaining renal perfusion, avoiding symptomatic hypotension, and achieving a stable weight. In the patient with more severe HF, metolazone, 2.5-5 mg given 30 minutes before furosemide, may improve diuresis. However, this drug combination may increase the potential for hypokalemia and hypomagnesemia. Other available loop diuretics include bumetanide, torsemide, and ethacrynic acid. The pharmacologic properties of these agents differ. The agent is chosen on the basis of an individual patient's condition and the expertise and experience of the attending physician or consultant. Treatment of systolic dysfunction The patient with HF caused by LV systolic dysfunction who has fluid volume overload should receive a loop diuretic. After fluid volume overload has been corrected (or if the patient does not have fluid volume overload), an angiotensin-converting enzyme (ACE) inhibitor should be given; the ACE inhibitor should be followed by a beta blocker. Digoxin may be added to improve symptoms and enhance quality of life. Spironolactone may be added cautiously in the patient with stable NYHA class III-IV HF who needs and wants all interventions that have been demonstrated to decrease mortality. Treatment of diastolic dysfunction Medication options for treating diastolic dysfunction include diuretics, nitrates, calcium channel blockers, beta blockers, and ACE inhibitors. The goals of intervention are to decrease fluid volume overload and treat elevated filling pressures. Many patients with HF caused by diastolic dysfunction have underlying hypertension, leading many experts to believe that blood pressure control may be the single most important treatment strategy for patients with diastolic dysfunction. Congestion can be reduced by means of salt restriction, diuretics, ACE inhibitors, and/or dialysis or plasmapheresis. To maintain atrial contraction, direct current or pharmacologic cardioversion and/or sequential atrioventricular pacing may be helpful. To prevent tachycardia and to promote bradycardia, beta blockers and radiofrequency ablation and pacing may be applied. The treatment and prevention of myocardial ischemia may require the use of nitrates, beta blockers, calcium channel blockers, bypass surgery, or angioplasty. Antihypertensive agents may be needed to control hypertension and to promote the regression of hypertrophy. To attenuate neurohormonal activation, beta blockers or ACE inhibitors may be administered. ACE inhibitors, spironolactone, and anti-ischemic agents may help prevent fibrosis and promote the regression of fibrosis. Phosphodiesterase inhibitors, systolic unloading, treatment of ischemia, and calcium blockers (in hypertrophic cardiomyopathy) may improve ventricular relaxation. Device therapyDevice therapy may involve the use of implantable cardiac defibrillators, biventricular pacing, ventricular-assist devices, or other devices. Implantable cardiac defibrillators Implantable cardiac defibrillators are now the treatment of choice for patients with LV dysfunction who have survived sudden cardiac death, who have symptomatic, sustained ventricular tachycardia, or who have asymptomatic and nonsustained but inducible ventricular tachycardia. Biventricular pacing One of the more interesting developments in the treatment of HF is the concept that LV or biventricular pacing may be beneficial in a subset of patients who have intraventricular conduction delay; these patients may include 30-50% of patients with advanced LV dysfunction. The biventricular pacing strategy is based on the fact that most patients with intraventricular conduction delay have asynchronous LV contraction, which results in a reduction in ventricular performance and an increase in regional wall stress. Ventricular assist devices In addition to their traditional role as a bridge to transplantation, ventricular assist devices have emerged as a potential treatment of chronic HF. Other investigational devices Several other devices in development may have a role in the treatment of HF. For example, external pneumatic counterpulsation, shown to be effective in treating angina, may have a role in treating HF. One of the more interesting approaches to the prevention of progressive remodeling is a device (the Acorn device) that physically prevents ventricular dilatation in animal models. Surgical therapiesSurgical therapy may involve cardiac transplantation, coronary artery bypass grafting (CABG), mitral valve reconstruction in cases involving LV dysfunction, or ventricular reduction surgery.7 Cardiac transplantation This procedure was the first definitive treatment developed for HF; that is, it was the first treatment that lowered mortality. The treatment is so successful in advanced or severe stage C or D HF that to this point, no randomized study has been ethically justified. Data from the enalapril arm of the Cooperative New Scandinavian Enalapril Survival (CONSENSUS) trial showed that the current survival of patients with severe stage D HF who underwent transplantation is superior to that of patients who underwent medical therapy. The biggest limitation of cardiac transplantation is not efficacy or safety but rather the limited supply of available donors. On the basis of the fact that in the United States, the upward limit of donors is 2000-3000 per year, it has been estimated that less than 10% of patients who would benefit from cardiac transplantation actually receive it. Therefore, transplantation is reserved for subjects who have stage D or late stage C HF and whose disease is progressing despite application of all medical therapy of proven benefit. Coronary artery bypass grafting Over 15 years ago, the Coronary Artery Surgery Study (CASS) demonstrated that, from a survival standpoint, CABG is superior to medical therapy for patients with symptomatic 3-vessel CAD whose LEVF is reduced but is not severely depressed. In recent years, the benefit of CABG has been extended to patients with LVEFs lower than the 0.35 cutoff used in CASS. Mitral valve reconstruction in LV dysfunction Mitral regurgitation occurs to a greater or lesser degree in the remodeled, dilated ventricle. Recently, surgical approaches to correct mitral regurgitation without valve replacement have been applied to the failing, remodeled ventricle; operative mortality has been low, and early clinical outcomes have been impressive. Thus, the role of mitral valve reconstruction in the setting of remodeling and mitral regurgitation is somewhat unclear. Ventricular reduction surgery The most controversial treatment of HF that has been developed in recent years is ventricular reduction surgery, originally known as the Batista procedure, after the surgeon who developed and popularized it. This procedure involves a direct, surgical approach to reversing remodeling by simply removing a large (20-40%) amount of the LV and reshaping it. Despite the considerable initial fanfare of this approach to HF, enthusiasm quickly waned when it was recognized that the combined rate of mortality, cardiac transplantation, or need for a LV assist device was on the order of 30%. Adjuvant therapiesOther appropriate interventions should be initiated as indicated. Other interventions by the interdisciplinary team may be helpful. For example, social services intervention is indicated if an advance directive needs to be drawn up or if family counseling would be helpful. Dietary counseling is critical in assessing the need for or extent of dietary salt limitations. A rehabilitation consultation may be indicated to develop an individualized restorative exercise program. It is also important that patients, families, and nursing staff receive education about the dietary needs of patients with HF and the side effects of medications used to treat HF, as well as about safety issues and environmental modifications. If prolonging life or decreasing exacerbations that lead to frequent hospitalizations is a goal of therapy, the consistent and aggressive application of the interventions outlined in this guideline and elsewhere is appropriate. However, for patients at or near the end of life, it may be appropriate to switch to a palliative or comfort mode of care in which the primary goal is to maintain quality of life. In such cases, each intervention for HF must be assessed for the comfort it provides and the intrusiveness and potential discomfort it entails. When the patient, family or advocate, and care team decide that palliative care is most appropriate, symptom relief and psychosocial and spiritual considerations become paramount. Management of end-of-life symptoms such as dyspnea, dry mouth, nausea, fatigue, pain, apprehension, and restlessness should be the main focus of the patient's care plan. Consultations with hospice or palliative care experts may be considered. Diuretics may be indicated as a palliative measure to address symptoms associated with fluid volume overload. Monitoring and surveillanceOngoing monitoring of the patient's condition and response to treatment is imperative. Fluid volume status should be assessed by monitoring weight at least 3 times a week (more frequently if the patient's condition is unstable). Levels of electrolytes, blood urea nitrogen, and creatinine should be monitored in patients receiving pharmacologic therapy. These measurements should be repeated as frequently as necessary, depending on the patient's condition and the combination of drugs the patient is receiving. Assessment by nursing staff of the patient's general functional status—including both activities of daily living and participation in recreational activities—is an important element of monitoring in the patient with HF who resides in a nursing facility. If a patient is not achieving the explicit goals set by the interdisciplinary team, the reasons should be documented in the patient's medical record. How the patient's care plan will be modified in an effort to reach the stated goals should also be documented. If it is determined that the goals cannot be achieved, the reasons for this should be documented, and more realistic goals should be set. In addition, if consultation with a cardiologist or with a center specializing in HF is indicated, the referral should be made. Components of monitoring HF patients include the following: signs and symptoms; weight and vital signs; functional performance; electrolyte levels, renal function, and magnesium level, when indicated; levels of drugs (eg, digoxin), when indicated. Medical/Legal Pitfalls
Special Concerns
FURTHER READINGSection 11 of 13
Chronic congestive heart failure. University of Texas Medical Branch Correctional Managed Care. 2000 Feb (revised 2003 Apr). 10 pages. NGC:003308 MULTIMEDIASection 12 of 13
REFERENCESSection 13 of 13
Congestive Heart Failure excerpt Article Last Updated: Sep 16, 2008 | |||||||||||||||||||
