ECG Blog #370 — A Post-Arrest Tachycardia ...

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 — was obtained from a previously healthy, elderly woman who collapsed in the hospital parking lot. 

• She underwent cardiopulmonary resuscitation for VT/VFib — with ROSC (Return Of Spontaneous Circulation) following defibrillation and treatment with Epinephrine and Amiodarone. 
• A series of cardiac arrhythmias were seen during the course of her resuscitation — including the interesting arrhythmia shown in the long lead II of Figure-1. The patient was hemodynamically stable with this rhythm.

QUESTIONS:

• How would YOU interpret this patient’s 12-lead ECG?
• What is the cardiac rhythm shown in the long lead II rhythm strip?

Figure-1: The initial ECG in today’s case — obtained from an elderly woman following successful resuscitation from cardiac arrest. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

When faced with interpreting a challenging 12-lead and a challenging rhythm — I favor starting my assessment with a quick look at the rhythm. To Emphasize — I do not necessarily complete full analysis of the rhythm in this “initial brief overview” — but rather aim to get a quick idea about whether immediate treatment (such as cardioversion) may or may not needed.

• The “good news” regarding today's case — is that we are told the patient was hemodynamically stable in association with the post-resuscitation rhythm shown in Figure-1.
• Looking quickly at all 12 leads — the QRS complex is narrow everywhere — which tells us the rhythm in Figure-1 is supraventricular. That said — QRS morphology does change a lot, in places with every-other beat (this best seen in the long lead II rhythm strip).
• The overall rate of the rhythm in Figure-1 is rapid (ie, over 100/minute). By definition, this defines the rhythm as some form of SVT (that is, some form of SupraVentricular Tachycardia).
• Although the rhythm is not completely regular — there is some form of “regular irregularity” (ie, group beating) that is seen through much of the long lead II rhythm strip, in that there are alternating short-long R-R intervals. Because most of these groupings in Figure-1 have 2 beats — there is a bigeminal rhythm for much of this rhythm strip.
• There is some form of atrial activity! Looking in front of each of the longer R-R intervals (ie, the R-R intervals before beats #2,3,5,7,9,10,12,14,16 and 18) — there does appear to be a P wave with a constant PR interval. This tells us that at least some of the P waves are conducted to the ventricles. That said — the P wave in the long lead II rhythm strip is not upright — which means that the mechanism of today's rhythm is not sinus.

To EMPHASIZE: I literally went through my "assessment thoughts" above regarding today's rhythm in slow motion! With experience, applying the Ps, Qs, 3R Approach (See ECG Blog #185) — to formulate the above steps in our initial assessment of the rhythm in Figure-1 can (should) be completed in less than 30 seconds!

• PEARL #1: Within a matter of seconds — we’ve already determined that the rhythm in Figure-1 manifests some form of bigeminal and non-sinus SVT rhythm, in which there is atrial activity — and in which at least some of the P waves are conducting! Since the heart rate is tachycardic (ie, ≥100/minute), but not excessively fast — and since the patient is hemodynamically stable — this more than suffices for our "initial brief overview" of the cardiac rhythm.

What about the 12-Lead ECG?

At about this point in the process — I like to take a closer LOOK at the 12-lead tracing, to ensure there is no acute ischemia or infarction that might need immediate attention.

• As already established — the QRS complex is narrow in all leads, so the rhythm is supraventricular.
• The QTc is not overly prolonged.
• The frontal plane axis is markedly leftward (ie, predominantly negative in each of the inferior leads). This qualifies as LAHB (Left Anterior HemiBlock).
• There is LVH (The R wave in lead aVL ≥12 mm — and there are very deep S waves in the anterior leads). At least some of the ST-T wave flattening in lateral leads may be the result of LV "strain".
• 
  
• Regarding Q-R-S-T Changes — QS complexes of uncertain significance are seen in the anterior leads (possible previous anterior MI) — R wave progression may be slightly delayed — and there are nonspecific ST-T wave changes in multiple leads — but nothing that looks acute! Therefore — there is time to assess today's rhythm in more detail!

Assessing the Cardiac Rhythm in More Detail:

Our brief "initial overview" of today's rhythm — was that there is some form of bigeminal and non-sinus SVT rhythm in Figure-1, with some form of atrial activity that is at least partially conducting.

• PEARL #2: Awareness of the common causes of a bigeminal rhythm helps to quickly narrow our differential diagnosis. These are reviewed in ECG Blog #343. For practical purposes — the fact that the rate of the rhythm in Figure-1 is relatively fast, with group beating for much of the rhythm strip (with conduction of at least those P waves that end the longer R-R intervals) — narrows the likely possibilities for the cause of today's rhythm to the following: i) Atrial Bigeminy; or, ii) Either Atrial Flutter or Atrial Tachycardia, with Wenckebach conduction accounting for the group beating.
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• PEARL #3: At this point — the most time-efficient step for solving today's rhythm will be to determine the nature of atrial activity. This can most EASILY be accomplished by using calipers! Simply set your calipers to the P-P interval between any 2 consecutive P waves that you can clearly see. Focusing our attention from Figure-1 on the long lead II rhythm strip — we can clearly see 2 consecutive P waves within the R-R intervals between beats #1-2 — and between beats #9-10 (RED arrows in Figure-2).

Figure-2: The EASIEST and most time-efficient way to assess atrial activity — is to set your calipers to the P-P interval between any 2 consecutive P waves that you can clearly see (ie, RED arrows within the R-R intervals between beats #1-2 — and between beats #9-10).

Labeling P Waves:

Once you have set your calipers to the P-P interval between 2 consecutive P waves that you clearly see — Try to walk out this P-P interval throughout the rest of the rhythm strip.

• Figure-3 reveals that walking out the P-P interval we determined in Figure-2 — allows us to verify that with 1 exception (ie, the ? after beat #15) — each progression of our calipers either falls on a negative deflection of atrial activity or falls within a part of a QRS complex where an "on-time" negative deflection might be hidden (RED arrows in Figure-3).

Figuring Out the Atrial Rhythm: The overall regularity of atrial activity highlighted by the RED arrows in Figure-3 — suggests there is an underlying regular atrial rhythm. By the every-other-beat Method (See ECG Blog #210) — the P-P interval for 2 consecutive P waves in Figure-3 is between 3-to-4 large ECG boxes — which means that about half the atrial rate is ~85/minute X 2 = 170/minute for the estimated atrial rate. 

• As already discussed — the finding of P wave negativity in lead II rules out a sinus mechanism for the rhythm in today's case.
• The rate of ~170/minute would be too slow for AFlutter (unless the patient was being treated with an antiarrhythmic agent that slows AV node conduction).
• This leaves ATach ( = Atrial Tachycardia) — as the most likely etiology for the rhythm in Figure-3. The finding of negative P waves in lead II — is perfectly consistent with an ectopic atrial rhythm such as ATach.

Figure-3: Walking out the P-P interval we set for our calipers in Figure-2 — suggests that with 1 exception (ie, the ? after beat #15) — the underlying atrial rhythm in today's tracing is regular!

PEARL #4: When certain elements of a complex rhythm appear to be more difficult to interpret — Save those elements for last! Instead — it's far more time-efficient to assess less difficult elements of the rhythm first. After doing so — the solution to those more difficult elements often becomes much easier to figure out!

• Applying this principle, I ignored the last part of today's rhythm (ie, what happens after beat #14) — and instead, I focused on the first 14 beats.
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• PEARL #5: The simple act of labeling P waves can be invaluable for solving an arrhythmia. For example, in Figure-4 — I labeled with YELLOW arrows those P waves that seem to have the least chance to conduct, because these P waves occur just after the QRS complex. Does doing so help you to recognize what is happening to the PR interval when you see 2 RED arrows in a row?

Figure-4: I've labeled with YELLOW arrows those P waves that seem to have the least chance to conduct. Does doing so help you to recognize what is happening to the PR interval when you see 2 RED arrows in a row? 

PEARL #6: Common things are common. IF we consider what we have determined about today's rhythm thus far — we know that there is a pattern of group beating through much of this SVT rhythm, in which there is an underlying regular ATach at ~170/minute (at least for the first 14 beats in this tracing).

• The finding of group beating, in which there is an underlying regular atrial rhythm — and each of the groups of beats begins with a similar PR interval — is characteristic of Wenckebach conduction.
• 2 SVT rhythms that very commonly manifest Wenckebach conduction are ATach and AFlutter. This is because the rapid atrial rates attained by these 2 arrhythmias is often too fast to allow continued 1:1 AV conduction. As a result — I always consider the possibility of Wenckebach conduction whenever I see a pattern of group beating (be this intermittent or continuous) — especially when there are a number of identical PR intervals at the beginning of some (or all) of the groups.

Applying PEARL #6 to the rhythm in Figure-4: 

• Aren't the PR intervals before beats #2,3,5,7,9,10,12 and 14 the same? 

QUESTION: Compared to the PR interval before beats #3,5,7,10,12 and 14 — What happens to the PR interval before beats #4,6,8,11,13 and 15?

• HINT: Answering this Question is facilitated by the BLUE arrows in Figure-5.

Figure-5: How do the BLUE arrows facilitate interpretation this rhythm?

Putting It All Together:

Focus on the rhythm in Figure-5, beginning with beat #2:

• The RED arrow negative P wave in front of beat #2 is conducted with a long PR interval — but the YELLOW arrow that occurs just after the QRS of beat #2 is not conducted.
• There follows the first 2-beat group in this tracing — that consists of beats #3 and #4. The RED arrow P wave in front of beat #3 is conducted with the same PR interval that preceded beat #2.
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• Isn't the PR interval of the BLUE arrow P wave before beat #4 longer than the PR interval of the RED arrow P wave before beat #3? And then the next P wave ( = the YELLOW arrow that is almost completely hidden within the QRS of beat #4) is not conducted. This is consistent with a Wenckebach cycle with 3:2 AV conduction ( = 3 P waves, with only 2 QRS complexes being conducted = beats #3 and 4).
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• After beat #4 — there follows a short pause until the RED arrow P wave before beat #5 begins the next cycle with a PR interval equal to the PR interval of other RED arrow P waves.
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• With the exception of what happens with beat #15 — a similar series of events occurs throughout the long lead II rhythm strip in Figure-5. Thus, we can say that the underlying rhythm in today's tracing is ATach at ~170/minute. There is Wenckebach conduction with 2:1 and 3:2 AV conduction ratios (2:1 AV conduction for beats #2 and 9 — and 3:2 AV conduction for beats #3,4; 5,6; 7,8; 10,11; 12,13; and 16,17).

Why are there 2 QRS Morphologies?

I noted earlier that QRS morphology changes slightly for a number of beats on today's tracing. Specifically — the QRS is slightly wider and the S wave deeper for beats #4,6,8,11,13 and 17.

• What all of these beats have in common — is that they all follow a longer R-R interval, and have a short coupling interval with the preceding QRS. These 2 features (ie, a longer preceding R-R interval — and a short coupling interval) — define what occurs with the Ashman phenomenon, that predisposes to aberrant conduction. Thus, these slightly different-looking beats almost certainly reflect an enhanced degree of LAHB (Left Anterior HemiBlock) aberration (See ECG Blog #70 for full review of the Ashman phenomenon).

LADDERGRAM Illustration of Today's Rhythm:

I conclude today's case with Figure-6 — which provides laddergram illustation of this patient's arrhythmia. For clarity — I have used the same coloration to depict conduction through the AV Nodal Tier corresponding to the colored P waves in the rhythm strip. The laddergram shows:

• The underlying ATach at ~170/minute.
• RED arrow P waves are conducted with a prolonged but constant PR interval.
• BLUE arrow P waves are conducted with a slight increase in PR interval.
• YELLOW arrow P waves are not conducted.
• The result is that there is ATach with 3:2 and 2:1 Wenckebach conduction through the AV Node.

Figure-6: Laddergram illustration of the mechanism in today's arrhythmia.

Beyond-the-Core: The Exception = Beat #15

Interpretation of today's rhythm as ATach with 3:2 and 2:1 AV Wenckebach conduction is more than sufficient for understanding and managing this patient. What follows are a number of advanced concepts for those with a desire to understand more: 

• The regular atrial rhythm in today's case is momentarily interrupted following beat #15. I believe the reason for this short-lived interruption — is that an Echo beat occurred. Instead of an on-time negative deflection for the next ATach impulse — a positive deflection is seen under the question mark that occurs right after beat #15.
• I reviewed the concept of Echo beats in ECG Blog #239. On occasion when the PR interval is prolonged — conditions may be "just right" that allow retrograde conduction back to the atria (ie, with production of an "echo" beat that is "returned" to the atria). Since forward-conducting P waves in today's ATach rhythm are negative in lead II — polarity of the retrograde echo beat produces a positive P wave (dotted BLUE lines in the laddergram).
• The reason there is a slight pause in the ATach rhythm — is that the retrograde P wave (echo beat) depolarizes the atria, temporarily delaying the next ectopic atrial impulse.
• It turns out that the PR interval of the RED arrow P wave before beat #16 is slightly shorter than all other RED arrow PR intervals! Presumably the reason for this is that the longer R-R interval between beats #15-16 allowed more complete recovery of atrial conduction properties, thus allowing slightly faster conduction of the P wave before beat #16 to the ventricles.

CASE Conclusion:

I lack detailed follow-up from today's case — other than knowing that the Atrial Tachycardia was controlled.

• KEY Point: Rather than calling today's arrhythmia as ATach with 2nd-degree AV "block" of the Mobitz I Type — I favor considering today's rhythm as ATach with Wenckebach conduction. This type of Wenckebach response that may be seen with atrial tachycardia (or atrial flutter) — is often physiologic, as a result of the rapid atrial rate that occurs with these arrhythmias. This usually does not represent a specific conduction defect — and Wenckebach conduction will often resolve once the ATach is controlled.

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Acknowledgment: My appreciation an anonymous clinician for the case and these tracings.

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ADDENDUM (3/24/2023): 

• The Audio Pearls below may help in assessment of today's case.

—  — 

ECG Media PEARL #51a (7:40 minutes Audio) — Simple Steps to Help for Interpretation of Complex Rhythms.

—  — 

ECG Media PEARL #54 (5:00 minutes Audio) — Reviews what Echo Beats are — and clinical applications of this ECG finding.

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Relevant ECG Posts to Today's Case:

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #210 — Reviews the every-other-beat Method for estimating the rate of regular rapid rhythms.
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• ECG Blog #186 — Highlights the importance of Group Beating — and reviews when to suspect the Mobitz I form of 2nd-Degree AV Block ( = AV Wenckebach).
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• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.
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• ECG Blog #343 — reviews common causes of a bigeminal rhythm.
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• ECG Blog #261 — A case of ATach with Wenckebach conduction.
• ECG Blog #55 — Acute inferior MI + AV Wenckebach.
• ECG Blog #154 — Acute inferior MI + AV Wenckebach. 
• ECG Blog #168 — Acute inferior MI + Wenckebach (dual-level) block. 
• ECG Blog #224 — Acute inferior MI + AV Wenckebach.
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• ECG Blog #240 — Reviews assessment of the Differential Diagnosis of the Regular SVT Rhythm.
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• ECG Blog #229 — Why is AFlutter so commonly overlooked? 
• ECG Blog #137 — AFlutter with an unusual conduction ratio. 
• ECG Blog #138 — AFlutter vs Atrial Tachycardia. 
• ECG Blog #40 — Another regular SVT that turned out to be AFlutter.
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• González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011 — Reviews making the distinction between AVNRT vs AVRT and other regular SVT rhythms in patients without WPW.
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• ECG Blog #239 — Reviews the concept of Echo Beats (and how Echo beats may sometimes end a Wenckebach cycle).
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• ECG Blog #70 — Reviews the Ashman Phenomenon. 

ECG Blog #369 — 10 Minutes Later ...

The ECG in Figure-1 was obtained from a man in his mid-60s — who presented with new chest pain.

• Should the cath lab be activated?

Figure-1: The initial ECG in today’s case. Should the cath lab be activated?

MY Thoughts on the Initial ECG:

The rhythm in ECG #1 — is sinus at ~70/minute. All intervals (PR, QRS, QTc) are normal. There is no chamber enlargement.

• There is significant LAD (Left Axis Deviation) — as the QRS is predominantly negative not only in lead aVF, but also in lead II. This results in a frontal plane axis of at least -40 degrees — which is consistent with LAHB (Left Anterior HemiBlock).

Regarding Q-R-S-T Changes:

• There are no Q waves (ie, There is a tiny-but-present initial positive deflection [r wave] — in both leads III and aVF).
• R Wave Progression overall is appropriate — in that Transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V3-to-V4.
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• PEARL #1: Although the zone of transition in the chest leads is appropriate — Note that the R wave in lead V2 increases abruptly in height (attaining 5 mm already by lead V2). This is relevant to today’s case (!) — as we will see momentarily.

Regarding ST-T wave abnormalities: 

• PEARL #2: It's most time-efficient to assess ST segment and T wave abnormalities together — and to do so at the same time for all leads in a given anatomic area. For example, in Figure-1 — My “eye” was drawn first to the inferior leads (II,III,aVF) — each of which show ST segment coving, followed by symmetric T wave inversion (BLUE lines that I've added to these leads in Figure-2).
• KEY Point: It is important to note that while inferior lead ST-T wave changes are clearly more marked in leads III and aVF — they are also present in the 3rd inferior lead ( = lead II). It is far less likely for a notable ST-T wave finding in leads III and aVF to be the result of a normal repolarization variant — IF a similar ST-T wave appearance is also seen in the 3rd inferior lead ( = lead II). 
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• PEARL #3: Confirmation that the abnormal inferior lead ST-T wave findings just described are “real” (and indicative of a recent or acute cardiac event) — is immediately forthcoming from assessment of lead aVL — which shows the mirror-image opposite ST-T wave picture as is seen in lead III (ie, not only scooped ST depression — but also terminal T wave positivity in lead aVL — as seen in Figure-2). 
• Further support that the picture in lead aVL represents true reciprocal ST-T wave changes to the abnormal inferior lead findings — is forthcoming from the similar ST-T wave shape (albeit a little less marked) for the ST-T wave depression in lead I.
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• To EMPHASIZE: My above description is intentionally made in “slow motion”. The total time it should take for you to arrive at this point in your interpretation (in which we already know that the cath lab needs to be activated) — should be less than 10 seconds.

Figure-2: I've labeled significant ST-T wave findings in the limb leads of ECG #1.

Assessment of ST-T Wave Changes in the Chest Leads:

• There is ST depression in leads V2-thru-V6 (See Figure-3). Leads V2 and V3 show terminal T wave positivity. The magnitude of ST-T wave change is maximal in lead V2 — with the insert in this lead showing a positive "Mirror" Test — that in this patient who presents with new chest pain, is diagnostic of acute posterior OMI — until proven otherwise.
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• PEARL #4: Normally, when there is acute posterior OMI — there is ST depression that is maximal in one or more of the leads between V2-to-V4. This ST depression sometimes extends more laterally (ie, to leads V5,V6 — as it does in Figure-3). That said — There should also be at least some ST depression in lead V1 with acute posterior OMI — unless something else is going on that results in ST elevation. The fact that instead of ST depression in lead V1, there is slight-but-real ST elevation (RED arrow in this lead in Figure-3) — strongly suggests that in addition to acute posterior OMI — there is also acute RV (Right Ventricular) involvement! (For more on this Pearl #4 — See the Audio Pearl and Figures-5 and -6 in the ADDENDUM below).

Putting It All Together:

In view of the history in today's case (ie, A man in his mid-60s who presents with new chest pain) — the ECG in Figure-1 is diagnostic of recent or ongoing acute infero-postero OMI.

• The fact that the amount of ST elevation in the inferior leads of ECG #1 is minimal (and associated with more impressive T wave inversion in leads III and aVF) — suggests that we are seeing reperfusion T waves from spontaneous reopening of the "culprit" artery.
• Consistent with the presence of reperfusion T waves in the inferior leads — is the modest amount of J-point ST depression in leads V2-thru-V4. The surprisingly tall terminal T wave positivity that we see in lead V2 almost certainly represents reperfusion in the posterior wall distribution.
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• To EMPHASIZE: Despite there not being "enough" ST elevation to satisfy millimeter-based criteria for an acute "STEMI" in ECG #1 — this initial ECG is absolutely diagnostic of OMI. The fact that spontaneous reopening of the occluded vessel has occurred in no way eliminates the risk that spontaneous reocclusion might at any time reoccur. Prompt cardiac cath is clearly indicated!
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• PEARL #5: We could probably get a better idea of the sequence of events in today's case with some additional history that correlates the timing of ECG #1 — with the timing of symptom onset — and — with the presence (as well as relative severity) of chest pain at the time the initial tracing in Figure-1 was done.
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• PEARL #6: The finding of slight-but-real ST elevation in lead V1 (RED arrow in this lead in Figure-3) — localizes the "culprit" artery to RCA (since the LCx does not supply the right ventricle).

Figure-3: Significant ST-T wave findings in the chest leads of Figure-1. The insert in lead V2 shows a positive "Mirror" Test indicative of acute posterior OMI. 

Today's CASE Continues: 

Approximately 10 minutes after ECG #1 was recorded — an ECG with right-sided chest leads was obtained ( = ECG #2).

• For clarity in Figure-4 — I've put the repeat ECG together with the initial tracing.

QUESTION:

• How do YOU interpret the repeat ECG?

Figure-4: Comparison of the initial ECG — with the repeat tracing obtained 10 minutes later using right-sided leads.

MY Thoughts on the ECGs in Figure-4:

• Although difficult to assess (because of artifact in lead V2R — and very low QRST amplitude in leads V3R-thru-V6R) — there is ST elevation in these last 4 right-sided leads. This confirms the acute RV involvement that we strongly suspected from the ST elevation in lead V1 of ECG #1.

Ideally, in addition to right-sided leads — a complete repeat 12-lead ECG with normal electrode lead placement would also have been done. Instead — we have no idea about what normally-placed leads V3-thru-V6 look like.

• Keeping in mind that ECG #2 was obtained just 10 minutes after ECG #1 — We now see dramatic ST elevation in each of the inferior leads in ECG #2, in association with comparable reciprocal ST depression in lead aVL. Even without knowing if the patient's chest pain was increased at the time ECG #2 was recorded — the inescapable conclusion is that just 10 minutes after seeing reperfusion T waves in the infero-postero leads — there has now been spontaneous reocclusion of the "culprit" RCA!
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• PEARL #7: It is good to remember that lead V1R corresponds to a normally-placed lead V2 (and lead V2R corresponds to a normally-placed lead V1). As a result — We can compare lead V2 in ECG #1 — with lead V1R in ECG #2. When we do — it should be obvious that a comparable amount of acute ST-T wave change as is seen in the limb leads — has also occurred in the posterior wall distribution (further supporting the inescapable conclusion of spontaneous reocclusion of the RCA).

CASE Conclusion:

On seeing ECG #2 — cardiac cath was expedited. The RCA was confirmed as the culprit artery — and PCI was promptly performed with good result. There was insignificant disease in the LAD and LCx.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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ADDENDUM (3/19/2023):

—  —

ECG Media PEARL #7 (4:50 minutes audio) — reviews the ECG findings of acute RV MI — as well as other pearls for determining the likely “culprit” artery.

FOR Other Examples of Acute RV MI:

• Discussion of the 12-lead ECG in Blog #187 —
• See Figure-4 in ECG Blog #80 (More on the "culprit" artery in this post) —
• See ECG Blog #141 —

Figure-5 (together with Figure-6): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).

 

 

Figure-6 (continued from Figure-5): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• 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 — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
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• ECG Blog #190 — Reviews the concept of RV MI.
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• 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).
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• ECG Blog #184 and ECG Blog #167 — illustrate the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL. 
•  
• 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. 
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• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
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• ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T waves).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• ECG Blog #262 — Potential significance of Low Voltage with acute MI.
• ECG Blog #272 — Significance of Low Voltage with acute MI.