Friday, May 26, 2023

20-something with huge verapamil overdose and cardiogenic shock

A 20-something presented after a huge verapamil overdose in cardiogenic shock.  

He had been seen at an outside institution and been given 6 g calcium gluconate, KCl, and a norepinephrine drip.

The initial K was 3.0 mEq/L and ionized calcium was 5.5 mg/dL (sorry, Europeans, for the weird units)

Here was the initial ED ECG:

There is a junctional rhythm with retrograde P-waves (see the dip in the T-wave in lead II across the bottom; you can follow that up to all the other leads and see the retrograde P wave).  

There is also Left Bundle Branch Block (LBBB). There is huge proportionally excessively discordant ST Elevation.  There is what appears to be a hyperacute T-wave in V4. 

This meets the Smith Modified Sgarbossa criteria, but the situation is wrong for diagnosing OMI!!

By the way, the PM Cardio Bot Queen of Hearts says this is Not OMI with High Confidence.  And she does not know that this is an overdose; she thinks it is a patient with chest pain!!

Case Continued:

He was stabilized on more calcium, pressors, and high dose insulin.  3 hours later, this was recorded at a K of 2.8 mEq/L and total calcium of 14.7 mg/dL:

The massive ST Elevation persists.

He was admitted to the ICU and was unstable, in shock, overnight.  He had this ECG recorded at 8 hours:

Now the ST Elevation is nearly gone

Another was recorded at 19 hours:

The ST Elevation is back!!  What is going on here?

Case continued

The patient has vasoplegia and was treated with, in addition to high dose insulin, multiple inotropic and vasopressor agents even including methylene blue for vasoplegia.

This was a very complex case and the details are too much for an ECG Blog, but suffice it to say that, shortly thereafter, the patient had an asystolic arrest and was resuscitated.  He was placed on ECMO.

Peak troponin I at 24 hours was 480 ng/L.

Assessment: In spite of apparent massive injury as seen on the ECG, there is no OMI here and only a mild amount of myocardial injury.  

Subsequent ECGs on ECMO:

ECG at 36 hours:

Junctional Rhythm with slightly wide QRS and Bizarre ST-T

At 48 hours:

Junctional Rhythm with more normal ST-T

On Day 4, the myocardium was contracting more normally by Echo, and the patient was weaning of of ECMO, with an normal neuro exam.  Here is the ECG on Day 4:

Junctional rhythm and otherwise only minimally abnormal.

The patient was discharged to psych neuro intact.

Comment on High Dose Insulin and Calcium Channel Blocker Overdose 

I do not have any explanation for the ST-T abnormalities here.  Verapamil overdose is complex and VERY dangerous.  It leads primarily to a cardiac depressant, and the treatment for this is high dose insulin in combination with other inotropic agents.  Although the primary effect is anti-chronotropic and anti-inotropic, at very high doses, verapamil loses some specificity and also has vasoplegic (vasodilatory, lowering systemic vascular resistance) effects similar to the dihydropyridine calcium channel blockers (such as amlodipine), which primarily result in vasodilation and vasoplegia.  Thus, since high dose insulin's (HDI) primary beneficial effect on calcium channel overdose is to as a positive inotrope, it does not work well for dihydropyridine overdose.  Complicating matters even more, HDI has vasodilatory effects of its own!  

Learning Points:

1. The ECG must always be interpreted in clinical context.  If the situation is not right for acute coronary occlusion, then the ECG findings probably do not represent acute coronary occlusion.

2. Severely ill patients from any etiology can have very abnormal ECGs

My Comment by KEN GRAUER, MD (5/26/2023):
There are more questions than answers in today's case. That said — I believe there are still a number of important teaching points to be made.

  • Today's patient is a young male who presented in cardiogenic shock following a massive verapamil overdose. Management of calcium channel toxicity is complex — with cardiovascular collapse, conduction defects and various bradyarrhythmias (including the asystolic arrest experienced by today's patient) among the common problems encountered. Details of management extend beyond the scope of this ECG Blog — with reviews by Atemnkeng at al (J Med Cases 12[9]:373-376, 2021) and Chakraborty & Hamilton (StatPearls, 2023) available for interested readers.
  • Despite the eye-catching ST-T wave changes that came-and-went a number of times — there was no acute coronary occlusion. We remain perplexed about the cause of these remarkable (and bizarre) ECG changes over the course of serial tracings — with the KEY lesson being to "Treat the Primary" (with the need for intervention directed primarily at cardiovascular support from the massive verapamil overdose). Amazingly, this patient stabilized and recovered with intact neurologic function.

  • Finally — I found the serial tracings in today's case interesting and illustrative of the gamut of rhythm and conduction disorders that may be seen with calcium channel blocker toxicity from verapamil or diltiazem overdose. I focus my comments purely on a few sophisticated concepts in arrhythmia recognition — fully aware that specific rhythm disorders with calcium channel toxicity need not be treated per se, beyond providing cardiovascular support. As occurred in today's case — rhythm and conduction defects largely resolved as the patient recovered and the effects of verapamil toxicity wore off (with the exception of the hemodynamically stable, albeit slightly accelerated junctional rhythm with narrow QRS on the final ECG at the time of hospital discharge)


— Did YOU Notice the Rhythm Disorder in Today's 2nd ECG?  

Take another LOOK at the first 2 tracings shown in today's case. For clarity in Figure-1 — I've reproduced and put these first 2 ECGs together.
  • What effects of verapamil toxicity do you see in these 2 tracings?

  • What is the rhythm in ECG #2?

Figure-1: The first 2 tracings in today's case.

MY Thoughts on the CHALLENGE: 
As noted above by Dr. Smith — the rhythm in ECG #1 appears to be a regular junctional escape rhythm at a rate of ~50/minute (ie, with a regular R-R interval almost exactly equal to 6 large boxes in duration).
  • Normal sinus P waves are absent. The QRS complex is wide — with QRS morphology consistent with LBBB. Although difficult to determine from this initial ECG alone — after consideration of ECG #2, I don't think there are retrograde P waves.

Did YOU see P waves in ECG #2?
  • If so — Are these P waves regular? 

ANSWER: Are there P waves in ECG #2?
  • I've illustrated the answer to this question in Figure-2.

Figure-2: I've added RED arrows to ECG #2 to illustrate the presence of regular sinus P waves in the long lead II rhythm strip. The atrial rate of these P waves in ECG #2 is ~75/minute (since the P-P interval remains close to 4 large boxes in duration throughout the long lead rhythm strip)
NOTE: The reason I didn't think retrograde P waves were present in ECG #1 — is that the terminal part of the QRS and the ST-T wave look similar in ECG #1 — to the terminal QRS and the ST-T wave for beats #3 and 6 in ECG #2, and that would not be the case if retrograde P waves were hiding there (ie, hidden retrograde P waves would disturb regularity of the RED-arrow P waves).

  • Are the RED-arrow P waves in Figure-2 related to neighboring QRS complexes?

In Figure-3 — I have color-coded P waves in the long lead II rhythm strip of ECG #2.
  • What do all P waves that share the same color in Figure-3 have in common?

Figure-3: I've color-coded P waves in the long lead II rhythm strip from ECG #2.

How Are the P Waves Color-Coded?
The easiest way to establish the relationships I cite below is by use of calipers.
  • As already noted — P waves in Figure-3 are fairly regular at a rate of ~75/minute (the P-P interval remains close to 4 large boxes in duration throughout this rhythm strip).
  • The QRS complex in Figure-3 is still wide, with LBBB morphology (as we previously saw in the 12-lead ECG shown in Figure-2).
  • The ventricular rhythm in Figure-3 is surprisingly Regular, with an R-R interval = 6.5 large boxes in duration. This corresponds to a ventricular Rate of ~46/minute for the long lead II rhythm strip of ECG #2, or a little bit slower than the ventricular rate for ECG #1.

  • KEY Point: Each of the colored-arrow P waves in Figure-3 — appears to be Related to its neighboring QRS complex, either by a constant PR interval with respect to the next QRS — or — by a constant RP' interval with respect to the preceding QRS. For example — the PR interval of the 3 RED-arrow P waves is prolonged, and appears to be of the same ( = 0.38 second) duration.

 Unlike the 6 other serial tracings in today's case — there are fairly regular sinus P waves in ECG #2. The fact that there appear to be repetitive PR intervals is unlikely to be due to chance — and instead suggests that there was at least some conduction of sinus impulses at the time ECG #2 was recorded.
  • This is consistent with ECG manifestations of verapamil overdose — which is known to produce conduction defects (such as the LBBB seen in the earlier tracings in today's case) — and — any of the various bradyarrhythmias that were seen in today's serial ECGs (ie, bradycardia, junctional escape, AV block — and the asystolic cardiac arrest that today's patient was resuscitated from).

Laddergram Illustration:
The mechanism of AV block in ECG #2 is complex. I suspect there is dual-level Wenckebach out of the AV Node — as shown by my proposed laddergram that I've drawn in Figure-3 (For more on the mechanism of dual-level AV block — CLICK HERE).
  • Acknowledgment: I can not be certain of the mechanism I've drawn in Figure-3. I don't even know serum electrolytes at the time this tracing was recorded (ie, If there was hyperkalemia — this electrolyte disturbance is notorious for causing highly unusual forms of AV block). In addition — I'd ideally want a longer period of monitoring to truly ensure the validity of what appears to be repetitive PR and RP' intervals that my color-coding suggests.

  • Learning POINTS: The specific mechanism that I've drawn out is much less important — than the reminder that it is EASY to overlook atrial activity and subtle forms of AV conduction disturbances. The way to prevent this — is to be systematic and always spend the 3-to-5 seconds it takes for your "educated eye" to start interpretation of every tracing you encounter — by looking at the long lead rhythm strip that accompanies the 12-lead tracing — to assess regularity, the presence (or absence) of atrial activity — and if P waves are present, whether they are (or are not) related to neighboring QRS complexes.
  • The mechanism I propose in my Figure-4 laddergram is complex. But deriving this mechanism is not necessary to recognize the likelihood of some form of 2nd-degree block because: i) An underlying sinus rhythm is present (ie, fairly regular arrow P waves); andii) There appear to be repetitive PR intervals, especially when 1st-degree AV block is present for conducted beats (RED-arrow P waves) — which usually suggests some form of Wenckebach conduction — be this with dual AV nodal pathways (given marked increment in conducting PR intervals between beats) or with dual-level Wenckebach conduction out of the AV node (as per my proposed laddergram).

  • To EMPHASIZE: The mechanism of the rhythm in ECG #2 was not important to management of today's case. Instead — the key was supportive therapy, with treatment directed at addressing the primary problem ( = verapamil toxicity). That said — there are times when today's Learning Point about regular use of a systematic approach to rhythm interpretation will make a big difference clinically! (ie, See My Comment in the April 6, 2023 post in Dr. Smith's ECG Blog — in which AFib and AV Wenckebach were repeatedly misinterpreted by a number of medical providers over a period of months, with obvious implications regarding optimal treatment decision-making).

Figure-4: My proposed laddergram for the rhythm in ECG #2

ADDENDUM by Ken Grauer, MD (5/27/2023):
I was delighted to receive an email from Dr. H.S. Cho (from Seoul, Korea) — regarding the mechanism of the rhythm in the long lead II rhythm strip from ECG #2.

  • Dr. Cho’s concern was twofold: i) That the intervals that I color-coded are not precisely equal; andii) That the R-R interval in this tracing is constant — and that typically when there is Wenckebach conduction, the R-R interval will show “group beating” with a pattern of variation in intervals, in which the BEST clue that a beat IS being conducted, is when an R-R interval occurs that is “shorter-than-expected”.
  • Although I was initially convinced about the mechanism I proposed in my Figure-4 laddergram — on my umpteenth “revisit” of this tracing (before I published my comment) — I experienced the identical concerns so astutely expressed by Dr. Cho. It was for this reason that I meticulously adjusted the wording of my commentary. You'll note that I wrote an "Acknowledgment" in my original comment, which states — I can not be certain of the mechanism I've drawn in Figure-3."

BOTTOM Line: I AGREE with Dr. Cho. My proposed laddergram may not be correct. 
  • The differences in interval measurement that I came up with are less than measurements by Dr. Cho. I think potential reasons for this are tiny differences in morphology of the low-amplitude P waves, and in the initial QRS inclination — which is why I wrote in my Acknowledgment“I'd ideally want a longer period of monitoring to truly ensure the validity of what appears to be repetitive PR and RP' intervals that my color-coding suggests.”
  • Distinction between 2nd-degree and 3rd-degree AV block is at times problematic — especially when the ratio of P-P and R-R intervals is such that it closely simulates a repetitive interval duration.
  • It will not always be possible to be 100% certain about the etiology of an arrhythmia from the single "snapshot" we get from a 10-second rhythm strip. This is certainly true in today's case — in which the effects of massive verapamil overdose raised havoc with cardiac impulse formation and properties of the conduction system that clearly "don't follow the usual rules".
  • That said, while I still maintain the possibility of dual-level Wenckebach — the consistent R-R interval is more consistent with Dr. Cho’s interpretation of complete AV block.

To Again EMPHASIZE: I welcome Dr. Cho’s concerns! It's always rewarding and mutually educational to discuss interesting aspects of arrhythmia interpretation. But as per my Learning Points from today’s case — specifics of the fascinating rhythm in ECG #2 did not alter management of this patient with massive verapamil overdose. As expected, the rhythm and QRS widening resolved as the effects of verapamil wore off (with exception of the slightly accelerated junctional rhythm at the time of patient discharge). 

  • Recognizing the correct rhythm will not always be needed for optimal treatment.
  • That said, as a teacher of clinical electrocardiography — I feel appreciation of the concepts discussed in today's case regarding the rhythm in ECG #2 will be useful for optimal arrhythmia management on certain occasions (such as the April 6, 2023 link I provided above) — in which attention to accurate arrhythmia interpretation WAS critical to optimal management.

THANK YOU again Dr. Cho for your comments! 

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