Scenario: This 12-lead electrocardiogram (ECG) was obtained in a 72-year-old man arriving in the emergency department with shortness of breath and dizziness. Prior medical history includes myocardial infarction (MI), heart failure (HF), chronic obstructive pulmonary disease (COPD), diabetes (type 2), and paroxysmal atrial fibrillation. Current prescribed medications include a β-blocker, aspirin, angiotensin-converting enzyme inhibitor, furosemide, and diltiazem. His blood pressure was 98/50 mm Hg, respiratory rate 24/min, and oxygen saturation as measured by pulse oximetry (Spo2) was 92% on 3 L of oxygen. He was most comfortable sitting up with his arms on the bedside table, and said he felt better after 40 mg of furosemide was administered intravenously.Sinus rhythm with premature atrial complexes (PACs), possible right and left atrial enlargement, prior inferior wall MI (q waves in leads III and aVF), incomplete left intraventricular conduction defect (fQRS waves), left ventricular hypertrophy, and ST-segment and T-wave abnormalities may suggest anterolateral ischemia.Although the underlying rhythm is irregular, suggesting atrial fibrillation, P waves are visible before every QRS complex; thus, this is sinus rhythm with frequent PACs. PACs are not uncommon in patients with structural heart disease and COPD, like this one. The pause after the PACs is a normal physiologic response and represents a compensatory pause associated with PACs. The ECG criterion for right atrial enlargement is a P-wave amplitude greater than 2.5 mm in leads II, III, and aVF (so-called P pulmonale) and can be seen with COPD. Left atrial enlargement is due to pressure or volume overload of the left atrium and can be assessed in V1 (biphasic P waves with negative terminal portion >40 ms long and >1 mm deep). Biatrial enlargement is consistent with this patient’s medical history (MI, HF, and left ventricular hypertrophy); however, ECG is not the reference standard method, so the diagnosis should be confirmed by echocardiography. The T-wave inversion and ST-segment depression most likely represent a “strain” pattern seen with left ventricular hypertrophy, but acute myocardial ischemia should be ruled out given the patient’s prior MI.Immediate management includes addressing the acute respiratory distress and low blood pressure, with HF exacerbation a likely source. This patient’s symptoms were somewhat relieved after the intravenous furosemide, which supports this diagnosis. Checking a venous blood sample for brain natriuretic peptide (BNP) to assess for HF, troponin to rule out myocardial ischemia, and electrolyte levels would help. A chest radiograph would be useful, as might arterial blood gas analysis, given his elevated rate of breathing and the 92% Spo2 with 3 L of oxygen. Findings on physical examination, especially lung and heart sounds, peripheral edema, and daily weight should be evaluated. Ultimately, this patient’s BNP level was 3400 ng/mL, which corroborates HF, and his troponin was negative for myocardial ischemia. He was discharged home 3 days later.