Pulmonary edema laboratory tests

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]


Laboratory findings consistent with the diagnosis of pulmonary edema include hypoxia, hypercapnia, acidosis. Elevated B-type natriuretic peptide (BNP) and cardiac enzyme is usually suggestive of cardiogenic pulmonary edema.

Laboratory Findings

Laboratory findings consistent with the diagnosis of pulmonary edema include:[1][2][3]

Arterial blood gas test:

Serum albumin:

  • Albumin may be low in pulmonary edema

Liver function tests:

Plasma brain natriuretic peptide levels :

  • A low BNP (<100 pg/ml) makes a cardiac cause very unlikely and is associated with non-cardiogenic pulmonary edema.

Pulmonary capillary wedge pressure(PCWP):

  • A wedge pressure of 18 mmHg or higher is usually suggestive of cardiogenic pulmonary edema.
  • A wedge pressure of less than 18 mmHg is usually suggestive of non-cardiogenic pulmonary edema.

Cardiac enzymes:

  • Elevated concentration of troponin, may suggestive of damage to myocytes, as underlying cause of cardiogenic pulmonary edema.

Shunt fractions (Qs/Qt):

  • Patients with non-cardiogenic pulmonary edema had greater shunt fractions(Qs/Qt) than patients with cardiogenic pulmonary edema.[4]
Differentiation of cardiogenic pulmonary edema and noncardiogenic pulmonary edema
Laboratory findings Cardiac enzymes BNP PCWP QS/QT
Cardiogenic pulmonary edema May be elevated High >18 mmHg Small elevated
Noncardiogenic pulmonary edema Usually normal Low <18 mmHg Large elevated


  1. Ware LB, Matthay MA (December 2005). "Clinical practice. Acute pulmonary edema". N. Engl. J. Med. 353 (26): 2788–96. doi:10.1056/NEJMcp052699. PMID 16382065.
  2. Sibbald WJ, Cunningham DR, Chin DN (October 1983). "Non-cardiac or cardiac pulmonary edema? A practical approach to clinical differentiation in critically ill patients". Chest. 84 (4): 452–61. PMID 6617283.
  3. Murray JF (February 2011). "Pulmonary edema: pathophysiology and diagnosis". Int. J. Tuberc. Lung Dis. 15 (2): 155–60, i. PMID 21219673.
  4. Siegel JH, Giovannini I, Coleman B (June 1979). "Ventilation:perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis". J Trauma. 19 (6): 432–60. PMID 448782.

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