population groups, and increased combined morbidity and mortality is similar to that of COPD and heart failure, or COPD and myocardial infarction (Incalzi et al 1997; Groe- newegan et al 2003; Lee et al 2003; Holguin et al 2005; Huiart et al 2005; Sin et al 2006). Lesser and Hartmann’s work conﬁrmed that PE does not appear to favor COPD (Lesser et al 1992; Hartmann et al 2000). Nonetheless, morbidity and mortality is increased at one year and while diagnosis is difﬁcult, an appreciation of the known morbidity of untreated thromboembolic disease makes acute detection of PE in the setting of COPD exacerbation important for improving clinical outcomes. Findings of PE prevalence in COPD are also helpful in the clinical setting when attempting to make evidence-based decisions for diagnosis and management. The current litera- ture suggests a one in four prevalence of PE in patients with atypical COPD exacerbation (Mispelaere et al 2002; Tillie- Leblond et al 2006). Twenty percent prevalence translates to at least 20% pretest probability in this patient group, which can be in addition to probabilities obtained by other clinical decision criteria, such as Wells or the Geneva score. The presumptive prevalence of PE in all COPD patients with infectious features is approximately 3% as found by Rutschmann and colleagues (2007) while DVT prevalence is estimated at 10% among all COPD patients according to Ambrosetti and colleagues (2003). Since DVT and PE are on the same spectrum of thromboembolic disease, accounting for DVT will increase the pretest probability of thromboem- bolic disease in those presenting with atypical exacerbations to a baseline of 30%, and those with typical features to 13%. Likelihood ratios for speciﬁc diagnostic tests can now be applied to obtain posttest probabilities for diagnosis of PE. As an example, Hartmann and colleagues (2000) found that V/Q perfusion scanning in patients with COPD yielded a 79% speciﬁcity and 92% sensitivity when the test was interpreted as high probability, translating to a positive likelihood ratio of 4.38 {sensitivity/(1 – speciﬁcity)}. Patients with atypical COPD exacerbation whom underwent V/Q perfusion scan- ning would have a posttest probability of 65%, while those with typical exacerbations would yield a posttest probability of 40%, doubling in both cases our initial pretest probability, but not enough to rule in a positive diagnosis. This conﬁrms again the ﬁnding that perfusion scanning, even when inter- preted as high probability for PE in the setting of COPD exacerbation, is a poor diagnostic choice in either patient population when clinical suspicion is low. In review, very little on physical exam delineates COPD and PE in patients with acute respiratory distress. Findings International Journal of COPD 2008:3(2) COPD and PE suggestive of underlying thromboembolic disease include dyspnea, absence of fever or sputum change, and tachycar- dia. Historical features such as prior DVT or PE, malignancy or decreased mobility are helpful and contributory to pre- test probability. Hypoxemia is notable and nondiagnostic, with rales and wheezes overlapping both diseases. While suspicion of PE in patients presenting with noninfectious COPD exacerbation is intuitive, further cohort studies look- ing directly at the presence of PE in patients with typical infectious features are needed to reveal further underlying prevalence. Laboratory and imaging studies in conjunction with clini- cal features contribute to pretest probability for PE. Though the presence of mildly elevated troponin and BNP in the setting of typical COPD exacerbation may provide clues as to underlying embolic disease, these values may be con- founded by right or left ventricular failure and acute ischemia, all possible sequelae of advanced obstructive lung disease. Appropriate echocardiography and serial troponins to rule out ischemia would be warranted. Echocardiography may help delineate right vs. left ventricular dysfunction and diastolic failure contributing to an elevated BNP. The arterial blood gas is nonspeciﬁc and improved hypercapnea or hypoxemia with treatment is helpful in supporting uncomplicated COPD. A decrease in PaCO2 on initial presentation in the setting of prior hypercapnea with known COPD has been advocated as an indicator of underlying thromboembolism (Lippmann and Fein 1981; Tillie-Leblond et al 2006). It appears that patients with COPD develop DVT at rates similar to patients in a medical intensive care unit (Pomper and Luchman 1991; Kummer 1998; Ambrosetti et al 2003). Knowing this, and the fact that D-dimer distribution is similar in patients with and without COPD, makes it a useful test in conjunction with low pretest probability for ruling out thromboembolism. While management does not differ in sub-massive PE and DVT, PE remains more difﬁcult to diagnose, and obtaining lower extremity Doppler ultrasound may clinch thromboembolic diagnosis faster than more extensive studies. V/Q scans are the default imaging study in the setting of acute or chronic kidney disease, but are diminished by increased frequency of nondiagnostic intermediate probability ﬁndings with COPD. Spiral CT has delineated similar prevalence of PE in patients with and without COPD, suggesting equivalent sensitivity of the test in both populations. Figure 1 suggests a diagnostic algorithm for respiratory decompensation in patients with known COPD. The approach utilizes clinical prediction criteria for PE, such as the Wells criteria or Geneva score, to obtain a pretest probability and 281