Monday, December 9, 2019

CO poisoning. Routine ECG recorded before hyperbaric therapy....Are they related?

This patient was working on his truck in a garage without ventilation and the vehicle was running. He felt dizzy and lost consciousness. The next thing he remembers is waking up in the ambulance. He was last seen normal at 09:00 AM and was found down at 10:30 AM. He denied chest pain, abdominal pain, SOB or any other symptoms, though he did endorse chest pressure when asked specifically.

He underwent a routine ECG prior to hyperbaric therapy for CO poisoning:
Obvious Massive STEMI, Proximal LAD Occlusion

His CO level returned at 34%.

Further h/o revealed that he had had a proximal LAD stent placed for a Non-Occlusion MI more than one year prior, and had been on clopidogrel for one year but was no longer on it.

The cath lab was activated.

The interventionalist told the patient that his ECG might be the result of CO poisoning only.

I shook my head because this would be nearly impossible from CO poisoning only.  It might be possible with an extremely severely tight stenosis in the proximal LAD, but such a STEMI is never the result of CO poisoning alone.

It was clear to me that this would be a proximal LAD occlusion, possibly at the site of the previous stent.

It was decided to go the cath lab first, and then to the hyperbaric chamber for hyperbaric oxygen.

Angiogram: Culprit Lesion (s): Thrombotic, in-stent occlusion of the proximal LAD

24 hour echo:
Regional wall motion abnormality-distal septum anterior and apex, akinetic.
Regional wall motion abnormality-anterolateral, akinetic.
Regional wall motion abnormality-anteroseptal, akinetic.

After intervention, the patient went for multiple rounds of hyperbaric oxygen therapy in our world class hyperbaric chamber (see the images at this link).  The patient is on 100% oxygen at 2 atmospheres pressure, so that the pO2 is may be over 1000 mm Hg.

The Hennepin County Medical Center hyperbaric chamber construction was organized by Dr. Cher Adkinson (retired HCMC Emergency Physician) and now run by our current outstanding HBO Emergency Medicine team, including HBO director Chris Logue.

48 hour ECG, after artery is opened and CO level is resolved:
This shows QS-waves and some persistent STE.  This is a bad sign, and suggests no reflow (downstream platelet fibrin aggregates obstructing small vessel flow) future aneurysm formation.

Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

Peak Abbott troponin I was 401.00 ng/mL (this is one of the highest troponins I have ever seen or heard of).

Another case of CO, with ST depression: What is the treatment for this subendocardial ischemia?

Carbon Monoxide displaces oxygen from hemoglobin, and thus effectively decreases oxygen saturation, in this case by 34%, down to 66%.  But it also binds with cytochrome oxydase to inhibit ATP formation.  Thus, its effect is the same as ischemia.

We consider cardiac ischemia (on the ECG, or by elevated troponin), by itself, to be an indication for emergent hyperbaric oxygen (HBO) even if there are no other indications such as neurologic disability, loss of consciousness, level greater than 40%, pregnancy, or other indications.

We treat many chronic conditions with hyperbaric oxygen, but are open 24/7/365 for emergencies including CO poisoning, air embolism, decompression sickness, and central retinal artery occlusion.

Dr. Adkinson's research here at HCMC, published in JAMA, found that myocardial injury (as indicated by troponin elevation, but also by ischemia on the ECG) is common in carbon monoxide poisoning and is independently associated with an increased risk of mortality at 7-year followup (38% vs. 15%).  A subsequent publication in JACC reported that myocardial injury was not at all predicted by CO level.

However, STEMI is rare in CO poisoning, with some case reports. All reports show coronary occlusion as the etiology.

So is it related to CO toxicity?

Some authors believe that CO toxicity increases platelet aggregation and thrombogenicity.  So it is possible that the CO toxicity resulted in the in-stent thrombosis and STEMI.

But the final common pathway for STEMI in CO toxicity is coronary occlusion, not the CO toxicity itself.  Such patients should go to the cath lab first, and to the hyperbaric chamber only after.


Late stent thrombosis secondary to carbon monoxide poisoning

A Case of Acute Carbon Monoxide Poisoning Resulting in an ST Elevation Myocardial Infarction

Ikeda H, et al. Free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries. J Am Coll Cardiol 1994; 24: 1749–1756.

Marius-Nunez AL. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest 1990; 97: 491–494.  This ECG showed diffuse ischemia, but no focal ST elevation. 

MY Comment by KEN GRAUER, MD (12/9/2019):
This case poses the intriguing question of whether CO poisoning by itself can be the cause of this patient’s acute STEMI?
  • Of note — this patient had a proximal LAD stent placed for non-occlusive MI more than 1 year prior.
  • He presented to the ED with loss of consciousness from acute CO poisoning (initial CO level = 34%). Although the patient denied “chest pain” — he later acknowledged “chest pressure" ...

I feel close scrutiny of the 2 ECGs shown in this case is worthy of additional discussion.
  • For clarity — I’ve reproduced these 2 tracings in Figure-1.
Figure-1: The 2 ECGs shown in this case (See text).

As per Dr. Smith — ECG #1 (which was the initial ECG obtained in the ED, prior to sending this patient for hyperbaric therapy) — showed an obvious, extensive STEMI, almost certainly the result of acute proximal LAD occlusion.

  • Question #— What are all of the specific ECG findings that YOU see in ECG #1?
  • Question #2  Why is ECG #1 likely to represent an acute proximal LAD occlusion?
  • HINT to Question #2: If you don’t see 5 reasons why ECG #1 is likely to represent acute proximal LAD occlusion — GO BACK and LOOK AGAIN.

ANSWERS: The following ECG findings support the likelihood that there is acute proximal LAD occlusion in ECG #1:
  • Ssegment elevation begins as early as in lead V1. When there is mid- or distal- LAD occlusion — precordial lead ST elevation typically begins later (ie, in lead V2 or V3). Considering the relatively small amplitude of the QRS complex in lead V1 — there is a substantial amount of ST elevation in this first chest lead. ST elevation then becomes extreme already by lead V2.
  • There is marked reciprocal Sdepression in each of the inferior leads. Reciprocal changes in the inferior leads are much less likely to be seen when acute anterior STEMI is due to mid- or distal LAD occlusion.
  • There is substantial Selevation in lead aVL — which is a near “mirror-image opposite” of the ST depression seen in lead III. Substantial ST elevation in lead aVL is less likely to be seen when acute anterior STEMI is due to mid- or distal LAD occlusion. There is also ST elevation in lead I — though lead aVL is a much more reliable indicator for suspecting proximal LAD occlusion.
  • There appears to be an incomplete RBBB pattern in ECG #1 — as manifest by the terminal R’ in lead V1, in association with a narrow terminal S wave in lead V6. Clearly, the QRS complex is not wide enough to qualify as complete RBBB — and there is no terminal S wave in lateral lead I. But normally, the QRS complex in lead V1 should be predominantly negative, and it most definitely is not in ECG #1.
  • There is LAHB — as manifest by predominantly negative QRS complexes in each of the inferior leads. In association with the new incomplete RBBB that we suspect — this potentially constitutes a new bifascicular block — and this combination of conduction defects, when new and occurring in association with acute anterior STEMI is a characteristic lesion of prognostic importance when there is acute proximal LAD occlusion. RBBB/LAHB (or IRBBB/LAHB) is less likely when LAD occlusion occurs at a more distal level.

To Finish Your Answer to Question #1: What additional ECG findings do YOU see in ECG #1 that have not yet been mentioned?
  • There are already Q waves in multiple leads in ECG #1. Although the Q wave in lead aVL is very small and narrow (and it could be a “normal” septal q wave) — in the setting of obvious extensive acute anterior STEMI with ST elevation in lead aVL — one has to assume that this Q wave in aVL is an “infarction Q wave”.
  • In addition — there are small-but-definitely-present Q waves in leads V1, V2 and even V3! The Q wave in lead V1 is the reason this incomplete RBBB pattern manifests a QR’ rather than an rSR’. And, even though the Q wave is small in lead V2 and tiny in lead V3 — there should be no Q wave at all in these leads given the incomplete RBBB pattern. These anterior Q waves are all “real” findings, and in association with the dramatic ST elevation, they portend what is soon to follow in ECG #2.
  • There is marked T-QRS-D (Terminal QRS Distortion) in leads V2 and V3. Morphologically, T-QRS-D is also present in lead V4 of ECG #1 — although we define T-QRS-D as the absence of both a J-wave and an S-wave in either lead V2 or V3, and not by the appearance in lead V4 (CLICK HERE for illustration and full discussion of the concept of T-QRS-D in My Comment at the bottom of this 11/14/2019 post in Dr. Smith’s ECG Blog). NOTE Obviously, T-QRS-D is not needed to diagnose the large acute anterior STEMI in this tracing. But ECG #1 provides an excellent example of this phenomenon, that may sometimes prove very important to recognize (SEE this 7/3/2018 casein which I summarize "the SHORT answer" in my Fig. 1 at the very END of that post, with detailed discussion above that by Dr. Meyers).

Now COMPARE ECG #1 to ECG #2: Dr. Smith summarized the ECG changes between these 2 tracings in the legend of the 2nd Figure in his discussion above. But to HONE your ECG interpretation skills — What are ALL of the specific ECG changes between these 2 tracings?

  • Although the amount of ST elevation in ECG #2 has dramatically decreased since ECG #1 was done — there still is 2-3 mm of ST elevation in leads V2-thru-V5, as well as a relatively large amount of residual ST elevation in leads I and aVL (especially considering the diminutive size of the QRS in these high lateral leads).
  • Similarly, although the amount of inferior lead reciprocal ST depression is decidedly less in ECG #2 — a worrisome amount of reciprocal ST-T wave change remains.
  • The small anterior Q waves we highlighted in ECG #1 — have evolved into large QS complexes in leads V1-thru-V3 of ECG #2. These are followed by substantial loss of R wave amplitude in lateral chest leads V4-thru-V6, as well as in high lateral leads I and aVL. Subtle Point: Despite loss of R wave amplitude in lead aVL — the Q wave in this lead has deepened and widened.
  • The leads which showed ST elevation in ECG #1 — now show deep T wave inversion. This is an evolutionary change.
  • The incomplete RBBB pattern seen in ECG #1 has resolved.
  • Criteria for LAHB are no longer met (ie, Considering the larger area under the R wave in lead II of ECG #2, compared to the smaller area within the skinny S wave in this lead — the frontal plane axis is now no morethan -20 degrees — or not enough to qualify as LAHB).
  • Bottom Line: As per Dr. Smith — the finding in ECG #2 of large QS complexes + loss of R wave amplitude this amount of persistent ST elevation at a point 48 hours after successful PCI is a very concerning prognostic sign.

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


  1. Great case, very good!!!In your remarkable explanation you have writed that there is marked T-QRS-D in leads V2 and V3, but i am confusing because i have seen a small J-wave in V2. In other words, are there T-QRS-D in V2 AND V3 or only in V3? Additionally,i realized that there is the presence of broad, notched (bifid) P waves in some leads, can i concern with this findings regarding P wave?

    1. @ Unknown — Thank you for your comment. At the least — there IS definite (if not dramatic) T-QRS-D in lead V3. In fact, the lowest point of the QRS descent is 4-5mm ABOVE the baseline in this lead V3! It is 3-4mm above the baseline in lead V2 — but technically, I agree with you that there IS a small J-notch in lead V2 — so lead V2 does not meet strict criteria for T-QRS-D. That said — we KNOW this is a hugh anterior STEMI from acute LAD occlusion — and qualitatively at least, the SHAPE of the distorted terminal portion of the QRS in leads V2, V3 and V4 is so clearly abnormal and obviously consistent with acute OMI even though we cannot use lead V4 in the definition of T-QRS-D (because confirming data in V4 is lacking) — and as you say, strict definition of T-QRS-D is not met in V2 because of that small J-notch. Otherwise — I agree that there is P wave notching in a number of leads (especially leads V3-thru-V6). That said, overall P wave amplitude is low, and morphology for either LAA or RAA (left or right atrial abnormality) is lacking. Most likely, this P wave notching reflects some intra-atrial conduction delay (whether this is acute and related to the MI, or longstanding). Given the overall low P wave amplitude, I chose not to mention this. Clinically, I don’t think it important in this case. For more on RAA/LAA/Intra-Atrial Conduction Defects — Please check out this LINK — — :)


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