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I. Acute Decompensated Heart Failure: What every physician needs to know.
Acute decompensated heart failure (ADHF), also known as acute heart failure, decompensated heart failure, acute heart failure syndromes, and hospitalization for heart failure is a common cause of hospitalization, rehospitalization, and mortality. There have been various definitions applied for ADHF.
The European Society of Cardiology defined ADHF as the rapid onset of symptoms and signs secondary to abnormal cardiac function. It may occur with or without previous cardiac disease.
Cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to pre-load and after-load mismatch. Acute decompensated heart failure has also been defined by the Heart Failure Society of America as new onset of decompensated heart failure or decompensation of chronic, established heart failure with symptoms sufficient to warrant hospitalization.
Other definitions include a gradual or rapid change in signs and symptoms compatible with heart failure, resulting in a need for new and urgent intravenous therapy or urgent significant augmentation of existing therapy in patients with established or newly developed left ventricular dysfunction. Acute decompensated heart failure represents a board spectrum of clinical presentations from acute onset of pulmonary edema to a gradual worsening of symptoms in a patient with established heart failure. The clinical classification of patients with ADHF continues to evolve and reflects ongoing changes in the understanding of the pathophysiology of this syndrome.
The clinical syndrome of ADHF may result from disorders of the pericardium, myocardium, endocardium, or great vessels, but the majority of patients with ADHF have symptoms due to an impairment of left ventricular function. Acute decompensated may be associated with a wide spectrum of left ventricular functional abnormalities, which may range from patients with normal left ventricular size and preserved ejection faction to those with severe dilatation and/or markedly reduced ejection fraction. In most patients, abnormalities of systolic and diastolic dysfunction coexist.
These symptoms are predominantly the result of systemic congestion due to elevated left ventricular filling pressures. Acute decompensated heart failure is known to occur in patients with preserved or reduced left ventricular ejection fraction and are a common cause of hospitalization and mortality.
Hospitalization for ADHF is independently associated with increased mortality risk. Patients with ADHF present frequently with other cardiovascular comorbid conditions, including coronary artery disease, hypertension, valvular heart disease, and arrhythmias, as well as noncardiovascular comorbid conditions, including renal dysfunction, pulmonary disease, and diabetes.
Several prognostic factors have been identified, including age, systolic blood pressure, serum sodium, and renal insufficiency. Timely and accurate diagnosis and assessment of ADHF is very important. Current guidelines recommend a comprehensive history and physical examination, laboratory testing, noninvasive evaluation of ventricular function, and in select patients functional and invasive testing.
The diagnosis of ADHF is based on clinical assessment. A thorough history and physical examination, as well as initial diagnostics are essential to developing an early management strategy.
Key components of the assessment include vital signs, electrolytes, renal function, and cardiac rhythm. Evaluation for precipitating factors and cardiovascular as well as noncardiovascular comorbid conditions is also important.
Common symptoms include symptoms of dyspnea, orthopnea, and fatigue, as well as signs such as peripheral edema and weight gain. Accurately establishing the diagnosis of ADHF is a critical first step, as delays in diagnosis and therapy may lead to worse outcomes in ADHF.
The initial assessment of patients presenting with ADHF should include a thorough history and physical examination focusing on the assessment of congestion, volume status, and perfusion. In addition, common factors that precipitate ADHF, including medication and dietary noncompliance, acute coronary syndromes, uncontrolled hypertension and diabetes mellitus, atrial fibrillation and other arrhythmias, recent addition of nonsteroidal antiinflammatory drugs, pulmonary emboli, excessive alcohol or illicit drug use, thyroid dysfunction, socioeconomic considerations, and concurrent infections, must be thoroughly assessed.
II. Diagnostic Confirmation: Are you sure your patient has Acute Decompensated Heart Failure?
The diagnosis of ADHF should be based primarily on signs and symptoms of heart failure being present. Clinicians need to determine as accurately as possible the volume status of the patient, the adequacy of circulatory support or perfusion, and the role or presence of precipitating factors and comorbid conditions. In the patient with previously established heart failure, efforts should also be directed toward understanding what has caused the apparent acute worsening of clinical symptoms.
When the diagnosis of ADHF is uncertain, determination of plasma brain natriuretic peptide (BNP) or NT-proBNP concentration should be considered in patients being evaluated for dyspnea who have signs and symptoms compatible with heart failure. The natriuretic peptide concentration should not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of ADHF.
However, it is important to highlight there is no single diagnostic test for ADHF because it is largely a clinical diagnosis that is based on a careful history and physical examination.
Features Associated with the Probability of ADHF
- Past history of heart failure (positive LR 5.8; 95% CI 4.1-8.0)
- The symptom of paroxysmal nocturnal dyspnea (PND) (positive LR 2.6; 95% CI 1.5-4.5)
- The sign of S3 gallop (positive LR 11.0; 95% CI 4.9-25.0)
- The chest radiograph (CXR) showing congestion (positive LR 12.0; 95% CI 6.8-21.0)
- Electrocardiogram (ECG) showing atrial fibrillation (positive LR 3.8; 95% CI 1.7-8.8)
- Absence of past history of heart failure (negative LR 0.45; 95% CI 0.38-0.53)
- Absence of the symptom of dyspnea on exertion (DOE) (negative LR 0.48; 95% CI 0.35-0.67)
- Absence of rales (negative LR 0.51; 95% CI 0.37-0.70)
- Absence of CXR showing CM (negative LR 0.33; 95% CI 0.23-0.48)
- Absence of any ECG abnormality (negative LR 0.64; 95% CI 0.47-0.88)
- Low serum BNP (<100 pg/ml) (negative LR 0.11; 95% CI 0.07-0.16)
A. History Part I: Pattern Recognition:
The cardinal manifestations of ADHF are dyspnea, fluid retention, and fatigue. Fluid retention, commonly leads to pulmonary congestion and peripheral edema in patients with ADHF.
Patients may present with progressive weight gain, lower extremity edema, increasing dyspnea on exertion, or dyspnea at rest. Patients may report orthopnea and/or paroxysmal nocturnal dyspnea.
Patients may note abdominal bloating or a decrease in appetite. Some patients may present with fatigue or even altered mental status. Some patients may present with sudden onset of dyspnea.
Common factors that precipitate ADHF may include noncompliance with medical regimen, sodium and/or fluid restriction, acute coronary syndromes, uncorrected high blood pressure, atrial fibrillation and other arrhythmias, pulmonary embolus, use of NSAIDs, excessive alcohol or illicit drug use, endocrine abnormalities, exacerbation of pulmonary diseases, or concurrent infections such as pneumonia.
Common causes of ADHF
Acute coronary syndrome
Hypertension urgency or emergency
Increase in afterload
Sodium or volume load
Decreased compliance with diuretics
Inflammation or infection
Lack of compliance with HF medications
New medication (NSAID)
B. History Part 2: Prevalence:
Acute decompensated heart failure causes considerable morbidity and mortality, and produces a tremendous burden on health care systems worldwide. In the United States, ADHF as the primary or secondary cause resulted in almost 3.6 million hospitalizations and translates into an annual estimated cost of $29 to $56 billion.
Studies have shown that ADHF represents a period of high risk for patients, during which their likelihood of death and rehospitalization is significantly greater than for a comparable period of chronic, but stable heart failure. The in-hospital mortality rates reported for ADHF have varied greatly, ranging from 2% to 20%.
Prognosis is also reported to be very poor postdischarge; the mortality risk after AHDF hospitalization has been reported to be as high as 11.3% at 30 days and 33.1% at 1 year in the U.S. Analysis of the case fatality rate for patients hospitalized with a principal diagnosis of ADHF in Scotland revealed a median survival of 1.47 years in men and 1.39 years in women. Studies from other countries also reveal a high mortality risk.
In addition, patients also face a very high risk of rehospitalization. In a study of almost 18,000 Medicare recipients, approximately 44% were rehospitalized one or more times in the 6 months following their index hospitalization.
Estimates of the risk of death or rehospitalization within 60 days of admission vary from 30% to 60%, depending on the population studied. These statistics emphasize the need for identifying prognostic markers and clinically practical methods of risk stratification for patients hospitalized with ADHF, as well as to develop and implement more effective strategies to manage ADHF.
Registry data from patients hospitalized for ADHF from the Acute Decompensated Heart Failure National Registry (ADHERE), the Euro Heart Failure survey, and the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) have provided insights regarding patients hospitalized with ADHF in the U.S. and Europe. Data from these registries show that 65% to 87% of patients hospitalized with HF have worsening of a previously diagnosed HF.
The median age of patients was 71 to 75 years, and approximately half were women. Among hospitalized patients with ADHF, two thirds have a history of coronary artery disease and one third of these patients have a history of prior myocardial infarction.
A history of hypertension is very frequent, present in 53% to 72% of patients. Diabetes is present in 27% to 44% and chronic obstructive pulmonary disease in approximately 30%.
Renal dysfunction is emerging as a critical feature of patients hospitalized with ADHF, as 18% to 30% of registry patients have a history of chronic renal insufficiency. Normal or mildly reduced systolic function (left ventricular ejection fraction [LVEF] >0.40) is present in 48% to 52% of the patients admitted with ADHF.
When a definition of LVEF >0.50 is used to designate preserved systolic function heart failure, the proportion of patients meeting this criteria is closer to 30% to 35%. Patients with ADHF and preserved ejection fraction are more likely to be female and 90% have a history of hypertension, coronary artery disease, and/or diabetes.
C. History Part 3: Competing diagnoses that can mimic Acute Decompensated Heart Failure.
- Pulmonary infection
- Acute chronic obstructive pulmonary disease (COPD)/asthma exacerbation
- Acute coronary syndrome
- Valvular heart disease
- Pulmonary emboli
- Pneumothorax, pleural effusions
- Aortic dissection
- Renal failure
D. Physical Examination Findings.
The physical exam should focus on several key features including vital signs, the cardiopulmonary examination, neck veins, and extremities. Patients may be tachycardic and have blood pressure derangements.
Hypertensive patients are more likely to have preserved systolic function, whereas hypotensive patients are more likely to be in a low-cardiac output state carrying a worse prognosis. Pulmonary examination often reveals crackles, consistent with interstitial pulmonary edema, or wheezing.
Examination of the neck veins provides diagnostic and prognostic information. Elevation of jugular venous pressure is indicative of elevated right-sided filling pressures, which in patients with advanced heart failure, predicts elevated left-sided filling pressures in 80% of cases.
Cardiac auscultation may reveal either a third and/or a fourth heart sound suggestive of cavitary dilation or decreased compliance of the left ventricle respectively. A new or changed murmur usually represents valvular abnormalities, which may reflect altered ventricular geometry.
Abdominal examination may reveal hepatomegaly as a result of passive congestion, hepatojugular reflux or ascites. Extremity examination may reveal peripheral edema, particularly in the dependent portions of the body. Perfusion may be assessed by capillary refill time and physicians’ perception of skin temperature (i.e., warm, suggestive of adequate perfusion, or cold, suggestive of poor perfusion) (Figure 1).
E. What diagnostic tests should be performed?
The initial evaluation of patients presenting with AHDF should include laboratory testing, including complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, fasting blood glucose (glycohemoglobin), lipid profile, liver function tests, and thyroid-stimulating hormone. A BNP or NT-BNP is indicated if the diagnosis is uncertain or for prognostic purposes.
Cardiac troponins should be obtained to evaluate for an acute coronary syndrome. A 12-lead electrocardiogram and chest radiograph (posterior-anterior and lateral) should be performed initially in all patients presenting with ADHF.
Two-dimensional echocardiography with Doppler should be performed during initial evaluation of patients presenting with ADHF to assess left ventricular ejection fraction, left ventricular size, wall thickness, and valve function. Radionuclide ventriculography can be performed to assess left ventricular ejection fraction and volumes.
In select patients, coronary arteriography should be performed in patients presenting with ADHF who have angina or significant ischemia unless the patient is not eligible for revascularization of any kind. Right heart catheterization is also indicated in select patients with ADHF.
There are multiple demographic, clinical, vital sign, and laboratory parameters that have prognostic significance. A number of risk models using these variables have been derived and validated for patients presenting with ADHF (Figure 2) (Figure 3).
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Initial laboratory evaluation of patients presenting with AHDF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, fasting blood glucose (glycohemoglobin), lipid profile, liver function tests, and thyroid-stimulating hormone. A BNP or NT-BNP is indicated if the diagnosis is uncertain or for prognostic purposes. Cardiac troponins should be obtained to evaluate for an acute coronary syndrome.
Measurement of natriuretic peptides is a Class I, Level of Evidence A recommendation of the ACC/AHA when the diagnosis of ADHF is in question. Evidence exists supporting their use for diagnosing, staging, establishing hospitalization/discharge decisions, and identifying patients at risk for clinical events.
B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP), which rise in response to an increase in myocardial wall stress, may be used for the diagnosis and management of ADHF. A normal level in an untreated patient has a high negative predictive value for ADHF, while elevated values despite optimal treatment portend a poor prognosis.
However, there is no definitive cut-off level recognized that ensures the diagnosis of ADHF. Conditions other than ADHF, which are associated with elevated BNP and NT-proBNP levels include: left ventricular hypertrophy, tachycardia, right ventricular overload, myocardial ischemia, hypoxemia, renal dysfunction, advanced age, liver cirrhosis, sepsis, and infection.
Cardiac biomarkers associated with myocardial injury, such as cardiac troponin I or T, are important prognostic markers in ADHF patients and should be obtained in patients in whom acute coronary syndrome is a concern, or in whom additional risk stratification is warranted. An increase in cardiac troponin indicates myocyte necrosis. Slight elevations in troponin have also been observed in patients with ADHF.
The laboratory assessment of patients with ADHF should include a complete blood count (white blood cells, hemoglobin, hematocrit, and platelets), serum electrolytes, renal indices (blood urea nitrogen, creatinine, estimated glomerular filtration rate), glucose, liver function tests, and urinalysis. The presence of anemia, hyponatremia, hyperkalemia, hypokalemia, and renal dysfunction are relatively common and are important both for immediate management considerations, as well as prognosis.
Anemia is an independent predictor of in-hospital mortality in ADHF patients. Hyponatremia occurs in approximately 25% of patients with ADHF and commonly remains uncorrected during hospitalization.
Patients with hyponatremia have a significantly greater risk of death in hospital and postdischarge. Admission serum sodium is an independent predictor of increased number of days hospitalized for cardiovascular causes and increased in-hospital and post-discharge mortality.
Markers of renal impairment including blood urea nitrogen, serum creatinine, blood urea nitrogen/creatinine ratio, and estimated glomerular filtration rate all have important prognostic importance in ADHF. Unfortunately, therapies to specifically target these renal function abnormalities to mitigate longer-term risk have yet to be established.
A fasting transferring saturation may be considered to screen for hemochromatosis. Screening for human immunodeficiency virus (HIV) should be considered for all high-risk patients. Serum titers of antibodies developed in response to infectious organisms are occasionally measured in patients with a recent onset of ADHF, especially in those with a recent viral syndrome.
Serum titers of Chagas disease antibodies should be checked in patients with nonischemic cardiomyopathy who have lived or traveled from an endemic region. Assays for connective tissue diseases and for pheochromocytoma should be performed if these diagnoses are suspected.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Echocardiography, including two-dimensional, pulsed and continuous wave Doppler, color Doppler, and tissue Doppler imaging, is the primary imaging tool for the structural and functional assessment of the ADHF patient. This imaging technique can rapidly provide information on left ventricular function, left atrial size, mitral regurgitation severity, and left ventricular filling pressures, as well as the presence or absence of regional wall motion abnormalities or left ventricular aneurysm.
The diagnosis of diastolic dysfunction via methodologies that demonstrate abnormal left ventricular relaxation or diastolic stiffness can also be used. Echocardiography combined with Doppler imaging may also be used to noninvasively assess hemodynamics (i.e., cardiac output by pulsed Doppler of the left ventricular outflow tract; pulmonary capillary wedge pressure (PCWP) by a regression equation involving mitral and pulmonary venous flow variables; pulmonary artery pressure from tricuspid valve velocities; and pulmonary vascular resistance from the previous measurements).
In addition, tissue Doppler imaging variables including the ratio of early transmitral velocity to tissue Doppler early mitral annular early diastolic velocity (E:E’) have been shown in some studies to correlate with left ventricular filling pressure, but other studies have not found this to be accurate.
Echocardiographic left ventricular (LV) dilatation (LV end-diastolic dimension >7.5 cm or LV index >4 cm/m2) is associated with a poor prognosis in AHFS patients. Pulmonary hypertension is commonly present in ADHF patients with both reduced and preserved ejection fraction.
Doppler echocardiography may be used to assess the presence of pulmonary hypertension with the estimation of pulmonary artery systolic pressure (PASP) by combining the right ventricular systolic pressure (as estimated by the modified Bernoulli equation) and the right atrial pressure, as estimated by the standardized echocardiographic features of the inferior vena cava.
Transesophageal echocardiography (TEE) is recommended in patients who have inadequate transthoracic echocardiographic windows, in complicated valvular patients, in suspected endocarditis, in congenital heart disease, or to exclude a thrombus in the left atrial appendage in patients with atrial fibrillation. Ultrasonic contrast agents may be an alternative option to enhance myocardial border definition in patients with unclear myocardial borders on transthoracic echocardiography.
Handheld echocardiography may also have a role in the care of HF patients, as it has been shown to be useful in detecting left ventricular pressures via inferior vena cava examination at the bedside.
Several noninvasive modalities can be used to identify myocardial ischemia in the ADHF patient, if indicated. These include stress echocardiography, nuclear imaging (single-photon emission computed tomography [SPECT], and positron emission tomography [PET]), and cardiac magnetic resonance (MR).
Noninvasive testing for ischemia can be considered as part of the initial assessment of ADHF patient particularly in patients with known coronary artery disease or an unknown coronary artery disease status. Dobutamine stress echocardiography detects ischemia through the induction of new or exaggerated left ventricular wall motion abnormalities, while increasing doses of intravenous dobutamine are administered.
Nuclear perfusion imaging with SPECT uses intravenously delivered radioisotopes (thallium-201 chloride, technetium-99m sestamibi, or technetium-99m tetrofosmin) to detect ischemia. Images obtained after stress and at rest are compared, and regions with defects following stress that normalize at rest (reversible) are indicative of ischemia.
Irreversible, or fixed, defects are indicative of myocardial infarction. Where available, PET may also be used to assess for the presence ischemia. PET detects ischemia by using rubidium-82, N13-ammonia, or O15-labeled water as tracers.
Cardiac MR is another modality available for the assessment of myocardial viability using different techniques including contrast enhanced cardiac MR, dobutamine stress cardiac MR, and assessment of LV end-diastolic wall thickness with resting cine cardiac MR. The most common MR technique for viability detection is the delayed-enhancement cardiac MR, which uses gadolinium-based contrast agents to detect nonviable areas of myocardium since they accumulate selectively in scar tissue.
The degree of delayed hyper enhancement is inversely proportional to the degree of myocardial viability.
In patients with ADHF, right heart catheterization may provide important hemodynamic data. It can be performed at the bedside or at the same time as left heart catheterization providing invasive measurements of right heart pressures, PCWP, cardiac output, and pulmonary artery pressures.
Right heart catheterization provides powerful prognostic data and hemodynamic targets for treatment in ADHF patients. Right heart catheterization may be considered in patients with severe heart failure and an unclear hemodynamic state (i.e., low output versus high output) in order to classify their ADHF and possibly monitor therapy.
An assessment of left and right sided cardiac function, pulmonary artery pressure, systemic vascular resistance, and cardiac output may guide initial therapies. Based on the ACC/AHA guidelines, right heart catheterization is a class I recommendation for patients with respiratory distress or in those with evidence of poor perfusion whose cardiac filling pressure cannot be ascertained from the physical examination and other clinical parameters.
It is a class IIA recommendation to perform right heart catheterization in patients who have persistent symptoms of ADHF, worsening renal function, or hypotension despite standard medical therapies, patients who require vasoactive agents, or patients who require consideration for advanced device therapies or heart transplantation.
Coronary angiography is the gold standard for the diagnosis and reassessment of coronary artery disease. The long-term prognosis of ADHF patients has been directly associated with the angiographic extent and severity of coronary artery disease.
Left heart hemodynamic measurements can also be obtained with left heart catheterization, which may impact the course of therapy. In addition, LV systolic function can be evaluated by left ventriculography. In select patients, coronary arteriography should be performed in patients presenting with ADHF who have angina or significant ischemia unless the patient is not eligible for revascularization of any kind.
What’s the Evidence for specific management and treatment recommendations?
Supporting guidelines for specific evaluation recommendations
Hunt, SA, Abraham, WT, Chin, MH. “2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines developed in collaboration with the International Society for Heart and Lung Transplantation”. J Am Coll Cardiol. vol. 53. 2009. pp. e1-e90. (National guidelines from ACC/AHA including recommendations on diagnosis, evaluation, and assessment of acute decompensated heart failure.)
Lindenfeld, J, Albert, NM, Boehmer, JP. “HFSA 2010 comprehensive heart failure practice guideline”. J Card Fail. vol. 16. 2010. pp. e1-194. (National guidelines from HFSA, including recommendations on diagnosis, evaluation, and assessment of acute decompensated heart failure.)
Dickstein, K, Cohen-Solal, A, Filippatos, G. “ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the task force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)”. Eur Heart J. vol. 29. 2008. pp. 2388-442. (International guidelines from ESC including recommendations on diagnosis, evaluation, and assessment of acute decompensated heart failure.)
Peacock, WF, Fonarow, GC, Ander, DS. “Society of Chest Pain Centers recommendations for the evaluation and management of the observation stay acute heart failure patient: a report from the Society of Chest Pain Centers Acute Heart Failure Committee”. Crit Pathw Cardiol. vol. 7. 2008. pp. 83-6. (Guidelines from SCPC including recommendations on the diagnosis, evaluation, and assessment of acute decompensated heart failure.)
Lloyd-Jones, D, Adams, RJ, Brown, TM. “Executive summary: heart disease and stroke statistics—2010 update: a report from the American Heart Association”. Circulation. vol. 121. 2010. pp. 948-54. (National health statistics documenting scope and outcomes for acute decompensated heart failure.)
Fonarow, GC, Stough, WG, Abraham, WT. “Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: a report from the OPTIMIZE-HF Registry”. J Am Coll Cardiol. vol. 50. 2007. pp. 768-77. (National registry study with presenting signs and symptoms of patients with acute decompensated heart failure.)
Adams, KF, Fonarow, GC, Emerman, CL. “Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE)”. Am Heart J. vol. 149. 2005. pp. 209-16. (National registry study with presenting signs and symptoms of patients with acute decompensated heart failure.)
Peacock, WF, Braunwald, E, Abraham, W, Gheorghiade, M, Pang, PS. “National Heart, Lung, and Blood Institute working group on emergency department management of acute heart failure: research challenges and opportunities”. J Am Coll Cardiol. vol. 56. 2010. pp. 343-51. (Consensus document of research challenges and opportunities for patients presenting with acute decompensated heart failure.)
Gheorghiade, M, Zannad, F, Sopko, G. “Acute heart failure syndromes: current state and framework for future research”. Circulation. vol. 112. 2005. pp. 3958-68. (Review article on the assessment and treatment of acute decompensated heart failure.)
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- I. Acute Decompensated Heart Failure: What every physician needs to know.
- II. Diagnostic Confirmation: Are you sure your patient has Acute Decompensated Heart Failure?
- A. History Part I: Pattern Recognition:
- B. History Part 2: Prevalence:
- C. History Part 3: Competing diagnoses that can mimic Acute Decompensated Heart Failure.
- D. Physical Examination Findings.
- E. What diagnostic tests should be performed?
- 1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- 2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- What's the Evidence for specific management and treatment recommendations?