A 65-year-old man who is in the hospital for treatment of a community-acquired pneumonia develops severe substernal chest pain. An ECG is obtained (ECG 25A), and as a result he is brought to the catheterization laboratory.

ECG A

There is a regular rhythm at a rate of 70 bpm. There is a P wave before each QRS complex (+) with a stable PR interval (0.16 second). The P wave is positive in leads I, II, aVF, and V 4 through V 6 . This is a normal sinus rhythm. The QRS complex duration is normal (0.08 second), and there is a normal morphology and axis about 0° (positive QRS complex in lead I and biphasic in lead aVF). Noted are T waves that are symmetrical in leads V 3 through V 6 (ie, upstroke and downstroke are equal). The normal T wave is asymmetrical and has a slower upstroke and a more rapid downstroke; these are hyperacute T waves. In addition, there is slight ST-segment elevation in leads V 2 through V 4 (↑). These are the earliest ECG changes seen with an acute transmural myocardial infarction. This is attributable to the presence of local hyperkalemia. With ischemia, membrane integrity is lost because of the lack of oxygen, which results in the breakdown of and failure to resynthesize ATP. As a result of the loss of the ATP-ase–dependent Na-K pump, potassium leaks out. Because there is no blood flow into or out of the affected area, local hyperkalemia develops. Therefore, this is an early acute ST-segment elevation myocardial infarction of the anteroapical area.

ECG B

There is a relatively stable rhythm at a rate of 90 bpm. There are 2 different QRS complex morphologies. The first 10 QRS complexes are wide (0.14 second) with a morphology that resembles neither a right nor a left bundle-branch block. In addition, there is an indeterminate axis between −90° and ±180° (negative QRS complexes in leads I and aVF). When there is a wide QRS complex, the presence of an indeterminate axis indicates direct myocardial activation, as occurs with a ventricular complex, a paced complex, or a preexcited complex (Wolff-Parkinson-White pattern). There are no P waves or pacing stimuli seen before or after any of these QRS complexes; thus these are ventricular in origin. There is a P wave (+) before the 10th QRS complex (^; PR interval=0.12 second), and this complex has a slightly different morphology and width (0.12 second) compared with the preceding wide QRS complexes. Complexes 11 to 13 have a different morphology. They have a normal duration (0.08 second) and morphology. There is a P wave before each of these QRS complexes (*) with a stable PR interval (0.16 second). Complex 10 (^) is a fusion complex, representing an impulse coming from the atria and through the AV node fusing with an impulse generated by the ventricular myocardium. The last QRS complex is slightly wider and has a different morphology (▲). Although there is a P wave before this complex (↓), the PR interval is shorter (0.14 second) than the conducted QRS complex; this is also a fusion complex. Therefore, the wide QRS complex rhythm is an accelerated idioventricular rhythm. It appears that as there is a slight increase in the sinus rate there is fusion and then capture, resulting in a sinus rhythm with captured complexes. With a slight slowing of the sinus rate, there is again a fusion complex, and likely there will be a recurrence of the idioventricular rhythm. An accelerated idioventricular rhythm is often a reperfusion arrhythmia, seen after therapy with a thrombolytic agent or percutaneous intervention.

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