Thursday, February 21, 2019

Computer often fails to diagnose atrial fibrillation in ventricular paced rhythm, and that can be catastrophic

Case 1.

An elderly patient presented with a massive hemiplegic ischemic stroke of 24 hours duration.  CT stroke series showed a middle cerebral artery thrombus.

He had an ECG recorded:

Case 1, ECG 1:
Computer: "Electronic Atrial Pacemaker.  Electronic Ventricular Pacemaker"
No other interpretation.
What do you think?

Answer: There is no atrial pacing spike.  This is atrial fibrillation (not diagnosed by the computer) but with a regular ventricular rhythm because the ventricle is regularly paced by an artificial pacemaker (ventricular paced rhythm, VPR).  This may easily deceive both the computer and the overreading physician because one of the primary means of identifying atrial fibrillation is by an irregularly irregular heart rate.

Case 2

This patient presented on the same day: She had a history of atrial fibrillation, CHF, COPD, HTN, CVA anticoagulated on Coumadin who presents for evaluation of shortness of breath.

Case 2 ECG (ECG 2):
Computer: "electronic ventricular pacemaker"
What do you think?

There is no mention of sinus rhythm, or any atrial rhythm diagnosis, even though sinus rhythm is obvious.  There is also, of course, VPR and PVCs.

Case 1, later in the day (ECG 3):
Now there is an irregular rhythm and so it is obviously atrial fib.  Because the AV node is conducting rapidly enough, the ventricle no longer needs to be paced, and there is an irregular rhythm.
There are also CNS T-waves (which is due to stress cardiomyopathy, common in acute severe stroke, and verified by multiple wall motion abnormalities on formal echo).

There were previous ECGs available for case 1 (the stroke patient):

Case 1, first previous ECG (ECG 4)
Computer and physician overread are:
"Electronic Atrial Pacer"
"Electronic Ventricular Pacer"
What do you think?

Again, there are no atrial pacer spikes.  There is probably underlying atrial fibrillation but neither the computer nor the physician diagnosed it.  The physician seemed to believe that if the computer detected it, it must be there. But this may not be an accurate assumption.

Another second previous ECG (ECG 5):
Computer and Physician overread:
"Ventricular Paced Rhythm.  Artifact makes interpretation difficult."

There are many little spikes.  These are artifact, and have nothing to do with a cardiac pacemaker. Sometimes you can see similar artifact from central nervous system devices.   Thus, ECG 5 also has atrial fibrillation that went undiagnosed.

Thus there are many failures of atrial rhythm diagnosis here, by both the computer and the overreading physician, because of the presence of VPR:

ECG 1 has atrial fibrillation (undiagnosed), not atrial pacing
ECG 2 has sinus rhythm, which is not mentioned.
Only ECG 3 has atrial fibrillation correctly diagnosed because there are no ventricular pacing spikes and the rhythm is irregular.
ECG 4 has atrial fibrillation misdiagnosed as an atrial pacer
ECG 5 has undiagnosed atrial fibrillation

Thus, for Case 1, 2 previous ECGs had failed to diagnose atrial fibrillation.  In one, the diagnosis was incorrect: "Electronic Atrial Pacemaker" diagnosed by both computer and overreading physician.  In the other case, no atrial diagnosis was given by either computer or physician.

Thus, the case 1 patient was never diagnosed with atrial fibrillation, even though it was present, and the atrial fibrillation ultimately resulted in catastrophic stroke.

This failure to diagnose atrial fib by the automated algorithm is very common.  In the setting of VPR, many conventional algorithms do not even attempt an atrial rhythm diagnosis.  And this leads physicians astray.  Below are a couple important articles on the topic.  There is a large literature on misdiagnosis of atrial fib by conventional computer algorithms.

Moreover, when a conventional algorithm does diagnose atrial fibrillation, it is an overdiagnosis in up to 20% of cases.  It is very common for these computer errors to go uncorrected by the overreading physician.

Learning Points:

1. All atrial rhythm diagnoses by the computer algorithm must be scrutinized.
2. The computer algorithm may not even attempt an atrial rhythm diagnosis in the presence of VPR.
3. Atrial fibrillation in the presence of VPR will usually have a regular rhythm, and thus be difficult to discern.
4.  Even a computer diagnosis of "atrial paced rhythm" may be a false positive.

Diagnostic performance of a computer-based ECG rhythm algorithm

Of the 4297 consecutive ECGs forming the basis of this report, 13.1% (565/4297) required revision of the computer-based rhythm interpretation. The most common errors were related to interpretive statements involving patients with pacemakers: of 343 ECGs with pacemaker activity comprising 8.0% of the study ECGs, 75.2% (258/343) required revision, so that 45.7% of all inaccurate rhythm statements in this population occurred in patients with pacemakers. The most common error in this subgroup was failure of the algorithm to detect evident underlying rhythms, such as sinus rhythm with dual chamber pacing or underlying atrial fibrillation, in 40.2% (138/343). Dual chamber pacing was an evident problem, with a specificity of 100% but a sensitivity of only 28.1% (73/260), most often caused by relatively minor mis-identification of these patients as simply ventricular paced. More important was complete failure to identify pacemaker activity in 10.2% of the paced patients (35/343). Because special diagnostic problems and special engineering solutions apply to pacemaker detection algorithms, these patients were eliminated from further data analysis, which focuses on the remaining 3954 consecutive unpaced ECGs in the group. Predominant physician-confirmed primary rhythms in this unpaced patient population include sinus rhythm (90.5%), atrial fibrillation (6.3%), atrial flutter (1.0%), and atrial tachycardia (0.9%).

Misdiagnosis of atrial fibrillation and its clinical consequences

PurposeComputer algorithms are often used for cardiac rhythm interpretation and are subsequently corrected by an overreading physician. The purpose of this study was to assess the incidence and clinical consequences of misdiagnosis of atrial fibrillation based on a 12-lead electrocardiogram (ECG).  MethodsWe retrieved 2298 ECGs with the computerized interpretation of atrial fibrillation from 1085 patients. The ECGs were reinterpreted to determine the accuracy of the interpretation. In patients in whom the interpretation was incorrect, we reviewed the medical records to assess the clinical consequences resulting from misdiagnosis.   ResultsWe found that 442 ECGs (19%) from 382 (35%) of the 1085 patients had been incorrectly interpreted as atrial fibrillation by the computer algorithm. In 92 patients (24%), the physician ordering the ECG had failed to correct the inaccurate interpretation, resulting in change in management and initiation of inappropriate treatment, including antiarrhythmic medications and anticoagulation in 39 patients (10%), as well as unnecessary additional diagnostic testing in 90 patients (24%). A final diagnosis of paroxysmal atrial fibrillation based on the initial incorrect interpretation of the ECGs was generated in 43 patients (11%).  Conclusion:  Incorrect computerized interpretation of atrial fibrillation, combined with the failure of the ordering physician to correct the erroneous interpretation, can result in the initiation of unnecessary, potentially harmful medical treatment as well as inappropriate use of medical resources. Greater efforts should be directed toward educating physicians about the electrocardiographic appearance of atrial dysrhythmias and in the recognition of confounding artifacts.

Monday, February 18, 2019

Chest pain and Convex ST Elevation in Precordial Leads

A 30-something y.o. male with PMH significant for anxiety, asthma, and alcohol use disorder presented with chest pain x 1 week.  Patient thinks he has an asthma flare, with wheezing. He subsequently developed fevers and chills, and then left-sided chest pain associated with a cough. His breathing and infectious sx then improved. Today, however, he developed constant chest pain radiating into left arm around 1345. He states the pain is improving now. He had associated "swimmy, head rush," which is no longer present. He denies associated shortness of breath, sweating, numbness, tingling. Onset of pain was while sweeping at work. He was able to ride bike on the day of presentation without difficulty.

No cardiac history. Non-smoker, no EtOH, no h/o DVT. No leg swelling. No risk factors for CAD.

Here is his ECG:
There is ST elevation, up to 2.5 mm in V2, with convexity.
Generally, STE with convexity in any of leads V2-V6 is abnormal and highly suggestive of ischemia (anterior MI, LAD occlusion).

As always, pre-test probability is critical.  And this patient's pretest probability was extremely low.

One is not supposed to use the formula that differentiates Normal Variant ST Elevation (often referred to as early repolarization) when there is convexity.  However, if one did, here is the result:

QTc = 428 ms
ST Elevation at 60 ms after the J-point in lead V3 (STE60V3) = 2.5 mm
R-wave amplitude in V4 (RAV4) = 12 mm
Total QRS amplitude in lead V2 (QRSV2) = 25 mm

4-variable formula value = 17.92.  This is below the cutoff for LAD occlusion (18.2), but not by a lot, so one must be careful.

There was a previous available.  I did not see it until writing this post:
The new one is changed.  Is that significant?

Although looking for change from an old ECG can be very helpful, it is not foolproof.

See this post and references below:
Kambara (see below) showed that early repolarization is dynamic; see this case and discussion: 

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

So we did a bedside echo:

Parasternal short axis shows excellent anterior wall contractility

A subsequent ECG approximately one hour later with continued chest pain:
Now there is an RSR', but the P-wave is inverted, so the RSR' is due to lead placement too high.
No evolution, no evidence of OMI/STEMI

QTc = 419
STE60V3 = 4.5
RAV4 = 19
QRSV2 = 17.5

Formula value = 18.83 (this is now consistent with LAD occlusion)

At this time, the first troponin I returned undetectable, below 0.010 ng/mL, which if the chest pain was acute, might be expected in OMI.  However, this patient had very prolonged chest pain.

So we waited for another, and a troponin drawn 2 hours later was still less than 0.010 ng/mL.

1.  The 1st ECG has false positive convexity.
2.  The 2nd ECG has a false positive 4-variable formula

I discharged the patient after excluding other serious causes of chest pain.

Learning points:
1.  Be skeptical of an apparently positive ECG when the pretest probability is extremely low.  (Do not be skeptical if the ECG is unequivocally positive!)
2.  Although the reperfusion decision does not depend on troponin in acute chest pain, an undetectable troponin in prolonged chest pain is strong evidence that the ST elevation is not ischemic.
3. Use Echo
4.  The formula does have false positives.
5.  Convexity rarely has false positives.

References on stability of early repolarization over time.

1. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

2. Mehta MC. Jain AC.  Early Repolarization on the Scalar Electrocardiogram.  The American Journal of the Medical Sciences 309(6):305-11; June 1995.

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

Comment by KEN GRAUER, MD (2/18/2019):
Excellent example by Dr. Smith of how use of other parameters (ie, pre-test probability; Echo at the bedside & serial troponins) may prove invaluable for ruling out acute cardiac disease. 
  • Although a previous ECG was found on this patient — this apparently was not available in the ED at the time acute decisions was done. I therefore focus my comments on the 2 ECGs that were done in the ED (Figure-1).

Figure-1: The 2 ECGs in this case that were done in the ED. Not included in Figure-1 is the previous ECG on this patient — as this tracing was not available at the time acute decisions were made (See text).
In my experience — there is a tendency (even among experienced interpreters) to jump at specific ECG findings, without first using a systematic approach to interpret the initial tracing — and then, failure to apply lead-to-lead comparison of this tracing with other ECGs in the case. I generally start with full evaluation of the initial tracing ( ECG #1which is the TOP tracing in Figure-1):
  • Rate & Rhythm: There is a fairly regular sinus rhythm at ~65-70/minute.
  • Intervals: The PR, QRS & QT intervals are all normal.
  • Axis: There is a rightward axis of ~100 degrees (ie, predominant negative deflection in lead I ).
  • Chamber Enlargement: None.
  • QRST Changes waves – wave progression – ST-wave changes)A small Q wave is seen in lead III — there is an rSR’ complex in lead V1, consistent with incomplete RBBB (narrow QRS; s waves present in both leads I and V6— Transition (ie, the place where the R wave becomes taller than the S wave is deep in the chest leadsdoes not occur until lead V6 (if then, as depth of the S in V6 looks to be equal to height of the R in V6 …). Perhaps the most remarkable finding in ECG #1 is the coved (and worrisome) ST elevation that is seen in leads V2-thru-V6.

IMPRESSION of ECG #1Sinus rhythm — right axis — incomplete RBBB — delayed transition — coved ST elevation in leads V2-thru-V6, albeit without reciprocal changes. Pre-test probability is low for acute cardiac disease (ie,younger age of this patient and a history more suggestive of an acute febrile illness rather than cardiac chest pain) — but, further evaluation is clearly indicated given ST elevation to rule out a worrisome cause (ie, MI, myocarditis).
  • There may be malposition of lead V3 in ECG #1. That’s because appearance of not only the QRS complex, but also the ST-T wave in lead V3 looks very different than in neighboring leads V2 and V4. In fact, the shape and amount of ST elevation looks quite similar in leads V2, V4 V5 — so the appearance of lead V3 just doesn’t “make sense”. That said, the overall “theme” of ECG #1 is clear regardless of whether lead V3 is or is not accurately placed.

What is Different in ECG #2?
In ECG #2 — there once again is sinus rhythm — right axis deviation — and an incomplete RBBB pattern. That said — ST elevation is clearly less compared to what had been seen in ECG #1. What Else is different between these 2 tracingsWhat might account for some of these differences?

It is much more likely that leads V1 and V2 were placed inappropriately high on the chest in ECG #2. This is because: ithe initial component of the P wave in both V1 and V2 in ECG #2 is negative (the initial component of the biphasic P wave in ECG #1 was positive; and the P was all positive in V2 in ECG #1); andiithere is now an rSr’ pattern alsoin lead V2 in ECG #2.
  • The zone of Transition is very different in ECG #2 !!! Note that there is already a substantial R wave by lead V4 — and the R wave clearly becomes predominant between V4-to-V5. In contrast, the R wave never became predominant in ECG #1.

IMPRESSION of ECG #2The shape and amount of ST-T wave elevation in lead V3 of ECG #2 looks to be similar to what it was in leads V2, V4 and V5 in ECG #1. It is possible that the reason the amount of ST elevation is less and the ST segment shape took on a more benign-looking appearance (ie, concave up) in leads V4-thru-V6 of ECG #2 may simply be a result of the fact that these 3 leads now all manifest a predominant R wave. There is probably no meaningful change in ST-T wave appearance between ECG #1 and #2.
  • The BEST evidence supporting the absence of any serious heart disease in this patient was forthcoming from the combination of — low pretest probability — completely normal Echo — negative troponin values. As a result, the patient was safely discharged from the ED.
  • It is likely that there was lead misplacement in both tracings — and probably a difference in the way in which chest leads were misplaced. Failure to recognize this might result in wrongly attributing the “change” in ST-T wave appearance between ECGs #1 and 2 as due to a dynamic change.
  • It would be extremely helpful to obtain another 12-lead on this patient after meticulously verifying lead placement. If this true “baseline” ECG (with verified lead placement) still results in a worrisome-looking convex ST elevation repolarization pattern — it would be good to have this on the chart in the event this patient returns to the ED with another episode of chest pain.
  • A useful PEARL to consider in patients with worrisome-looking baseline tracings — is to GIVE THE PATIENT miniaturized copy of their ECG to carry on their person, so that they can then show this to medical providers in the event of a subsequent trip to the ED.

Our THANKS to Dr. Smith for presenting this case.
  • For “My Take” on use of the Systematic Approach to ECG Interepretation — CLICK HERE.
  • For more on recognizing Lead V1, VMalposition — CLICK HERE.

Saturday, February 16, 2019

How much time are you willing to wait for OMI to become STEMI (if it ever does)?

Written by Pendell Meyers, few edits by Smith

A man in his 60s with history of stroke and hypertension but no known heart disease presented with chest pain that started on the morning of presentation at around 8am.

Here is his triage ECG when he presented at 1657:
What do you think?

There is sinus rhythm with normal QRS complex and ST depression in V2-V5, maximal in V3-V4. There is no ST depression in V6, II, III, or aVF, and no significant ST elevation in aVR, all confirming that the ST vector is not consistent with diffuse subendocardial ischemia, but rather a focal ST vector pointed at the posterior wall. It is posterior OMI until proven otherwise.

This ECG is quite obvious for long-time readers, and you may think this far too easy to be presented on this blog.

But in actual practice, similar patients are routinely missed and under-treated, as you will see as this case progresses. "Posterior STEMI" may not even technically exist according to the current (2013) ACC/AHA STEMI guidelines, as it is not described as a "STEMI equivalent" and the only relevant statement in the guidelines is: "In addition, ST depression in 2 precordial leads (V1-V4) may indicate transmural posterior injury."  JACC 61(4):e78-140; page e83.

Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it.

It is true that other documents occasionally describe "abnormal ST segment elevation" in the posterior leads (commonly accepted criteria is 0.5 mm in just one lead V7-9), but as far as I can tell all of these documents specifically avoid calling this condition STEMI and specifically avoid using any terminology similar to "STEMI equivalent."  The once exception I have found is the NCDR guidelines, which actually do give a definition: "ST elevation in the posterior chest leads (V7 through V9), or ST depression that is maximal in V1-V3, without ST segment elevation in other leads, demonstrating posterobasal myocardial infarction, is considered a STEMI equivalent and qualifies the patient for reperfusion therapy." I find this definition problematic because the maximal STD in posterior OMI frequently extends out to V4 rather than V3.

So it is very unclear to me whether or not "posterior STEMI" is actually a recognized entity under our current guidelines. It is my opinion that this lack of clarity is part of the reason why patients with posterior OMI are frequently underecognized and undertreated. Regardless of its formality, the more important problem is that it is certainly not recognized in widespread current practice.

Back to the case:

As is unfortunately common practice, a repeat ECG was only performed after the initial troponin T returned elevated at 0.19 ng/mL 1.5 hours after arrival.

Persistent posterior injury. The ST depression which was present in V5-V6 is now gone, which may be either resolution or relative ST elevation of the lateral wall (which would be common with posterior involvement), either way it is dynamic and further proves the existence of ACS.

This was interpreted as "no significant change." Cardiology was called, but elected not to take the patient to the cath lab for some reason, but instead simply admitted him.

The second troponin returned at 0.25 ng/mL. There is no mention of whether the patient had ongoing symptoms. The records show that heparin drip had been ordered in addition to aspirin which had already been given.

The third troponin returned at 22:05 at 0.92ng/mL. A repeat ECG is recorded at 2333, along with a posterior ECG minutes later:

Leads labelled V4-V6 are actually V7-V9 on the posterior thorax. Obvious inferoposterior STEMI.

At this time, just before midnight, the cath lab was activated. The acute finding is reported as a 100% thrombotic lesion of the proximal left circumflex (TIMI 0 flow). In the views below, I would have guessed that this vessel was a ramus intermedius as it seems to be the middle vessel of a trifurcation of the left main, but I will simply defer to the true angiographers. See the occlusion here:

Here is the ECG after intervention showing resolution:

The peak troponin T was 2.35 ng/mL (fairly large MI). The patient had no further complications. Unfortunately an echo was not available.

I hope you are surprised at this case, but I fear that most readers recognize this as the sad reality that exists across many institutions as of 2019. I attribute this mostly to the inadequate current paradigm of myocardial infarction which inspires failure for all such cases that are not obvious according to the STEMI criteria. If this case were an acute occlusion of ANY other important artery (say for example, the superior mesenteric artery, or the middle cerebral artery), 7 hours from arrival to diagnosis despite ongoing evidence of occlusion would be seen as an important and unacceptable delay to diagnosis. Yet in our STEMI vs. NSTEMI paradigm this is simply not understood as an emergent arterial occlusion syndrome. "Time is muscle," but somehow only for occlusions that cause STEMIs, not for occlusions that are more subtle.

Hopefully fixing the paradigm by reframing this disease as an acute arterial occlusion will help people understand this problem. This patient had an Occlusion MI (OMI) and needed emergent reperfusion therapy. It is common sense that such patients have a higher probability of survival and of myocardial preservation if such an OMI is reperfused early, and there is no study that contradicts this notion.

Cases like this will be carefully quantified and studied in our ongoing retrospective study designed to quantify the difference in accuracy between advanced ECG interpretation and the current STEMI criteria. Specifically, cases such as this one will detail the difference in time between diagnosis of Occlusion MI by expert ECG interpreter vs. the current STEMI criteria. This case, for example, would be nearly 7 hours of ischemic time between arrival and cath lab activation.

How much time are you willing to wait for OMI to become "STEMI" (if it ever does)?

Comment from K. Wang:

Very clinically important point is being made by this case as usual. What is "STEMI"? It's an ECG manifestation of transmural MI from an occluded coronary artery registered in the ECG leads FACING the infarcted ventricular wall. Yes, a transmural MI occurs in the posterior wall, too,  The only reason we don't see ST elevation in the "routine" 12 lead ECG is because it does not include posterior chest leads, which are the leads FACING the infarcted wall. Do we have to take posterior chest leads to see it then? No, we already have it . It's in the anterior chest leads registered reciprocally, i.e. upside down, as ST depression. If one wants to confirm it, just pick up the tracing, turn it upside down and look at it against light. There, one sees typical STEMI to one's satisfaction. I agree with Dr. Smith that, if current ACC guidelines are not clear about posterior STEMI, it should be clarified for better patient care.
K. Wang.

Comment by KEN GRAUER, MD (2/16/2019):
The importance of early recognition of an acute OMI (instead of waiting until it becomes a “stemi” ) can not be overstated! The consequences of failing to appreciate this critical concept is made painfully evident in this case by Dr. Meyers — in which it took over 6 hours until this man with new chest pain was finally taken to the cath lab. Superb review (above) by Dr. Meyers about the details of this case. I focus My Comments on 3 of the ECGs that were shown in this case (Figure-1).
Figure-1: The 1st, 3rd and 4th ECGs shown in this case (See text). 
The crux of this case — is the failure to appreciate that acute posterior OMI was clearly evident in the initial ED ECG ( = ECG #1). The abnormal findings in ECG #1 are localized (ie, ST depression in leads V2-thru-V5) — and, in the setting of new chest pain — ECG #1 should be interpreted as acute posterior OMI until proven otherwise. Had the treating clinicians recognized these concepts — they would have: iobtained a 2nd ECG long before 18:33 (~ 1 1/2 hours after ECG #1 was done); and, iithey would have advocated for activating the cath lab.
  • SUGGESTION: Consider use of the Mirror Test”. I’ve been teaching this concept for over 36 years (since including it in my first ECG publication that I wrote in 1983). The mirror test is a simple visual aid: It helps the clinician recognize acute posterior infarction. The mirror test is based on the concept that none of the standard 12 leads directly view the posterior wall of the LV — BUT — the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the mirror-image” of leads V1, V2 and V3. It should be readily apparent that the mirror-image view of leads V2 and V3 in ECG #1 (just to the right of ECG #1 in Figure-1— shows a QRST complex that is almost shouting out, “I’m having an acute posterior OMI (ie, large Q waves; coved ST elevation and symmetric T wave inversion in this mirror-image). With a little bit of practice — use of the Mirror Test should facilitate near-instant recognition of subtle changes such as the slightly-taller-than-expected anterior R waves in leads V2 and V3 of ECG #1 (which “become” Q waves in the mirror image view) — and the “shelf-like” shape (ie, nearly straight) ST depression in leads V2,V3 of ECG #1 (which “becomes” ST elevation in the mirror-image view).
ECG #2 (which is not shown in Figure-1— was done ~1 1/2 hours after ECG #1. It showed slightly less ST depression than was seen in ECG #1 — but no sign of ST elevation (ie, no “stemi” ).
Review of ECGs #3 and #4 is especially interesting. ECG #3 was done 6+ hours after ECG #1. It shows downward slanting and slightly greater ST depression in a number of chest leads compared to ECG #1 — but still NO ST elevation in the inferior leads, and NO reciprocal ST depression in lead aVL.
  • ECG #4 was done just a few minutes after ECG #3 for the purpose of directly assessing posterior leads V7, V8 and V9. These posterior leads show obvious ST elevation. But DID YOU SEE that this 4th ECG (done just minutes after ECG #3) now shows: iST elevation in leads III and aVF that was not present in ECG #3; iireciprocal ST depression in lead aVL that was not present earlier; andiiisignificantly more ST-T depression in leads V1, V2, V3 compared to what was seen JUST MINUTES EARLIER in these same leads in ECG #3. This means we are just now in ECG #4 catching acute evolutionary changes, that are evolving in front of us over these very few minutes between the time when ECGs #3 and 4 were done.
  • KEY POINT Although many providers advocate for doing posterior leads when looking for acute posterior involvement — realize that the magnitude of ST elevation that you are likely to see in posterior leads with acute posterior infarction is usually modest. The reason the amount of ST elevation in leads V7, V8 and V9 in ECG #4 is as large as it is — is because this ECG #4 was obtained during the very moments that acute evolution was developing (ie, Note there is now inferior lead ST elevation in ECG #4 — and note how profound is the downsloping ST depression in leads V2 and V3).
  • Finally — Note how obvious acute posterior infarction is in the Mirror Test of leads V1, V2, V3 in ECG #4 (insert to the right of ECG #4 in Figure-1). While use of posterior leads (V7,V8,V9) clearly showed ST elevation in ECG #4 — Are posterior leads really needed to make the diagnosis of a STEMI in this case? I am not saying that you should never do posterior leads — but rather, that with a little bit of practice — it’s possible to make the diagnosis of acute posterior OMI much more quickly by just using the standard 12 lead ECG. COMMENT  I don’t think I’ve seen a case in which posterior leads told me something that I did not immediately know from use of the standard 12-lead ECG (with Mirror Test of the anterior leads).
Our THANKS to Drs. Meyers and Smith for presenting this highly insightful case.
  • For another example of the Mirror Test CLICK HERE.

Recommended Resources