How effective is PaO2 level on ABG analysis in predicting pulmonary embolism (PE)?

Answer

In most settings, fewer than half of all patients with symptoms suggestive of pulmonary embolism actually turn out to have pulmonary embolism as their diagnosis. In such a population, if any reasonable level of PaO₂ is chosen as a dividing line, the incidence of pulmonary embolism will be higher in the group with a PaO₂ above the dividing line than in the group whose PaO₂ is below the divider. This is a specific example of a general truth that may be demonstrated mathematically for any test finding with a Gaussian distribution and a population incidence of less than 50%.

Conversely, in a patient population with a very high incidence of pulmonary embolism and a lower incidence of other respiratory ailments (eg, postoperative orthopedic patients with sudden onset of shortness of breath), a low PO₂ has a strongly positive predictive value for pulmonary embolism.

The discussion above holds true not only for arterial PO₂ but also for the alveolar-arterial oxygen gradient and for the oxygen saturation level as measured by pulse oximetry. In particular, pulse oximetry is extremely insensitive, is normal in the majority of patients with pulmonary embolism, and should not be used to direct a diagnostic workup.

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Media Gallery

A large pulmonary artery thrombus in a hospitalized patient who died suddenly.
Pulmonary embolism was identified as the cause of death in a patient who developed shortness of breath while hospitalized for hip joint surgery. This is a close-up view.
Lung infarction secondary to pulmonary embolism occurs rarely.
Posteroanterior and lateral chest radiograph findings are normal, which is the usual finding in patients with pulmonary embolism.
High-probability perfusion lung scan shows segmental perfusion defects in the right upper lobe and subsegmental perfusion defects in right lower lobe, left upper lobe, and left lower lobe.
A normal ventilation scan will make the noted defects in the previous image a mismatch and, hence, a high-probability ventilation-perfusion scan.
Anterior views of perfusion and ventilation scans are shown here. A perfusion defect is present in the left lower lobe, but perfusion to this lobe is intact, making this a high-probability scan.
A segmental ventilation perfusion mismatch is evident in a left anterior oblique projection.
A pulmonary angiogram shows the abrupt termination of the ascending branch of the right upper-lobe artery, confirming the diagnosis of pulmonary embolism.
A chest radiograph with normal findings in a 64-year-old woman who presented with worsening breathlessness.
This perfusion scan shows bilateral perfusion defects. The ventilation scan findings were normal; therefore, these are mismatches, and this is a high-probability scan.
This ultrasonogram shows a thrombus in the distal superficial saphenous vein, which is under the artery.
A posteroanterior chest radiograph showing a peripheral wedge-shaped infiltrate caused by pulmonary infarction secondary to pulmonary embolism. Hampton hump is a rare and nonspecific finding. Courtesy of Justin Wong, MD.
Computed tomography angiogram in a 53-year-old man with acute pulmonary embolism. This image shows an intraluminal filling defect that occludes the anterior basal segmental artery of the right lower lobe. Also present is an infarction of the corresponding lung, which is indicated by a triangular, pleura-based consolidation (Hampton hump).
Computed tomography angiography in a young man who experienced acute chest pain and shortness of breath after a transcontinental flight. This image demonstrates a clot in the anterior segmental artery in the left upper lung (LA2) and a clot in the anterior segmental artery in the right upper lung (RA2).
Computed tomography angiogram in a 55-year-old man with possible pulmonary embolism. This image was obtained at the level of the lower lobes and shows perivascular segmental enlarged lymph nodes as well as prominent extraluminal soft tissue interposed between the artery and the bronchus.
Computed tomography venograms in a 65-year-old man with possible pulmonary embolism. This image shows acute deep venous thrombosis with intraluminal filling defects in the bilateral superficial femoral veins.
The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
A spiral CT scan shows thrombus in bilateral main pulmonary arteries.
CT scan of the same chest depicted in Image 18. Courtesy of Justin Wong, MD.
Longitudinal ultrasound image of partially recanalized thrombus in the femoral vein at mid thigh.
Sequential images demonstrate treatment of iliofemoral deep venous thrombosis due to May-Thurner (Cockett) syndrome. Far left, view of the entire pelvis demonstrates iliac occlusion. Middle left, after 12 hours of catheter-directed thrombolysis, an obstruction at the left common iliac vein is evident. Middle right, after 24 hours of thrombolysis, a bandlike obstruction is seen; this is the impression made by the overlying right common iliac artery. Far left, after stent placement, image shows wide patency and rapid flow through the previously obstructed region. Note that the patient is in the prone position in all views. (Right and left are reversed.)
Lower-extremity venogram shows outlining of an acute deep venous thrombosis in the popliteal vein with contrast enhancement.
Lower-extremity venogram shows a nonocclusive chronic thrombus. The superficial femoral vein (lateral vein) has the appearance of 2 parallel veins, when in fact, it is 1 lumen containing a chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it effectively causes the venous valves to adhere in an open position, predisposing the patient to reflux in the involved segment.
Pulmonary embolus.

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Author

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director, Pulmonary Medicine General Practice Unit (F2), Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Received research grant from: Sanofi Pharmaceutical.

Coauthor(s)

Annie Harrington, MD Fellow in Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center

Annie Harrington, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians

Disclosure: Nothing to disclose.

Nader Kamangar, MD, FACP, FCCP, FCCM Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care Medicine, Vice-Chair, Department of Medicine, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: Academy of Persian Physicians, American Academy of Sleep Medicine, American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of Specialty Professors, California Sleep Society, California Thoracic Society, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, Trudeau Society of Los Angeles, World Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Judith K Amorosa, MD, FACR Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital

Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology