Thursday, February 28, 2019

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). 
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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 etiologyconfirms 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.


9 comments:

  1. What is the most basic difference between the Hyperacute T of Hyperkalemia and MI ? Is there a definite criteria ? or one just have to recognize the pattern ?

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    1. you really just have to see it over and over again. You can see dozens of examples here.

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    2. I saw your question and it is a question that I (and I'm sure Steve and Ken) have been asked many, many times. Steve is absolutely right! You have to see a lot of them to develop a sense of which one you are dealing with. The best hint is the context within which you are seeing the patient. Is the patient having classic ACS-type chest pain or did they miss their last 4 dialysis appointments? The internet is filled with examples of both kinds of T waves. Find them, print them out and study them.

      Next, don't fixate on tall, narrow peaked T waves as hyperkalemic. They are only going to be present 22% of the time - that means that 78% of the time you won't see them - even with significant hyperkalemia. Focus more on the QRS complexes and get a good idea when something doesn't seem right for a bundle branch block or even a "slow" v-tach. Typical hyperkalemic T waves are tall, very narrow and sharply peaked. But they CAN be relatively short with bases that aren't at all narrow and peaked but not sharply peaked. They do tend to be symmetrical. The T waves in these two tracings are excellent examples of that.

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  2. Steve...

    Thanks again for great learning/teaching experience with this ECG (and one of my favorite topics). And the points outlined by Ken were spot on! However... I do have a few things to add.

    Ken, in your comments under the section " What is the Rhythm in ECG #1?" you mention that beat #6 is a junctional escape beat "because it ends a short pause..." I think you meant it ends a LONG pause. Granted, we've all seen longer pauses, but this pause is long for this tracing.

    The rhythm perplexes me as much as it did both of you. Here's my take on it: I think it is junctional in both ECGs though ECG #1 may be manifesting some late sinoventricular conduction that is about to give way to a junctional ectopic rhythm. The inverted P' waves noted in the bottom rhythm strip I think are actually a manifestation of the junctional rhythm. When a junctional rhythm manifests inverted P' waves BEFORE the QRS under more normal circumstances, the P'-R interval is typically very, very short. But here we have a rather profound hyperkalemia that is adversely affecting conduction velocities throughout the heart. I think there appears to be more delay going toward the ventricles than back into the atria. That could also explain the constant P'-R intervals when they are visible (due to the fact that they are equally part of the junctional complex). Here's what really perplexes me: the fact that there are retrograde P' waves present at all! The mere presence of sinoatrial conduction means that the working atrial myocytes can no longer repolarize and are thus paralyzed by the hyperkalemia. Perhaps ECG #1 captured that moment just before all the atrial myocytes were left in a depolarized state but most of the conduction was sinoatrial. I have no confident answer for that.

    Regarding ECG #2, I agree completely that it is a junctional rhythm. Conduction is much faster now and the QRS intervals are much narrower; this allows the retrograde P' waves to be hidden in the QRS intervals as they usually are. It was suggested that it could still be sinoventricular but I doubt it. If the sinus node had recovered enough to produce a regular rhythm at a rate around 75/min, I would expect the atria to have recovered enough to produce a P wave or two. I still think it's junctional - AV dissociation by usurpation.

    I totally agree with Ken that QRS axis in the presence of hyperkalemia is "anyone's guess." Hyperkalemia affects the conduction velocity of different myocardial tissues in different ways. The mean QRS axis is likely going to be a perplexing surprise. I think that QRS complexes in Lead I in both tracings demonstrate a net negativity amd thus right axis deviation in both tracings.

    There are two other things I think that clinicians interpreting ECGs should be aware of:

    First, hyperkalemia can produce ST elevation that is very impressive. However, the STE typical of hyperK+ (to me) looks much more like the elevation one sees in Brugada syndrome. In retrospect, that seems somewhat appropriate because Brugada Syndrome is caused by a Na+ channel defect and hyperkalemia exerts its effect by depolarizing the myocytes and rendering their Na+ channels inactive.

    Second, if you have a fairly young patient (<45-50 years) with risk factors for hyperkalemia (hypertensive, diabetic, early renal disease, elevated serum myoglobin due to muscular injury) and you see a 1st degree AV block, perhaps in addition to some T waves of which you are only mildly suspicious - be aware that this may be an additional suggestion of hyperkalemia. Don't immediately write-off 1st degree AV block in a young person as benign; it is present in only about 1% of the population below age 50. If it's present in someone under the age of 50 yrs, it is probably there for a specific reason. Granted, above age 50 it becomes somewhat common but below age 50 - be careful!

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    1. THANKS as always (!) for your comments Jerry — which are always excellent for educational purposes. I’ll respond to a few of them. The R-R interval preceding beat #6 = 1.5 second. I called it a “pause” because it is the longest R-R interval we see (can’t be sure about what happens before beat #1 or after beat #9), and because this longer R-R interval occurs unexpectedly given the cadence of other beats. I called it “short”, because 1.5 second is relatively short for a pause.

      Your thought that beats #4, 5, 7, , 8 and 9 (each preceded by a small negative P wave with constant PR interval) are junctional in the lead II rhythm strip at the bottom of ECG #1 is interesting — and I had a similar thought. The reason I opted to call these atrial beats, is that I otherwise did not know what to call beats #3 and 6, which are not preceded by any P waves at all — and in addition these 5 beats (that are each preceded by a negative P wave) are more irregular than is usually seen with junctional escape rhythms — especially given how so soon afterward (in ECG #2) we have what looks like a regular junctional escape rhythm. Of course, ANYTHING is possible given marked hyperkalemia — which affects conduction in so many sites and in so many ways.

      I agree that the rhythm in ECG #2 is most likely accelerated junctional. The reasons I postulated as a possibility (not probability) that the rhythm in ECG #2 might be sinoventricular are: i) If the underlying rhythm in ECG #1 was ectopic atrial — then why after treatment would the site of impulse formation shift to a lower location (in the AV node); and ii) My suspicion that perhaps the actual degree of hyperkalemia was much more severe than is likely to occur at a serum K+ level of 7.1 mEq/L, which is high — but not so high as one might expect given the number and severity of conduction disturbances that we see in ECG #1. Unfortunately, details about when blood levels were drawn, how severe the acidosis of cardiac arrest & PEA really were, how long the patient went before treatment, etc are missing — but I theorized that given the situation we were told — that serum K+ might have been much higher than 7.1 mEq/L, and therefore that much more likely to produce a sinoventricular rhythm. Again, I agree with you & Steve that a junctional rhythm is still the most probable rhythm in ECG #2.

      I agree entirely with you that hyperkalemia may produce sometimes very impressive ST elevation. But given that hyperkalemia IS a cause of Brugada phenotype — don’t we then get into the difficulty of distinguishing between ST elevation from hyperkalemia itself vs hyperkalemia producing a secondary Brugada ECG pattern that then results in ST elevation? The “good news” (one of the points I tried to emphasize in my comments) — is that while ECG patterns and rhythms associated with hyperkalemia may be perplexing — they usually “go away” after hyperkalemia has been corrected.

      Finally — I’d add to your comment regarding 1st degree AV block — that as with most (almost all) conduction disturbances — clinical significance depends in LARGE part on the clinical situation in which it occurs.

      THANKS again Jerry for your intriguing comments. It is always fun and educational to debate these issues with you! — :)

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  3. Ken...

    I think your sentence "Of course, ANYTHING is possible given marked hyperkalemia — which affects conduction in so many sites and in so many ways" pretty much says all there is to say about dysrhythmias during hyperK+!

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    1. Thanks Jerry! I've stopped trying to figure out "mechanisms" for some of these hyper-K+ arrhythmias, as they defy my interpretation ability (and they most often resolve once K+ returns to normal) — :)

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  4. the base of T wave looks too broad for hyper K

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    1. @ Abdullah — When the QRS widens because of marked hyperkalemia — the ST-T wave may also widen, in which case the base of the T wave may not be so narrow. But T waves are still quite peaked (almost pointed) in many leads of ECG #1 here — which given the degree of QRS widening, IS a T wave change consistent with marked hyperkalemia. I find looking for a narrow T wave base in association with T wave peaking to be most helpful when the QRS complex is still narrow.

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