PE Detection: Role of the ABG and aA Gradient ============================================== þ From the Internet emed-l thread: -------------------------------- In a study of PE published in Circulation in 1973 (Urokinase Pulmonary Embolism Trial) the clinical and laboratory findings of those with PE was tabulated. The percent distribution of pO2 was as follows: <40 7.7% 40-49 8.5% 50-59 25.4% 60-69 32.3% 70-79 14.6% >=80 11.5% Your comment about overdiagnosing PE in the otherwise healthy young female and underdiagnosing it in the chronically ill or infirm are well taken. This was essentially the conclusion of a review article written many years ago in the Annals of Internal Medicine (Overdiagnosis and Overtreatment of Pulmonary Embolism: The Emporer May Have No Clothes 87:775;1977). How pertinant his observations are today with improvements in technology I'm not really sure however. Ultimately the physician's judgment of pre-test probability of PE looms large in terms of the final disposition of these patients. Even patients with low probability scans who CLINICALLY have a high probability of PE have a substantial risk of ultimately having one (I believe that it's about 15% for the category low probability scan--high clinical suspicion). Although I could not find my original reference for this one I did come across reference 2 below which says pretty much the same thing. (References: H. Louzon MD ------------------------------------------------------------ When Dave Overton and I did our study in 1988, we went back through 20 years of angios at a 1000 bed aggressive teaching hospital in order to get 194 patients who had pulm angios done. Of these, 1/3 did not have room air gases (probably ok - we were reamed for having a trauma CXR with a pneumo and no chest tube) about half had negative angios (you can see the numbers keep getting smaller). We found three patients (out of the 68 left) with normal A-a gradients and postive angios. One had a huge saddle embolus and a low prob V/Q...all had a PCO2>36 and PO2s of 89, 91, and 87..."this was a well done study, but used a skewed set of patients. Patients with atypical presentations and all comers, not those who already had enough suspicion to get a VQ, may have different results. A (very) large prospective study needs to be done." I thought it would be of interest to present a followup article by the same author a year later, which concluded that no single ABG value showing normoxia, normocarbia, or a normal A-a gradient, nor any combination thereof, was of benefit in ruling out a pulmonary embolism. Scary stuff. As other members of the group have previously concluded, an ABG is essentially useless in the workup of suspected pulmonary embolism. --James Li, MD [Stein PD, Goldhaber SZ, Henry JW et al. Arterial Blood Gas analysis in the Assessment of Suspected Acute Pulmonary Embolism. Chest 1996 Jan;109(1):78-81.] ABSTRACT: Conclusion: With various combinations of the PaO2 of 80 mm Hg or more, the PaCO2 of 35 mm Hg or higher, and the P(A-a)O2 gradient of 20 mm Hg or less, PE could not be excluded in more than 30% of patients with no prior cardiopulmonary disease and PE could not be excluded in more than 14% of patients with prior cardiopulmonar disease. Blood gas levels, therefore, are of insufficient discriminant value to permit exclusion of the diagnosis of PE. More on the Aa gradient: