Wednesday, March 30, 2022

ECG Blog #294 — One Hour Later


The patient whose ECGs are shown in Figure-1 — was a 55-year old man who presented with new chest pain of ~2 hours duration. ECG #1 was obtained on arrival at the ED (Emergency Department). His symptoms continued — and an hour later, ECG #2 was obtained.

QUESTIONS:
  • How would YOU interpret these 2 serial tracings?
  • "Culprit" artery? (Be as specific as you can.).
  • Was there any hint in ECG #1 that just 1 hour later we'd see the picture shown in ECG #2?

Figure-1: The first 2 ECGs in today's case, which were done just 1 hour apart (See text).


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NOTE: Some readers may prefer at this point to listen to my 10-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review My Thoughts on ECG #1 (that appear below ECG MP-10).

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Today’s ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MIshould replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.



MY Thoughts on the 2 ECGs in Figure-1:
I was sent the tracings in today's case — and I looked first at ECG #1. I saw sinus rhythm at ~65-70/minute — normal intervals (PR, QRS, QTc) and normal axis (about +20 degrees). No chamber enlargement.
  • Regarding Q-R-S-T Changes in ECG #1 — there were no Q waves — R wave progression was normal, with slightly delayed transition (the R does not become taller than the S wave is deep until between leads V4-to-V5).
  • The only ST-T wave findings of note are seen in the inferior leads. There is nonspecific ST-T wave flattening in lead aVF, and to a lesser extent in lead II. There is shallow, symmetric T wave inversion in lead III — but given that the QRS complex is predominantly negative in this lead, this is not necessarily an abnormal finding (especially given the absence of T wave inversion in the other 2 inferior leads).

  • BOTTOM LINE for ECG #1: There are some nonspecific ST-T wave abnormalities in the inferior leads — but I saw nothing to indicate what was soon to occur in ECG #2.


Regarding ECG #2:
Sinus rhythm is again present at a rate similar to that seen in ECG #1. Intervals and the axis are again normal. There is no chamber enlargement. BUT — the rest of the interpretation has dramatically changed in the space of an hour. Specific ECG findings that are now seen on ECG #2 include the following:
  • Marked ST elevation in each of the inferior leads (with ST elevation in lead III clearly greater than in lead II). Small q waves in leads II and aVF + a large, wide Q wave in lead III.

  • Marked reciprocal ST depression in high-lateral leads I and aVL (with shape of the ST-T wave in lead aVL being the mirror-image opposite picture from the shape of the ST elevation in lead III).
  • Marked shelf-like ST depression in leads V2, V3, V4 (ie, positive Mirror Test) — but virtually no ST depression at all in lead V1.

  • BOTTOM Line for ECG #2: In this patient with new chest pain — this ECG is diagnostic of an acute infero-postero STEMI, from acute proximal RCA  (Right Coronary Artery) occlusion

  • PEARL #1: In addition to acute infero-postero MI — acute RV (Right Ventricular) involvement is highly likely, given the absence of any ST depression in right-sided lead V1 in this tracing with such marked ST depression in neighboring leads V2,V3 (ie, ST elevation from RV MI in lead V1 is probably attenuated by what otherwise would have been ST depression in this lead from acute posterior MI). It is this acute RV involvement that for practical purposes localizes the site of acute coronary occlusion to the proximal RCA — because the LCx (Left Circumflex) coronary artery does not supply the RV wall (See ECG Blog #190for more on acute RV MI).

  • PEARL #2: It is sometimes quite humbling to see how quickly dramatic ECG signs of infarction may develop. The case I presented in ECG Blog #115 showed a similar dramatic evolution from subtle ST-T wave changes — to full-blown ST elevation in the space of only 8 minutes. The MESSAGE is clear: Serial ECGs can change extremely rapidly. IF concerned about an acutely evolving OMI (Occlusion-based MI), especially if the patient's chest pain is ongoing — ECGs may sometimes need to be repeated as often as every 10-20 minutes, until a definitive diagnosis is made.

Follow-Up to this Case:

The facility where this patient was seen did not have acute cardiac catheterization capability. The patient was instead immediately treated with thrombolytic therapy (Streptokinase). Chest pain resolved — and ECG #3 (shown in Figure-2) was obtained.


QUESTIONS:

  • Was thrombolytic therapy successful? If so — HOW can you tell?
  • What would you expect subsequent ECGs to show?


Figure-2: Comparison of ECG #2 — with the ECG obtained following completion of Streptokinase.


ANSWERS:
When promptly administered to appropriate patients — thrombolytic therapy can be extremely effective. Features of today's case that suggest a very favorable response to Streptokinase include the following:
  • The patient's chest pain resolved following use of thrombolytic therapy.
  • The dramatic inferior lead ST elevation has improved greatly. High lateral lead reciprocal ST depression in leads I and aVL has largely resolved.
  • ECG changes of acute posterior infarction (ie, shelf-like ST depression in leads V2,3,4) are no longer present. A more normal picture of shallow T wave inversion is now seen in lead V1.
  • Inferior lead Q waves have only minimally increased in size.

 

What to Expect in subsequent ECGs?
In addition to resolution of chest pain, with marked reduction in the amount of ST elevation and depression — reperfusion of the occluded coronary artery is typically marked by development of fairly deep T wave inversion in those leads that manifested ST elevation.
  • The opposite is seen with reperfusion of acute posterior OMI — with development of tall, peaked T waves in the anterior leads (instead of T wave inversion).
  • It would not be surprising to see transient AIVR (Accelerated IdioVentricular Rhythm) — as this is an extremely common reperfusion arrhythmia (See ECG Blog #194).
  • An example of reperfusion T wave changes can be seen in ECG Blog #268 . 


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Acknowledgment: My appreciation to M Shah (from Srinagar, India) for the case and this tracing.

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ADDENDUM:

  • Included below are a series of links and other material relevant to detection of the “culprit” artery — and my thoughts for making the case to replace the term “STEMI” with “OMI”, in the hope of substantially increasing detection of acute coronary occlusion. 

 

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

  • PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
  • PDF File: Posterior MI and the “Mirror Test” —

 


Figure-3: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.





Today’s ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.



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Relevant ECG Blog Posts to Today’s Post: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 

  • ECG Blog #184  That magical inverse relationship between leads III and aVL.
  • ECG Blog #167 — More on that "magical" lead III-aVL relationship.
  • ECG Blog #183 — deWinter-like T waves.
  • ECG Blog #190 — How to recognize acute RV MI.
  • ECG Blog #56 — Posterior MI; Mirror Test
  • ECG Blog #80 — What's the Culprit Artery? + the Mirror Test.
  • ECG Blog #82 — What’s the Culprit Artery?
  • ECG Blog #162 — What’s the Culprit Artery?
  • ECG Blog #193 — Reviews a case with a probable dominant LCx culprit.
  • ECG Blog #194 — Reviews how to tell IF the "culprit" artery has reperfused (with an example of AIVR).

  • 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 #246 — Reviews the Mirror Test for diagnosis of Posterior MI (Also check out the Audio Pearl in this post).
  • ECG Blog #266 — How to distinguish between deWinter T waves vs reperfusion T waves with Posterior MI.

  • ECG Guru (9/3/2019) — See My Comment regarding acute occlusion of 1st or 2nd Diagonal Branch of the LAD.
  • Acute OMI that wasn’t accepted by the Attending — See My Comment at the bottom of the page in the November 21, 2020 post on Dr. Smith’s ECG Blog.
  • Another overlooked OMI (Cardiologist limited by STEMI Definition) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog.
  • 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 T-QRS-D (Terminal QRS Distortion) as a sign of acute OMI — See My Comment at the bottom of the page in the November 14, 2019 post on Dr. Smith's ECG Blog.
  • LVH vs a Repolarization variant vs LAD OMI (and looks like Wellens' after reperfusion) — See My Comment at the bottom of the page in the October 23, 2020 post on Dr. Smith's ECG Blog.
  • Repolarization Variant vs Acute OMI (even repolarization variants may sometimes manifest "dynamic" ECG changes!) — See My Comment in the August 22, 2020 post on Dr. Smith's ECG Blog.
  • Diagnosis of an OMI from the initial ECG — Serial tracings with spontaneous reperfusion — then reocclusion! — See My Comment at the bottom of the page in the October 14, 2020 post on Dr. Smith's ECG Blog.
  • And for more on the Mirror Test — See My Comment at the bottom of the page in the September 21, 2020 post and, in the February 16, 2019 post on Dr. Smith's ECG Blog.

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Saturday, March 26, 2022

ECG Blog #293 — What Diagnoses to Suspect?


You are given the ECG in Figure-1 — but without the benefit of any history.
  • How would YOU interpret this tracing?
  • What clinical diagnoses do you suspect?

Figure-1: ECG you are given without the benefit of any history.


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NOTE #1: I'm repeating Video PEARL-22, that is relevant to today's case. Some readers may prefer at this point to watch to this Video Pearl before reading My Thoughts that appear below, regarding the ECG in today's case.

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Today’s ECG Media Pearl #22 (13:15 minutes Video) — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds.

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NOTE #2: I have excerpted a written summary of today's Video Pearl in the Addendum below (in Figure-2 through Figure-7).

  • CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).

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My THOUGHTS on the ECG in Figure-1:
It would be extremely helpful to know the clinical history in today's case. That said — sometimes we are asked to interpret ECGs without the benefit of any history, as we are in Figure-1. My thoughts on today's tracing were as follows:
  • The rhythm in ECG #1 is rapid, irregular — and with a QRS complex that is obviously wide.
  • Although small-amplitude deflections in the baseline are seen in lead II during the short pause at the beginning of the tracing — there are no clearly defined P waves in any of the 12 leads.
  • More than simply being irregular — the rhythm in Figure-1 is irregularly irregular. That is, despite looking “almost regular” in certain parts of this tracing — careful observation confirms slight-but-definite differences in the R-R interval from one-beat-to-the-next throughout the ECG.
  • IMPRESSION: The above description defines the rhythm in Figure-1 as AFib (Atrial Fibrillation), here with a rapid ventricular response (average rate well over 120/minute). Although VT (Ventricular Tachycardia) is not always regular — VT is rarely as irregularly irregular as we see here when QRS morphology is constant throughout the tracing. Thus, the rhythm in Figure-1 is AFib with QRS widening and not VT.

Continuing with My Systematic Approach:
Since the rhythm in Figure-1 is supraventricular and the QRS complex is wide — we next need to determine WHY the QRS is wide before proceeding further with our systematic approach. This is because ECG crtieria for axis, chamber enlargement and ischemia/infarction will all be different, depending on the type of conduction defect (See Figures-2 thru -7 in the Addendum below).

  • QRS morphology for the ECG in Figure-1 is most consistent with complete LBBB (Left Bundle Branch Block). This is because: i) The QRS is ≥0.12 second in duration; ii) The QRS complex in lateral leads I and V6 manifests a monophasic (all upright) R wave; and, iii) There is predominant negativity for the QRS in right-sided lead V1and — the angle of descent for anterior S waves is extremely steep. Although most of the time with LBBB, the initial R wave in other anterior leads (ie, leads V2, V3) is not as large as is seen in ECG #1 — QRS morphology is otherwise extremely typical, such that best description of the conduction defect for this tracing is complete LBBB.

Regarding other features of the ECG in Figure-1:
  • Chamber Enlargement: Criteria for the ECG diagnosis of LVH are different when there is complete LBBB. This is because this conduction defect alters the sequence of electrical depolarization — such that the usual voltage criteria for assessing LVH are no longer valid when there is LBBB. That said — the finding of extremely deep anterior S waves (ie, greater than 25-30 mm in V1, V2 and/or V3) is highly correlated with LVH in patients with this conduction defect.

  • Axis: Calculation of the frontal plane axis is of little use in patients with LBBB. This is because the left bundle branch is an extensive conduction fascicle — which when damaged, may result in development of LBBB from a variety of anatomic lesions (depending on where in the common left bundle branch and/or in the left anterior or posterior hemidivisions the conduction block occurs). As a result — a variety of axis deviations are possible with LBBB.

  • R Wave Progression: By definition — IF there is true LBBB — then R wave progression will be delayed in the chest leads. This explains the delay in Transition that is seen in Figure-1 — in which the R wave does not become taller than the S wave is deep until between leads V5-to-V6.

  • ST-T Wave Changes: It follows that since LBBB alters the sequence of electrical depolarization — the sequence of repolarization will also be changed. As a result — the appearance of ST-T waves in a patient with complete LBBB will look different than what one would otherwise expect. Thus, ST-T wave depression that may be seen in lateral leads with LBBB (ie, in leads I, aVL, V6) — will not necessarily reflect LV "strain" or ischemia — but may instead simply be the result of secondary ST-T wave changes that are to be expected in lateral leads with LBBB. Similarly, some ST elevation with T wave peaking in anterior leads in association with LBBB will often simply reflect an expected reciprocal finding from the conduction defect.
 

Final Interpretation:

The ECG in Figure-1 shows rapid AFib + complete LBBB + probable LVH. I suspect that there are no acute ST-T wave abnormalities in this tracing. Instead — the ST-T wave depression in lateral leads I, aVL and V6 probably reflects normal repolarization changes of LBBB. The modest amount of J-point ST elevation and T wave peaking in leads V1-thru-V4 is most probably the result a combination of factors including: i) The tachycardia (which may often produce some transient ST elevation that resolves when the rate slows); ii) The LBBB itself; and, iii) The tremendous increase in QRS amplitude in leads V1-thru-V4 (such that the height of anterior T wave peaking is probably not disproportionate given how deep S waves in leads V1-thru-V4 are).

  • Clinical correlation will be essential in order to know what to do with this tracing.

 



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Acknowledgment: My appreciation to M Shah (from Srinagar, India) for the case and this tracing.

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Relevant ECG Blog Posts to Today’s Post: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 

  • ECG Blog #282 — for a case that reviews the application of modified Smith-Sgarbossa Criteria in the setting of a patient with LBBB and acute symptoms.

  • ECG Blog #198 — An Irregular WCT (LBBB or IVCD).
  • ECG Blog #162 — LBBB with obvious STEMI.
  • ECG Blog #146 — LBBB with Acute ST-T Wave Changes.
  • ECG Blog #145 — RBBB with Diffuse Subendocardial Ischemia.

  • The January 31, 2022 post in Dr. Smith's ECG Blog — Reviews subtle signs of acute OMI in a patient with LBBB (Please see My Comment at the bottom of the page).

 

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ADDENDUM (3/26/2022): In the following 6 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of BBB.

  • CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).

 

Figure-2: Intro — Using the Algorithm for QRS Widening to determine the type of conduction defect.


 


Figure-3: ECG Findings with typical RBBB.



Figure-4: ECG Findings with typical LBBB.



 

Figure-5: Incomplete LBBB — ECG Findings with IVCD.


 

Figure-6: Expected ST-T wave changes with RBBB and LBBB.


 

Figure-7: RBBB-Equivalent Patterns — Incomplete RBBB.



Monday, March 21, 2022

ECG Blog #292 — Why Did the Patient Die?


The 2 ECGs shown in Figure-1 were obtained from a man in his 30s — who presented to the ED (Emergency Department) with chest pain that began several hours earlier. ECG #2 was recorded 1 hour after ECG #1. Initial troponin was negative.

Cardiac cath was advised — but the patient refused. Instead, he left the hospital — only to be found dead at home 36 hours later
  • How would YOU interpret the serial tracings shown in Figure-1?
  • WHY did the patient die?

Figure-1: The 2 ECGs in today's case (See text).


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NOTE: I'm repeating the following Audio PEARLS that are relevant to today's case. Some readers may prefer at this point to listen to these Audio Pearls before reading My Thoughts that appear below, regarding the ECGs in today's case.

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ECG Media PEARL #39a (4:50 minutes Audio) — 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 Media PEARL #46a (6:35 minutes Audio) — Reviews HOW to compare Serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).




My THOUGHTS on Today's Case:
There are lessons to be learned from today's case. These include:
  • What is meant by the term, "dynamic" ECG changes?
  • How to compare serial tracings?
  • Are "dynamic" ECG changes seen in Figure-1?
  • What is the most likely reason this patient died?
  • Can we determine a "culprit" artery?

What is Meant by the term, "Dynamic" ECG Changes?
The goal of obtaining serial ECGs in patients suspected of evolving an acute coronary event — is that tracings obtained early on may look relatively normal. This picture may rapidly change, sometimes over the course of minutes! When initial ECG changes are subtle — they may be most easily recognized by lead-to-lead comparison of 1 tracing with another.
  • IF ECG changes evolve in a way that corresponds to the coming and going of chest pain symptoms — this is important information. It tells us there is an active, ongoing process — and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter-definition of a STEMI has been satisfied.
  • The problem is — that the "culprit" artery may spontaneously open and close more than once during its process of arriving at a final result — so that even if ST elevation resolves in association with resolution of chest pain — this spontaneous reopening of the vessel, may just-as-easily be followed by spontaneous closure again — and this time, perhaps without spontaneous reopening.
  • It is this active evolution of ST-T wave changes that may occur with the coming and going of symptoms that we define as "dynamic" ECG changes. ST segments elevate with the onset of chest pain (signaling acute coronary occlusion) — and ST segments return toward their baseline, often followed by "reperfusion" changes of T wave inversion that signal reopening of the "culprit" vessel. The importance of recognizing these "dynamic" ECG changes — is that this indicates an unstable situation at risk of evolving further to permanent coronary occlusion.

How to Compare Serial Tracings?
The method I favor for comparing serial tracings — is to pick one of the ECGs — and to interpret that tracing in its entirety by whatever systematic approach you are using. I usually start with the earliest tracing that was recorded — because you then know that any changes seen on a subsequent tracing are "new".
  • We are looking for changes in the shape and amount of ST elevation and depression between the tracings that we are comparing.
  • The challenge with ECG comparison — is that we have to distinguish between differences from one ECG to the next that are likely to be due to a worsening or improvement in the patient's coronary diseaseversus — ECG changes that are likely the result of technical factors (ie, a shift in frontal plane axis or QRS morphology changes due to a difference in lead placement or in the degree of elevation of the patient's bed [some acutely ill patients are unable to lie flat]).
  • After full interpretation of the initial ECG you looked at — I go lead-to-lead when I compare serial tracings, holding both tracings right next to each other. This is because IF, for example — the QRS complex is predominantly positive in lead III or in lead aVF on the 1st tracing — but then becomes more-negative-than-positive on the 2nd tracing — then the frontal plane axis has shifted!and — you'll need to consider this axis shift when determining whether any differences in ST-T wave morphology are likely to be due to technical factors or "true" evolution of the patient's cardiac condition.



My THOUGHTS on the Initial ECG in Figure-1:

I began assessing today's case with interpretation of the initial ECG in the ED ( = ECG #1). As always — I used a Systematic Approach (See ECG Blog #205 for details):

  • Rate & Rhythm: There is a fairly regular sinus rhythm at ~80-85/minute.
  • Intervals (PR, QRS, QTc) — Normal.
  • Axis: Normal (about +65 degrees — given slight negativity of the QRS in lead aVL).
  • Chamber Enlargement: None. 

 

Regarding Q-R-S-T Changes:

  • Q Waves: No Q waves of note. There appears to be a small initial r wave in lead III (which manifests an rsR' complex). The Q waves seen in leads aVR and V1 are so common (and normal) that I generally don't mention them. No other Q waves.
  • R Wave Progression: Normal. Transition (where height of the R wave exceeds depth of the S wave in the chest leads) occurs normally (ie, here between leads V3-to-V4).

 

Regarding ST-T Wave Changes:

  • There is nonspecific ST-T wave flattening in leads III and aVF.


IMPRESSION: Overall, I thought ECG #1 was unremarkable for a patient who presented with new chest pain. The nonspecific ST-T wave flattening seen in leads III and aVF is often seen in patients without chest pain.



My THOUGHTS on ECG #2:

As noted in Figure-1ECG #2 was obtained 1 hour after ECG #1 in this 30-something year-old man, who presented to the ED with several hours of chest pain.

  • Once again — My assessment of the ST-T wave appearance in ECG #2 for this patient with chest pain was fairly unremarkable — and by itself, did not suggest acute changes. 




CHALLENGE:
What I did not do in my description above — was to compare these 2 tracings, looking for changes that may have occurred during the hour after ECG #1 was done. Please go back and TAKE ANOTHER LOOK at these 2 tracings (which for clarity, I reproduce below in a 2nd look at Figure-1). Please GO lead-by-lead in your comparison.
  • Do YOU see any differences in ST-T wave morphology in any of the 12 leads?
  • What clinical information do we need to know in order to optimally interpret these 2 tracings?

Another Look at Figure-1: The 2 ECGs in today's case.



ANSWER: Comparison of ECG #1 and ECG #2:
As emphasized in the above Audio Pearl-46a — the KEY for accurate comparison of serial tracings is to assess whether the frontal plane axis and chest lead electrode placement are comparable.

  • In the Limb Leads: QRS morphology and amplitude, as well as the frontal plane axis — are virtually identical in ECG #2, compared to what was seen in ECG #1.
  •  
  • In the Chest Leads: Considering that half-standardization was used to record the chest leads in ECG #2 — I saw no significant difference in R wave progression or QRS morphology between the 2 tracings.

  • KEY Point: Knowing that frontal plane axis and chest lead electrode placement is comparable in ECG #1 and ECG #2 greatly facilitates comparison of these serial tracings. This tells us that any significant change that we see between ECG #1 and ECG #2 is likely to be real.


Lead-by-Lead Comparison:
Careful comparison between the 2 tracings shown in Figure-1 does show a number of differences:
  • In the High-Lateral Leads: The T waves in leads I and aVL of ECG #1 were slightly larger (more upright) in this earlier tracing — than they are in ECG #2.
  • In the Inferior Leads: Although I do not see any difference in the ST-T wave appearance in lead II — T waves in the other 2 inferior leads (leads III and aVF) are more upright in ECG #2, compared to what they were in ECG #1.
  • In the Chest Leads: Even accounting for the change in standardization — the T waves in leads V2-thru-V6 are flatter in ECG #2 than they were in ECG #1. The T wave in lead V1 is less deeply inverted in ECG #2.
Conclusion: Admittedly — the above described differences in ST-T wave appearance between ECG #1 and ECG #2 are subtle. But the fact that despite no appreciable change in either frontal plane axis or chest lead QRS morphology — no less than 10/12 leads do show differences is undeniable!
  • The KEY clinical information missing in this case — is an account of what happened to the severity of this patient's chest pain between the time that these 2 ECGs were recorded.
  • IF there was in fact a change in the severity of this patient's symptoms — this would strongly support the premise that there are ongoing dynamic ST-T wave changes. For example — IF chest pain was significantly less at the time ECG #2 was recorded, this might indicate evolution of acute LAD (Left Anterior Descending) occlusion, in which spontaneous reperfusion signaled what was soon to become anterior reperfusion T waves ( = anterior T wave inversion).
  • In this case — IF an ECG had been recorded a bit before ECG #1, perhaps it might have revealed "tell-tale" anterior ST elevation.
  • BOTTOM Line: Without knowing details about the course of this patient's chest pain — it's impossible to predict a probable "culprit" artery. But IF there was indeed a significant change in the severity of this patient's symptoms between the time that ECGs #1 and #2 were recorded — this would have been clear indication for prompt cath.

  • "Take-Home" Message #1: The course of acute coronary occlusion is sometimes stuttering. That is, the "culprit" artery may completely occlude — only to spontaneously open a short time later. IF the duration of complete occlusion is brief (ie, minutes) — then even high-sensitivity troponin may not necessarily elevate. When ST-T wave changes correlate with the "coming-and-going" of symptoms — these ECG findings strongly suggest onging change in the patency of the "culprit" artery. The reason these dynamic ST-T wave changes are indication for prompt cath — is that what was totally occluded (and is now open) — might just as easily occlude again at any time, until the final state of the culprit artery is ultimately reached.
  • "Take-Home" Message #2: The ECG findings in today's case are subtle — and neither ECG #1 nor ECG #2 alone suggested an ongoing acute event. But when one considers that no less than 10/12 leads show a subtle-but-real difference in ST-T wave morphology in this patient with new chest pain — the strong indication for prompt cath that was advised is undeniable. This patient might still be alive IF he had not ignored this recommendation.

  • Final "Take-Home" POINT: Recognition of dynamic ST-T wave changes sometimes requires meticulous lead-by-lead comparison of serial ECGs, interpreted in association with the serial course of the patient's symptoms.

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Acknowledgment: This case was anonymously sent to me ...
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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 #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript). 
  • ECG Blog #222 — Reviews the concept of Dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • ECG Blog #260 — Reviews another case that illustrates the concept of "dynamic" ST-T wave changes.

  • 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 "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes.
  • The January 9, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case is remarkable for the dynamic ST-T wave changes that are seen. It's helpful to appreciate: i) That acute ischemia/infarction is not the only potential cause of such changes (cardiac cath was normal); ii) That changes in heart rate, frontal plane axis and/or patient positioning can not always explain such changes; and, iii) That entities such as repolariztion variants, LVH and/or acute myopericarditis may all contribute on occasion to produce an evolution of challenging dynamic ST-T wave changes on serial ECGs.

  • The August 22, 2020 post in Dr. Smith's ECG Blog — which illustrates another case of dynamic ST-T wave changes that resulted from a repolarization variant

  • The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.
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