ECG Challenge: A 67-year-old man with new-onset heart failure is seen in the hospital and is begun on therapy with an angiotensin-converting enzyme inhibitor, a β-blocker, furosemide, and spironolactone. One week later, he presents with weakness, nausea, and lightheadedness. His blood urea nitrogen and creatinine are significantly elevated to 62/2.8 in comparison with baseline 24/1.3. An ECG is obtained.
There is a regular rhythm at a rate of 50 bpm. There are no P waves seen before or after any of the QRS complexes. The QRS complex duration is very prolonged (0.26 s) (↔). The QT/QTc intervals are prolonged (600/550 ms), but are normal when the prolonged QRS complex duration is considered (440/400 ms). Because the QT interval includes the QRS complex, and the ST segment and T wave, as well, prolongation of the QRS complex duration needs to be considered when establishing the QTc interval. The amount of widening of the QRS complex that is above the normal width needs to be subtracted from the QT-interval measurement before the QT is corrected for heart rate. A QRS complex width that is >0.24 ms is a result of hyperkalemia, regardless of the etiology of the QRS complex. Also noted are hyperacute T waves that are not just tall and peaked, but more importantly are symmetrical (ie, the upstroke and downstroke are equal). In contrast, the normal T wave is asymmetrical with an upstroke that is slower than the downstroke. Although there are no P waves seen, the etiology of the QRS complex is not clear (ie, it may be sinus, atrial, junctional, or ventricular). The atria are more sensitive to the effects of hypokalemia, and, as a result, the atrial myocardium may not respond to electric stimuli, resulting in atrial asystole. Hence it is possible that this is a sinus rhythm and with the absence of atrial activity it would be termed a "sino-ventricular rhythm.
- © 2013 American Heart Association, Inc.