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!

The rhythm includes a short burst of narrow-complex tachycardia at 150/minute certainly capable of producing symptoms of palpitations.

Portion of lead II rhythm strip with section of tachycardia

Notice that the 3rd complex of this rhythm strip is a typical PAC with the early P wave slightly altering the T wave of the 2nd complex. What follows is a regular narrow-complex tachycardia at 150/minute with an inverted P-wave preceding each QRS complex. The rate of 150/minute raises the consideration of atrial flutter with 2:1 conduction, but in the lead II rhythm strip there is no indication of flutter waves at a rate of 300/minute. The regular, deeply-inverted P waves in lead II suggest an ectopic rhythm, and thus this short run of tachycardia is an ectopic tachycardia.

The rhythm is irregularly irregular with a wide-complex QRS – atrial fibrillation with aberrancy, pre-existing bundle, or conduction down a bypass tract of Wolfe-Parkinson-White syndrome. [see EKG Discussion regarding the differential of tachycardias on this website]

This rhythm is fairly uncommon but very important to recognize. Two features of this tachycardia strongly suggests involvement of a bypass tract – 1) the extremely rapid rate with R-R intervals at a rate of 300/minute or more, and 2) the varying morphology of the QRS complexes.

Treatment of this rhythm depends on the stability of the patient. If unstable, electrical cardioversion is always the right answer. This may require proceeding with defibrillation as the rapid complexes may not allow synchronized cardioversion.

Medical management is precarious because typical options for atrial fibrillation may cause deterioration of the rhythm causing ventricular fibrillation. Any medication that causes AV node blocking will increase conduction down the bypass tract often precipitating v. fib. So, avoid:

Adenosine
Beta-blockers
Calcium-channel blockers
Digoxin

Amiodarone has had a controversial recent history, with removal from the 2010 ACLS recommendation following multiple case reports of deterioration due to precipitation of ventricular fib. More recently expert opinions again endorse the use of amiodarone. Another acceptable alternative, and the board exam answer, is procainamide.

The clue to this rhythm lies within the compensatory pause following the PVC at the end of the tracing. Notice a P-wave with a significant 1° AV block (PR of 400msec) – a complex that has actually been masquerading as a T-wave in the remaining EKG. Without this opportune advantage one might easily interpret the rhythm as junctional (absence of P-waves) with a prolonged QT interval.

It pays to carefully scrutinize every part of the 12-lead EKG and the rhythm strip. As in this case it can truly alter the interpretation.

The differential diagnosis of conditions that produce inverted T waves is worth reviewing. It includes more than ischemia and subendocardial infarction!

Differential of T-wave inversion
1° T-wave changes
Normal variants, like juvenile T-wave pattern
CNS events (can be impressive, diffuse, and deep)
Takotsubo cardiomyopathy
Coronary vasospasm
2° T-wave changes
Bundle branch blocks
WPW pre-excitation
Ventricular pacing (memory T-waves)
Acute pulmonary embolism (especially V1-4)

This woman presented with chest pain and shortness of breath after the stressful argument with her daughter. She was taken to the cath lab which revealed clean coronary arteries but left ventricular apical ballooning – Takotsubo cardiomyopathy.

From the differential diagnosis, there are really only four things that can produce such striking, deeply inverted T waves: coronary vasopspasm, subendocardial ischemia, CNS events (stroke or subarachnoid hemorrhage), and Takotsubo cardiomyopathy.

Hayden GE, Brady WJ, Perron AD, et al. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. Am J Emerg Med 20:252, 2002.

Prasad A, Lerman A, Rihad CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 155:408, 2008.

The rhythm is sinus with an alternating QRS complex morphology – every other QRS is wide with a LBBB morphology. Further evaluation of the wide QRS complex also reveals a short PR interval – this is Wolff-Parkinson-White syndrome with a bypass tract that conducts intermittently. Thus it is a great comparison of a normal AV node conducted complex with the altered complex of Wolff-Parkinson-White (a “fusion” of AV node-His-Purkinje conduction with abnormal ventricular depolarization via a bypass tract).

The trick to this EKG is to recognize WPW as the cause for the wide complex beats – it might be tempting to diagnose bigeminy, or even, intermittent LBBB.

EKG interpretation:
Irregularly irregular narrow complex at 115/minute – ? rhythm
Axis – normal
Intervals – there is a P wave in many R-R spaces, of varying PR
No chamber enlargement, ischemia or infarct patterns

There are two irregularly irregular rhythms – atrial fibrillation and multifocal atrial tachycardia (MAT). MAT is defined as >3 ectopic atrial foci with P waves of differing P wave morphology and differing PR intervals. The R-R intervals are necessarily irregularly irregular. In many of the R-R intervals in this lead II rhythm strip, notice that the T wave is “deformed” by the addition of a P wave.

MAT is often seen in COPD, especially during exacerbation. Other causes are any critical illness, especially with depletion of electrolytes and cations. There is no specific treatment of MAT – first, remedy any underlying process like hypoxia, exacerbation of COPD, fluid status.

And remember this sneaky rhythm when atrial fibrillation with very rapid ventricular rate doesn’t respond to usual treatment for a fib – it may be misdiagnosed multifocal atrial tachycardia (MAT)!