Tuesday, November 30, 2021

ECG Blog #265 (73) — VT or Something Else?

The patient whose ECG is shown in Figure-1 was admitted for carbon monoxide poisoning. The computer interpreted the rhythm in this tracing as VT (Ventricular Tachycardia).



  • Do you agree with the computer interpretation?
  • If not — How would YOU interpret the ECG in Figure-1? 


Figure-1: Initial ECG in the ED from a patient admitted with carbon monoxide poisoning.



NOTE: Some readers may prefer at this point to listen to the 5:40-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on these tracings (that appear below ECG MP-73).


Today's ECG Media PEARL #73 (5:40 minutes Audio) — Reviews the concept of "Shark Fin" Selevation and depression as a sign of extensive acute infarction.




MY Approach to the ECG in Figure-1:

As always — I favor a Systematic Approach for interpretation of every ECG that I encounter (This Systematic Approach is reviewed in ECG Blog 205).

  • Rate & Rhythm: The computerized interpretation of the rhythm is wrong. This is not VT. Instead, the mechanism of the rhythm is sinus — as determined by the presence of regular upright P waves in lead II (as per the RED arrow in lead II of Figure-2). Sinus P waves are also seen in lead V1 (RED arrow in this lead in Figure-2) — as well as in a number of other leads. Overall, QRS complexes are regular at a rate of ~110/minute — therefore the rhythm is sinus tachycardia.
  • Intervals: The principle teaching point for this tracing lies with assessment of QRS duration. I initially thought the QRS complex was wide. On closer inspection — I realized that the QRS is not wide — but that instead, there was "Shark Fin" ST segment elevation in multiple leads, making it appear that the QRS was wide!

Figure-2: I've labeled key findings from Figure-1 (See text).

What is Shark Fin Morphology?

It's important to be aware of the pattern of "Shark Fin" ST segment elevation — in which the QRS complex looks wide, because it blends in with ST segments that show extreme ST elevation in multiple leads. As a result — the boundary between the end of the QRS complex and the ST segment becomes indistinguishable in those leads showing marked ST elevation or depression.

  • As discussed in detail in today's Audio Pearl (above) — "Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion. Consideration of prompt cardiac cath is essential for clarifying the anatomy — since in many (most) cases, prognosis is likely to be poor unless there is prompt reperfusion.
  • The KEY for confirming that "Shark Fin" morphology is the cause of the striking ECG picture this produces — is to find 1 or 2 leads in which you can clearly define the limits (end point) of the QRS complex. The most helpful lead for doing this in today's case is lead V1 — in which I've drawn in a RED line parallel to the heavy ECG grid line in simultaneously-recorded leads V1,V2,V3. Note that I've extended this line down to the corresponding complex in the long lead II rhythm strip (Figure-2).
  • The reason for continuing the RED line all the way down to the corresponding beat in the long lead II rhythm strip — is that this tells you where the QRS complex ends and the ST segment begins in the long lead II rhythm strip.
  • Knowing this landmark for the complexes in the long lead II rhythm strip — allows us to draw in and extend upward the PINK lines parallel to the heavy ECG grid line in the other 3 sets of simultaneously-recorded leads (PINK lines in Figure-2).
  • Putting IAll Together: The ECG in Figure-2 shows sinus tachycardia at ~110/minute with massive (ie, "Shark Fin" morphology) ST elevation in leads I, II, aVF — and in leads V2-thru-V6. A lesser degree of ST elevation is seen in leads III and aVL. Marked (ie, "Shark Fin" morphology) ST depression is seen in lead aVR, with a lesser degree of ST depression in lead V1.


Technical Points about this Tracing:

Unfortunately — the ECG in today's case is significantly angled. Presumably, this occurred because a picture of this ECG was taken and sent via smart phone, in the hope of expediting a 2nd opinion on this case.

  • It's important to appreciate the effect that an angled tracing may have in distorting ECG measurements. That said — one can compensate for this angling by drawing in your reference line for assessing simultaneously-occurring events parallel to the ECG heavy grid line in whatever lead(s) you are looking at (as was done with the RED and PINK lines in Figure-2).
  • NOTE: The reason I deviated from my Systematic Approach (as outlined in ECG Blog #205) — was my concern about QRS widening. This is because parameters for Axis, Chamber Enlargement and assessment of ST-T wave changes all depend on determining the reason for QRS widening. Figuring out that the cause of the unusual ECG picture in today's case was "Shark Fin" morphology with a normal QRS duration completely changed my assessment of this tracing.



Back to the HISTORY in Today's Case:

We were told that the patient in today's case was admitted for carbon monoxide poisoning. 

  • QUESTION: How should we interpret the ECG in Figure-2 in light of this history?





  • Brief review of carbon monoxide poisoning provides insight on how best to clinically interpret the ECG in Figure-2.


Cardiac Toxicity from CPoisoning:

The clinical presentation of acute CO (Carbon MonOxide) poisoning can be subtle. The gas is colorless, odorless, tasteless and non-irritating — so it can easily go undetected. Initial symptoms are varied, and often nonspecific (ie, headache, weakness, dizziness, nausea or vomiting, shortness of breath, mental confusion). 

  • The mechanism of CO toxicity stems from its exceedingly high affinity for binding with hemoglobin (~200 times greater than oxygen) — which leads to formation of carboxyhemoglobin, thereby substantially reducing the oxygen-carrying capacity of the blood.
  • Toxic effects from CO poisoning most severely affect the cardiovascular system and central nervous system — because of the increased oxygen demand of tissues in these organ systems. 
  • Cardiac Toxicity from CO poisoning includes an increased incidence of cardiac arrhythmias, conduction defects, myocardial ischemia/injury, and impaired LV (left ventricular) function (Zaky et al — Cardiovasc Regen Med, 2015). Although myocardial infarction may occur — this most often is the result of supply-demand mismatch (ie, "Type II" infarction) and not from acute coronary occlusion. That said — Hsu et al have documented that acute LAD occlusion from CO poisoning can occur (Kaohsiung J Med Sci 26:271-275, 2010).



Clinical details are lacking in today's case. What is known, is that the patient was intubated (therefore unable to provide any history) — and — in refractory shock at the time the ECG in Figure-2 was obtained. Unfortunately, this leaves us with more questions than answers. That said — My Thoughts are the following:

  • As noted above — most infarctions that occur as a result of carbon monoxide poisoning are not the resut of acute coronary occlusion. Given that the patient in today's case was in refractory shock at the time ECG #1 was obtained — I interpreted the massive ST elevation in multiple leads (with marked ST depression in leads aVR and V1) — as representing diffuse subendocardial ischemia from severe CO poisoning, resulting in markedly impaired LV function.
  • I was then provided with a follow-up ECG on this patient, who unfortunately remained in refractory shock (Figure-3):


Figure-3: Comparison of the initial ECG in today's case — with a follow-up tracing (See text).



The follow-up ECG ( = ECG #2) shows a rapid sinus tachycardia at ~135-140/minute, consistent with the patient's refractory shock state.

  • There is very poor R wave progression in ECG #2 — with no more than a tiny r wave in leads V1, V2 and V3.
  • Although the overall amount of ST segment deviation (elevation and depression) is markedly less in ECG #2 compared to what it was in ECG #1 — 3-4 mm of ST elevation persist in lead V3. The dfference between the 2 tracings in Figure-3 — is that the diffuse ST elevation seen on the initial ECG is now localized in ECG #2, primarily to the anterior leads (ie, leads V2, V3, V4) — with a much lesser degree of ST elevation in selected limb leads (ie, leads I, II, aVL, aVF). This made me wonder if rather than diffuse subendocardial ischemia — there may have been LAD (Left Anterior Descending) coronary artery occlusion at some point during the evolution of this case.



"Take-Home" PEARL:

Be aware of the entity of "Shark Fin" morphology — which can easily be mistaken for QRS widening.

  • Look closely in all 12 leads for the 1 or 2 leads that allow you to precisely define the limits of the QRS complex (as described in explaining Figure-2).
  • Realize that the massive ST segment elevation (and/or reciprocal ST depression) of "Shark Fin" morphology is most often the result of acute coronary occlusion.



Acknowledgment: My appreciation to Ehab Abdoh Bahgaat (from Hofuf, Saudi Arabia) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
  • The November 22, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was cardiac arrest, ischemic Osborn waves, with massive Shark Fin ST deviation from acute STEMI.
  • The June 12, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB) in addition to Shark Fin ST elevation & depression
  • The January 24, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LAHB) in addition to Shark Fin ST elevation & depression — followed by progressive Low Voltage due to Myocardial Stunning from the huge infarct.

  • The May 13, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews ECG recognition and the differential diagnosis of diffuse subendocardial ischemia.

Thursday, November 25, 2021

ECG Blog #264 — The 2 Major Findings?

The ECG shown in Figure-1 was obtained from a 60-ish year old man who presented to the ED (Emergency Department) with chest pain.

  • How would you interpret this tracing?
  • What are the 2 major ECG findings?
  • Extra Credit: What is the rhythm?

Figure-1: ECG obtained from a 60-ish year old man with chest pain. What are the 2 major findings?

The Case Continues:

Twenty minutes later — a repeat ECG was obtained on this patient with chest pain (Figure-2). 

  • What are the differences between these 2 tracings (ie, between ECG #1 and ECG #2 in Figure-2)?
  • Extra Credit: Has there been evolution?


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




NOTE: Some readers may prefer at this point to listen to the 5:45-minute ECG Audio PEARL before reading My Thoughts regarding the first 2 ECGs in today's case. Feel free at any time to refer to My Thoughts on these tracings (that appear below ECG MP-72).


Today’s ECG Media PEARL #72 (5:45 minutes Audio) — Reviews how to suspect Limb Lead Reversal (especially LA-RA lead reversal).



PEARL #1 = My 1st Impression of ECG #1 ...

There is global negativity (of the P wave, QRS complex and T wave) in lead I. This is virtually never normally seen — and should immediately suggest either: i) LA-RA (Left Arm-Right Arm) Lead Reversal; or, ii) Dextrocardia (Discussed in detail in the above Audio Pearl).

  • Standard lead I is a left-sided lead. Since the heart lies toward the left — predominant electrical activity will almost always be directed toward the left. Even in the setting of a large lateral infarction — it is rare to see a predominant Q wave in lead I.
  • More than just the predominant Q wave in lead I of ECG #1 — is the fact that both the P wave and T wave in this lead are negative (ie, there is global negativity of the P, QRS and T wave in lead I).
  • In contrast — the P wave in ECG #1 is upright in lead aVR (whereas with sinus rhythm, the P wave will be negative in lead aVR).
  • In Figure-1 — the reason for global negativity of the P, QRS and T wave in lead I is not dextrocardia — because a significant R wave does develop in lateral chest lead V6 (whereas with dextrocardia — there should be "reverse" R wave progression, with lack of significant R wave throughout the chest leads). As a result — I strongly suspected LA-Rlead reversal.
  • KEY Point: There are potentially hyperacute T waves (with some ST elevation) in the inferior leads of ECG #1 — as well as some possible reciprocal changes. Given the history of chest pain — this ECG should be immediately repeated to clarify what is going on. I suspected an acute OMI (Occlusion-based Myocardial Infarction) — but given the probable technical error (of LA-RA lead reversal) — accurate assessment of the situation was difficult from inspection of ECG #1.


MY Thoughts on the ECGs in Figure-2:

To answer the question I posed at the beginning of this case — the major ECG findings in Figure-1 are: iProbable LA-RA lead reversalandii) Acute inferior OMI until proven otherwise (with need for a technically correct tracing for accurate assessment of ECG findings).

  • Compared to ECG #1 — ECG #2 in Figure-2 appears to be technically correct because: i) The P wave, QRS complex and T wave in lead I are now all positive; ii) Global negativity (of the P wave, QRS complex and T wave) is now seen in lead aVR, as should be expected with normal electrode lead placement; andiii) A normal, upright sinus P wave is now seen in lead II (whereas no upright P wave had been seen in ECG #1).
  • Regarding the Extra Credit Question that I posed earlier — it is likely that the mechanism of the rhythm in ECG #1 was sinus — and that the reason we did not see an upright P wave in lead II is LA-RA lead reversal. I provide support to this theory below (in Figure-5, in which I show what ECG #1 should-have-looked-like IF all extremity electrode leads were properly placed).



MY Interpretation of ECG #2:

Now that we've verified that ECG #2 (in Figure-2is technically correct — I interpreted this tracing in light of the history that this patient presented to the ED with new chest pain. As always — I favor the use of a Systematic Approach (which I review in ECG Blog #205).

  • Rate & Rhythm: Although we do not have a long lead rhythm strip — we can see that the rate is slow and slightly irregular. An upright P wave is seen in lead II — and the PR interval in all leads remains constant — so the rhythm in Figure-2 is sinus bradycardia with sinus arrhythmia
  • Intervals (PR/QRS/QTc): The PR interval is normal — the QRS complex is narrow — and, the QTc is not prolonged — so all intervals are normal.
  • Axis: The frontal plane QRS axis is normal (I'd estimate at about +60 degrees — given maximal positivity in standard lead II — with an isoelectric QRS complex in lead aVL).
  • Chamber Enlargement: None. If anything — QRS amplitude is reduced throughout, though not quite satisfying criteria for low voltge (since several of the limb leads exceed 5 mm in amplitude).


Regarding Q-R-S-T Changes in ECG #2:

  • Q Waves — Very small and narrow normal septal q waves are seen in leads I and V6.
  • R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) is slightly delayed, occurring between leads V4-to-V5.
  • ST-T Wave Changes — In view of this patient's presentation (ie, with chest pain as his chief complaint in the ED) — I'd interpret the T waves in each of the inferior leads as hyperacute, because these T waves are much taller than expected (ie, taller than the R wave in leads III and aVF!) — as well as being fatter-at-their-peak and wider-at-their-base than one would expect given R wave amplitude in these leads. There is also at least 1 mm of ST elevation in each of the inferior leads (most marked in lead III).
  • Proof that these inferior lead changes are acute is forthcoming from reciprocal ST-T wave inversion in lead aVL, and in anterior leads V1, V2, V3.
  • PEARL #2: Although viewed by itself — the T wave in lead V6 might not necessarily seem abnormal — in the context of the clearly hyperacute inferior lead T waves — and progressive increase in T wave "volume" from lead V4 — to V5 — to V6 — the T wave in lead V6 is fatter-at-its-peak and wider-at-its-base than one would normally expect.


Impression of ECG #2:

In a patient with new-onset chest pain — this ECG suggests an acutely evolving infero-postero-lateral STEMI. Prompt cath lab activation for acute reperfusion is indicated.

  • PEARL #3: Note the "magical" mirror-image opposite relationship of the ST-T waves between leads III and aVL in ECG #2 (This concept discussed in detail in ECG Blog #184). Although subtle — there is J-point ST depression in lead aVL that is the mirror-image of the ST elevation in lead III. This relationship confirms the acute ongoing inferior OMI.
  • PEARL #4: Assessment of the ST-T waves in ECG #2 provides superb illustration of the concept of proportionality. Although amplitude of the inverted T wave in lead aVL is only 3 mm — this T wave amplitude is double the size of the tiny R wave in this lead! Similarly — we know the T waves in each of the inferior leads are hyperacute, because they are disproportionately tall compared to the R waves in these leads.



LA-RLead Reversal: What Should ECG #1 Look Like?

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 on their web site regarding 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 types of 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 ArmelectrodesThis is the mix-up that occurred in todays case. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-3

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

MY Approach for Recognizing Lead Misplacement — What has helped me over the years to rapidly recognize most cases of lead misplacement is attention to the following parameters:

  • Lead I — usually manifests a predominantly positive QRS complex, because this left-sided lead normally sees the heart’s electrical activity as traveling toward lead I. It is of course possible to have right axis deviation — but you will virtually never see an all-negative (ie, QS) complex in lead I unless there is: i) lead reversal; or iidextrocardia. 
  • It is also extremely uncommon for there to be a very deep and wide Q wave in lead I. Of course, there are exceptions (ie, a large lateral MI) — but I always consider the possibility of lead misplacement whenever there is a predominant initial negative deflection (ie, a large and wide Q wave) in Lead I.
  • IF there is global negativity” (ie, negative P wave, QRS complex and T wave) in lead I — then the diagnosis of either lead reversal or dextrocardia is virtually assured!
  • Lead aVR — usually manifests a predominantly negative QRS complex, because this right-sided lead normally views the heart’s electrical activity as traveling away from the remote (looking down from the right shoulder) viewpoint of lead aVR. Clearly, there are instances in which the QRS manifests positive activity in lead aVR — but the finding of an all negative QRS in lead I with an all positive QRS in lead aVR is virtually diagnostic of either lead reversal or dextrocardia!
  • The P wave should always be upright in lead II when there is sinus rhythm. The only 2 exceptions (ie, when there may be sinus rhythm without the P in lead II being upright) — is when there is either lead reversal or dextrocardia.
  • Finally — the way to distinguish between lead reversal vs dextrocardia on ECG is to look at R wave progression. When there is dextrocardia — there will be reverse R wave progression (ie, a modest R wave in lead V1 will quickly become smaller and disappear as you move across left-sided chest leads). Repeating the ECG with right-sided leads when the patient has dextrocardia will normalize R wave progression.

  • PEARL #5: With true Dextrocardia — Not only is there "reverse" R wave progression (in that the R wave in the chest leads gets smaller as you move across the precordium) — but because you are moving further and further away from the heart (that lies in the right side of the thorax) — the amplitude of the QRS becomes smaller and smaller as you approach lead V6!

  • PEARL #6: Although with LA-RA lead reversal (and also with Dextrocardia) — we tend to think of lead I being all negative (P wave, QRS and T wave) and lead aVR as being the "opposite" (ie, all positive)IF there is a frontal plane inferior axis (such that lead aVL is predominantly negative) — you may not necessarily see a predominantly positive QRS complex in lead aVR with LA-RA lead reversal (because as shown in Figure-4leads aVL and aVR "switch" places).

  • PEARL #7: The finding of a negative P wave in Lead II tells you that you do not have sinus rhythm unless there is: i) Lead Reversal (most commonly LA-RA lead reversal); or, ii) Dextrocardia! That said — the reverse is not true! By this I mean that you may can an isoelectric or negative P wave in lead II with either dextrocardia or lead reversal. 

  • BOTTOM LINE: When I see a negative P wave in lead II — I think about non-sinus rhythms (ie, junctional, low atrial) and/or lead reversal or dextrocardia. I look to see if the R wave is positive in lead aVR (although as per Pearl #6 — it doesn't have to be with lead reversal or dextrocardia). But I know that there should never normally be global negativity in lead Inor should there normally be reverse R wave progression. IF in doubt: i) Listen to hear if heart sounds are on the right or the left; ii) Take another look at the chest X-ray; and, iii) Verify lead placement — and repeat the ECG!

Figure-4: The initial ECG in the ED — with features of LA-RA lead reversal written below the tracing (See text).


Let’s now take another look at the initial ED ECG ( = ECG #1A) in this case (Figure-4):

  • For clarity — I’ve added the effects listed in Figure-3 that LA-RA lead reversal manifests under the initial ECG.
  • CHALLENGE: In your “mind’s eye” — TRY TO ENVISION what this initial ECG in Figure-4 would have looked like IF the limb leads were correctly placed.
  • Applying MY Approach to ECG #1A — The most striking finding in this tracing is the global negativity of the QRS complex in lead I (with negative P wave, huge Q wave and inverted T wave). This immediately tells you something is wrong! Coupled with a positive P wave in lead aVR, but lack of a positive P wave in lead II — tells you in less than 5 seconds that there most probably is either lead reversal or dextrocardia. Development of a significantly positive R wave by lead V6 rules out dextrocardia — which essentially rules in LA-RA lead reversal.



What the initial ECG Should Look Like: 

I illustrate what the initial ECG in today's case should look like in Figure-5 — in which I have: i) Inverted lead I from ECG #1A; ii) Switched positions for leads II and III; and, iii) Switched positions for leads aVL and aVR.

  • ECG #1B shows what the initial ECG would have looked like IF all extremity electrode leads had been correctly placed! Note that the normal expected relationships have all been restored (ie, the P wave, QRS complex, and T wave in lead I are now all positive — and, there is now global negativity of P wave, QRS and T wave in lead aVR).
  • In addition — there is now an upright P wave in lead II of ECG #1B, as should be expected with sinus rhythm!


Figure-5: Comparison of the initial ECG in the ED ( = ECG #1A) — with what this ECG would look like (as shown in ECG #1B) IF: i) Lead I was inverted; ii) Leads II and III switched places; and, iii) Leads aVR and aVL switched places (See text).



Beyond-the-Core: As an advanced point — I'll draw attention to the subtle differences between ECG #1A and ECG #1B in leads aVR and aVL.

  • In ECG #1A (with LA-RA lead reversal) — there was in lead aVR a positive (albeit small) P wave — and — a small initial positive deflection in the QRS (r wave). Neither of these findings is expected in lead aVR when there is sinus rhythm with correct electrode lead placement. Confirmation that these subtle morphologic abnormalities result from LA-RA lead reversal is forthcoming in the PQRST appearance in lead aVR with ECG #1B — which now shows the typical global negativity (of P wave, QRS and T wave) that we expect in lead aVR with normal electrode lead placement.
  • The PQRST appearance in lead aVL of ECG #1B — is also much more consistent with what we'd expect with an acute inferior OMI (ie, with J-point ST depression that is the mirror-image opposite picture of the ST elevation seen in lead III). Note that there was no ST depression in lead aVL of ECG #1A.



The Case Continues:

Now that we know what the initial ECG in today's case should-have-looked-like — I thought it would be of interest to compare that tracing with the repeat ECG that was done 20 minutes later (Figure-6).

  • NOTE: We previously (in our discussion of Figure-2) reviewed our interpretation of ECG #2. Now that we have derived in ECG #1B what the initial ECG in today's case should-have-looked-like — Take another look at these 2 ECGs together!



  • In Figure-6 — Has there been evolution of the acute OMI in the 20 minutes since the initial ECG was obtained?
  • HINT: Be sure to go lead-by-lead in your comparison — and remember to apply the concept of "proportionality" (discussed above in Pearl #4).

Figure-6: Comparison of what the initial ECG in the ED should-have-looked-like (ie, If electrode leads were correctly placed) — with the repeat ECG done 20 minutes later ( = ECG #2). Has there been any evolution?


ANSWER to Challenge Question:

The importance of recognizing dynamic ST-T wave changes on serial ECGs — is that in a patient with chest pain, seeing ECG changes of acute evolution confirms the need for prompt cath to determine IF acute reperfusion is needed. I've reviewed these concepts in ECG Blog #222 and ECG Blog #230. At times — these evolutionary ST-T wave changes can be subtle. Comparison of the first 2 ECGs in today's case provides a superb example of such changes:

  • At 1st Glance — the ST-T wave changes in the 2 tracings seen in Figure-6 look similar. However, on closer inspection — there are definite (albeit subtle) changes, suggesting that there has been evolution of the acute OMI during these 20 minutes — thereby confirming the need for prompt cath.
  • Sinus bradycardia with sinus arrhythmia is seen in both tracings.
  • QRS morphology in the limb leads is similar in both ECGs — suggesting no change in the frontal plane axis. However, R wave progression is slightly different — with transition (where the R wave becomes taller than the S wave is deep) occurring slightly sooner in ECG #2. This difference in R wave progression between these 2 tracings is small and probably not clinically important for the final result in today's case. But it is essential when comparing serial tracings to always look to see if frontal plane axis and R wave progression are similar — since significant change in either of these parameters can sometimes alter the accuracy of our assessment.
  • The hyperacute T waves in the inferior leads are more marked in the 2nd ECG. This is best appreciated by applying the concept of "proportionality" — in that the T wave looks "fatter"-at-its-peak and relatively taller (with respect to R wave amplitude in each of the inferior leads) in ECG #2. Specifically — T wave amplitude in ECG #1B is clearly not as tall as the R waves in leads II, III and aVF — whereas T wave amplitude in ECG #2 surpasses R wave amplitude in leads III and aVF, and almost does so in lead II.
  • Similarly — the relative amount of ST-T wave inversion is greater in lead aVL and in leads V1,V2,V3 of ECG #2 compared to ECG #1B.



The Case Continues:

Based on the above described serial ECG changes between ECG #1B and ECG #2 — the patient was taken to cath. A 3rd ECG was obtained just before cardiac cath was done (Figure-7).

  • Cardiac Cath revealed complete occlusion of the proximal RCA (Right Coronary Artery) — which was treated.

Figure-7: Comparison of the 2nd and 3rd ECGs done in today's case.

Comparison of ECG #2 and ECG #3:

Today's case concludes with comparison of the 2nd ECG — with a 3rd ECG done just before cardiac catheterization. Of note — both the frontal plane axis and R wave progression in the chest leads look similar in these 2 tracings shown in Figure-7. This suggests that lead-by-lead comparison for assessment of ST-T wave changes is valid (ie, that we are "comparing apples with apples"). I noted the following:

  • Sinus arrhythmia remains in ECG #3 — but the heart rate is a little faster than it had been in the first 2 ECGs of today's case.
  • There has been marked progression of acute ST-T wave changes in virtually all 12 leads of ECG #3 — consistent with acute evolving infero-postero-lateral STEMI.


PEARL #8: Recognition of hyperacute T waves is of invaluable assistance for determining if there is ongoing acute OMI in a patient with new symptoms (this concept discussed in ECG Blog #218 — with focus on this topic in the Audio Pearl of that post). Comparison of the 2 ECGs shown in Figure-7 provides insight into the evolution of hyperacute T waves:

  • In our assessment of ECG #2 — We interpreted the T waves in each of the inferior leads as "hyperacute" — because these T waves are clearly taller-than-expected (with respect to R wave amplitude) — as well as being "fatter"-at-their-peak and wider-at-their-base than what is normally seen. Similarly — the reciprocal ST-T wave depression in lead aVL of ECG #2 was also interpreted as "hyperacute", in that it is clearly disproportionate in size considering how tiny the QRS complex is in this lead.
  • In ECG #3  Note how these hyperacute changes have progressed! The amount of J-point elevation above the baseline in each of the inferior leads has been accentuated — the ST segment takeoff has straightened (compared to the upward concavity of the ST segment that had been seen in ECG #2) — and the peak of these hyperacute inferior lead T waves is so much "fatter" than it had been previously.
  • Similar progression of hyperacute T wave changes is now seen in leads V5 and V6 (compared minimal changes seen previously in these leads).
  • Note that there is also striking evolution in the leads showing T wave inversion in ECG #3. This hyperacute T wave inversion shows mirror-image opposite changes to the inferior lead ST-T wave elevation, with deepening J-point depression and rounding out of the deepest part of these inverted T waves.



Acknowledgment: My appreciation to Tsao Jian-Hsiung (from Taipei, 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". NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.
  • 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 #222 — Reviews the concept of Dynamic ST-T wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated)
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?")
  • ECG Blog #218 — Reviews when a T wave becomes Hyperacute (vs the T wave seen with repolarization variants).
  • 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 #175 — shows a case of true Dextrocardia! (and reviews the basics about the many different forms of Dextrocardia!).

  • The November 19, 2020 post in Dr. Smith's ECG Blog — in which I present an easy-to-overlook but important case in which LA-Llead reversal was missed (with the "tip-off" being recognition of a taller P wave in lead I > lead II).
  • The August 28, 2020 post in Dr. Smith's ECG Blog — My Comment (in my Addendum, at the very bottom of the page) reviews expected findings when there is LA-Llead reversal (Tipoff = the P in lead I is larger than the P in lead II).

  • The July 29, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there were technical errors that multiple physicians failed to recognize ( = LA-RA lead reversal and too high placement of leads V1, V2 on the chest). 
  • The February 11, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there was LA-Rlead reversal.