Sunday, March 17, 2024

Why is the angiogram normal?

Written by Willy Frick

A man in his 50s with a 15 pack-year smoking history presented to his primary care physician's office complaining of intermittent headache. He also complained of intermittent mild chest pain radiating into into both shoulders and his back, as well as occasional unexplained sweating. (Although radiation into the left arm is most classic for coronary ischemia, radiation into both arms is actually modestly more predictive). The primary care physician's note indicates low suspicion for cardiac ischemia, but "for completion, check troponin and ECG." If an ECG was obtained in the office, it was not saved. The patient had his blood drawn that morning, and troponin I was 6.496 ng/mL (ref. < 0.033). The PCP's office called the patient and advised him to present to the ER immediately. His ECG is shown.

ECG 1


Readers of this blog will have no trouble recognizing this as an OMI with some early reperfusion. Looking through the ECG in detail, we see:
  • STE and HATW in II, III, aVF with terminal reperfusion TWI
  • STD in aVL with overly upright T waves, reciprocal to inferior reperfusion
  • ST flattening with subtle depression in V1 and probably V2, plus overly upright T waves suggestive of reperfused posterior occlusion
  • Subtle coved STE in V6 with terminal TWI (and to a lesser extent V5) consistent with reperfused lateral occlusion
He underwent emergent angiography, which showed normal coronary arteriesHis troponin peaked at 10.310 ng/mL and trended down.  (Smith: a typical peak troponin for an OMI is above 10 ng/mL)

What happened?


Answer: This is MINOCA -- Myocardial Infarction with Non-Obstructive Coronary Arteries. The name is self-explanatory. But MINOCA is more of an observation than a diagnosis, per se. The immediate next question is why? Possible etiologies (depending on your definition) include: plaque rupture with spontaneous recanalization, coronary artery vasospasm, spontaneous coronary artery dissection, or other rarer causes. Most sources exclude myocarditis.

When coronary artery vasospasm is suspected, it can be assessed in the cath lab with intracoronary acetylcholine. Comprehensive coronary evaluation (with testing for vasospasm and microvascular dysfunction) was shown in the randomized trial CorMicA to significantly improve angina, quality of life, and diagnostic accuracy. Unfortunately, this is not performed in most cath labs, and was not done in this case. The patient underwent cardiac MRI which demonstrated transmural infarction of the inferolateral wall as expected.

He was managed medically with aspirin, clopidogrel, and atorvastatin. In addition, his cardiologist suspected vasospastic angina and therefore started amlodipine. He had no further chest pain. Repeat ECG at follow up in clinic a few weeks later is shown. Clear inferior and posterior reperfusion.

ECG 2


Six years later: He presented to the ER with recurrence of his prior symptoms. He described mild substernal chest pain, again radiating into both shoulders with occasional sweating. He said the pain would come and go, sometimes lasting only a few seconds. In the ER, his symptoms had remitted. He stopped taking all his medications about a year prior. ECG is shown.

ECG 3


In isolation, this ECG is suggestive of possible reperfused inferoposterolateral OMI (inferior and lateral precordial TWI with ST flattening and overly upright T waves in V1-3 reciprocal to posterior leads). However, knowing that this patient had a prior infarct in this territory, it is unclear what these findings represent. (That is to say, this could be his baseline ECG.) Initial troponin I was 0.013 ng/mL (ref. < 0.033), repeat 2 hours later 0.016. At this point, the ER consulted cardiology who requested repeat ECG. The patient told the cardiologist that his symptoms had not returned since arriving at the hospital.

ECG 4


In the context of resolved chest pain, this was interpreted as confirmation of inferolateral reperfusion, and the patient was loaded with aspirin and clopidogrel and started on continuous heparin infusion with plan for catheterization. Serial cTnI values were 0.019 ng/mL and 0.027 ng/mL, rising but still within the reference range (< 0.033). The patient reported transient return of his pain, and repeat ECG was obtained.

ECG 5


Like ECG 3, this ECG could be mistaken for being non-specific. However, in this clinical context and especially following ECG 4, the current ECG actually represents re-occlusion! It is a snapshot of the T waves during their transition from deeply inverted reperfusion T waves to upright, hyperacute T waves. If the ECG had been recorded a few minutes later when the T waves were slightly more upright, it would have appeared pseudonormal. At this point, the patient went for angiography. The RCA is shown below.


Below is a still frame with a red arrow pointing to an area of focal vasospasm in the proximal RCA


Repeat angiogram after intracoronary nitro showing resolution of vasospasm:


The left coronary artery system was angiographically normal. The patient was restarted on amlodipine. Repeat cTnI remained within normal limits and trended down.

This finding at angiography explains both the present and prior presentations. In his index presentation years prior, he suffered type 2 MI secondary to vasospasm which was suspected but not confirmed at the time, and had resolved by the time angiography was performed. His symptoms were controlled by amlodipine for years, but he stopped taking it and his symptoms returned. At discharge, he was restarted on amlodipine and given a prescription for varenicline to help with smoking cessation. One final ECG was obtained 24 hours after symptoms had resolved.

ECG 6


This ECG confirms persistent reperfusion of the RCA. Some clinicians who see this ECG mistakenly believe it is worsened compared to ECG 5 since the T wave inversion is "worse." But readers of this blog understand the phenomenon of reperfusion, and recognize this change as reassuring evidence of adequate reperfusion.

Learning points:
  • Vasospasm is one cause of MINOCA. It can be tested for, and CorMicA showed that doing so improves diagnostic accuracy and reduces angina.
  • Calcium channel blockers and smoking cessation improve symptoms in patients with vasospastic angina.
  • "Normal" cath does not rule out OMI, which is a clinical diagnosis.
  • Vasospastic angina is commonly the worst in the morning and at night. Unlike classic angina pectoris, it does not always present as pain that is worse with exertion and improved by rest (since vasospasm can occur and resolve independent of activity and oxygen demand).

Thursday, March 14, 2024

Three patients with chest pain and “normal” ECGs: which had OMI? Which were normal? And how did the Queen of Hearts perform?

Written by Jesse McLaren

Three patients presented with acute chest pain and ECGs that were labeled by the computer as completely normal, and which was confirmed by the final cardiology interpretation (which is blinded to patient outcome) also as completely normal. 

What do you think?

 

Case 1:



Case 2:



Case 3:


Triage ECGs labeled ‘normal’

There have been a number of small studies suggesting that triage ECGs labeled ‘normal’ are unlikely to have clinical significance, and therefore that emergency physicians should not be interrupted to interpret them, and that such patients can safely wait to be seen. These have all been small studies, studying very few patients with ACS, and often used final cardiology interpretation rather than patient outcome. The most recent study found a NPV of 100% of triage ECGs labeled ‘normal’ or ‘otherwise normal’ for final hospital diagnosis of ACS, and concluded that avoiding physician interruption would “alleviate interruptions in workflow and improve patient safety.” 

Smith: This study had such low risk patients that not a single patient was ultimately diagnosed with ACS.  It is well known that NOMI usually has a normal ECG or nonspecific ECG.  The fact that not a single one of these patients had ACS shows that the population studied could not possibly support their conclusion.  It should never have been published.

According to this data a triage ECG labeled ‘normal’ rules out the possibility of acute coronary occlusion.

This is obviously unreliable data, as Dr. Smith’s Blog has published 51 cases of OMI with ECGs labeled ‘normal’, 35 of which were identified by the Queen of Hearts – with 10 examples here. We also studied 7 years of Code STEMI patients requiring emergent reperfusion, and found that 4% presented with an ECG labeled ‘normal’, often confirmed by the final blinded interpretation. This was just published in print in this month's Academic Emergency Medicine:

McLaren, Meyers, Smith and Chartier. Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review. Acad Emerg Med 2024;31:296-300

Many of these 'normal' ECGs had signs of OMI, and those that were identified in real time by the treating emergency physician had faster reperfusion than those that were missed. This study only included patients admitted as Code STEMI, which likely underestimates the false ‘normal’ rate because it doesn’t include those admitted as ‘non-STEMI’ who had delayed reperfusion for OMI. So not interrupting the physician, or physician reliance on a computer 'normal' ECG will lead to preventable delays to reperfusion that would threaten patient safety.

These three cases are from this study, and this prior post shows 4 more. For all cases, see the supplement from the online version of the article.

Now let’s see how these patients were managed in real time, and the patient outcome. These ECGs were not only labeled normal by the computer but also the final blinded cardiology interpretation—which according to some studies would designate these ECGs as not clinically relevant. We can compare these interpretations with the actual patient outcome, and with the blinded interpretation of the Queen of Hearts which is expert-trained to identify OMI.

Case 1:

 

There’s ST elevation in V1-2. The large S wave in V1 may account for some of the ST elevation in this lead, and there is no reciprocal ST depression in V6 (swirl pattern). But the convex ST elevation and bulky T wave in V2 is disproportionate to voltage and indicates OMI until proven otherwise - either LAD or RCA. The Queen calls this OMI with high confidence:

This was missed, and the patient was only seen after the first troponin came back at 100 ngL (normal < 26 in males and <16 in females), and a repeat ECG was done:


Some reperfusion T wave inversion not only in V2 but V1-3, confirming OMI, but still doesn’t meet STEMI criteria. A stat cardiology consult led to cath lab activation, with door-to-cath time of 202 minutes. Despite some reperfusion at the time of the repeat ECG, at the time of the angiogram there was 100% mid LAD occlusion, with peak troponin of 19,049 ng/L. Queen of Hearts could have reduced reperfusion delay by 2 hours for this 100% LAD occlusion that was mislabeled ‘normal.’

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

Case 2:

There is a subtle biphasic T wave in aVL, reciprocal to down/up tall T waves inferiorly, suggesting high lateral reperfusion.


A truly normal or non-OMI ECG would be labeled "not OMI, high confidence" but instead the Queen calls this "OMI low confidence", suggesting the ECG is concerning but not yet diagnostic. The emergency physician who was shown the ECG identified the same concerns and asked for a repeat ECG, which was done 30 minutes later:

The reperfusion TWI in aVL is now upright (pseudonormalization) with reciprocal ST depression inferiorly. There is also ST elevation and hyperacute T waves V1-2 with reciprocal ST depression V5-6 (precordial swirl). Now the ECG is STEMI(+)OMI, diagnostic of proximal LAD occlusion, and was identified by the computer. Cath lab was activated, with door-to-cath time of 118 minutes. There was 95% proximal LAD occlusion, with first troponin of 31 ng/L and peak of 11,894 ng/L. This infarct would have been much worse if the physician had not been interrupted to interpret the initial ‘normal’ ECG, and had not identified the subtle abnormalities.

Case 3:

There’s hyperacute T waves V2-4, with a small Q in V3 and potentially terminal QRS distortion in V3 (at least by the third beat, where there is no S wave), indicating LAD occlusion. The Queen calls this OMI with high confidence.


Fortunately this was also identified by the emergency physician, who asked for a repeat ECG immediately:


Now there’s deWinter waves in V3-4. Cath lab was activated, with door-to-cath time of only 44 minutes. First troponin was 4ng/L which is normal and just above the limit of detection of 2. But peak troponin was greater than 50,000 ng/L despite very rapid reperfusion. This case could have been a disaster if the emergency physician had not been interrupted to review the ECG or if they trusted the ‘normal’ interpretation, and if they waited for and relied on the first troponin which was normal.


None of these were Normal!!  

All were diagnostic of OMI!! 

Do not pay attention to the conventional algorithm!


Take away

1.     ECGs labeled normal by the conventional computer algorithm are unreliable, even if confirmed by the final blinded interpretation. The reliability of these ECGs should be based on patient outcome.

2.     Emergency physicians should be interrupted to review all triage ECGs, even those that labeled ‘normal’, and should look beyond STEMI criteria for signs of OMI – including acute Q waves, terminal QRS distortion, convex ST segments, hyperacute T waves, and reciprocal change

3.     Expert-trained AI can accurately identify OMI and lead to faster reperfusion

Wednesday, March 13, 2024

A man in his 40s with 3 days of stuttering chest pain

Written by Willy Frick

A man in his early 40s with BMI 36, hypertension, and a 30 pack-year smoking history presented with three days of chest pain. It started while he was at rest after finishing a workout. He described it as a mild intensity, nagging pain on the right side of his chest with nausea and dyspnea. It woke him the next day and radiated into his back. He was only able to sleep while sitting in a chair. He went to urgent care and had an ECG (not available) which was interpreted as normal, and was sent home. His pain returned, and he went back to the urgent care but was sent to the ER. His ECG is shown:

What do you think?






Here is the Queen's verdict and translator:

For me, it is hard to make much of this ECG. The most troublesome lead is aVL which shows abnormal ST flattening and perhaps even a very tiny of depression. With no context, I would call it sinus rhythm with non-specific ST&T wave abnormalities.

Smith: there is a bit of STE in inferior leads, and aVL has not only some STD, but it is downsloping, which is very worrisome for inferior OMI.

High sensitivity troponin I (hsTnI) obtained around that time was 5548 ng/L (ref. < 35). This is enough to cause serious alarm. Distilling this case into its most salient components, a man with multiple risk factors for coronary disease is presenting with several days of chest pain and markedly elevated troponin with no other reason to explain the lab abnormality (e.g. sepsis). It is impossible to overstate the importance of putting the ECG and troponin into the context of the clinical history.

Smith: at this point, the ECG becomes irrelevant.  The patient has ACS by history, active pain, and an elevated troponin.  There is acute MI with persistent symptoms.  This is an indication for the cath lab regardless of the ECG.  Nevertheless, learning these ECGs is critical because the next time such a patient presents, it might be acute, before there is any troponin elevation.  Activate the cath lab!  Do not wait for repeat troponins or ECGs.

Already, we should be asking ourselves whether this could be OMI. And since the ECG does not define the disease, the answer is of course it could be. Troponin is not specific for acute coronary syndrome, but in a case like this when we have nothing else to explain it, we must rule out the deadliest (reasonably likely) possibility. Repeat ECG was obtained and is shown below:



Here is the Queen's verdict and translator:

I sent these ECGs along with the troponin trend to our group chat, and Dr. Nossen said "With those troponins retrospectively, this is an inferoposterior OMI. It would be hard to call without the previous ECG for comparison, but the inferior leads are worrisome." Dr. Hellerman agreed and mentioned the inferior ST elevations with reciprocal depression in aVL. Dr. Smith (catching up on the discussion) saw ECG 1 and commented that it looked like "very subtle inferior OMI."

Dr. Nossen also pointed out that with voltage this high in the limb leads, you would typically expect some degree of inferior/inferolateral ST depression (the so-called "LVH strain" pattern), and in fact this patient did have severe LVH on subsequent echocardiogram (which Dr. Nossen did not know at the time). Therefore, the finding of any STE inferiorly is doubly alarming.

Here they are side by side:

The T waves in the inferior leads have significantly increased in volume, and the mostly flat ST segment in aVL now has more of a down-up morphology.

Around this time, the patient received aspirin 324 mg. Repeat hsTnI was 10497 ng/L, and this was interpreted as "likely NSTEMI." Note that this patient has elevated troponin with dynamic change and chest pain. By definition, this is acute myocardial infarction, the only question now is the etiology.

Given radiation of pain into the patient's back, he underwent CTA which showed no evidence of aortic dissection or any other acute pathology. It is not clear exactly what symptoms the patient may have been experiencing at this time, but the notes indicate that he then developed "worsening" pain, suggesting he had likely had ongoing angina the whole time. Recall that medically refractory angina is itself a Class I indication for immediate angiography (see Figure 8). (It is hard to call this medically refractory at this point as the patient had not received any anti-anginal therapy.)

At this point, the patient was treated with 1 inch of nitro paste (Smith: this is a worthless treatment and the ACC guidelines even say so!) and morphine 4 mg IV (Smith: this is even more worthless, and just hides the fact that the patient is having ongoing ischemia and infarction), and repeat ECG was obtained. (Treating angina with morphine and continuing non-emergent management is like taking the batteries out of an actively alarming smoke detector during a house fire and going back to sleep.)

Another ECG was recorded:




Here is the Queen's verdict and translator:

Compared to the first two ECGs, and especially in the context of chest pain and rapidly rising troponin, we see progressively increasing area under the curve in the inferior T waves, and the ST segment in aVL now has much clearer reciprocal depression.

A third hsTnI was 17809 ng/L, and the patient was started on IV heparin as well as sublingual and IV nitroglycerin. Due to persistent pain, he received a second dose of morphine 4 mg IV. Repeat hsTnI was 25763 (ten hours after the initial result).

Brief aside: Remember that the overwhelming benefit of reperfusion therapy is attained if performed within 2-3 hours. By 6 hours, most of the salvageable myocardium has infarcted. This is WHY refractory angina should prompt immediate angiography. If you wait until the ECG and troponin are "convincing," you are sacrificing a lot of myocardium.

Due to persistent pain, the patient received a third dose of morphine 4 mg IV. A fourth ECG is shown below.



Here is the Queen's verdict and translator:


If any doubt remained, we are now completely certain that the inferior T waves are hyperacute, especially with the reciprocal changes in aVL. Although this ECG is obvious to the Queen of Hearts, it was read by cardiology as sinus rhythm with non-specific ST&T wave abnormality.

At this point, due to refractory pain, the patient was taken for left heart catheterization. It is not clear why it was only considered refractory after topical, sublingual, and intravenous nitroglycerin plus morphine 12 mg IV over the course of over 10 hours. But unfortunately, this is not surprising, only about 6% of patients with refractory angina receive immediate angiography as recommended.

Thirteen hours after the first troponin was drawn, the following angiogram was performed.


The troponin peaked at 25749 ng/L. Echocardiogram showed akinesis of the mid to basal inferior and inferoseptal walls, and hypokinesis of the inferolateral wall. One final ECG performed after cath shows obvious inferoposterior reperfusion. (Deep TWI in the inferior leads with reciprocal overly upright T waves in I and aVL, plus posterior reperfusion T waves in V1-2 at least.)




False negative by Queen of Hearts: All ECGs like this will be reviewed in detail by Powerful Medical, and these "critical misses" will be rectified in the algorithm! 

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.




Learning points:
  • ECG owes you nothing in OMI, and may be completely normal, or show only impossibly subtle findings.
  • Fortunately, ECG is not the only diagnostic information to clue you into the possibility OMI! There is history, physical, troponin, and bedside echo.
  • There are many causes of elevated troponin, but unexplained troponin elevation in a patient with ongoing chest pain is OMI until proven otherwise.
  • Patients with medically refractory angina should undergo immediate angiography.

Saturday, March 9, 2024

Acute chest pain and ST Elevation. CT done to look for aortic dissection.....

Written by Willy Frick

A 67 year old man with a history of hypertension presented with three days of chest pain radiating to his back. He had associated nausea, vomiting, and dyspnea.

What do you think?








This ECG together with these symptoms is certainly concerning for OMI, but the ECG is not fully diagnostic, and another consideration could be acute pericarditis. Mistaking OMI for pericarditis is a much more harmful error than the converse. Still, in the interest of studying the ECG, here are some findings that could support pericarditis:

  • Absence of large T-waves (flat ST segments)
  • There is no reciprocal depression anywhere (except aVR and V1, the rightward facing leads).
  • STE spanning from lead I (0°) all the way to lead III (120°), i.e. diffuse.
  • There is appreciable PR depression in a few leads (I, II, V4-6).
  • There is Spodick's sign (downsloping TP segment) in a few leads (V3, V4).
  • The STE has a more concave morphology (vs the more ischemic coved appearance).
  • Ongoing pain despite terminal TWI in a few leads (II, aVF, V5, V6). If this were OMI, that should indicate reperfusion and improving pain.
  • There is end QRS slurring in II, aVF, V6 (vs the more ischemic checkmark sign).
  • The STE in II is greater than the STE in III.
  • The rate is tachycardic, which is uncommon in OMI and common in pericarditis.
There is also low voltage across the ECG.

Important note: None of these findings proves pericarditis. All of them can be seen in OMI. But seeing them all together is more suggestive that pericarditis could be possible.

Due to the chest pain radiating into the patient's back, the ER physician ordered CTA chest to rule out aortic dissection. While awaiting the results of the CT, the physician called cardiology. The cardiologist agreed that the ECG was suggestive of STEMI, but the facility's cath lab was apparently not available and he therefore recommended emergent transfer to a cath capable facility.

A representative still from the CT scan is shown below:


This shows a very large pericardial effusion, which fits with the diagnosis of pericarditis. Recall that pericarditis is diagnosed clinically by any 2 of the following:
  • Characteristic pain (pleuritic, worse with deep inspiration and supination)
  • Friction rub
  • New widespread ST elevation
  • New or worsening pericardial effusion
This patient now has at least two of the above (effusion plus STE), making the diagnosis of pericarditis quite likely. This would have been fairly easy and much more expedient to diagnose with bedside echocardiogram. The constellation of dyspnea, tachycardia, and (relatively) low voltage on ECG should prompt immediate evaluation for pericardial effusion and tamponade.

After transfer to a cath capable facility, and before he was taken to lab, repeat ECG was performed and is shown:




Over just an hour or so, the Queen's certainty has improved significantly, and she now has mid confidence that this is not OMI. The patient underwent pericardiocentesis with drainage of 1500 mL of serous fluid! No further ECGs were obtained. Troponin I was serially undetectable.

____________________________

This is Version 1 of the Queen of Hearts, which was not trained on pericarditis.  Version 2, coming soon, was trained on many pericarditis ECGs and version 3 on even more.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.


Learning Points:
  • Calling OMI pericarditis is much more harmful mistake than the converse
  • Bedside echo demonstrating pericardial effusion can strongly support a diagnosis of pericarditis (and is seen in 60% of cases of acute pericarditis)
  • Pericarditis can only be ruled in after proving
    • Absence of reciprocal changes (other than V1 and aVR), particularly aVL
    • Absence of STE III > II
    • Absence of checkmark sign
    • Presence of PR depression
    • Presence of Spodick's sign
  • When you see dyspnea, tachycardia, and lowish voltage, rule out pericardial effusion and tamponade with bedside echocardiogram 

Thursday, March 7, 2024

Young man with Gunshot wound to right chest with hemorrhagic shock, but bullet path not near heart. A case of irregular accelerated idioventricular rhythm (AIVR)

A young man presented with a gunshot wound to the right chest, with hemo-pneumothorax and hemorrhagic shock.

He got a chest tube and intubation and massive transfusion and stabilized.

CT of chest showed the bullet path through his right lung but nowhere near his heart.

But he did get an EKG:

What is this?  There were times when it would be usurped by sinus tachycardia, then return to this rhythm.


















There is a wide complex.  It is irregular.  It is not fast (cannot be VT).  There is no atrial activity to suggest atrial fibrillation.  

There are what could be interpreted as delta waves if, and only if, there were P-waves or other atrial activity preceding the QRS (pre-excitation can only happen when there is an impulse originating in the atria).  Therefore, these are NOT delta waves and this is NOT pre-excitation!

I could only conclude that this was an irregular accelerated idioventricular rhythm.  I concluded that it is safe and did not require treatment and to leave it alone unless it became too slow, at which point atropine would be indicated to increase the sinus rate to let that sinus rate take over.

AIVR should never be treated with anti-dyrrhythmics!!  It is a stable rhythm.  Atropine is ok to improve the sinus rate if the heart rate is too slow.

All troponins were negative.

Formal echo was normal.

Here are 4 more ECGs recorded over the ensuing hours:


Another irregular AIVR


Back to sinus rhythm


This is a normal regular AIVR



Another normal regular AIVR




On that first ECG, I was not entirely certain, since I have never seen nor heard of irregular AIVR, nor can I find a report of it in the literature.  But I have seen AIVR in young people with trauma (see case below)


So I sent it to Ken Grauer and here are his comments:
============================
For clarity — I've reproduced in Figure-1 the ECG that Dr. Smith sent me (Ken Grauer, MD — 3/7/2024).
============================
Figure-1: The ECG sent to Ken Grauer (showing some semblance of "group" beating).


Hi Steve. This looks VERY bizarre … I don’t see P waves. With a GSW to the chest and what certainly looks like abnormal ST changes (including marked ST elevation in I,aVL) — there is presumably significant cardiac injury that could cause weird rhythms.
  • The QRS is VERY wide — and the very wide Q in lead I (showing marked axis deviation) certainly suggest a ventricular etiology. Lots of leads almost look like delta waves — but I hate to diagnose delta waves when there are no P waves.
  • This does NOT seem irregularly irregular enough for AFib … Instead — there is almost “group beating” with “Wenckebach periodicity”. That is, R-R intervals are decreasing within groups — and the pauses (ie, between beats #3-4; 8-9; and 13-14) are less than twice the shortest R-R interval. 
  • My guess is this is an irregular Accelerated Ventricular Rhythm (which can occur when there is “triggered” activity) — perhaps with Wenckebach conduction out of the ectopic ventricular focus.
  • That said — it is not impossible for AFib + complete AV block to manifest Wenckebach conduction out of the AV nodal escape (We used to see this when Dig toxicity was common … ) — but my guess in this case is “triggered” activity irregular AVR … 
  • In any event — I don’t think I’d try and treat this rhythm given the reasonable ventricular rate (and I’d hope the rhythm improves as the GSW to chest is treated … ).

============================


I had a previous case of an adolescent with trauma and chest pain who also had AIVR:

An adolescent with trauma, chest pain, and a wide complex rhythm

From this blog post: "AIVR is NOT common in otherwise healthy children. I’ve attached an article and an abstract (that article is in Japanese unfortunately … ) that do document that you CAN however on occasion find AIVR in otherwise healthy children — and I suppose that IS what we have here. Perhaps the circumstances surrounding the ED visit cause slight acceleration in the ventricular escape rate to allow this all to happen."


Here the full text of the article:



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