ECG Blog #443 — A 40s Man with CP and Dyspnea

The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?

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

MY Thoughts on this CASE:

Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1. I see the following:

• There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
• Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
• There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).

Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2). 

• PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7, -8, -9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".

• Sinus Tachycardia and RAD — as already noted above.
• PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.
• 
  
• Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).
• 
  
• S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE. 
• 
  
• PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
• As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).
• 
  
• PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2 in Figure-2).

PEARL #5: The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history. 

• Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis. 
• Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).
• 
  
• ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; and, ii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).

Figure-2: I've labeled the initial ECG in today's case.

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QUESTION: 

Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.

• What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?

ANSWER:

• A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
• The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).

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The ECHO on Today's Patient:

In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?

Figure-3: Still picture of the Echo 4-chamber view.

Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.

Figures-3 and -4 on Today's Echo:

For orientation — the 4 chambers are shown in Figure-3:

• The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".
• 
  
• PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE. 
• 
  
• A McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber); and, ii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."
• 
  
• References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.

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Diagnostic CTPA on Today's Patient:

Final confirmation of acute PE in today's case was obtained by CTPA ( = Pulmonary Angiography in Figure-5). 

• Excellent review of diagnostic testing for acute PE (Moore et al — Cardiovasc Diagn Ther 8(3):225-243, 2018).
• For a 10-minute video review on reading Pulmonary CT Scan — WATCH_this_VIDEO by Dr. Jake Gibbons.

Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries.

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CASE Follow-Up:

The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.

• PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.

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Repeat ECG After Thrombolytic Therapy:

I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).

• Sinus tachycardia has resolved.
• Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
• RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
• Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
• S waves no longer persist through to lead V6.

Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #313 and ECG Blog #435 — Review cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
• 
  
• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 

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ADDENDUM #1 (8/16/2024): 

I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".

Figure-7: ECG Findings associated with acute PE (from ECG Blog #435).

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PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).

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Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub).

Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

 

ADDENDUM #2 (8/17/2024): 

My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.

• The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
• Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?

Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case). 

ANSWER:

The ECG in Figure-10 shows the following findings in favor of acute PE:

• Sinus tachycardia.
• S1Q3T3.
• Persistent precordial S waves (through to lead V6).
• Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.

ECG Blog #442 — And then the Patient Arrested ...

I was sent the ECG shown in Figure-1 — told only that that this middle-aged woman noted chest tightness and nausea an hour earlier.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• 
  
•    — IF told that this patient arrested shortly after ECG #1 — Does this change your interpretation?

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

MY Initial Thoughts on Today's CASE:

To emphasize — the only information I was provided with was that this middle-aged woman had chest tightness and nausea about an hour before ECG #1 was recorded.

• PEARL #1: The importance of the History can not be overestimated. Knowing that this patient sought medical assistance because of "chest tightness" — immediately places her in a higher-risk prevalence group for having an acute event. As a result — our scrutiny of less marked ST-T wave changes is heightened.
• PEARL #2: If at all uncertain as to whether a patient with subtle ECG findings is having an acute event — Repeat the ECG soon! (ie, within ~10-20 minutes — continuing to repeat the ECG often until such time that you arrive at more certainty as to whether or not an acute event is evolving). In today's case — I believe the patient arrrested before a repeat ECG could be done.

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Regarding the ECG in Figure-1 that was sent to me ...  

  My Reply: "Since this patient is having chest tightness — this ECG is potentially worrisome.

• Leads V1,V2 may be placed too high on the chest. This is relevant to today's case — because IF the picture we see in V1,V2 is not accurate — then we may overlook posterior OMI.
• PEARL #3: While not 100% predictive — seeing a significant negative component to the P wave in these leads (as per the YELLOW arrows in Figure-2) — suggests that the V1,V2 electrodes may be placed 1 or 2 interspaces too high on the chest (See ECG Blog #274 — for more on too high placement of the V1,V2 electrode leads).

Continuing with My Reply regarding ECG #1:

• The rhythm is sinus at ~70-75/minute. Intervals (PR-QRS-QTc) are normal. The frontal plane axis is slightly leftward (negative QRS in aVF) — but not enough to qualify as LAHB (positive QRS in lead II) — thereby placing the axis at about -10 degrees. No chamber enlargement.
• There are no Q waves — and R wave progression is appropriate, with transition (where the R wave becomes taller than the S wave is deep) between leads V2-to-V3.

The most striking abnormality as shown in Figure-2 — is in lead V3 (within the RED rectangle):

• PEARL #4: Normally in leads V2 and V3 — there should be slight, gently upslopinng ST elevation. As per PEARL #3 — We have lost the diagnostic utility of lead V2 (because of probable malposition of this lead). That said, as per the RED lines I have drawn in Figure-2 — the ST segment in lead V3 is inappropriately flat (if not, slightly depressed).
• 
  
• PEARL #5: The BEST way to verify subtle abnormality in a given lead — is to carefully scrutinize neighboring leads to see if similar abnormalities are also seen there. As suggested within the BLUE rectangle — similar ST segment flattening with angulation between the end of the ST segment and the ascending limb of the T wave is seen in lead V4. Subtle-but-real ST segment straightening is also seen in leads V5 and V6.
• 
  
• PEARL #6: The more leads there are that show ST-T wave abnormalities — the greater the likelihood that these ST-T wave abnormalities are of clinical significance (This is true even when these ST-T wave findings are subtle). 
•   KEY Point: In the absence of new chest tightness and the clearly abnormal ST-T waves in leads V4-thru-V6 — I would probably not have been impressed by the limb lead findings in Figure-2. But, given my heightened clinical suspicion — there is no denying ST segment straightening in leads I and aVL, as well as in the inferior leads. 

Putting It All Together:

• In the context of new "chest tightness" — I thought today's ECG was highly suspicious for an acute cardiac event.
• If feasible — it would have been helpful to obtain valid information from leads V1 and V2 — by repeating the ECG immediately after verifying electrode lead placement.
• I was suspicious of acute posterior OMI — because of maximal ST-T wave change in leads V3,V4 (See links to multiple posterior OMI cases below in the References).
• Given how commonly posterior and inferior OMI occur together (because of the common blood supply these areas of the heart share) — I interpreted the unexpectedly terminal T wave positivity in each of the inferior leads as a hyperacute change (with greatest disproportionality of T wave to QRS amplitude seen in lead aVF) — thereby suggesting acute infero-postero OMI.
• Finally — the fact that virtually all leads in Figure-2 manifest ST segment flattening and/or depression (with ST elevation in lead aVR) — suggests there is DSI (Diffuse Subendocardial Ischemia) from multi-vessel disease.
• 
  
• BOTTOM Line: The above noted ECG findings are admittedly subtle. But in the context of new "chest tightness" — it can be understood why this patient arrested soon after this tracing was recorded.

Figure-2: I've labeled the initial ECG in today's case.

CASE Conclusion:

The patient was successfully resuscitated — and was doing better on follow-up.

• There are lessons to be learned from today's case ...

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Acknowledgment: My appreciation to Heba Metawea (from Dubai, UAE) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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

• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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

• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• 
  
• ECG Blog #433 — for another subtle OMI case!
• 
  
• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes (and also DSI = Diffuse Subendocardial Ischemia).
• 
  
• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
• 
  
• ECG Blog #274 — How to tell if leads V1,V2 are misplaced.
• 
  
• ECG Blog #351 — Blog #285 — Blog 246 — Blog #80 — for examples of acute posterior OMI.
• ECG Blog #317 — reviews another case regarding use (or not) of Posterior Leads.

ECG Blog #441 — What to Learn from this Case?

The ECG in Figure-1 was obtained from a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with a 1-hour history or new CP (Chest Pain). 

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Should the cath lab be activated?  And, if not — What would you do?

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

MY Thoughts on this CASE:

This is difficult. The ECG findings in Figure-1 are extremely subtle. That said — the initial ECG in today's case is not normal!

• It's important to start with the premise that since this middle-aged woman presented for emergency care with new-onset CP — she is automatically in a higher-risk group for an acute cardiac event. As a result — our threshold for interpreting ECG findings as potentially consistent with a recent or ongoing acute is lowered. 
• By way of contrast — our suspicion for an acute event would not be as high if this patient's symptoms were less typical for new-onset chest pain.

As to the ECG in Figure-1: 

• The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes: 

• There are no Q waves (a tiny initial r wave [and not a Q wave] is seen in lead aVL). 
• R wave progression is normal (with Transition, where the R wave becomes taller than the S wave is deep — occurring normally between lead V2-to-V3).

The ECG abnormalities relate to ST-T wave findings:

• In a patient with new CP — my "eye" was immediately drawn to lead V2 (within the RED rectangle in Figure-2). As I often emphasize in this ECG Blog — there should normally be slight, gently upsloping ST elevation in leads V2 and V3. This is clearly missing in lead V2. Instead — the ST segment in lead V2 is flat without any J-point elevation — and with a biphasic T wave showing terminal positivity.
• In the context of the definitely abnormal ST-T wave in lead V2 — neighboring lead V3 (within the BLUE rectangle) is also abnormal because its ST segment shows flattening and no J-point ST elevation.

KEY Point: Although the remaining 10 leads in Figure-2 might understandably be thought of as insignificant — in this patient with new CP — the subtle-but-definitely-abnormal ST-T wave abnormalities in leads V2 and V3 suggest the possibility of acute posterior OMI until proven otherwise.

• By itself — I would not have interpreted the negative ST-T wave in lead V1 as abnormal, since this ST-T wave shape in lead V1 may sometimes be seen normally. But in the context of suspecting posterior OMI (from the appearance of ST-T waves in neighboring leads V2,V3) — the ST-T wave in lead V1 could reflect a continuation of this process.
• Posterior OMI is very commonly associated with inferior OMI — since blood supply to these 2 areas of the heart is similar (arising from either the RCA or LCx). Therefore, the ST segment coving seen in leads III and aVF of Figure-2 (albeit without any ST elevation) could reflect recent inferior OMI.
• The final subtle finding I noted in Figure-2 — relates to straightening of ST segment in lead V6. In the context of the above noted other ST-T wave abnormalities — this could represent a hyperacute T wave in this lateral chest lead.

BOTTOM Line: I don't know that I would have necessarily activated the cath lab on the sole basis of the ECG in Figure-2. That said — in this middle-aged woman with new CP — we need to appreciate the possibility of recent or ongoing infero-postero-lateral OMI.

• Sometimes — "Ya gotta be there." If this patient's CP was severe and persistent in association with the ECG recorded in Figure-2 — this may have been enough to activate the cath lab at that time (ie, unrelieved ischemic CP is an accepted indication for cardiac cath!).
• At the least — a repeat ECG should have been obtained within 15-30 minutes of ECG #1 — with continued frequent serial ECGs being recorded until it can be comfortably determined IF an acute OMI was or was not ongoing (with recording of frequent serial ECGs also serving the goal of convincing a reluctant interventionist on the need for prompt cath).
• 
  
• Given the history of new CP and the ECG findings highlighted above — any elevation in Troponin needs to be taken as evidence of an ongoing event until proven otherwise (especially if serial Troponins show a continued increase).
• 
  
• Stat Echo in the ED at the time of CP — can provide additional objective evidence of an acute evolving event (ie, If there is a localized wall motion abnormality on Echo). 
• To Emphasize: If the patient is no longer having CP at the time that the Echo is done — then a normal Echo does not rule out anything. The patient must be having CP at the time of the Echo for a normal result to be used as evidence against an acute event.

Figure-2: I've labeled the initial ECG in today's case.

The CASE Continues:

• The ECG was not repeated in the ED ...
• The initial Troponin was slightly elevated. There was slight increase with the 2nd Troponin, though the total level was still under 2.0 ng/mL.
• Echo was not part of initial evaluation.
• Information regarding the status of the patient's CP was not available from chart review.

Cardiac Cath was done the next day — presumably because of slow-rising Troponin levels that attained ~10 ng/mL.

• Cath showed 100% occlusion of the 1st Obtuse Marginal Branch of the LCx (Left Circumflex) coronary artery, which was felt to be the "culprit" artery. PCI was successful in restoring flow.
• Echo done around the time of cardiac cath showed no wall motion abnormality, and an excellent ejection fraction of 72%.
• The patient did well clinically — and was discharged with a diagnosis of "NSTEMI".

The repeat ECG (that was done after cath with PCI) — is shown together with the initial ECG in Figure-3.

Figure-3: Comparison between the 2 ECGs in today's case.

COMMENT:

Putting together the “pieces” of today’s case that we are aware of — it appears that this patient did have an acute OMI. The cath finding of acute coronary occlusion of a branch of the LCx is consistent with the above-noted infero-postero-lateral changes seen in ECG #1.

• A repeat ECG was apparently only done after a successful PCI procedure was completed (shown in comparison to the initial ECG in Figure-3). The principal changes in this post-PCI are seen in the chest leads — and feature: i) A decidedly earlier increase in R wave amplitude, which is now predominant already in lead V2 (consistent with a completed posterior OMI); ii) Return of a more normal-looking appearance to the ST-T waves in leads V2 and V3, which now feature slight J-point ST elevation and upright T waves (consistent with posterior reperfusion T waves); and, iii) T wave “deflation” in lateral chest leads V4,V5,V6 (also consistent with reperfusion).
• 
  
• Concluding Thoughts: PCI was “successful” in reperfusing the “culprit” vessel in today’s case. That said — cardiac cath was only performed the following day, whereas the diagnosis of acute OMI could have been made much sooner (potentially salvaging significantly more myocardium). 
• Among the Lessons-to-be-Learned include those noted in interpretation of the subtle findings in the initial ECG and the BOTTOM Line reflections noted in my above discussion. Today’s case covers many similar aspects recently covered in ECG Blog #433.
• 
  
• P.S.: As noted above — the final discharge diagnosis in today's case was that "the patient had a NSTEMI". But as happens in all-too-many cases — the history, elevated troponin, cath finding of 100% occlusion of the 1st Obtuse Marginal Branch of the LCX — and the post-cath ECG findings consistent with a completed posterior MI (ie, the predominant R wave seen in lead V2 of Figure-3 — as well as the serial ECG changes consistent with reperfusion T waves) — the "real" diagnosis is that the patient had an infero-postero-lateral OMI that was overlooked by the treatment team (similar in regard to misdiagnosed "NSTEMIs" in ECG Blog #337 and ECG Blog #400).

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Acknowledgment: My appreciation to 張三毛 = JJ (from Taiwan) for the case and this tracing.

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

Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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

• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes (and also Diffuse Subendocardial Ischemia).
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• ECG Blog #337 and ECG Blog #400 — Examples of "NSTEMI" that were really ongoing OMIs.
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• ECG Blog #274 — How to tell if leads V1,V2 are misplaced.
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• ECG Blog #351 — Blog #285 — Blog 246 — Blog #80 — for examples of acute posterior OMI.
• ECG Blog #317 — reviews whether to use Posterior Leads?