For the past three weeks, a 56-year-old man has experienced shortness of breath, fever, and night sweats. During the past two days, he has had a nonproductive cough that now causes left chest wall discomfort. He denies hemoptysis or hematemesis.

Medical history is remarkable for an ischemic cardiomyopathy, congestive heart failure (New York Heart Association functional class II), diffuse coronary artery disease, paroxysmal atrial fibrillation, and hyperlipidemia. The patient’s most recent left ventricular ejection fraction was 38%. He has a history of chronic obstructive pulmonary disease and was hospitalized last year with bilateral pulmonary emboli. He is also obese and has obstructive sleep apnea. 

Surgical history includes three-vessel coronary artery bypass graft surgery (left internal mammary artery to left anterior descending artery, reverse saphenous venous grafts to the second obtuse marginal artery and to the posterior descending artery) five years ago. Social history is notable for tobacco use (half a pack per day for 30 years) and moderate alcohol use.

The patient’s medication list includes aspirin, digoxin, amiodarone, metoprolol, hydralazine, isosorbide mononitrate, metolazone, potassium chloride, spironolactone, and pravastatin. He is allergic to ACE inhibitors and refuses to take warfarin or low-molecular-weight heparin.

Vital statistics include a height of 5’4”; weight, 211 lb; blood pressure, 108/88 mm Hg; temperature, 38.4°C; respiratory rate, 22 breaths/min; and O2 saturation, 94% on 2 L of oxygen. The physical examination reveals an anxious, disheveled man in moderate distress. Pulmonary examination is notable for rales in both bases and consolidation in the left upper lung fields. The neck veins are elevated to 8 cm, and there is a grade III/VI systolic murmur at the left sternal border. The extremities demonstrate 2+ pitting edema bilaterally.

A chest x-ray shows a left upper lobe opacity with numerous ill-defined (ground glass) nodules bilaterally. An ECG shows the following: a ventricular rate of 83 beats/min; QRS duration, 108 ms; QT/QTc interval, 398/467 ms; R axis, –45°; and T axis, 146°. A PR interval is not reported. What is your interpretation of this ECG?

ANSWER

The ECG shows atrial flutter with a controlled rate of 83 beats/min. Typical (type I or isthmus-dependent) atrial flutter is characterized by the absence of P waves, biphasic flutter (F) waves with a range between 240 and 340 beats/min, and F waves with an axis of ± 90° that are usually prominently negative in leads II, III, and aVF. The F wave–to–R wave relationship in this case is variable (2:1, 3:1) due to respiratory rate and the presence of AV nodal blocking agents.

Recall that the patient is taking amiodarone and digoxin, both of which can control the ventricular rate during a supraventricular tachycardia. ST- and T-wave abnormalities are consistent with digitalis effect. Finally, the QT interval is prolonged; however, this is probably due once again to amiodarone.

The patient has a history of paroxysmal atrial fibrillation. The onset of atrial flutter (which subsequently converted to atrial fibrillation) may have been precipitated by the physiologic stress of Aspergillus pneumonia, which was diagnosed through additional testing.