eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Pulmonary Edema, Cardiogenic: Differential Diagnoses & Workup

Author: Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, University of California at Los Angeles; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Contributor Information and Disclosures

Updated: Apr 22, 2008

Differential Diagnoses

Acute Respiratory Distress Syndrome
Pneumocystis Carinii Pneumonia
Asthma
Pneumonia, Bacterial
Cardiogenic Shock
Pneumonia, Viral
Chronic Obstructive Pulmonary Disease
Pneumothorax
Emphysema
Pulmonary Edema, High-Altitude
Goodpasture Syndrome
Pulmonary Edema, Neurogenic
Myocardial Infarction
Pulmonary Embolism
Myocardial Ischemia
Respiratory Failure

Other Problems to Be Considered

CPE should be differentiated from pulmonary edema associated with injury to the alveolar-capillary membrane caused by diverse etiologies. Damage to alveolar capillary barrier can be seen in various direct lung injuries (pneumonia, aspiration pneumonitis, toxin inhalation, pulmonary contusion, radiation, drowning and fat emboli) or indirect lung injuries (sepsis, shock and multiple transfusions, acute pancreatitis, anaphylactic shock).

In addition, several conditions related to noncardiogenic pulmonary edema (NCPE) primarily affect Starling forces rather than the alveolar-capillary barrier. These conditions include decreased oncotic pressure of the plasma due to various etiologies and increased negativity of interstitial pressure due to rapid removal of pneumothorax. Lymphatic insufficiency (eg, lymphangitic carcinomatosis, fibrosing lymphangitis, lung transplantation) is another important pathophysiologic mechanism of NCPE.

Several features may differentiate CPE from NCPE. In CPE, a history of an acute cardiac event is usually present. Physical examination shows a low-flow state, an S3 gallop, jugular venous distention, and crackles on auscultation. Patients with NCPE have a warm periphery, a bounding pulse, and no S3 gallop or jugular venous distention. Definite differentiation is based on PCWP measurements. The PCWP is generally >18 mm Hg in CPE and <18 mm Hg in NCPE, but superimposition of chronic pulmonary vascular disease can make this distinction difficult.

Workup

Laboratory Studies

  • Blood count: The CBC with differential helps in assessing for severe anemia and may suggest sepsis or infection if a markedly elevated WBC count or bandemia is present.
  • Serum electrolyte measurements
    • Patients with chronic CHF often use diuretics. Therefore, they are predisposed to have electrolyte abnormalities, especially hypokalemia and hypomagnesemia.
    • Patients with chronic renal failure are at high risk for hyperkalemia, especially when they are noncompliant with hemodialysis sessions.
  • BUN and creatinine determinations: These tests help in assessing for renal failure and the anticipated response to diuretics. In low-output states, such as systolic dysfunction, decreased BUN and creatinine levels may be secondary to hypoperfusion of the kidneys.

Imaging Studies

  • Chest radiography is helpful in distinguishing CPE from other pulmonary causes of severe dyspnea.
  • An enlarged heart, inverted blood flow, Kerley lines, basilar edema (vs diffuse edema), absence of air bronchograms, and presence of pleural effusion (particularly bilateral and symmetrical pleural effusions) are features that suggest CPE versus NCPE and other lung pathologies.
  • Chest radiography is somewhat limited in patients with CPE of abrupt onset because the classic radiographic abnormalities may not appear for as long as 12 hours after dyspnea begins.
  • Echocardiography: A bedside echocardiogram in a patient with decompensated CHF is an important diagnostic tool in determining the etiology of pulmonary edema. Echocardiography can evaluate LV systolic and diastolic function, valvular function, and assess for pericardial disease. It is especially helpful in identifying a mechanical etiology for pulmonary edema (eg, acute papillary muscle rupture, acute ventricular septal defect [VSD], cardiac tamponade, contained LV rupture, valvular vegetation with resulting acute severe mitral, aortic regurgitation).

Other Tests

  • Arterial blood gas analysis
    • This test is more accurate than pulse oximetry for measuring oxygen saturation.
    • The decision to start mechanical ventilation is mainly based on clinical findings and rarely arterial blood gas results.
  • Pulse oximetry
    • Pulse oximetry is useful in assessing hypoxia and, therefore, the severity of CPE.
    • It is also useful for monitoring the patient's response to supplemental oxygenation and other therapies.
  • Electrocardiography
    • Left atrial enlargement and LV hypertrophy are sensitive, though nonspecific, indicators of chronic LV dysfunction.
    • The ECG may suggest an acute tachydysrhythmia or bradydysrhythmia as the cause of CPE.
    • The ECG may suggest acute myocardial ischemia or infarction as the cause of CPE.

Plasma brain-type natriuretic peptide (BNP) and NT-proBNP testing

Both BNP and NT-proBNP are derived from pre-proBNP, a 134-amino-acid precursor synthesized by cardiac myocytes. A number of triggers including wall stretch, ventricular dilation, and/or increased pressures stimulate a 26-amino-acid signal peptide sequence to be cleaved from the precursor’s N-terminus to produce proBNP (108-amino-acid). This hormone is further cleaved by a membrane-bound serine protease (corin) into the inactive N-terminal fragment (NT-proBNP) and the active BNP (32-amino-acid) fragment. Both NT-proBNP and BNP testing are clinically available and have exhibited parallel changes across broad ranges of age, ejection fraction, diastolic CHF, and renal function. 

  • NT-proBNP testing 
    • Ventricular myocytes secrete proBNP in response to muscle-wall tension.
    • NT-proBNP has a longer half-life (120 min) than that of BNP (20 min)
    • NT-proBNP is less studied than BNP, but its levels are well correlated with BNP levels.
    • The cutoff value of NT-proBNP >450 pg/mL in patients younger than 50 years correlates to values of BNP >100 pg/mL. NT-proBNP is less accurate than BNP in patients older than 65 years.
  • BNP testing
    • CHF is the most common form of CPE.
    • Several observational studies and clinical trials have shown the important diagnostic value of BNP measurements in differentiating heart failure from pulmonary causes of dyspnea.
    • BNP testing decreases the total cost of treatment and the length of hospitalization. This is a cost-effective diagnostic test in this setting.
    • Although reports differ, a cutoff value of 100 pg/mL is generally accepted. By using this cutoff value, measurement of BNP has a high negative predictive value. That is, in patients with BNP value of <100 pg/mL, heart failure is unlikely.
    • The level of BNP increases with age and is slightly higher in women than men. BNP levels also tend to be lower in obese patients.
    • In a recent study, a cutoff point of 250 pg/mL was the most accurate for elderly patients (mean age, 80 y).
    • Renal dysfunction may be associated with a significantly increased level of BNP.
    • In the Breathing Not Properly Multinational Study, the mean BNP level in patients without heart failure and with a glomerular filtration rate (GFR) below normal was 300 pg/mL.
    • Although the predictive value of BNP measures with cutoff value of 100 pg/mL is high, its positive predictive value is not as high as its negative predictive value. This means that mildly to moderately elevated levels of BNP should be interpreted in accordance to the patient's clinical status and other diagnostic results.
    • Values of 100-400 pg/mL may be related to various pulmonary conditions, such as cor pulmonale, COPD, and pulmonary embolism.
    • Atrial fibrillation is another factor that may mildly increase the cutoff value of BNP in diagnosing heart failure. Important information to know is the patient's baseline heart function. Patients with chronic heart failure and BNP values of £ 400 pg/mL may have pulmonary causes of dyspnea without an exacerbation of their CHF.
    • Until additional studies establish the precise cutoff values for different conditions, the threshold of 100 pg/mL is recommended, with the exceptions noted above. This cutoff value has an accuracy of 80-85%, a sensitivity of 90%, and a specificity of about 75% along with other appropriate clinical and laboratory findings.
    • One study of ICU patients who required invasive hemodynamic monitoring showed that they had markedly elevated BNP values, but the correlation between BNP values and PCWP was weak.

Procedures

  • PCWP can be measured by using a pulmonary arterial catheter (Swan-Ganz catheter). This method helps in differentiating CPE from NCPE.
    • NCPE occurs secondary to injury to the alveolar-capillary membrane rather than to alteration in Starling forces.
    • A PCWP exceeding 18 mm Hg in a patient not known to have chronically elevated left atrial pressure indicates CPE.
    • In patients with chronic pulmonary capillary hypertension, capillary wedge pressures exceeding 30 mm Hg are required to overcome the pumping capacity of the lymphatics and produce pulmonary edema.
  • Large V waves are sometimes observed in the PCWP tracing with acute mitral regurgitation because large volumes of blood regurgitate into a poorly compliant left atrium.
    • This condition raises pulmonary venous pressure and causes acute pulmonary edema.
    • The pulmonary artery waveform appears falsely elevated because of the large V wave reflected back from the left atrium through the compliant pulmonary vasculature.
    • The Y descent of the waveform is rapid, as the overdistended left atrium quickly empties.
  • Cardiogenic shock is the result of a severe depression in myocardial function.
    • Cardiogenic shock is hemodynamically characterized by a systolic BP <80 mm Hg, a cardiac index <1.8 L/min/m2, and a PCWP >18 mm Hg.
    • This form of shock can occur from a direct insult to the myocardium (large acute MI, severe cardiomyopathy) or from a mechanical problem that overwhelms the functional capacity of the myocardium (acute severe mitral regurgitation, acute ventricular septal defect). Although the pulmonary artery catheter is commonly used in ICU patients with severe acute decompensated CHF, it is not clear whether this technique improves mortality rate and clinical outcome. The results of the recent ESCAPE trial showed no mortality benefit or decrease in the number of hospitalized days in the group of patients who underwent PAC insertion.1 This matter needs further investigation.

More on Pulmonary Edema, Cardiogenic

Overview: Pulmonary Edema, Cardiogenic
Differential Diagnoses & Workup: Pulmonary Edema, Cardiogenic
Treatment & Medication: Pulmonary Edema, Cardiogenic
Follow-up: Pulmonary Edema, Cardiogenic
Multimedia: Pulmonary Edema, Cardiogenic
References
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Further Reading

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Keywords

PE, pulmonary edema, cardiogenic pulmonary edema, pulmonary edema cardiogenic, CPE, congestive heart failure, CHF, decompensated heart failure, heart failure, increased capillary hydrostatic pressure, increased capillary permeability, decreased plasma oncotic pressure, lymphatic obstruction, noncardiogenic pulmonary edema, NCPE

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Contributor Information and Disclosures

Author

Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, Heart Rhythm Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, University of California at Los Angeles; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, and American Society of Echocardiography
Disclosure: Pfizer Honoraria Speaking and teaching

Medical Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC, Sidney W and Marilyn S Lassen Professor of Cardiovascular Medicine, Chief, Section of Cardiology, Director, Cardiovascular Center of Excellence, Tulane University; Professor of Physiology, Chair, Department of Medicine, Tulane University School of Medicine
Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Diabetes Association, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Endocrine Society, European Society of Cardiology, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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