Disclosure
Background: Congestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump blood at a rate required by the metabolizing tissues or in which the heart can do so only with an elevated filling pressure. The heart's inability to pump a sufficient amount of blood to meet the needs of the body tissues may be due to insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanisms increase blood volume and also the cardiac filling pressure, heart rate, and cardiac muscle mass to maintain the pumping function of the heart and cause a redistribution of blood flow. Despite these compensatory mechanisms, the ability of the heart to contract and relax declines progressively, and the 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 the ventricle 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. Pathophysiology: Clinical manifestations of HFThe clinical manifestations of HF arise as a consequence of inadequate cardiac output and/or 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 maintaining cardiac output at a normal level:
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 reduction in glomerular filtration rate and in part by activation of the renin-angiotensin-aldosterone system. Reduced cardiac output is associated with a lowered glomerular filtration rate and an increased elaboration of renin, which, through the activation of angiotensin, results in the release of aldosterone. The combination of impaired hepatic function, owing to hepatic venous congestion, and reduced 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 glomerular filtration rate) may be normal in many patients with HF, particularly when they are at rest. However, during stress, such as 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, only to 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 endocarditis, a marked reduction in cardiac output occurs. This is associated with symptoms due to inadequate organ perfusion and/or acute congestion of the venous bed behind the affected ventricle. If the same 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, and these allow the patient to adjust to and tolerate not only the anatomical 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 in 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 with 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 can be caused by an abnormality in systolic function leading to a defect in the expulsion of blood (eg, systolic HF) or by an abnormality in diastolic function leading 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 due to 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 elevation of the ventricular filling pressure, and the high venous pressure upstream to the ventricle, causing pulmonary and/or systemic congestion (backward HF). Many examples of pure systolic or diastolic HF exist. Examples of the former are patients with acute massive MI or pulmonary embolism, whereas examples of the latter are patients with hypertrophic or restrictive cardiomyopathy. Community-based, epidemiologic studies have demonstrated that diastolic HF is more common than was previously thought and 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 due to the ventricle's reduced compliance caused by replacement 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 (Ho, 1993), the diagnosis of CHF requires that either 2 major criteria or 1 major and 2 minor criteria be present concurrently. 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 based on 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 the same patient at different times. In addition, the NYHA class has proven to be a strong, independent predictor of survival in patients with chronic HF. The severity of HF can be symptomatically classified according to the amount of effort needed to produce HF symptoms, as follows:
Reports about the effects of drug treatment for 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 than a 50-year-old patient with equally severe disease. Frequency:
Mortality/Morbidity: In the US, approximately 45,000 deaths each year are primarily caused by CHF and HF is listed as a contributing cause in 260,000 deaths. This trend may be partly due to the aging of the population and partly due to the improved survival of patients with cardiovascular disease. Race:
Sex: According to the American Heart Association, 80% of men and 70% of women younger than 65 years 65 who have CHF will die within 8 years (AHA, 2004).
Age:
Clinical Details: Symptoms and signs Symptoms that suggest HF include the following:
Signs that suggest HF include the following:
In cardiogenic cases, clinical findings include cold and clammy peripheral structures due to low cardiac. Jugular venous pressure is elevated, and a ventricular gallop (S3) is present. Lung examination reveals crackles. In noncardiogenic cases, the periphery is usually warm due to 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 cardiac enzymes, such as creatine phosphokinase (CPK and CPK-MB) and troponins, may be increased in the plasma. Edema fluid 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 to plasma protein 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 can often be found. Preferred Examination: Echocardiography Echocardiography is the preferred examination. Two-dimensional and Doppler echocardiography can be used to determine systolic and diastolic LV performance, the cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. Echocardiography also can be used to identify clinically important valvular disease. Radiography In cardiogenic cases, the radiographs may show cardiomegaly, pulmonary venous hypertension and pleural effusions. Pulmonary venous hypertension (PVH) can be divided into 3 grades. Grade I PVH demonstrates redistribution of blood flow to the nondependent portions of the lungs, upper lobes in an upright examination. Grade II PVH shows evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, interlobular septal thickening. Grade III PVH results in perihilar and lower-lobe airspace filling with the typical features 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 areas. 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 large acute MI and infarction of the mitral valve, support apparatus that atypical patterns of pulmonary edema may arise that can mimic noncardiogenic edema in patients who in fact have cardiogenic edema. Multidetector-row gated CT scanning can provide excellent analysis of the heart and nature of the pulmonary edema in cases that are clinically troublesome. 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 may be inadequate in 8-10% of cases, and the results are is difficult to interpret in patients with lung disease.
CAD (angina or MI)
Findings: Two principal features of the chest radiograph are useful in the evaluation of patients with HF: (1) the size and shape of the cardiac silhouette and (2) edema at the lung bases. 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 determined on the 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, and the relationship is not clinically useful in the individual patient. In the presence of normal pulmonary capillary and venous pressure, the lung bases are better perfused than the apices in the erect position, and the vessels supplying the lower lobes are significantly larger than are those supplying the upper lobes. With elevation of left atrial and pulmonary capillary pressures, interstitial and perivascular edema develops and 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 occurs into non-dependent portions of the lung, (ie, further constriction of vessels leading to the lower lobes and dilatation of vessels leading to the upper lobes in an upright patient). When pulmonary capillary pressures exceed 20-25 mm Hg, interstitial pulmonary edema occurs, grade II PVH. Grade II PVH shows evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, interlobular septal thickening. The interlobular septal thickening is also referred to as Kerley B lines. Early blunting of the lateral and posterior costophrenic angles may occur, indicating 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 peri-hilar 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 can be accommodated with fewer clinical and radiologic signs, presumably due to enhanced lymphatic drainage. In a study of 22 patients with advanced HF who were referred for cardiac transplant evaluation and pulmonary capillary wedge pressures of 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 Confidence: The degree of confidence is low. The weak negative correlation between cardiothoracic ratio and 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/Negatives: False negative findings are frequent. |
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Findings: CT of the heart is usually not required in the routine diagnosis, and management of HF. Multichannel CT scanning is useful in delineating congenital and valvular abnormalities; however, both echocardiography and MRI can provide similar information without exposing the patient to ionizing radiation. Degree of Confidence: The degree of confidence is moderate. False Positives/Negatives: The rate of false-positive and false-negative findings is low.
Findings: MRI is infrequently used in the work-up of CHF. Its main use involves delineation of congenital cardiac abnormalities and valvular heart disease, among other conditions. The widespread acceptance of echocardiography has made the use of MRI infrequent. Degree of Confidence: The degree of confidence is high. False Positives/Negatives: The rate of false-positive and false-negative findings is low.
Findings: Two-dimensional echocardiography is recommended as an initial part of the evaluation in patients with known or suspected CHF. Ventricular function can be evaluated, and both primary and secondary valvular abnormalities can likewise be accurately assessed. Doppler echocardiography can play a valuable role in determining diastolic function and establishing the diagnosis of diastolic HF. HF 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 can be used to determine: systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. Echocardiography can also be used to identify clinically important valvular disease. Degree of Confidence: The degree of confidence is high. False Positives/Negatives: The rate of false-positive and false-negative findings is low.
Findings: ECG-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 can 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 exercise-induced myocardial perfusion defects. On ECG-gated SPECT images, regional wall thickening can be quantified as percent wall thickening in comparison to end-diastole. Commercially available and validated software packages exist 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 determined with other modalities. Quality assurance is important. LVEF determined with gated SPECT can be less accurate, even invalidated, by an irregular heart rate, low count density, intense extracardiac radiotracer uptake adjacent to the LV, and small LV. Combined interpretation of perfusion and function on ECG-gated images substantially increases the confidence of interpretation. Taillefer and associates reported that interpretation of stress and rest end-diastolic section rather than summed ungated sections may enhance the overall sensitivity of detecting mild CAD. ECG-gated images are also useful for recognizing artifactual defects caused by attenuation (breast and diaphragm) and thus adds to 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 have the potential for improvement in function after adequate revascularization. Two important practical issues need to be addressed when patients with presumed ischemic dysfunction are evaluated: (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 can expect recovery of function after revascularization. (2) One should also 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 according to 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 using 99mTc. The intravascular label is affixed to the patient's own red blood cells by using 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 using 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 also 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 views provide optimal qualitative information concerning contraction of the inferior wall and posterobasal segment. Ventricular aneurysm can be assessed best 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 can easily be combined with additional physiological stress testing or provocation, which may be in the form of either physiological stress such as exercise, pharmacological stress with positive inotropic agents such as dobutamine or isoproterenol, or psychological stress. Degree of Confidence: The degree of confidence is moderately high. False Positives/Negatives: False-positive and false-negative findings are infrequent.
Findings: Cardiac catheterization and coronary angiography has a useful role in patients with CHF, those with valvular heart disease, patients with congenial heart disease, and those with other conditions. In patients with CHF, cardiac catheterization and coronary angiography are clearly indicated in these situations:
For these patients, the procedures are frequently indicated when systolic dysfunction with unexplained cause is present despite noninvasive testing or when normal systolic function with but episodic HF suggests ischemically mediated LV dysfunction. In patients with valvular heart disease, cardiac catheterization and coronary angiography are clearly indicated in these situations:
In patients with congenital heart disease, cardiac catheterization and coronary angiography are clearly indicated in these situations:
For these patients, the procedures are frequently indicated before corrective open heart surgery for congenital heart disease in an adult whose risk profile increases the likelihood of coexisting CAD. In patients with other conditions, cardiac catheterization and coronary angiography are clearly indicated in these situations:
For these patients, the procedures are frequently indicated in these situations:
Degree of Confidence: The degree of confidence is moderately high. False Positives/Negatives: The rate of false-positive and false-negative findings is low.
Intervention: General medical treatmentFirst treat the chronic underlying cardiac condition. 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 quality-of-life considerations into account. No convincing evidence confirms that vitamin C and flavonoids are helpful in HF, and evidence only suggests that vitamin E, coenzyme Q, and thiamine are helpful. If edema is present, one should consider 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. Specific medical treatmentsTreatment of fluid overload Treat fluid volume overload if present. 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. In the patient with fluid volume overload, start a loop diuretic immediately. Diuretics improve symptoms and quality of life but do not necessarily prolong life. However, all available loop diuretics have altered pharmacodynamics and diminished effectiveness in patients with severe HF. These agents also have profound effects on electrolyte balance and renal function. Consider 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. Each of these agents has somewhat different pharmacologic properties. The choice of agent is based on 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), start an angiotensin-converting enzyme (ACE) inhibitor 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 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 can 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 can 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 in 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 HF is the concept that LV or biventricular pacing may be beneficial in a subset of subjects with intraventricular conduction delay, which may include 30-50% of subjects with advanced LV dysfunction. The biventricular pacing strategy is based on the fact that most subjects 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 Ventricular assist devices have emerged as a potential treatment of chronic HF, beyond their traditional role as a bridge to transplantation. 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 preventing 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 LV dysfunction, or ventricular reduction surgery. Cardiac transplantation This procedure was the first definitive treatment developed for HF, that is, 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 could have been ethically justified. The current survival of severe HF stage D subjects from the enalapril arm of the Cooperative New Scandinavian Enalapril Survival (CONSENSUS) trial showed that survival after transplantation is superior to that with medical therapy. The biggest limitation of cardiac transplantation is not efficacy or safety, but rather, the limited supply of donors available to apply the treatment. It has been estimated that less than 10% of subjects who would benefit from cardiac transplantation can actually receive it on the basis of the upward limit of 2000-3000 donors per year in the United States. Therefore, transplantation is reserved for subjects who have reached stage D or late stage C HF and are 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 CABG is superior to medical therapy from a survival standpoint in subjects with symptomatic 3-vessel CAD and reduced but not severely depressed LVEFs. In recent years, the benefit of CABG has been extended to patients with LVEFs lower than the 0.35 cutoff 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 correction of mitral regurgitation without valve replacement have been applied to the failing, remodeled ventricle with low operative mortality and impressive early clinical outcomes. 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 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 appreciated that the combined rate of mortality, cardiac transplantation, or need for a LV assist device was on the order of 30%. Adjuvant therapiesInitiate other appropriate interventions 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 to 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 maintaining quality of life is the primary care goal. 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 surveillanceMonitor the patient's condition and response to treatment. Ongoing monitoring of the patient's condition and response to treatment is imperative. Assess fluid volume status by monitoring weight at least three times a week (more frequently if the patient's condition is unstable). Monitor levels of electrolytes, blood urea nitrogen, and creatinine in patients receiving pharmacologic therapy. Repeat these measurements 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 nursing facility patient with HF. If a patient is not achieving the explicit goals set by the interdisciplinary team, document the reasons in the patient's medical record. Also document how the patient's care plan will be modified in an effort to reach the stated goals. If it is determined that the goals cannot be achieved, document the reasons for this and set more realistic goals. Also, if consultation with a cardiologist or center specializing in HF is indicated, make the referral. Components of monitoring HF patients include the following: signs and symptoms; weight, vital signs; functional performance; electrolytes, renal function, and magnesium when indicated; levels of drugs (eg, digoxin) when indicated. Medical/Legal Pitfalls:
Special Concerns:
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