Most commonly shows hypoxemia and hypocapnea (respiratory alkalosis) due to hyperventilation, keep in mind, however, that despite these “classic” findings, arterial blood gas analysis is NOT useful in diagnosis of pulmonary embolism.
The more massive the obstruction, the more severe the hypoxemia is likely to be, with an SpO2 < 95% on room air being predictive for increased morbidity and mortality. However, many other conditions also cause hypoxemia, and embolism often does not cause hypoxemia or even a widening of the alveolar-arterial Po2 difference. Hypocapnia usually is present with embolism; hypercapnia, on the other hand, is rare. A massive PE may cause a combined respiratory (hypercapnea) and metabolic acidosis due to hemodynamic collapse. 18% of patients will have a PaO2 85-105 mmHg and 6% will have a normal A-a gradient.
Pulmonary Embolism and ABG
- Classic finding: hypoxemia and hypocapnea (respiratory alkalosis)
- Normal ABG: 18% will have PaO2 > 85 mm Hg and 6% will have normal A-a gradient
- Mixed Acidosis: in setting of hemodynamic collapse
- Utility of ABG: minimal, even when combined with other modalities (see Roger MA et al., below)
- Outcome: SpO2 < 95% on room air may be predictive of poor outcome, however
M A Rodger, M Carrier, G N Jones, P Rasuli, F Raymond, H Djunaedi, P S Wells Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism. Am. J. Respir. Crit. Care Med.: 2000, 162(6);2105-8
Jeffrey A Kline, Jackeline Hernandez-Nino, Craig D Newgard, Dana N Cowles, Raymond E Jackson, D Mark Courtney Use of pulse oximetry to predict in-hospital complications in normotensive patients with pulmonary embolism. Am. J. Med.: 2003, 115(3);203-8
P D Stein, M L Terrin, C A Hales, H I Palevsky, H A Saltzman, B T Thompson, J G Weg Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest: 1991, 100(3);598-603