YES! This is an acute anterolateral STEMI occurring with a RBBB. Unlike its cousin, a LBBB, a RBBB does not obscure ischemia and infarct patterns. Again, it is important to be familiar with some expected repolarization changes with a RBBB (essentially T-wave inversion in V1-3, leads with the most obvious depolarization changes).

This EKG is impressive for the ST-segment elevation in leads V2-4, including “giant R waves” in V4-5, the earliest signs of STEMI. There does seem to be subtle, probably early, reciprocal ST-segment depression in the inferior leads, supporting the diagnosis of STEMI.

If you were questioning, or not embracing, this unique and fairly rare EKG of a RBBB with an acute STEMI, look at the second EMS transmission that occurred 10 minutes later…

ST-segment elevation in V2-5, as well as ST- and T-wave changes in I, aVL and V6; notice also the T-wave inversion in III, a reciprocal change to the anterior-lateral infarct.

There are two premature beats seen in this rhythm tracing (#4 and #7). Although they appear similar in morphology to supraventricular beats, both are PVCs by criteria that define the difference between PVC and PAC.

Both beats are followed by a pause – in these beats, a compensatory pause, which implies that the next P wave was undisturbed by the premature beat. Another way of saying the same thing is that the sinus P waves “march through” the premature beat, or that the sinus metronome marked by regular P and QRS complexes is undisturbed. Each of these descriptions say the same thing – these premature beats are both PVCs!

This bradycardic rhythm is wide-complex and regular at 22/minute. There are no discernible P waves. Without further information this rhythm is best described as a slow junctional rhythm.

However, we do have more information. This young woman has SLE with renal failure requiring dialysis. Even if she has not missed a dialysis session, one must assume this bradycardic wide-complex rhythm is due to hyperkalemia.

Hyperkalemia has several predictable effects on the EKG. The P-wave, QRS-complex, and T-wave are all targets of this “poison” that effects normal depolarization and repolarization. These effects occur in a predictable sequence. The first sign seen is increased amplitude of the T waves – a peaked, narrow-based T wave. As the level of potassium continues to rise, the next changes are prolongation of the QRS complex and then diminution of the P wave. With further QRS prolongation, the EKG complex begins to resemble the pre-terminal sin wave of critically severe hyperkalemia.

After treatment with Ca++ gluconate

This EKG is important for emergency medicine providers. It is commonly seen in presentations of chest pain, and it is one of the most difficult of EKG patterns for ED physicians to interpret definitively.

Let’s return to a systematic review of the EKG…
Rate 60/minute
Rhythm Sinus rhythm with no ectopy
Axis Leftward axis at -30°
Intervals PR – 160msec, QRS – 110msec (slightly prolonged), QTc – normal
Chamber enlargement – LVH voltage because R≥12mm in aVL
Ischemia & Infarct – slight ST-elevation V1-3

While ST-segment elevation in the anterior leads may be the most concerning feature of this EKG on a cursory evaluation, there may be an alternative, and more appropriate, explanation.

In this EKG we have LVH by voltage criteria, plus several factors that suggest the diagnosis of severe LVH. These include:
1. ST-depression/T inversion in lateral leads – a “strain pattern”
2. left axis deviation
3. prolongation of the QRS complex (delayed depolarization due to increased size of the ventricle)
4. repolarization changes, including ST-elevation in anterior leads
As LVH becomes more severe, the changes on the EKG begin to resemble those of LBBB. Notice, however, that normal small Q waves (“septal Q waves”) remain in the lateral leads (I, aVL, V5-6). These Q waves signify that the LBBB is still functioning and provides depolarization of the septum!

Sometimes it takes some skill and confidence to NOT call a consultant!