A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB).

A patient arrived after PEA arrest, with ROSC after intubation and chest compressions.

Here is the initial 12-lead ECG:

What is the appropriate therapy?

This ECG is all but diagnostic of hyperkalemia.  There is an irregular, slow, wide complex rhythm.  Is it ventricular escape? (no, because it is irregular and there appear to be conduced P-waves).  Or atrial fib with slow ventricular response? (no, because it is irregular and there appear to be conducted P-waves).

Because you can see some conducted atrial activity in lead II across the bottom, you know that it is of supraventricular origin.  So then it is clear that there is Right Bundle branch block (RBBB).  However, it is extremely wide (the computer measured it at 193 ms, and I think this is correct), much wider than RBBB should be.  Also, you can see peaking of the T-waves in many leads.


The physicians did not recognize this, but they did think to give calcium empirically.  The K returned at 7.1 mEq/L and complete therapy for hyperK was given.

Here is the ECG after therapy:

Probable junctional rhythm
RBBB
QRS of 133 ms by computer (looks correct)

See more similar cases here:
https://hqmeded-ecg.blogspot.com/2018/04/is-this-just-right-bundle-branch-block.html


QRS duration in RBBB and LBBB
RBBB by definition has a long QRS (at least 120 ms).  But very few are greater than 190 ms.  Literature on this is somewhat hard to find, but in this study of patients with RBBB and Acute MI, only 2% of patients with pre-existing RBBB had a QRS duration greater than 200 ms.  This study only reported durations in 10 ms intervals up to 150 ms, but one might extrapolate from it that approximately 10% of patients with baseline RBBB have a QRS duration greater than 160 ms.  193 ms would be quite unusual.

The point of this is that if you see BBB with a very long QRS, you must suspect hyperkalemia or sodium channel blockade (e.g, flecainide).  Then of course the peaked T-waves should tip you off.   Unless a patient has severe hypercalcemia (this should be evident by a short QT on the ECG as seen at the bottom of this post), or severe hyperphosphatemia (which is very unusual), treatment with calcium is harmless if you read an ECG falsely positive for hyperkalemia.

So don't wait for the laboratory K or you might be resuscitating a cardiac arrest (see the case at this post with ECGs #3 and #4 of this post).

How about LBBB?

In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms. 



Hypercalcemia (courtesy of K. Wang)

Notice the very short QT interval, and very short ST segment

https://hqmeded-ecg.blogspot.com/2018/04/is-this-just-right-bundle-branch-block.html

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Comment by KEN GRAUER, MD (2/28/2019):

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The important theme of recognizing the many “faces” of Hyperkalemia is wonderfully illustrated in this case by Dr. Smith. I’d like to amplify some of the points highlighted by Dr. Smith — and explore some of them in further detail.

• POINT #1: IF the rhythm is supraventricular, but the QRS complex is overly wide — Think of Hyperkalemia! It’s too easy to overlook this diagnosis if you are not actively considering it as a possibility each time you see a supraventricular rhythm that appears to be wider-than-you-think-it-should-be.
• POINT #2: Once you consider the possibility of Hyperkalemia — Look extra carefully at the T waves. They may not be as tall or “classically peaked” with narrow T wave base as is common in earlier stages of hyperkalemia (ie, when the QRS complex is still narrow) — but it is easier to appreciate T waves that are probably-more-peaked-than-they-should-be IF you are looking for them.
• POINT #3: Severe Hyperkalemia sometimes results in T wave inversion rather than peaked T waves! This may be in only a few leads — as opposed to the positively peaked T waves that tend to be more generalized. The T wave inversion I have seen with severe hyperkalemia is often a near “mirror-image” of the positive T wave peaking (ie, negatively peaked T waves).
• POINT #4: Severe Hyperkalemia commonly results in reduced P wave amplitude. Ultimately, there may be a sinoventricular rhythm — in which despite the disappearance of P waves on the ECG, conduction from the SA node through the atria and ventricles continues. This may result in the paradox that despite a regular wide QRS rhythm without P waves — sinus mechanism may be preserved.
• POINT #5: Severe Hyperkalemia commonly results in bradycardia (which may be severe) — and all kinds of unusual conduction blocks. Many of these arrhythmias defy logical interpretation. That said, precise determination of the rhythm is not clinically important — because treatment of the severe hyperkalemia is often all that is needed to restore a normal sinus rhythm.
• POINT #6: In addition to marked QRS widening — severe Hyperkalemia may distort QRS morphology, including marked axis deviation.
• POINT #7: You have NO IDEA about what the underlying QRS complex and ST-T wave really look like — until you correct the severe Hyperkalemia. For example, preexisting severe diffuse ST depression might attenuate diffusely tall and peaked T waves from severe hyperkalemia — resulting in a deceptively benign picture. Only after serum K+ has been normalized might it become apparent that there was preexisting severe ischemia.

For clarity — I’ve put the 2 ECGs in this case together to illustrate the above points (Figure-1):

Figure-1: The 2 ECGs in this case (See text). 

I think it could be EASY to overlook the etiology of the TOP tracing ( = ECG #1) in Figure-1. That’s because the QRS complex does not look so wide in many of the leads! The problem arises because of the difficulty of knowing where the QRS complex ends ...

• The 2 KEY leads in ECG #1 are leads V1 and V2. These are the 2 leads on this 12-lead tracing for which there is NO doubt about where the QRS begins and ends. I have drawn vertical RED lines to show where the QRS complex ends in simultaneously-obtained lead V3, as well as in the long lead II rhythm strip at the bottom of the tracing.
• Using this exact QRS duration that I measured with these vertical RED lines — I’ve drawn in vertical BLUE lines in the remaining leads on this tracing to illustrate the limits of the QRS complex. So, rather than profound ST segment depression in leads V4, V5 and V6 — this patient with severe hyperkalemia manifests a bizarre QRS morphology.
• And once we realize how wide and bizarre the QRS complex in ECG #1 really is (which means we need to be considering hyperkalemia) — it becomes easier to appreciate that although wide in base, the T waves in leads I, II, aVL, aVF, and V3-thru-V6 do look pointed ...

What is the Rhythm in ECG #1?

The long lead II rhythm strip at the bottom of ECG #1 shows the 9 beats in this tracing to be irregular. This is not sinus rhythm — because there is no upright P wave in lead II. But consistent atrial activity in the form of a tiny amplitude negative P wave is present in front of 5 of the beats (RED arrows).

• We know that these non-sinus P waves are conducting — because the PR interval preceding beats #4, 5, 7, 8 and 9 is constant! Therefore, despite marked QRS widening — this is a supraventricular rhythm.
• Beat #6 is a junctional escape beat — because it ends a short pause, and manifests QRS morphology identical to that of the atrial-conducted beats. No preceding P wave is seen in any of the simultaneously-recorded leads (ie, No P waves precedes beat #6 in leads V1, V2, V3 or in the long lead II).
• No P wave precedes beats #1 and #3 — so these are presumably also junctional beats.
• I’m not sure what beat #2 is. It occurs earlier-than-expected, but the large preceding T wave may (or may not) be hiding atrial activity.
• BOTTOM LINE: This is an unusual rhythm. That said, the important point was highlighted by Dr. Smith — namely, that despite marked QRS widening and definite irregularity — the fact that a number of P waves are conducting (even though not of sinus etiology) confirms this to be a supraventricular rhythm.
• Clinically: It does not matter what this rhythm is — because it will probably convert to sinus rhythm once hyperkalemia is corrected and the patient has stabilized.

What do We See in ECG #2?

As per Dr. Smith — duration of the QRS complex has decreased significantly in ECG #2. QRS morphology now looks much more typical for RBBB (rsR’ complex in lead V1; narrow R wave with wide terminal S waves in leads I and V6). But now there is no atrial activity at all ...

• Presumably the rhythm in ECG #2 is junctional, with underlying RBBB. That said, given the clinical scenario (ie, extended cardiac arrest with PEA prior to ROSC) — I think it quite possible that there was significant associated acidosis, which may well have resulted in even more severe hyperkalemia than the initial lab value of 7.1 mEq/L suggests (? depending on when labs were drawn with respect to the ongoing resuscitation). There can be a lag between laboratory electrolyte correction and normalization of the cardiac rhythm — so — Could this be a sinoventricular rhythm?
• I think it is interesting to compare QRS morphology in ECG #1 and ECG #2. Isn’t the initial part of the QRS complex almost identical in both tracings?
• There was clearly more of a rightward axis in ECG #1. On occasion, I have seen bizarre axis deviations with marked hyperkalemia — including an all negative complex in lead I that totally resolved after correction of the electrolyte disturbance.
• We are not told what the final serum K+ value was. Almost regardless of what it was — I suspect there has not yet been true stabilization of this patient at the time ECG #2 was done — as T waves in ECG #2 still appear more prominent and more-peaked-than-they-should-be with simple RBBB. In addition — the T wave inversion in leads V1 and V2 of ECG #2 is deeper and more pointed than typical secondary ST-T wave changes of RBBB. Although this could be ischemic — it might also reflect residual ST-T wave effect from resolving severe electrolyte disturbance. We won’t know the answer to this, until more time has passed, and until an additional ECG or two is done.
• Finding a prior baseline tracing on this patient might help to resolve some of the questions I just raised in the preceding bullet point ...

Our THANKS to Dr. Smith for presenting this interesting case.