Friday, June 22, 2018

A 60-something year old man with chest pain and a wide QRS

Written by Pendell Meyers, with edits by Steve Smith


A man in his 60s with history of CAD s/p PCI, HTN, presented with chest pain which started while doing construction on his house several hours prior to arrival.

Here is his ECG on arrival at 2052:
What do you think? Should you activate the cath lab?














Yes, because there is an acute coronary occlusion causing OMI of the inferior wall. This is evident based on the LBBB with excessively discordant STE in leads II, III, and aVF, with reciprocal findings in I and aVL.

But the current guidelines do not use the modified Sgarbossa criteria, but rather the original Sgarbossa criteria. Because the STE in the inferior leads does not meet the 5mm threshold, it is negative by the original Sgarbossa criteria, as there is no concordant STE or STD.


The patient was given ASA and NTG drip with improvement but not full resolution of pain.

Initial troponin T was undetectable.

Troponin T at 2200 was 0.10 ng/dL (elevated).

Here is his repeat ECG several hours later at 0022:
There has been interval marked improvement of OMI findings, implying the artery has reperfused.


 Another repeat at 0248:
Still no signs of reocclusion.

Troponin T at 0306 was 0.80 ng/dL.

Troponin T at 0649 was 1.60 ng/dL.

The patient was admitted to cardiology for urgent cath.

1629: Cath shows an acute thrombotic ostial RCA in-stent restenosis culprit, 95% stenosed at the time of cath with TIMI 3 flow. Stent placed with good angiographic result. He also had a 70% chronic mid LAD stenosis, as well as 30% LCX.
Left main, LCX, and LAD, no large vessel occlusions.
LAD lesion described above.

RCA showing 95% ostial stenosis immediately after the tip of the catheter.

Another view showing the ostial RCA stenosis.

Intervention on ostial RCA lesion underway.

Post intervention with good angiographic result.



Troponin T peaked at 3.75 ng/mL the next morning (large MI). The characteristics of this lesion and the highly elevated troponin meet our definition of acute coronary occlusion surrogate criteria (when the angiogram is not performed at the time of the occlusion) used in the derivation and validation of the modified Sgarbossa criteria studies.


I looked back in the chart and found an almost identical presentation 4 years prior. He presented at that time with chest pain.


Presentation ECG at 2317:
Even more obviously positive for the modified Sgarbossa criteria with very excessive discordant STE in II, III, and aVF, with reciprocal findings in aVL and I. Notice how the original Sgarbossa criteria are falsely negative in this case both times.

0124
Cath showed a 90% in stent thrombosis in the proximal RCA, described as "severely thrombotic." TIMI flow was increased from 2 to 3 after intervention.

0253
Findings resolving.

0937
Ongoing resolution with a hint of terminal T wave inversion in the inferior leads.


Serial Troponin T rose from undetectable to 3.63 ng/dL over the course of about 16 hours.



Learning Points: 

Use the modified Sgarbossa criteria to look for OMI in LBBB. The modified criteria are more sensitive than the original criteria as evidenced by cases like this.

Just because there is not complete occlusion at the time of cath does not mean there wasn't complete occlusion at the time of the ECG prior to cath. This is why we have criteria for OMI when the angiogram is not performed at the same time as the ECG evidence of occlusion. Finally, complete transmural ischemia (what happens when there is OMI without collateral circulation) does not even require complete occlusion. A near-occlusion with TIMI 1 flow without collateral circulation may result in similar amount and speed of myocardial loss, and therefore similar benefit of immediate reperfusion therapy until proven otherwise.

Unlike most diagnostic tests, the modified Sgarbossa criteria are also more specific than the unweighted Sgarbossa criteria.  It is unusual to find a test that is both more sensitive and specific than the original test, but this is one.  

Here is the table from the validation cohort:
Compare lines 1 and 4
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Comment by KEN GRAUER, MD (6/23/2018):
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Highly insightful case by Drs. Meyers & Smith regarding the clinical utility of Modified Smith-Sgarbossa Criteria for diagnosis acute OMI in the setting of LBBB. Details in the paper by Dr. Smith et al on use of these modified criteria is found under the Rules + Equations Tab on this blog. I will play “Devil’s Advocate", and offer the following points:
  • As emphasized by Dr. Meyers — Use of the Modified Smith-Sgarbossa Criteria are clearly diagnostic in this case!
  • Another way to arrive at the same conclusion that the 1st ECG (@ 20:52) is diagnostic of acute OMI is qualitative — by recognizing the presence of ST segment elevation in leads in which it just should not be there. This is seen in all 3 inferior leads in ECG #1 (Figure-1). Support that this ST elevation is acute is provided by the presence of “mirror-image” reciprocal ST-T wave changes in lead aVL.
  • IF any doubt existed about the acuity of the initial ECG — lead-to-lead comparison with the 2nd ECG that was done (@ 00:22) should have clarified the picture. While slight-but-definite differences in QRS morphology make interpretation of ST-T wave changes challenging for the chest leads in the 2 tracings shown in Figure-1 — there is unmistakable reduction in inferior lead ST elevation, and in high lateral lead (ie, leads I, aVL) reduction in reciprocal changes. Given associated reduction in chest pain — the clinical picture of OMI with spontaneous reperfusion is irrefutable with this 2nd ECG done at 00:22.
Figure-1: Simultaneous view of the 1st 2 ECGs in this case to facilitate lead-to-lead comparison and appreciation of qualitative ST-T wave changes.
My purpose in posting the first 2 ECGs recorded together in Figure-1, is that this combination tells a story. For those clinicians not yet as comfortable with qualitative ST-T wave assessment — a picture is worth 1,000 words.
  • Although correctly classified as LBBB — ECG #1 is an atypical form of LBBB because: i) there is excessive fragmenting; ii) there is no predominant upright R wave in any of the lateral leads; and iii) the initial Q waves seen in the inferior leads are not “normal” for LBBB in view of the positive, then negative deflections that follow (ie, a qrS is not a “normal” inferior lead morphology with simple LBBB). In this context — there is inferior ST elevation that should not be there in each of the 3 inferior leads in ECG #1.
  • Perhaps the most markedly abnormal-appearing ST-T wave in ECG #1 is seen in lead I. Despite the artifact and tiny overall QRS complex in this lead — the depressed and straightened ST segment “shelf”, that then rises to a disproportionately tall and peaked terminal T wave has to be assumed acute until you prove otherwise.
We often learn the most from challenging cases that do not go the way we might optimally want them to go. Soul-searching is tough work. Armchair quarterbacking the next day is far easier. Our THANKS to Drs. Meyers and Smith for this highly insightful and instructive case, in which the cath lab should have been activated after ECG #1 (@ 20:52) — and if for any reason not then — then after ECG #2. In the “retrospectoscope” — a 2nd tracing would have been ordered before 00:22. Finally, appreciation of qualitative ST-T wave changes can facilitate optimal application of modified Smith-Sgarbossa Criteria.


Wednesday, June 20, 2018

You Diagnose Pericarditis at your Peril (at the Patient's Peril!)

The source of this case is anonymous.

A 40 something woman with a history of hyperlipidemia and additional risk factors including a smoking history presented with substernal chest pain radiating to "both axilla" as well as the upper back.  She was reportedly "pacing in her room while holding her chest".

The initial tracing (EKG 1) was obtained.
Clinician and EKG machine read of acute pericarditis.
What do you think?
















There is sinus rhythm.  There is diffuse ST elevation in II, III, aVF and V3-V6.  One might agree with the computer and the clinician because there is inferolateral ST elevation without any reciprocal ST depression.  While it is true that inferior MI has ST depression in aVL 99% of the time (Bischof and Smith), and that inferolateral ST elevation is the most common distribution for pericarditis, the ST elevation in V3 has "terminal QRS distortion (TQRSD)," (diagnostic of LAD occlusion)


Paper published: Terminal QRS distortion not found in any ECG of Early Repolarization

TQRSD is defined as the absence of BOTH an S-wave and a J-wave in leads V2 or V3.  While I have shown that early repolarization never has this feature which is common to LAD occlusion, no one has ever studied it in pericarditis.  I strongly suspect that pericarditis does not have this feature, and would never assume that it might.  When I see this feature, the ECG represents LAD occlusion until proven otherwise.


First, this is so clearly an LAD occlusion that I would simply activate the cath lab.  However, if you were prevented from doing that, then an emergent contrast echo is indicated.  If there is no wall motion abnormality, then you can be confident that it is not an LAD occlusion.


Why is there diffuse ST elevation (also in inferior leads?).  This is almost certainly due to a type 3 ("wraparound") LAD that supplies the inferior wall.

How about the use of the LAD occlusion formula?  

This formula was developed comparing early repol to LAD occlusion, so it may not apply when the DDx is pericarditis vs. LAD occlusion.    

1. Forget about diagnosing pericarditis here; it is too rare and it is too dangerous to diagnose it in lieu of MI.  

2.  Much of what is called pericarditis is really early repolarization.  
See this case, written by Pendell Meyers when he was a student: 

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!


3.  TQRSD is a sign of obvious LAD occlusion.  These cases were excluded from the study that derived and validated the formulas, and so you should not rely on the formula when there is TQRSD.  Just diagnose LAD occlusion!


Nevertheless, here are the values if you use the formula:

QTc = 431, STE60V3 = 2 mm, RAV4 = 5 mm, QRSV2 = 5 mm
  
3-variable: 26.2 (greater than 23.4 is LAD occlusion)
4-variable: 22.4 (greater than 18.2 is LAD occlusion)


Clinical course 

Later, the first troponin I returned at 2.67 ng/mL (quite elevated).  

Comment: If you are still somehow convinced that this ECG represents pericarditis, then you must at least change your diagnosis to myo- pericarditis (because the elevated troponin shows myocyte necrosis).  But in patients with ST elevation due to myocarditis, there will be a wall motion abnormality and elevated troponin, so it usually can't be differentiated from MI without an angiogram.  


Another ECG was recorded:
Is it true that there is "no significant change"?






In the intervening 3 hours, new Q-waves have developed in leads V3 and V4, and deepened in V5 and V6.


The patient was admitted to medicine service for pericarditis where she had intermittent pain throughout the rest of the night.  The medicine note documents that the patient had worsening pain with lying flat and relief with leaning forward.  There was no history of preceding viral symptoms.

Another ECG was recorded at t = 6 hours:
The Q-waves are more pronounced and now the computer sees it.
Also, the ST elevation has diminished as myocardium infarcts

Outcome and comments by the source of the case:

"The following morning the cardio consult service saw the patient.  The repeat TnI at that time was 19.20 ng/mL and an official echo showed: 'Severe hypokinesis to akinesis of the apical 1/3 anteroseptal wall with partial wall thinning c/w apical anterospetal MI.'"

"Cath showed a 100% mid LAD lesion which was successfully intervened upon."

"TnI peaked at 67.10 ng/mL post PCI."

"I know from reading your blog that you "diagnose pericarditis at your own peril", but are there any signs on that initial ECG that would make you think ischemia?  No PR depression, no Spodicks sign, but concave segments which are diffusely elevated... no reciprocal depressions (aVL looks isoelectric to me, maybe make an argument for slight depression?)."

"In the clinical context I would have performed a bedside echo and had I seen the RWMA the diagnosis would have been made, but in the absence of this I thought that initial ECG looked like pericarditis."

2 comments

1. 40-50% of acute LAD occlusion have upwardly concave ST segments in all of V2-V5.   
--Smith SW.  Upwardly Concave ST Segment Morphology Is Common in Acute Left Anterior Descending Coronary Artery Occlusion.  Journal of Emergency Medicine 2006; 31(1):67-77. 

2. 40-50% of LAD occlusion have zero reciprocal ST depression.
--> --Walsh B.  Grauer K.  Smith SW.  Proximal RCA occlusion producing anterior ST segment elevation, Q-waves, and T-wave inversion.  Journal of Electrocardiology 2018.


Did absence of reciprocal ST depression in aVL lead to this erroneous diagnosis?

That may be the case.  The absence of STD in aVL should only be reassuring when you are trying to differeniate the inferior ST elevation of MI from that of pericarditis.  If that were the differential diagnosis, then pericarditis would be a reasonable thought, and one should look for PR depression (not present), STE in II greater than III (which is present), Spodick's sign (downsloping TP segment - to my knowledge this has never been verified as a true sign of pericarditis), as well as clinical factors such as a rub or effusion.  However, in almost every case, one should confirm absence of OMI (Occlusion MI) at least by contrast ultrasound.

But absence of ST depression in aVL is not meant to rule out anterior MI!  

Positive troponin: this transformed the differential Dx from MI vs. pericarditis to MI vs. myocarditis.  Myocarditis is virtually indistinguishable in the ED from MI.  These patients may have ECGs, troponin profiles, and echo exams that are identical to acute OMI.  If there is ST elevation, they almost always need an angiogram to rule out OMI.

Learning Points:

It is very dangerous to diagnose pericarditis unless there is overwhelming evidence to support it.  This ECG was diagnostic of OMI (not pericarditis).  Even if it was a more ambiguous ECG, a more detailed investigation would be warranted because OMI is far more common and it cannot be missed!

Final thought:

In my experience, I have noticed that clinicians love to make the diagnosis of pericarditis, and will use any evidence, no matter how weak, to support that diagnosis if they think of it. I am not sure why this bias exists, and don't even know what kind of bias it is. Confirmation bias? But confirming what?  And why do they want it confirmed?

See this case:


Pericarditis, or Anterior STEMI? The QRS proves it.


Pendell Meyers comment: when teaching interns, I tell them to think about pericarditis (but not myocarditis or pericarditis with pericardial effusion) as a wastebasket diagnosis, almost on the same level as "costochondritis," as if that were a thing. It appears to me that the only reason pericarditis exists is to trick emergency physicians into missing OMIs (and less commonly PEs, dissections, etc). Like costochondritis or GERD, it is a diagnosis from which nothing good can come. Pericarditis (without myocarditis or pericardial effusion) simply does not matter in the grand scheme of things. The treatment for pericarditis (which probably doesn't relieve the pain of pericarditis any more than placebo or tylenol or anything else) is simply NSAIDs (which can have complications) or colchicine (which some toxicologists believe should simply never be used given the astounding mortality of its overdose). Nothing good comes from diagnosing pericarditis, and there are huge risks of doing so, as illustrated by this case and so many others on this blog. If you correctly diagnose 99 patients with pericarditis and misdiagnose 1 OMI as pericarditis, you have failed, because the harm of missing OMI far outweighs the nearly nonexistent harms of missing pericarditis. Just say no to diagnosing pericarditis, and the problem is solved. Dr. Smith appropriately wonders what type of bias this is that makes clinicians so obsessed with diagnosing pericarditis. I'm not sure if this bias has been described before, but it seems to me to be related to the fun of making a relatively rare, "interesting" diagnosis. So maybe it should be called the "shiny distracting zebra bias." That seems to be what's happening - the shiny fun diagnosis of pericarditis is distracting us from the actual emergencies.




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Comment by KEN GRAUER, MD (6/20/2018):
-----------------------------------------------------------
Great case & supporting comments by Drs. Smith & Meyers. I’d add the following:
  • Dr. Smith’s concept of terminal QRS distortion is worth repeat emphasis (link to his paper given above in the text). A picture is worth 1,000 words — and lead V3 illustrates this concept to perfection. Like visual recognition of what a Brugada-1 ECG pattern looks like — the picture of terminal QRS distortion in a patient with new chest pain (as seen in lead V3 of this 1st ECG) is a pattern to be memorized by all emergency care providers.
  • I love Dr. Smith’s quote, “You Diagnose Pericarditis at Your Peril (and at the Patient’s Peril!)”. I use this quote often when questions regarding this diagnosis arise. But not only is acute pericarditis a diagnosis of exclusion — the clinician should also be knowledgeable about how acute pericarditis (on those occasions when it does occur) presents. The most common form of acute pericarditis is associated with recent viral infection — and, the nature of the chest pain is typically positional (worse in supine position) and pleuritic (aggravated by deep inspiration). Although a pericardial friction rub is not always present — it should always be carefully listened for, because if you do hear a rub in the right clinical setting — then you have made the diagnosis. Why then in the literally hundreds of suspected cases that I’ve seen ECGs posted on the internet in recent years with a query about pericarditis — is it so very rare for anyone to ever describe the nature of the patient’s chest pain? — and rarer still to even mention having thought about listening with a stethoscope to see if a rub might be present? 




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Monday, June 18, 2018

A Wide Complex Rhythm in an Intoxicated Patient

This patient presented with altered mental status and was thought to be intoxicated.  He did not have any other apparent medical issues.

I'm not certain why an ECG was recorded, but it was:
The computer and the overreading physician diagnosed "Sinus rhythm with LVH."
What is it?

















This is an accelerated idioventricular rhythm (AIVR).  There is also isorhythmic dissociation (P-waves and QRS co-incidentally going the same rate, but without the P-waves consistently conducting through the AV node because frequently the ventricular rhythm usurps it (comes too early for the P-wave to conduct).

I point out the salient features on the annotated image below:
There is a wide QRS that is at regular intervals at a rate of about 65.
They are either not preceded by a P-wave, or by a P-wave that is too close to be conducting.
Black arrows points to normal P-wave that conducts to a normal QRS.
Green Arrows point to upright sinus beats that are close to the QRS and create a "fusion" beat, in which the ventricular beat and the normal beat meet up (fuse) and create a hybrid QRS that is longer than a normal one, but shorter than the idioventricular ones.
Red Arrows point to retrograde P-waves.  The idioventricular rhythm conducts up the AV node to the atrium, creating an upside down P-wave after the QRS.
Blue arrows point to upright P-waves that are within or after the QRS; they occurred too late to affect the QRS (they did not fuse).

See below how this resembles WPW and why it is not WPW.


AIVR is an automatic ventricular rhythm that is:
1.  Faster than a normal ventricular escape rhythm (which is also automatic at rates as high as 50).  AIVR is caused by enhanced automaticity (faster than normal automaticity).
2.  Slower than ventricular tachycardia (less than 100-120).  VT is a re-entrant rhythm.

It is a benign rhythm but may be seen in dangerous pathologies, particularly in the reperfusion phase of acute STEMI, digoxin toxicity, and sympathetic overload.

Clinical course

Although the overreading physician did not see the AIVR, the resident did diagnose "Idiopathic Ventricular Rhythm without Tachycardia," which does pretty well (but not exactly) describe the ECG, but does not conform to the standard terminology.  "AIVR" is much more accurate and precise.

The patient had negative troponins in the ED.   He was not on digoxin.  He did not have other evidence of sympathetic overload.

He metabolized his toxin, whatever it was, and was discharged.

It is important to know that AIVR can occur any time and does not necessarily imply significant pathology.

Since there is a great and succinct article on AIVR at Life in the Fast Lane, I do not feel the need to explain in greater detail: https://lifeinthefastlane.com/ecg-library/aivr/


The QRSs do resemble those of WPW; is this intermittent WPW? 
  
However, here we do not see the typical slurred upstroke (delta wave) of WPW; the QRS is uniformly wide, whereas a delta wave has a slower initial upstroke that later. 

Moreover, an interpretation of WPW would require there to be P-waves prior to these abnormal QRSs.

So it is not WPW.

Here is an example of intermittent WPW:
http://hqmeded-ecg.blogspot.com/2016/06/it-is-easy-to-be-led-astray-by-computer.html
In this case, the computer also interpreted "Normal"
But complexes 3, 4, 5 have delta waves and a short PR interval.

Here is a case of WPW in which the QRSs do resemble those of AIVR:
Looks similar, right?  But here there are P-waves before every QRS and the first part of the QRS is more slurred.
You can read here why the PR interval is not short in this case of WPW:

A large R-wave in lead V1. And why is the PR interval not short?


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Comment by KEN GRAUER, MD (6/18/2018):
-----------------------------------------------------------
Interesting case in which an ECG was probably not essential to management — but for which we are thankful, since it provides such an instructive teaching case! As per Dr. Smith — AIVR is generally a benign rhythm that will often be seen in dangerous pathologies (most commonly as a “reperfusion rhythm” in occlusion-related infarction). As Dr. Smith also emphasized — AIVR may on occasion be seen in otherwise healthy individuals who do not have underlying heart disease. So, as is the case with most cardiac rhythms — the clinical setting is KEY to determining the significance (or lack thereof) of the arrhythmia! I’ll offer a different viewpoint to one aspect of Dr. Smith’s interpretation:
  • I suspect there are no retrograde P waves here (which if present, might then be expected to reset the sinus rate). Instead, I favor the hypothesis that all colored arrows in Figure-1 represent sinus-generated P waves — with the underlying rhythm being sinus arrhythmia.
  • We see evidence of this variation in sinus rate at the beginning of the tracing. Thus the P-P interval between the 1st black and 1st green arrows measures 960 msec (corresponding to a rate of ~62/minute) — which is clearly longer than the P-P intervals once normal sinus conduction resumes for the last 2 beats on the tracing. Thus, the P-P intervals for these last few sinus beats = 740 and 720 msec (corresponding to a faster sinus rate of 81 and 83/minute, respectively).
  • It is because of this sinus arrhythmia with bradycardia that AIVR is seen! With periods of sinus rate slowing (as occurs at the beginning of Figure-1) — once the sinus rate drops below the 65/minute threshold of the slightly accelerated ventricular escape focus — AIVR takes over — until, the sinus rate speeds back up toward the end of the tracing.
Figure-1: Perhaps all P waves are sinus-initiated — with an underlying sinus arrhythmia + bradycardia leading to intermittent AIVR? (Details in my Comment above).
P.S.— AIVR is not always completely benign. As a result of “takeover” by this ventricular rhythm — the “atrial kick” is lost. In some settings — this loss of atrial contribution to cardiac output may result in hypotension. In those rare instances in which excessive slowing of sinus P waves results AIVR with hemodynamic compromise — Atropine may be the drug of choice. That said, in the vast majority of cases — AIVR will not produce symptoms, and no specific treatment is needed.



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