COPD alone (Lesser et al 1992). Other overlapping features of COPD and PE on exam include tachypnea, tachycardia, and fever. Cough productive of sputum is less common in acute PE and more indicative of COPD exacerbation (Tillie-Leblond et al 2006; McGee 2001; Pineda et al 2001). Consequently, sub-acute PE may be overshadowed by or confound a bona ﬁde COPD exacerbation, escaping suspicion for diagnosis on physical exam. Chest X-ray Findings supportive of COPD on CXR include increased lung volumes and hyperinﬂation. The presence of diffusely diminished lung markings suggests obliteration of supportive bronchial structures and correlates well with COPD; how- ever, the CXR is otherwise nonspeciﬁc. Stein’s evaluation of chest radiographs in 117 patients diagnosed with PE and no prior lung disease found 68% had nonspeciﬁc parenchymal abnormalities. The majority of ﬁnd- ings were atelectasis and small pleural effusions (Stein et al 1991). Classic features of PE on CXR, such as Westermark’s sign or Hampton’s hump, had poor sensitivity in the setting of COPD (Sharma and Sasahara 1975). The CXR is of value for the evaluation of other acute causes of dyspnea including pneumonia, pleural effusion, pulmonary edema, or pneumothorax. The acutely dyspneic patient with minimal parenchymal ﬁndings points towards vascular or bronchial etiologies such as asthma, COPD exacerbation, or thromboembolic disease. Arterial blood gas Arterial blood gas ﬁndings in COPD are nonspeciﬁc, but are characterized by hypoxemia and hypercapnea, with elevated bicarbonate indicative of chronic metabolic correction of respiratory acidosis. In the acute setting, hypercapnea may be increased secondary to worsened deadspace ventilation and ventilation/perfusion (V/Q) mismatch caused by increased mucus production, bronchial constriction, or worsened alveo- lar-capillary interface destruction with disease progression. With pulmonary embolism, Stein and colleagues (1991) found the PaO2 to be less than 80 mmHg in 74% of patients without underlying pulmonary disease. The A–a gradient was greater than 20 mmHg in 76% of patients (Stein et al 1991). PaCO2 was commonly lower due to tachypnea, except in the presence of increased deadspace ventilation. In a case report of 3 patients with known COPD complicated by PE, Lipmann and Fein (1981) suggested a drop in PaCO2 of 10mmHg or more in otherwise previously hypercapneic COPD patients as indicative of thromboembolism. The mean increase in International Journal of COPD 2008:3(2) COPD and PE A–a gradient was 20 (±13) mmHg with poor response to conventional bronchodilator therapy (Lippmann and Fein 1981). Tillie-Leblond and colleagues (2006) supported the ﬁndings of Lipmann and Fein with a drop in PaCO2 of 5 mmHg or more as statistically indicative of concomitant PE (Tillie-Leblond et al 2006). On the other hand, Lesser and col- leagues (1992) reported 108 patients presenting with a history of COPD and newly diagnosed PE to have no difference in the A–a gradient or reduction in PaCO2, despite prior hypercapnea on arterial blood gas (Lesser et al 1992). Hypoxemia remained a shared blood gas ﬁnding nonspeciﬁc to either disease. The correction of hypoxemia with oxygen or positive pressure ﬂow may support the diagnosis of COPD, while major pulmonary embolism with intrapulmonary or intracardiac shunt may be resistant to correction (Pineda et al 2001). D-dimer In conjunction with pretest probability, the D-dimer is the preferred diagnostic tool in the outpatient setting and emer- gency department for DVT and PE. A low pretest probability and negative D-dimer effectively excludes thromboembolic disease. Work by Hartmann and colleagues (2000) found similar distribution of D-dimer results in 313 patients with and without COPD, suggesting COPD had no inﬂuence on the diagnostic accuracy of the test for thromboembolic dis- ease. This also suggested there was no increased prevalence of elevated D-dimer with COPD exacerbation. Sohn and colleagues (2006) found the combination of a low pretest probability and negative D-dimer among subsets of patients with increased age, prior malignancy, heart failure, or COPD sufﬁcient in ruling out PE in 98% of all-comers. Missed diagnoses were most prevalent among subsets of patients with known malignancy (Sohn et al 2006). A systematic review found a negative D-dimer to be as diagnostically useful as a normal lung perfusion scan or negative duplex ultrasonography in the setting of low pretest probability (Stein et al 2004). B-type natriuretic peptide B-type natriuretic peptide may be elevated in any disorder, causing right ventricular dilatation including acute PE, COPD, pulmonary hypertension with corpulmonale, or left-to-right shunting, causing ventricular overload. Such elevations are usually smaller than those appreciated in left ventricular heart failure and negligible or absent in uncom- plicated COPD exacerbation (Bando et al 1999). In the setting of PE, brain natriuretic peptide (BNP) has served more as a prognostic tool relating severity of 279