Wednesday, May 31, 2023

Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mass delusion (and Opiate pain relief).

I received the following text message with these 3 EKGs (providers text me ECGs all day every day; most are false positives; many are subtle true positives):

"Hi Steve, here are 3 EKGs for you (my colleague's case).  A 67 yo f developed chest pain this morning."

EKG #1

Followed 15 minutes by this #2 EKG:

Then the patient received aspirin and Dilaudid (hydromorphone, same effect as morphine) and the pain went away and there was this 3rd ECG:

Smith comment: hydromorphone will make any pain go away (or improve) without any improvement in the underlying pathology.  Do NOT give it unless you are committed to the cath lab!!

"Cath attending is aware.  I think it is OMI; am I right?  Cath lab declined as it is not a STEMI."

Smith Interpretation: there is diffuse ST depression followed by a hyperacute T-wave. This is classic de Winter pattern, and here it involves both anterior and inferior walls, so this is probably OMI of the mid LAD that also supplies the inferior wall (a "wraparound," or "Type III," LAD because it wraps around to the inferior wall).  There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves).

I sent the last one to the Queen of Hearts #PMCardio app and here is the verdict:

My response: 

"It’s not even subtle.  It is one of the few OMI patterns that is really well described: de Winter’s T-waves. And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! They are simply Hyperacute T-waves with depressed ST takeoff.  Even described in the New England Journal.  This is one that even cardiologists with no knowledge of subtle OMI should know.  LAD Occlusion.

Often, with this pattern, there is a trickle of flow through the LAD. So I doubt it was 100% Occluded. But the flow was greatly diminished and the infarct will be large.

So I encouraged her to be sure the patient goes to the cath lab emergently.

Many hours later, I asked what the angiogram showed.  

Here is her astonishing reply:

"Well, they still haven’t taken her to the Cath Lab yet!!!!  Trop at 5000 by now."

I asked: "Is this at the University of YYYYYYYY?"  

She answered: "I am so embarrassed to say that yes it is. I was not the attending, but I feel very bad for this patient who couldn’t defend herself." 

Smith Comment: This is all too common.  Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset.  It is a mass delusion.  

The patient did finally go to the cath lab and had a 99% Mid LAD Occlusion.

My response was: "This interventionalist should find a job that he/she enjoys doing."

This cardiologist has directly violated the ACC Guidelines on STEMI equivalents, and the patient will likely suffer increased morbidity and mortality as a result.

Opiates are associated with worse outcomes in Myocardial Infarction.

See this case: A man his 50s with chest pain. What happens when you treat with morphine rather than with reperfusion?

----See this study showing an association between morphine and mortality in ACS:
Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4. Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149:1043–1049.

And Another that we wrote:

----Bracey, A.  Meyers HP.  Smith SW.  Wei L. Singer DD.  Singer A.  Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion Myocardial Infarctions. Academic Emergency Medicine 27(S1): S220; May 2020.  Abstract 556.
Main result: STEMI(-) OMI Patients

65 (23.9%) patients were found to have STEMI(-) occlusion myocardial infarction (OMI) at the time of cardiac catheterization. The 45 patients with STEMI(-) OMI without pre-cath opioids had a door-to-balloon time of 75 minutes, vs. 684 minutes for the 25 STEMI(-) OMI with pre-cath opioids.

My Comment by KEN GRAUER, MD (5/31/2023):
I focus my comment on counting the ways that today's case should have been recognized as clear indication for prompt cath immediately on seeing the initial ECG — and at the very latest, 15 minutes after this when the 2nd ECG was recorded.
  • For clarity in Figure-1 — I reproduce today's initial tracing.

Figure-1: The initial tracing in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The Need for Prompt Cath: — Way #1 —
In a 67-year old patient with several hours of new chest pain — ECG #1 clearly fits the description of deWinter T waves. As per Dr. Smith — this entity is now formally endorsed as a "STEMI-equivalent" pattern in the 2022 ACC Guidelines.
  • In discussing deWinter T waves — I find it helpful to return to the original commentary by deWinter and colleagues (N Engl J Med 359:2071-2073, 2008) — in which they described a “new ECG pattern" without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.
  • To quote the authors’ original description of the new ECG pattern they reported on: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”
  • The authors went on to say: i) That the QRS complex was usually not widened (or no more than minimally widened); — andii) That most patients in their experience also manifested 1-2 mm of ST elevation in lead aVR.

  • To illustrate the spectrum of ECG findings — the authors included in their 2008 NEJM manuscript a composite picture taken from 8 representative tracings of patients in their study who manifested deWinter T waves. PEARL — I often refer to this composite picture (that I put in Figure-2) — as it serves to remind us of variations on the "theme" of deWinter T waves.

Figure-2: The deWinter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms.

MY OBSERVATIONS regarding De Winter T Waves: Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

  • Many (most) of these cases do not fit strict definition of “deWinter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, the number of leads that manifest giant T waves is limited.
  • I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. I suspect that to a large extent — what is seen on ECG depends greatly on when during the process the ECG is obtained. That said, for the practical purpose of promptly recognizing acute OMI — I feel ( = my opinion) that it matters less whether STEMI-criteria are satisfied or whether a "true" deWinter T wave pattern is present — vs the presence of simply "hyperacute" T waves (that are deWinter-like — and which indicate acute coronary occlusion all the same)


The Need for Prompt Cath: — Way #2 —
Giant T waves were not seen in each of the chest leads of the initial tracing in Figure-1. But regardless of whether you wanted to accept ECG #1 as consistent with a deWinter T wave pattern (or a "deWinter-like" pattern) — in a patient with new cardiac chest pain, this initial ECG is clearly indication for prompt cath:
  • There is J-point ST depression in 6 leads ( = leads I,II,III; aVF; V4,V5,V6). This ST depression is marked in most of these leads — in association with marked ST elevation in lead aVR, suggesting at the least diffuse ischemia.
  • ST coving and elevation is seen in leads V1 and V2. While the amount of ST elevation in these leads is not marked — its presence is clearly abnormal in lead V1, and the ST segment straightening in lead V2 in a patient with new chest pain suggests an ongoing acute process.
  • Hyperacute T waves (ie, much fatter-at-their-peak and wider-at-their-base than they should be) — are especially prominent in leads V3 and V4, and to a lesser extent in leads I,II; and V5,V6.
  • Although the QRST complex in lead aVL is tiny — the ST segment is elevated in this lead, and the T wave is hyperacute.
  • Reciprocal ST depression is seen in each of the inferior leads.

  • BOTTOM Line: In a patient with new chest pain — the findings in ECG #1 have to be interpreted as suggestive of acute proximal LAD occlusion until proven otherwise. Without a prior tracing for comparison — it's impossible to know if the QS complexes in leads V1-thru-V3 represent new anteroseptal infarction? — an old infarction? — or, a new infarction superimposed on a prior infarction. But even if this patient had a prior anterior infarction — the abnormal ST-T waves in literally all 12 leads is clear indication for prompt cath!


The Need for Prompt Cath: — Way #3 —
For ease of comparison in Figure-3 — I've put the first 2 tracings from today's case together.
  • Has there been any change during the 15 minutes that passed in the time between the recording of ECG #1 and ECG #2?

    Figure-3: Comparison between the first 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

    Comparison Between ECG #1 and ECG #2:
    Only 15 minutes passed between the recording of ECG #1 and ECG #2. But — Isn't there a significant difference between these 2 tracings?
    • I see no significant difference between these 2 tracings in the limb leads.
    • But in the Chest Leads — Lead-to-lead comparison suggests to me that there has been progression of ST-T wave abnormalities in each of these 6 chest leads! While the increase in ST elevation in leads V1 and V2 is subtle — there is clearly more J-point ST depression in leads V3 and V4 of ECG #2 — and — there is increased hyperacuity of the T waves in leads V3-thru-V6 that is most easily appreciated by comparing relative height of T waves in these leads, with amplitude of the QRS complex.

    • BOTTOM Line: The fact that ST-T wave changes have increased during the 15 minutes between the recording of these 2 ECGs qualifies as dynamic ST-T wave change — which in a patient with new chest pain, by itself is indication for prompt cath. 

    Tuesday, May 30, 2023

    Chest pain and shock: Is there a right ventricular OMI on this ECG? And should he undergo trancutaneous pacing?

    A 50-something man presented in shock with severe chest pain. His prehospital ECG was diagnostic of inferior posterior OMI.

    The patient was in clinical shock with a lactate of 8.  BP was 108 systolic (if a cuff pressure can be trusted) but appeared to be maintaining BP only by very high systemic vascular resistance.

    He appeared gray in color, with cool skin.

    Here is his ED ECG:

    There is bradycardia with a junctional escape.  
    What is the atrial activity?  Is it sinus arrest with junctional escape?  Or is it atrial fibrillation with complete AV block and junctional escape?  

    There is an obvious inferior posterior STEMI(+) OMI.  
    But also some STE in lateral leads.  
    So inferior, posterior, and lateral OMI.

    Is there also a right ventricular OMI (RV OMI, or RV MI)?

    How would one tell?

    On the initial 12-lead, any STE in V1 in the setting of inferior OMI is very specific and about 70% sensitive for right ventricular OMI.  This is because V1 sits directly over the RV.

    HOWEVER, this only applies when there is NO ST depression in V2.  STD in V2 "pulls down" the ST segment in V1 thus negating any sign of RV MI.

    In fact, if there is significant STD in V2, but NONE in V1, that is a sign of probable RV MI, as you would expect associated STD in V1 with such a posterior OMI.

    This is also true of V4R: its sensitivity drops greatly in the presence of posterior OMI.  See Kosuge reference below.

    Thus, the absence of STE in V1 does not by any means exclude RV MI, and even absence of STE in V4R would not exclude it.

    What to do?

    We recorded an ECG in which V1-V3 were put in the position of V4R-V6R, and V4-6 were placed in V7-9 to (academically) confirm posterior OMI.  I say academically because the STD in V2 is diagnostic -- posterior leads are NOT necessary.

    Here it is:
    There is STE and hyperacute T-waves across the right chest leads, and STE in posterior leads.
    This confirms inferior, posterior, lateral, and RV MI

    RV  MI often leads to shock and (systolic) hypotension.  Because the RV pressure is normally low (unlike the LV), it is perfused by systolic blood pressure in addition to diastolic, so hypotension is very bad for the RV.  Fortunately for this patient, even though his cardiac output was terrible, his SVR was keeping his BP high enough for the RV.  If it did not do so, norepinephrine would be indicated to maintain systolic BP

    As for the escape rhythm:
    It is narrow complex, and therefore it is in the His bundle or above (not below the His bundle).   When narrow (above His bundle), it is likely to be atropine responsive.

    Case continued

    A bedside ultrasound showed diminished LV EF and of course bradycardia.

    1 mg of Atropine was given and the heart rate increased transiently to 60.

    RVMI explains part of the shock.  IV fluids for more preload are indicated, but not too much, as the RV can be overloaded with fluid, cause the septum to bow into the LV, and then harm LV stroke volume and cardiac output, leading to worsening hypotension, worse RV perfusion, worse RV function, and more RV failure..

    Transcutaneous pacing was considered while the patient waited for the cath team.   And also intubation for both airway protection and facilitation of the external pacing.  The interventionalist was worried that if pacing were done, and then was interrupted for some reason, that it might result in asystole.  

    It is indeed a real worry that pacing can take away the escape rhythm.  I asked our electrophysiologist about this and he said that it primarily a worry when the escape is BELOW the His bundle.  Anyway, he said he would have just kept giving atropine as long as it worked.  However, raising the pulse to 60 is hardly "working" for a patient who needs a lot more cardiac output.

    Fortunately, the patient made it to the cath lab alive without pacing or intubation.


    Culprit Lesion (s): Thrombotic occlusion of the proximal RCA -- stented.  

    Comment: Proximal means proximal to the Right Ventricular Marginal Branch supplying the RV.  Not all proximal occlusions result in RV OMI because many people have collaterals from the LAD to the RV.


    Initial:                     29 ng/L (this is in normal range, as URL </= 35 ng/L)

    Then after PCI:   > 36,000 ng/L

    Post PCI ECG:

    Q-waves, Reperfusion, and Atrial Fib

    Later that day:

    Sinus with PACs and Q-waves with reperfusion

    And the next day:


    Learning Points:

    1. RV MI due to proximal RCA occlusion occurs in a significant proportion of RCA inferior OMI.

    2. Not all proximal RCA occlusion results in RV MI (i.e., it does not always result in STE in right side leads with poor RV function because of LAD collaterals.)

    3. ST Elevation in V1 is moderately sensitive for RV MI, but not sensitive at all when there is STD in V2

    4. STD in V2 without STD in V1 is a sign of RV MI

    5. RV MI can cause hypotension. 

    6. The RV is supplied during systole as well as diastole. 

    7. The RCA supplies the SA node and RCA OMI can result in sinus arrest.

    8. Atropine usually works in junctional rhythm with a narrow complex

    9. You can try right chest leads to help diagnose RV MI

    10. Transcutaneous pacing should not result in subsequent pacing insensitivity unless the escape is infra-Hissian (below the bundle of His).  Such an escape would have a wider complex.

    Literature cited

    In inferior myocardial infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction



    In the presence of inferior myocardial infarction (MI), ST depression (STD) in lead I has been claimed to be accurate for diagnosis of right ventricular (RV) MI. We sought to evaluate this claim and also whether ST Elevation (STE) in lead V1 would be helpful, with or without STD in V2.


    Retrospective study of consecutive inferior STEMI, comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. STE and STD were measured at the J-point, relative to the PQ junction. The primary outcomes were sensitivity/specificity of 1) STD in lead I ≥ 0.5 mm and 2) STE in lead V1 ≥ 0.5 mm, stratified by presence or absence of posterior (inferobasal) MI, as determined by ≥0.5 mm STD in lead V2, for differentiating RVMI from non-RVMI.


    Of 149 patients with inferior STEMI, 43 (29%) had RVMI and 106 (71%) did not. There was no difference in the presence or absence of at least 0.5 mm STD in Lead I between patients with (37/43, 86%) vs. without RVMI (85/106, 80%, p = 0.56). In those with, vs. without, RVMI, (15/43, 35%) had STE in V1, versus (17/106, 16%) (p = 0.015). Specificity of STE in V1 for RVMI was 84%; sensitivity was 35%. Sensitivity was higher without (69%), than with (35%), STD in V2.


    Among inferior STEMI, the presence of any ST depression in lead I does not help to diagnose RVMI. ST elevation ≥0.5 mm in lead V1 is specific for RVMI, and moderately sensitive only if concomitant STD ≥ 0.5 mm in V2 is not present. Although STE in V1 is quite specific, overall the diagnostic characteristics of the standard 12‑lead ECG are inadequate to definitively diagnose, or exclude, RVMI, as defined angiographically.


    Kosuge M, Ishikawa T, Morita S, Ebina T, Hibi K, Maejima N, Umemura S, Kimura K. Posterior wall involvement attenuates predictive value of ST-segment elevation in lead V4R for right ventricular involvement in inferior acute myocardial infarction. J Cardiol [Internet]. 2009;54:386–393. Available from:

    BACKGROUND: ST-segment elevation of >/=1.0 mm in the right precordial chest lead V4R (ST upward arrowV4R) has been shown to be a reliable marker of right ventricular involvement (RVI) in inferior acute myocardial infarction (IMI). However, the impact of left ventricular posterior wall involvement (PWI) on the relation between ST upward arrowV4R and RVI is unknown. METHODS: We studied 267 patients with recanalized IMI due to the right coronary artery (RCA) occlusion within 6h after symptom onset. A 12-lead electrocardiogram, lead V4R, and leads V7-9 were recorded on admission. RVI was defined as occlusion proximal to the first major right ventricular branch of the RCA. The perfusion territory of the RCA was assessed by angiographic distribution score, and PWI was defined as a score of >/=0.7. Patients were stratified according to the presence or absence of PWI and RVI. RESULTS: RVI was associated with higher peak creatine kinase and a higher rate of impaired myocardial reperfusion, defined as a myocardial blush grade of 0 or 1 after recanalization, in the presence or absence of PWI, especially the former. RVI was associated with a higher rate of ST upward arrowV4R in the absence, but not in the presence, of PWI. ST upward arrowV4R identified RVI with sensitivities of 34% and 96% (p<0.001), and specificities of 83% and 82% (NS) in the presence and absence of PWI, respectively. CONCLUSIONS: In patients with recanalized IMI, RVI is associated with larger infarction and impaired myocardial reperfusion in the presence or absence of PWI, especially the former. However, the presence of PWI attenuates the predictive value of ST upward arrowV4R for RVI.

    My Comment by KEN GRAUER, MD (5/30/2023):
    Illustrative case on the effects of acute proximal RCA (Right Coronary Artery) occlusion with RV involvement. I focus my comments on some additional aspects of ECG interpretation from this case.

    • In Figure-1 — I've reproduced the initial ECG in today's case. As per Dr. Smith's discussion above — ECG #1 shows an acute infero-postero-lateral STEMI with a junctional escape rhythm.

    How to Determine the "Culprit" Artery?
    Statistically, approximately 80-90% of patients have a "right-dominant" circulation. In these patients, after supplying the RV (right ventricle) — the RCA continues as the PDA (Posterior Descending Artery) along the undersurface of the heart to supply the posterior and inferior walls of the LV (left ventricle) — and sometimes the lateral wall with postero-lateral branches off the PDA. 
    • In contrast, about 15% of patients have a left-dominant circulation, in which the RCA is less prominent. To compensate, the LCx (Left Circumflex) artery is a relatively larger vessel, and it (rather than the RCA) provides most (or all) of the blood supply to the PDA. As a result, not only the lateral — but also the inferior and posterior walls of the LV are predominantly supplied by LCx artery in patients with a left-dominant circulation. 
    • Therefore — Acute occlusion (OMI) of either the RCA or the LCx may result in acute infero-postero-lateral MI (although statistically — the RCA will much more commonly be the "culprit" artery).

    PEARL #1: Among the ECG features that further support the likelihood of the RCA as the "culprit" artery are: i) ST elevation in lead III>II;ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III>V6; and, iv) Evidence of acute RV involvement. All of these features are present in ECG #1 from today's case.
    • KEY Point: The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the "culpritartery (since the RV is supplied by this initial part of the RCA).
    • While ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI — lead V1 is a right-sided lead. As a result — lead V1 in a standard ECG may on occasion provide insight as to the likelihood of RV MI.

    Dr. Smith has provided data showing when ST elevation in lead V1 is indicative of acute RV involvement. While fully appropriate to obtain right-sided leads in today's case — We could be almost certain that the "culprit" artery in today's case was the proximal RCA (with associated RV involvement) from ECG #1 correlated to the clinical scenario.
    • The marked "shelf-like" ST depression in lead V2 is by itself diagnostic of acute posterior MI (as per Dr. Smith's point that posterior leads are not necessary to diagnose this!).
    • With isolated posterior MI — there is usually at least some ST depression in neighboring leads V1 and V3. Instead — the J-point in both of these leads is no more than minimally depressed.
    • With knowledge from the above ECG features pointing to the RCA as the "culprit" artery (ie, ST elevation in III>II — marked reciprocal ST depression in aVL — ST elevation in III>V6) — and — the patient's presentation of shock (relative hypovolemia with hypotension being common with RV MI) — and — the lack of ST depression in lead V1 — the most logical conclusion is to assume acute RV involvement associated with proximal RCA occlusion (with ST elevation from the RV MI attenuating what otherwise would have been ST depression in lead V1).

    Figure-1: I've reproduced the initial ECG in today's case.

    Lead V2 as a "Transition" Lead:
    I found it interesting that ST depression in the initial ECG was mainly found in lead V2. I interpreted this as lead V2 serving as a "transition" lead:
    • As mentioned above — the relative ST-T wave flattening in lead V1 in association with acute RCA occlusion suggests likely RV involvement.

    • Rather than comparable ST depression in leads V3,V4 as was seen in lead V2 — there is no more than minimal J-point depression in lead V3 — andbeginning ST elevation in lead V4 that clearly increases as we move laterally toward lead V6. It was therefore no surprise to see the continuation of increasing ST elevation as more lateral and posterior leads were assessed (ie, leads V7,V8,V9 — in ECG #2aas shown in Figure-2).

    In addition to confirming acute posterior and RV MI — there is one more new major ECG finding in ECG #2a.
    • WHAT is this new ECG finding in the repeat ECG in Figure-2?

    • HINT: If the "culprit" artery is the RCA — WHY in ECG #2a is there now more ST elevation in lead II than in lead III?

    Figure-2: I've reproduced the first 2 tracings in today's case — with substitution of left-sided chest leads with right-sided leads V4R,V5R,V6R — and posterior leads V7,V8,V9.

    ANSWER to the CHALLENGE Question:
    The reason there is now more ST elevation in lead II than in lead III in ECG #2a — is that there is LA-RA Lead Reversal in this repeat tracing! 
    • My favorite on-line Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, LITFL Lead Reversal in the Search bar — and the link comes up instantly.
    • This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
    • By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodesThis is the mix-up that occurred in ECG #2a. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-3.

    • PEARL #2: As noted in the "Quick Guide" at the bottom of Figure-3 — LA-RA Lead Reversal is EASY to recognize when you see "global negativity" in lead I (ie, When the P wave, QRS complex and T wave are all negative in lead I ). It's instructive to realize that these "tell-tale" findings may be absent when there are no P waves (because the rhythm is junctional) — when there is marked reciprocal ST depression in lead I — and when the QRS in lead aVR is of small amplitude and nearly biphasic — as occurred in today's case!

    Figure-3: LA-RA Lead Reversal (adapted from LITFL). 

    What Should the Repeat ECG Look Like?
    For clarity — I've taken the repeat ECG in today's case ( = ECG #2a) — and inverted lead I — switched leads II and III — and switched leads aVL and aVR ( = ECG #2bwhich is the lower tracing in Figure-4).
    • Doesn't ECG #2b now look perfectly consistent with what we might expect the limb leads in today's case to look like?

    • Now LOOK aFigure-5 — which compares the "corrected" repeat tracing ( ECG #2b) — with the initial ECG in today's case. The virtually identical QRST morphology in the limb leads between these 2 tracings confirms that there was LA-RA Lead Reversal in ECG #2a. As discussed earlier — substitution in the chest leads of ECG #2b with right-sided and posterior leads confirms RV and posterior MI.

    Figure-4: Applying the manipulations specified in Figure-3 for LA-RA Lead Reversal — reveals in ECG #2b what the repeat tracing should have looked like if the LA and RA electrodes had been properly placed in ECG #2a.

    Figure-5: Comparison of the "corrected" repeat tracing ( = ECG #2b) — with the initial ECG in today's case. The virtually identical QRST morphology in the limb leads between these 2 tracings confirms that there was LA-RA Lead Reversal in ECG #2a. As discussed earlier — substitution in the chest leads with right-sided and posterior leads confirms RV and posterior MI.

    OTHER Examples of Lead Reversal on Dr. Smith's Blog:
    Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — we'll continue to periodically publish clinical examples of lead misplacement. For review — GO TO:

    Recommended Resources