How do we put these observations together? Although the exact mechanism is unknown, we would like to postulate that the initial trigger for most COPD exacerbations is an infection. The accompanying upregulation of systemic inflammation, oxidative stress, and/or heightened output of the autonomic neurohumoral system may result in cardiac failure and fluid shifts into the lung. Depending on the gravity of the situation, pulmonary edema, alveolar flooding, and peribronchiolar cuffing may develop during an acute COPD exacerbation, leading to ventilation/perfusion mismatch, impaired gas exchange, and increased work of breathing. Particularly when the changes are mild, cardiac failure during acute COPD exacerbations can be difficult to diagnose clinically, as symptoms of increased dyspnea, cough, and wheezing are uniformly present in exacerbations. Even careful clinical examination by experienced physicians looking for the third heart sound may not be rewarded. Routine chest radiographs to detect pulmonary venous congestion in patients with COPD may be insensitive.10 Despite these challenges, if our postulate is correct, it would be important to make the correct diagnosis of heart failure, so that we can intervene with pharmacologic agents to treat not only the lung attack but also the cardiac failure. So, how can we diagnose heart failure in patients with COPD during a lung attack? A high index of suspicion followed by a careful cardiac assessment is needed throughout the episode of exacerbation. Learned societies, such as the American College of Cardiology, in collaboration with the American Heart Association, have advocated the use of biomarkers, such as BNP or pro-BNP, and echocardiography for ejection fraction as diagnostic aids for heart failure.2 In the technically challenging case, nuclear medicine scan, cardiac MRI, and cardiac catheterization may be needed.