Scenario: The rhythm strip below was printed from the bedside monitor of a 71-year-old man admitted to the intensive care unit for hypoxemic respiratory failure, fluid overload, and septic shock. The patient’s history includes coronary artery disease, hypertension, diabetes, paroxysmal atrial fibrillation after successful cardioversion (prescribed at-home apixaban), alcoholic cirrhosis, heart failure (ejection fraction, 50%), and chronic obstructive pulmonary disease (COPD). When this electrocardiogram (ECG) was generated, his blood pressure was 119/63 mm Hg, heart rate was 95/min, and oxygen saturation was 97% while receiving mechanical ventilation with a fraction of inspired oxygen of 0.8. The nurse noted that the rhythm looked like either a heart block or multifocal atrial tachycardia (MAT) and decided to record a 12-lead ECG (see next page). What is your interpretation?Atrial flutter (AFL) with 3:1 conduction with a ventricular rate of ~100/min and right bundle branch block (RBBB).Atrial flutter is common in patients with hypertension, diabetes, COPD, alcohol misuse, and atrial fibrillation (risk factors in this scenario) and is typically initiated or terminated by a premature complex (atrial or ventricular) or rapid atrial pacing. When a premature stimulus excites an area in the atrium, it travels in a single stable reentry circuit (either clockwise or counterclockwise) that is long enough to allow initially depolarized myocardial tissue to recover and then be capable of depolarizing again owing to the reentered stimulus. This mechanism can be seen in this example, particularly in leads III and aVF, as regular, uniform flutter waves (or F waves). The typical atrial rate for AFL is 200-350/min and is characterized by the absence of an atrial diastolic interval, as is seen in sinus rhythm.The rhythm strip displayed only leads II and V1 and showed upright P waves in V1 with various PR intervals, which could be confused with third-degree heart block. In lead II, the P wave is negative, suggesting a junctional rhythm with retrograde conduction of the atria. However, the sharp negative P wave in lead II raises the suspicion of AFL, which was confirmed on the 12-lead ECG. The unique feature of F waves (ie, “sawtooth” pattern) associated with AFL can be seen clearly in leads III and aVF. The F waves that are negative in the inferior leads but positive in V1 indicate the AFL is moving in a counterclockwise direction, which is most common (~75% of cases). The flutter waves should not be confused with MAT, which typically exhibits at least 3 different P-wave morphologies and is irregular because of multiple focal sites of atrial impulse formation. In contrast, AFL is a self-sustaining macroreentrant atrial arrhythmia without focal sites of impulse formation. The ventricular rate in AFL is usually a multiple of the FF interval. In this case, the F waves occur at a rate of 300/min and result in a ventricular rate of ~100/min and can be slightly irregular.Left ventricular hypertrophy in the presence of RBBB can be examined by using an S wave >2 mm in V1 or an R wave >15 mm in V5 or V6, both of which are absent on this ECG.Clinical management is focused on converting AFL to normal sinus rhythm, which will reduce the heart rate and prevent embolic stroke. In this case, the cardiology service was consulted, and ibutilide, an antiarrhythmic, was prescribed with a return to normal sinus rhythm. The patient’s anticoagulant was changed to clopidogrel, an antiplatelet. Given this patient’s underlying risk factors and the risk of prolonging QT with ibutilide, the QT interval should be closely monitored to prevent torsades de pointes. The patient's hospital course was complicated by continued respiratory distress and acute alcohol withdrawal. He was later transferred to the step-down unit.