Pulmonary edema laboratory tests

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

Overview

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]

Acidosis:
- PH < 7.35 nEq/liter
- Early ﬁndings of pulmonary edema may be respiratory alkalosis because of hyperventilation

Elevation in alanine aminotransferase, aspartate aminotransferase and bilirubin may be seen in right ventricular failure as underlying cause of cardiogenic pulmonary edema

B-type natriuretic peptide (BNP) is elevated in the patient with cardiogenic pulmonary edema.

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.

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

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

References

↑ 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.
↑ 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.
↑ Murray JF (February 2011). “Pulmonary edema: pathophysiology and diagnosis”. Int. J. Tuberc. Lung Dis. 15 (2): 155–60, i. PMID 21219673.
↑ 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.

Overview