A patient with cardiac arrest, ROSC, and right bundle branch block (RBBB).

A patient arrived after PEA arrest, with ROSC after intubation and chest compressions.

Here is the initial 12-lead ECG:

What is the appropriate therapy?

This ECG is all but diagnostic of hyperkalemia.  There is an irregular, slow, wide complex rhythm.  Is it ventricular escape? (no, because it is irregular and there appear to be conduced P-waves).  Or atrial fib with slow ventricular response? (no, because it is irregular and there appear to be conducted P-waves).

Because you can see some conducted atrial activity in lead II across the bottom, you know that it is of supraventricular origin.  So then it is clear that there is Right Bundle branch block (RBBB).  However, it is extremely wide (the computer measured it at 193 ms, and I think this is correct), much wider than RBBB should be.  Also, you can see peaking of the T-waves in many leads.


The physicians did not recognize this, but they did think to give calcium empirically.  The K returned at 7.1 mEq/L and complete therapy for hyperK was given.

Here is the ECG after therapy:

Probable junctional rhythm
RBBB
QRS of 133 ms by computer (looks correct)

See more similar cases here:
https://hqmeded-ecg.blogspot.com/2018/04/is-this-just-right-bundle-branch-block.html


QRS duration in RBBB and LBBB
RBBB by definition has a long QRS (at least 120 ms).  But very few are greater than 190 ms.  Literature on this is somewhat hard to find, but in this study of patients with RBBB and Acute MI, only 2% of patients with pre-existing RBBB had a QRS duration greater than 200 ms.  This study only reported durations in 10 ms intervals up to 150 ms, but one might extrapolate from it that approximately 10% of patients with baseline RBBB have a QRS duration greater than 160 ms.  193 ms would be quite unusual.

The point of this is that if you see BBB with a very long QRS, you must suspect hyperkalemia or sodium channel blockade (e.g, flecainide).  Then of course the peaked T-waves should tip you off.   Unless a patient has severe hypercalcemia (this should be evident by a short QT on the ECG as seen at the bottom of this post), or severe hyperphosphatemia (which is very unusual), treatment with calcium is harmless if you read an ECG falsely positive for hyperkalemia.

So don't wait for the laboratory K or you might be resuscitating a cardiac arrest (see the case at this post with ECGs #3 and #4 of this post).

How about LBBB?

In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms. 



Hypercalcemia (courtesy of K. Wang)

Notice the very short QT interval, and very short ST segment

https://hqmeded-ecg.blogspot.com/2018/04/is-this-just-right-bundle-branch-block.html

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Comment by KEN GRAUER, MD (2/28/2019):

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The important theme of recognizing the many “faces” of Hyperkalemia is wonderfully illustrated in this case by Dr. Smith. I’d like to amplify some of the points highlighted by Dr. Smith — and explore some of them in further detail.

• POINT #1: IF the rhythm is supraventricular, but the QRS complex is overly wide — Think of Hyperkalemia! It’s too easy to overlook this diagnosis if you are not actively considering it as a possibility each time you see a supraventricular rhythm that appears to be wider-than-you-think-it-should-be.
• POINT #2: Once you consider the possibility of Hyperkalemia — Look extra carefully at the T waves. They may not be as tall or “classically peaked” with narrow T wave base as is common in earlier stages of hyperkalemia (ie, when the QRS complex is still narrow) — but it is easier to appreciate T waves that are probably-more-peaked-than-they-should-be IF you are looking for them.
• POINT #3: Severe Hyperkalemia sometimes results in T wave inversion rather than peaked T waves! This may be in only a few leads — as opposed to the positively peaked T waves that tend to be more generalized. The T wave inversion I have seen with severe hyperkalemia is often a near “mirror-image” of the positive T wave peaking (ie, negatively peaked T waves).
• POINT #4: Severe Hyperkalemia commonly results in reduced P wave amplitude. Ultimately, there may be a sinoventricular rhythm — in which despite the disappearance of P waves on the ECG, conduction from the SA node through the atria and ventricles continues. This may result in the paradox that despite a regular wide QRS rhythm without P waves — sinus mechanism may be preserved.
• POINT #5: Severe Hyperkalemia commonly results in bradycardia (which may be severe) — and all kinds of unusual conduction blocks. Many of these arrhythmias defy logical interpretation. That said, precise determination of the rhythm is not clinically important — because treatment of the severe hyperkalemia is often all that is needed to restore a normal sinus rhythm.
• POINT #6: In addition to marked QRS widening — severe Hyperkalemia may distort QRS morphology, including marked axis deviation.
• POINT #7: You have NO IDEA about what the underlying QRS complex and ST-T wave really look like — until you correct the severe Hyperkalemia. For example, preexisting severe diffuse ST depression might attenuate diffusely tall and peaked T waves from severe hyperkalemia — resulting in a deceptively benign picture. Only after serum K+ has been normalized might it become apparent that there was preexisting severe ischemia.

For clarity — I’ve put the 2 ECGs in this case together to illustrate the above points (Figure-1):

Figure-1: The 2 ECGs in this case (See text). 

I think it could be EASY to overlook the etiology of the TOP tracing ( = ECG #1) in Figure-1. That’s because the QRS complex does not look so wide in many of the leads! The problem arises because of the difficulty of knowing where the QRS complex ends ...

• The 2 KEY leads in ECG #1 are leads V1 and V2. These are the 2 leads on this 12-lead tracing for which there is NO doubt about where the QRS begins and ends. I have drawn vertical RED lines to show where the QRS complex ends in simultaneously-obtained lead V3, as well as in the long lead II rhythm strip at the bottom of the tracing.
• Using this exact QRS duration that I measured with these vertical RED lines — I’ve drawn in vertical BLUE lines in the remaining leads on this tracing to illustrate the limits of the QRS complex. So, rather than profound ST segment depression in leads V4, V5 and V6 — this patient with severe hyperkalemia manifests a bizarre QRS morphology.
• And once we realize how wide and bizarre the QRS complex in ECG #1 really is (which means we need to be considering hyperkalemia) — it becomes easier to appreciate that although wide in base, the T waves in leads I, II, aVL, aVF, and V3-thru-V6 do look pointed ...

What is the Rhythm in ECG #1?

The long lead II rhythm strip at the bottom of ECG #1 shows the 9 beats in this tracing to be irregular. This is not sinus rhythm — because there is no upright P wave in lead II. But consistent atrial activity in the form of a tiny amplitude negative P wave is present in front of 5 of the beats (RED arrows).

• We know that these non-sinus P waves are conducting — because the PR interval preceding beats #4, 5, 7, 8 and 9 is constant! Therefore, despite marked QRS widening — this is a supraventricular rhythm.
• Beat #6 is a junctional escape beat — because it ends a short pause, and manifests QRS morphology identical to that of the atrial-conducted beats. No preceding P wave is seen in any of the simultaneously-recorded leads (ie, No P waves precedes beat #6 in leads V1, V2, V3 or in the long lead II).
• No P wave precedes beats #1 and #3 — so these are presumably also junctional beats.
• I’m not sure what beat #2 is. It occurs earlier-than-expected, but the large preceding T wave may (or may not) be hiding atrial activity.
• BOTTOM LINE: This is an unusual rhythm. That said, the important point was highlighted by Dr. Smith — namely, that despite marked QRS widening and definite irregularity — the fact that a number of P waves are conducting (even though not of sinus etiology) confirms this to be a supraventricular rhythm.
• Clinically: It does not matter what this rhythm is — because it will probably convert to sinus rhythm once hyperkalemia is corrected and the patient has stabilized.

What do We See in ECG #2?

As per Dr. Smith — duration of the QRS complex has decreased significantly in ECG #2. QRS morphology now looks much more typical for RBBB (rsR’ complex in lead V1; narrow R wave with wide terminal S waves in leads I and V6). But now there is no atrial activity at all ...

• Presumably the rhythm in ECG #2 is junctional, with underlying RBBB. That said, given the clinical scenario (ie, extended cardiac arrest with PEA prior to ROSC) — I think it quite possible that there was significant associated acidosis, which may well have resulted in even more severe hyperkalemia than the initial lab value of 7.1 mEq/L suggests (? depending on when labs were drawn with respect to the ongoing resuscitation). There can be a lag between laboratory electrolyte correction and normalization of the cardiac rhythm — so — Could this be a sinoventricular rhythm?
• I think it is interesting to compare QRS morphology in ECG #1 and ECG #2. Isn’t the initial part of the QRS complex almost identical in both tracings?
• There was clearly more of a rightward axis in ECG #1. On occasion, I have seen bizarre axis deviations with marked hyperkalemia — including an all negative complex in lead I that totally resolved after correction of the electrolyte disturbance.
• We are not told what the final serum K+ value was. Almost regardless of what it was — I suspect there has not yet been true stabilization of this patient at the time ECG #2 was done — as T waves in ECG #2 still appear more prominent and more-peaked-than-they-should-be with simple RBBB. In addition — the T wave inversion in leads V1 and V2 of ECG #2 is deeper and more pointed than typical secondary ST-T wave changes of RBBB. Although this could be ischemic — it might also reflect residual ST-T wave effect from resolving severe electrolyte disturbance. We won’t know the answer to this, until more time has passed, and until an additional ECG or two is done.
• Finding a prior baseline tracing on this patient might help to resolve some of the questions I just raised in the preceding bullet point ...

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

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.


K. Wang comment:

When we read a ventricularly paced ECG and see regularly occurring QRSs after each pacer spike, we are satisfied saying that  the pacemaker is functioning normally and the ECG reading ends there. However, it is very important to see what the atria are doing; are they in sinus rhythm (with or without association with the QRS)?, retrogradely conducting?, fibrillating?, fluttering? If fibrillating, the patient has the same risk of systemic embolization as in non-paced (ordinary) atrial fibrillation. V1 lead is the best lead to see what the atria are doing (see case 2 ECG 2 above). By the way, it looks like we are also dealing with hyperkalemia in case 2.

K. Wang.

Diagnostic performance of a computer-based ECG rhythm algorithm

https://www-sciencedirect-com.ezp2.lib.umn.edu/science/article/pii/S0022073605000488

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

https://www.sciencedirect.com/science/article/pii/S0002934304004784

Purpose: Computer 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).  Methods:  We 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.   Results: We 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.

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.

Therefore:
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.

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Comment by KEN GRAUER, MD (2/18/2019):

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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).

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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 #1, which 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 ( = Q waves – R wave progression – ST-T 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 leads) does 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 #1: Sinus 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.

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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 tracings? What might account for some of these differences?

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ANSWER:

It is much more likely that leads V1 and V2 were placed inappropriately high on the chest in ECG #2. This is because: i) the 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); and, ii) there 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 #2: The 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 a 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.

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FOR MORE:

• For “My Take” on use of the Systematic Approach to ECG Interepretation — CLICK HERE.
• For more on recognizing Lead V1, V2 Malposition — CLICK HERE.