ECG Blog #319 — QRS Alternans?

The ECG in Figure-1 — was obtained from a 59-year old man who presented to the ED (Emergency Department) with new-onset chest pain.

• How would YOU interpret the ECG in Figure-1?
• Why is QRS morphology changing?
• Should you activate the cath lab?

Figure-1: The initial ECG in the ED.

MY Thoughts on the ECG in Figure-1:

The underlying rhythm appears to be sinus — at a rate just under 100/minute. Of note is the observation that QRS morphology changes every-other-beat. This alternating QRS morphology is more apparent in some leads compared to others.

• Despite the changing QRS morphology — sinus P waves remain precisely regular throughout this tracing (RED arrows in the long lead II rhythm strip in Figure-2).
• What is different — is that every-other-beat, the PR interval shortens and we see delta waves that prolong the QRS. Delta waves are both positive and negative — and they are present in virtually all leads (BLUE arrows).
• 
  
• BOTTOM Line: The rhythm in Figure-2 is sinus at a rate just under 100/minute. The patient has WPW (Wolff-Parkinson-White) Syndrome — and every-other-beat is conducted with preexcitation!

PEARL #1: The 2 entities to consider in the differential diagnosis of the rhythm in Figure-2 are: i) Ventricular bigeminy with late-cycle PVCs; and, ii) Electrical alternans. 

• Precise regularity of sinus P waves in the long lead II rhythm strip (RED arrows) — with the identical distance from the onset of P waves until the end of the QRS tells us that the odd-numbered beats do not occur early (ie, that odd-numbered beats are not PVCs).
• Rather than true electrical alternans — the rhythm in Figure-2 is a form of "pseudo-alternans". True electrical alternans would not develop delta waves (and would be unlikely to manifest as dramatic a change in QRST morphology as is seen in a number of leads).

Figure-2: I've labeled P waves (RED arrows) — and delta waves (BLUE arrows) from the initial ECG (See text).

Assessment of ST-T Wave Changes in ECG #1:

In my experience — it is rare that we are able to identify acute infarction in a patient with WPW. It is possible to see acute ST-T wave changes during preexcitation (See ECG Blog #157) — but most of the time in patients with WPW, acute ST-T wave changes of infarction will be hidden within the QRST complex.

• Today's case is unique — in that it provides us with an insightful opportunity to assess the effect that preexcitation may have in a patient with acute infarction.

Even-numbered beats in Figure-2 are conducted normally:

• Focusing attention on simultaneously-recorded beats #2,4,6 and 8 in the limb leads — We see relatively low-voltage, narrow QRS complexes with left axis deviation consistent with LAHB (predominant negativity for the QRS  of beats #2 and 4 in lead II).
• There is T wave inversion in leads III and aVF (ie, for beats #2,4; and 6,8).
• There appears to be ST segment flattening, and perhaps a hyperacute T wave in lead I (for beats #2,4).
• 
  
• In the chest leads — There is a QS complex in leads V1,V2 — with no more than a tiny positive r wave in lead V3 (for beats #10,12). Transition never occurs — as the R wave in lateral chest lead V6 remains smaller than the S wave in this lead (for beats #14,16).
• The most remarkable finding in the chest leads — is the 2-3 mm of J-point ST elevation in leads V1,V2,V3 (for beats #10,12) — with an abnormally straightened ST segment takeoff in lead V1 — and disproportionately tall and peaked T waves in leads V2,V3.
• Disproportionately tall and peaked (hyperacute) T waves continue in leads V4 and V5 (for beats #14,16).
• 
  
• IMPRESSION: Given the history of new-onset chest pain — I interpreted the chest lead ST-T wave changes as consistent with deWinter-like T waves — if not frankly consistent with recent or acute LAD (Left Anterior Descending) coronary artery occlusion. 
• 
  
• PEARL #2: As discussed in ECG Blog #183 — Typical deWinter T waves manifest 1-3 mm of upsloping J-point ST depression in at least a few leads, prior to continuing into tall, peaked T waves. I favor the term, "deWinter-like" T-waves when this J-point ST depression is lacking (as it is in ECG #1) — since the concept (ie, LAD occlusion) is the same, with the probable reason ST depression is missing being dependent on the timing of the ECG with respect to evolution of the process.
• 
  
• PEARL #3: ECG findings in favor of a more proximal location of LAD occlusion include: i) Onset of ST elevation as soon as lead V1; ii) Maximal T wave peaking in leads V2,V3; iii) Hyperacute lateral limb lead changes (ie, Considering modest QRS amplitude — I interpreted the T waves of beats #2,4 in lead I and the T wave of beats #6,8 as hypervoluminous); and, iv) Reciprocal ST-T wave changes in the inferior leads (especially in leads III and aVF).
• 
  
• PEARL #4: Did you notice slurring in the initial downslope of the QS complex in lead V2? This subtle-but-real fragmentation of the initial QS downslope suggests "scar" — which in the context of the ST-T wave changes seen in ECG #1, suggests anterior infarction has already taken place.

Returning to interpretation of ST-T wave changes in ECG #1 — the odd-numbered beats in Figure-2 show preexcitation:

• Most of the preexcited beats show nonspecific ST-T wave changes that are not indicative of recent infarction. The exceptions are beats #9 and 11 in leads V1 and V2 — both of which manifest marked (and unexpected) ST elevation. The shape of the ST-T wave for preexcited beats #9 and 11 in lead V1 clearly looks different than what one would expect with simple preexcitation.

The CASE Continues:

A prior ECG (recorded 3 years earlier) was found (Figure-3).

• Compare QRS and ST-T wave morphology of the preexcited beats in ECG #1 — with the baseline ECG #2 (that was recorded 3 years earlier).
• In retrospect (ie, with the benefit of this baseline tracing) — which leads in ECG #1 showed acute ST-T wave changes in those beats that conducted with preexcitation?

Figure-3: Comparison of the initial ECG — with a baseline ECG obtained 3 years earlier. What differences do you see?

Comparison with the Prior ECG:

The prior ECG recorded 3 years earlier ( = ECG #2 in Figure-3) — showed preexcitation of every beat! This confirmed our presumption that this patient has WPW.

• The most striking difference in ST-T wave morphology between preexcited beats in ECG #1 — and preexcitation in ECG #2 — was in leads V1 and V2. The fact that there was no ST elevation at all in these leads in the baseline tracing confirms that the J-point ST elevation seen in beats #9 and 11 of ECG #1 was acute!
• In addition — Note that the very tall, peaked T waves seen for preexcited beats in leads V2-thru-V5 of ECG #1 were not present in the baseline ECG. This confirms that deWinter-like T waves were indeed manifest in the preexcited beats of ECG #1.

CASE Follow-Up:

Troponin came back markedly elevated. Cardiac cath was performed — and revealed single-vessel disease in the form of a high-grade proximal LAD stenosis, consistent with recent infarction.

• Take-Home Point: Although most of the time you will not be able to recognize acute infarction when there is preexcitation — On occasion, ST-T wave changes may be so abnormal as to allow this diagnosis. Such was the case for preexcited beats in leads V1 and V2 of ECG #1.

================================== 

Acknowledgment: My appreciation to 林柏志 (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 #83 — Reviews the concept of Electrical Alternans.
• 
  
• ECG Blog #153 — What IF WPW is incidentally discovered?
• ECG Blog #121 — WPW with intermittent Delta Waves (ie, the Concertina Effect).
• ECG Blog #157 — Reviews a case of WPW that simulates acute MI.
• 
  
• ECG Blog #183 — Reviews the concept of deWinter-like T waves.

ECG Blog #318: Stroke but No Chest Pain (TQRSD)

The ECG in Figure-1 — was obtained from a 65-year old man who was admitted to the hospital for unilateral weakness that began a number of days earlier. No chest pain. Hemodynamically stable. His stroke symptoms had stabilized at the time this ECG was recorded.

• In view of this clinical history — How would YOU interpret the ECG in Figure-1?
• 
  
• Beyond-the-Core: What is T-QRS-D?

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

MY Thoughts on the ECG in Figure-1:

The rhythm in ECG #1 — is sinus bradycardia at a rate just under 60/minute. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +10 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are no significant Q waves. In leads III and aVF — we see the interesting phenomenon that a large and wide Q wave is present for the 3rd beat in these leads — but there is no Q wave for the 1st, 2nd and 4th beats in these leads. Instead — we see a multiphasic (ie, fragmented) complex with an initial positive deflection (r wave). 
• Leads III and aVF "look up" at the heart from the perspective of the diaphragm — and are therefore subject on occasion to this type of variation in QRS morphology as a result of diaphragmatic motion. Clinically — I interpret this variation of QRS morphology that we see in these 2 leads of Figure-1 as indicative of no significant Q waves.
• 
  
• Regarding R wave progression — Transition occurs early, with abrupt development of and all positive QRS complex as early as in lead V2.
• 
  
• The most remarkable finding in ECG #1 — relates to the very tall and peaked T waves in the chest leads. These T waves tower over their respective R waves in leads V2 and V3. T waves remain disproportionately peaked in multiple other leads. For example — the T waves in limb leads II and aVF are almost twice the amplitude of the tiny R wave in these leads.
• In addition to T wave peaking — there is significant J-point ST elevation in multiple leads. This is most marked in leads V2 and V3 (attaining 3 mm!) — but is also considerable in leads V1 and V4, and present to a lesser extent in lead V5. Considering how tiny the QRS complex is in lead V1 — the ST segment is markedly elevated.
• Finally — U waves of uncertain significance are present in leads V2-thru-V5.

IMPRESSION: 

Despite the absence of chest pain — the obvious concern regarding interpretation of ECG #1 — is whether these ST-T wave findings indicate a recent (and possibly still acutely ongoing) cardiac event:

• T waves in the chest leads resemble deWinter T waves in terms of their chest lead location — and the truly giant size that some of these T waves attain. In the original deWinter et al. NEJM description of this ECG finding (See ECG Blog #183 for details) — the tall, peaked T waves represented a "static pattern" indicative of high-grade LAD narrowing or occlusion that persisted until reperfusion was achieved. This might explain persistence of the ST-T wave changes seen in ECG #1, that was recorded almost a week after the onset of stroke symptoms.
• That said — the T wave picture in Figure-1 differed from that typically seen with deWinter T waves, in that there was no J-point ST depression in any of the leads with tall, peaked T waves. Instead — there was frank ST elevation in several of these leads. 
• While serum K+ clearly needs to be checked — the ST-T wave appearance in Figure-1 was not particularly suggestive of hyperkalemia because of the ST elevation and the fact that the base of many of the peaked T waves was wider-than-expected for pure hyperkalemia.
• 
  
• BOTTOM Line: Given the history of stroke symptoms beginning days before the ECG in Figure-1 was recorded — I found it difficult to know how to interpret this tracing (especially given the absence of chest pain). My best assessment was that the remarkable ST-T wave changes in ECG #1 represented deWinter-like T waves — with need to assume a recent (or still ongoing) acute cardiac event until proven otherwise.

A Final ECG Finding to Consider = T-QRS-D!

The concept of Terminal QRS Distortion (T-QRS-D) was unknown to me prior to my active participation as an Associate Editor in Dr. Smith's ECG Blog. Since then I've seen many patient cases that validate the clinical utility of this ECG finding promoted by Dr. Stephen Smith. When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction). I illustrate the ECG finding of T-QRS-D below in Figure-2, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. To review:

• T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3. Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-2 from previous cases posted on Dr. Smith’s ECG Blog:

• TOP in Figure-2 — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
•  BOTTOM in Figure-2 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Figure-2: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).

Is there T-QRS-D in Figure-1?

Return to the initial ECG in today's case that was shown in Figure-1. Take another look at the ST-T waves in leads V2 and V3.

• Is T-QRS-D present in either of these leads?

ANSWER:

For clarity in Figure-3 — I've enlarged and have labeled the QRST complexes in leads V2 and V3 from today's tracing.

• In Lead V2: The ST elevation is not consistent with T-QRS-D — because there is prominent J-point notching (BLUE arrow).
• 
  
• In Lead V3: There is T-QRS-D — because there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

PEARL #1: Overall in my experience — T-QRS-D is not a common finding among patients with acute coronary occlusion. That said — the potential value of this finding when it is present, is indisputable (as was seen in today's case when this ECG finding provided strong support in favor of recent infarction).

Figure-3: Blow-up view of the QRST complexes from leads V2 and V3 of today's tracing (See text).

Putting It All Together:

While the absence of chest pain makes it difficult to determine the timing of events in today's case — the dramatic deWinter-like T waves in the chest leads of ECG #1, that occur in association with the T-QRS-D seen in lead V3 — suggested to me the need to presume recent LAD occlusion with resultant infarction until proven otherwise.

• Whether the infarction occurred before the stroke (perhaps causing the stroke) — is uncertain from the limited information known.
• That said — Today's case presumably provides an insightful example of a "silent" MI (ie, no chest pain) — with this MI only being recognized because the patient had a stroke (See ECG Blog #228).

CASE Follow-Up:

Unfortunately — Follow-up of today's case is somewhat limited. What can be said is: i) Serum K+ at the time the initial ECG was recorded was not elevated; and, ii) The ECG abnormalities described above were promptly recognized — so Cardiac Cath was performed. This revealed 3-vessel disease with the following specific findings:

• LMain (Left Main coronary artery) — atheromatous, but no significant lesion.
• 
  
• LAD (Left Anterior Descending) — 80-90% tandem lesion, extending from the proximal LAD to the mid-LAD. TIMI Flow = Grade 2-to-3 (ie, partial flow) — suggesting that there had been obstruction (and that the proximal LAD had been the "culprit" artery) — but that this vessel had spontaneously reperfused. This tandem lesion was successfully stented.
• 
  
• PEARL #2: This case illustrates how to presume the occurrence of a recent infarction despite the absence of 100% coronary occlusion at the time cardiac cath is performed. Clinical correlation of the timing of symptoms with troponin values and serial ECGs — together with appreciation of how commonly spontaneous reperfusion occurs — are KEY for making this determination.
• 
  
• LCx (Left Circumflex) — 70-80% tandem lesion, extending from the proximal LCx to the mid-part of this vessel. Coronary flow was normal (ie, TIMI Grade 3) — and the LCx was not felt to be a "culprit" vessel. PCI of the LCx was deferred to the near future.
• RCA (Right Coronary Artery) — 60-70% proximal stenosis — but normal ( = TIMI Grade 3) flow. No stenting was deemed necessary for this vessel.
• 
  
• For brief review of TIMI Grade Flow —> Go To — Sarkar et al: Stat Pearls, NIH, 2022.

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

Acknowledgment: This case was anonymously submitted to me for use in my ECG Blog.

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

 

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEM manuscript).
• 
  
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 
• ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.
• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
• 
  
• ECG Blog #228 — Reviews the concept of "Silent" MI.
• 
  
• ECG Blog #215 — Reviews a case with T-QRS-D.
• 
  
• The November 14, 2019 post in Dr. Smith’s ECG Blog (Please scroll down to the BOTTOM of the page for My Comment and illustration of the phenomenon of T-QRS-D = Terminal QRS Distortion).

ECG Blog #317 — 80yo man-CP- The Culprit?

The ECG in Figure-1 — was obtained from an 80-year old man who presented to the ED (Emergency Department) with new-onset chest pain.

• How would YOU interpret the ECG in Figure-1?
• Is there a "culprit" artery?

Figure-1: The initial ECG obtained from an 80-year old man with new-onset chest pain.

MY Thoughts on the ECG in Figure-1:

Obviously — ECG #1 shows an acute STEMI, based the "eye-catching" ST elevation in leads V5,V6. That said — there are abnormal findings in virtually every lead! However, I thought the most interesting part of today’s case was contemplating the answer to my 2nd Question — namely, predicting the “culprit” artery.

• There is much baseline artifact in this initial ECG, especially in the limb leads. That said — we are still able to accurately interpret this tracing.
• The rhythm in ECG #1 looks to be a fairly regular sinus at ~85/minute. All intervals (PR, QRS, QTc) are normal.
• The frontal plane QRS axis is normal at +60 degrees.
• There is no chamber enlargement.

 

PEARL #1: Did YOU notice the Low Voltage in the limb leads? (ie, the QRS complex does not exceed 5 mm in any of the 6 limb leads).

• When contemplating the diagnosis of acute or recent infarction — it is important to remember that myocardial "stunning" from a large MI is one of the causes of acute low voltage (More on this subject in ECG Blog #262 and ECG Blog #272).

Regarding Q-R-S-T Changes:

• I'm uncertain if the small, fragmented QRS complex in lead aVL begins with a small q wave. I otherwise see no sign of Q waves in other leads.
• R wave progression is appropriate — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V3. Of note — the R wave in lead V3 is surprisingly tall (ie, ~19 mm). This is relevant to today's case, but easy to overlook because of overlap with the very deep S wave in lead V2 (See RED and BLUE outlines of QRS complexes in these leads in Figure-2).

The most remarkable findings in ECG #1 relate to ST-T Wave Changes:

• As already mentioned — there is "eye-catching" coved ST elevation in lateral chest leads V5 and V6.
• 
  
• PEARL #2: There is also ST elevation in lead V4. While minimal in amount — we know this is real because: i) By the principle of "neighboring leads" — we know there is marked ST elevation in adacent lead V5, and the coved shape of the ST segment in lead V4 manifests similarity to that seen in lead V5; and, ii) There is ST depression in lead V3 that lies next to V4 — so even the small amount of J-point ST elevation seen in lead V4 is definitely real.
• 
  
• There is subtle-but-real ST elevation in 3 of the limb leads. This is perhaps best seen in lead I — but is also present in leads II and aVF (albeit not in leads III and aVL).
• 
  
• PEARL #3: Note how the presence of artifact complicates assessement of ST-T wave changes in the limb leads! For example — the shape of the ST-T wave changes from 1 beat-to-the-next for each of the 3 complexes in leads I,II,III and aVF. Some of these complexes clearly look more worrisome than others! When this common artifactual phenomenon occurs — I favor a "Gestalt" approach — in which you survey the "overall picture", realizing that our information is imperfect. In Figure-2 — my "Gestalt" is that there is subtle-but-real ST elevation in leads I, II and aVF.
• 
  
• Finally — there is marked ST depression in anterior leads V1,V2,V3. Note the shelf-like (flat) ST segment appearance in leads V2 and V3 — with terminal positivity in these leads! This appearance results in a positive “Mirror Test” — that in the context of the new chest pain experienced by the patient in today's case, is diagnostic of acute posterior MI (See Figure-2).

Figure-2: I've added the mirror-image of anterior leads V1,V2,V3 to Figure-1 — to illustrate how the initial ECG in today's case manifests a positive “Mirror Test”. As discussed in ECG Blog #193 (with many additional illustrative links to the Mirror Test provided below) — this test serves as my favorite visual aid to facilitate recognition of acute posterior MI. The mirror-image view of anterior leads provides insight to the perspective of what the posterior wall of the left ventricle sees. The shape of the ST depression seen in leads V1,V2,V3, when vertically flipped (as shown in the Mirror Test here to the right of ECG #1) — suggests deepening Q waves, a worrisome shape of ST elevation — and already deep T wave inversion in lead V2.

What Do YOU See in ECG-2?

Shortly after ECG #1 was recorded — the ECG was repeated with posterior leads (ie, leads V7,V8,V9) being substituted for leads V4,V5,V6 (See Figure-3).

QUESTIONS:

• Were posterior leads needed to make the diagnosis of acute posterior MI?
• 
  
• Extra Credit: What is the most useful finding in the repeat ECG that is shown in Figure-2?

Figure-3: Shortly after ECG #1 was recorded — a 2nd ECG was obtained with posterior leads (V7,V8,V9) being substituted for leads V4,V5,V6. Does this 2nd ECG help to clarify the clinical picture? If so — HOW specifically does it help?

PEARL #4: Posterior Leads Were Not Needed ...

In my experience over the years since 1983 (when I first published on the utility of the Mirror Test for recognizing acute posterior MI) — I have never seen an example of an ECG in which acute posterior MI diagnosed by posterior leads was not already evident in the standard 12 leads with use of the Mirror Test.

• QRST amplitudes with posterior leads are reduced compared to mirror-image anterior lead amplitudes — because assessment of electrical activity from posteriorly placed V7,V8,V9 electrodes has to traverse the thick back musculature before it can pick up the heart's electrical activity.
• 
  
• Isn't the mirror-image picture to the right of ECG #1 in Figure-2 more convincing than the lesser amount of ST deviation seen in leads V8 and V9 of Figure-3?
• 
  
• NOTE: I am not against those who prefer to obtain posterior leads because they feel this helps in their interpretation. I am simply saying that with minimal practice using the Mirror Test — that equal information is obtained faster without the need to apply additional leads. (Actually — more information is obtained — since there are times when the Mirror Test is positive despite negative posterior leads).

Take Another LOOK: How Does ECG #2 Help in Today's Case?

Unfortunately — the 2nd ECG in today's case substituted leads V7,V8,V9 for leads V4,V5,V6. I would have been more interested in seeing what progression there was in leads V4,V5,V6 from ECG #1 (instead of seeing leads V7,V8,V9 which do not provide new information).

• BUT — Knowing that ECG #2 was obtained shortly after ECG #1 is important — because there is now increased ST elevation in lead I — new (and marked) ST elevation in lead aVL — and new (and marked) reciprocal ST depression in each of the inferior leads.
• 
  
• Putting It All Together: Given the history of new chest pain in association with the sequential ECG changes seen in ECG #1 and ECG #2 — there is active evolution of a large acute postero-lateral STEMI. As discussed in ECG Blog #193 — this type of distribution strongly suggests a dominant LCx (Left Circumflex) as the "culprit" artery.

CASE Follow-Up:

Cardiac cath confirmed the above ECG impression — showing acute proximal LCx occlusion (as shown in Panel A of Figure-4). 

• Panel B in Figure-4 shows the result of successful PCI — reestablishing perfusion in the "culprit" vessel.

Figure-4: Cath images pre- and post successful PCI.

Final QUESTIONS:

• In light of ECGs #1 and #2 — How would YOU interpret ECG #3, obtained the day after hospital admission? (Figure-5).
• 
  
• CHALLENGE: HOW MANY relevant ECG changes can you identify in ECG #3?

Figure-5: Comparison of the 3 ECGs obtained in today's case. What changes do you see in ECG #3, obtained the next day?

Final Thoughts on the 3 Serial ECGs:

There are a number of interesting findings in ECG #3, obtained the next day. These changes are best assessed in the context of ECGs #1 and #2, that were both recorded prior to PCI (Figure-5):

• ECG #3 shows marked evolutionary changes of the extensive postero-lateral STEMI, that now shows reperfusion T waves in these lateral leads (ie, in leads I,aVL; and in V4,V5,V6).
• There has been marked loss of QRS amplitude in each of the limb leads (compared to the already reduced limb lead amplitudes evident in ECGs #1 and #2). This is consistent with apparent loss of significant myocardium from this extensive infarction.
• There is no longer any R wave at all in lead V6 of ECG #3! Assuming this is not the result of lead placement error (which is unlikely given similar T wave inversion in both leads V5,V6) — the loss of R wave in lead V6 is one more indication of the extensive myocardial damage.
• 
  
• The frontal plane axis has been displaced rightward — and is now clearly indeterminate (ie, predominantly negative in both leads I and aVF). Whether this reflects development of LAHB (Left Anterior HemiBlock), with predominant negativity of the QRS in all inferior leads — or simply profound loss of QRS amplitude from the large infarction is uncertain.
• NOTE: The fact that the P wave in lead I of ECG #3 is positive — tells us that the reason for predominant negativity of the QRS in lead I is not LA-RA lead reversal. Instead, it reflects loss of QRS amplitude from extensive infarction.
• 
  
• There is now a predominant R wave (R>S) in lead V1 — that was not present in ECG #1. This is consistent with evolution of posterior infarction.
• The anterior lead ST depression evident on the initial ECG — has been replaced by positive T waves in each of these anterior leads! Note in particular how tall the positive T wave is in lead V1 of ECG #3. These are reperfusion T waves in the posterior wall of the left ventricle (which produce the mirror-image opposite picture of the deep, symmetric T wave inversion seen in leads V4,V5,V6 that reflects lateral wall reperfusion). 

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

Acknowledgment: My appreciation to 林柏志 (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 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery.
• 
  
• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
• 
  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
•  
• The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
• 
  
• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
• 
  
• ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).
• 
  
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• 
  
• ECG Blog #262 — Potential significance of Low Voltage with acute MI.
• ECG Blog #272 — Significance of Low Voltage with acute MI.