Friday, August 27, 2021

ECG Blog #247 (61) — Why is the PR Interval Decreasing?

The ECG in Figure-1 was obtained as part of a routine exam of an otherwise healthy and asymptomatic 30-year old man.



  • What are the abnormal findings in Figure-1?
  • Are any of the P waves conducted to the ventricles?
  • Clinically — HOW should this patient be treated?


Figure-1: ECG obtained from an otherwise healthy and asymptomatic 30-year old man. Can you explain the abnormal findings?




NOTE: Some readers may prefer at this point to listen to the 5:45-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 this tracing (that appear below ECG MP-61).


Today's ECG Media PEARL #61 (5:45 minutes Audio) — Reviews HOW to Tell IF a P Wave is Conducting? Being able to answer this question is KEY for determining the etiology of complicated AV Block/AV Dissociation tracings.




MY Sequential Thoughts on the ECG in Figure-1:

As always — I favor the use of a Systematic Approach for interpreting ECG findings in the 12-lead (which I review in ECG Blog #205— and — the Ps, Qs & 3Rs Approach for initial assessment of the cardiac rhythm, especially when the rhythm is complicated (as reviewed in ECG Blog #185).

  • My initial impression of the rhythm, as seen in the long lead II rhythm strip in Figure-1 — was that the QRS complex was narrow — that fairly regular P waves were seen — that the ventricular rhythm was for the most part regular (at a rate of ~80-85/minute) — and, that most of the P waves looked to be conducting. And then I noticed that the PR interval was decreasing ... This suggested that the mechanismo of this rhythm was more complex than what I initially thought.


PEARL #1: It's fine to make a quick, initial hypothesis. The experienced clinician routinely does this in virtually all aspects of medicine — often suggesting a preliminary diagnosis to us within seconds of seeing the patient. But after this brief, almost intuitive impression — what should then follow, is a far more specific series of inquiries and assessments that either confirm or negate our initial impression.

  • In the field of arrhythmia interpretation — IF your initial impression is wrong (as mine was for the rhythm in Figure-1)  GO BACK to the BASICS (which means step-by-step assessment by the Ps, Qs & 3R Approach).
  • Number the beats in the rhythm strip.
  • Use calipers to determine IF there are regular (or at least fairly regular) P waves throughout the rhythm strip (Figure-2).


Figure-2: I have numbered the beats in the long lead II rhythm strip from Figure-1. I then used calipers to facilitate labeling P waves throughout this tracing.


  • Is the atrial rhythm regular (or at least almost regular)?
  • Are any of the P waves in Figure-2 being conducted to the ventricles?



MY Thoughts:

We have already established that the QRS complex is narrow — which tells us that the rhythm in Figure-2 is supraventricular.

  • Definite evidence for regular sinus P waves is seen under all RED arrows in Figure-2. The exceptions for where sinus P waves are less obvious are highlighted by the 3 PINK arrows.
  • Reasons why I believe these 3 PINK arrows in Figure-2 also indicate where sinus P waves are falling are: iThe PINK arrow coinciding with the QRS of beat #7 highlights a downward deflection in the terminal portion of this QRS that is not seen in any other QRS complex; ii) The T wave of beat #8 is "fatter"-at-its-peak than any other T wave in this tracing (and — in simultaneously-occurring leads V2 and V3, there is "telltale" notching of the ST segment of beat #8); iii) There is subtle-but-real initial slurring of the QRS of beat #14 that is not seen for any other QRS complex in this long lead II rhythm strip; andiv) Using calipers allows us to walk out a fairly (albeit not completely) regular P wave rhythm for each of the arrows in the long lead II that is consistent with sinus arrhythmia. Postulating an underlying sinus mechanism with no more than slight irregularity is far more common (and far more logical) than having to postulate sudden loss of sinus P waves.


PEARL #2: It may sometimes be extremely challenging to try and figure out if certain P waves on a tracing are (or are not) being conducted to the ventricles. In such cases — Start with what you know!

  • What We Know — is that the P wave that coincides with beat #7 can't be conducting — because it begins afterthis QRS complex.
  • We Also Know — that the PR intervals preceding beats #6, 13 and 14 are clearly too short to conduct.
  • Considering the PR intervals preceding beats #2, 3; and 10, 11 — it would seem that the PR intervals preceding beats #4 and 12 are probably also too short to conduct. Therefore — Many (if not the majority) of P waves in the long lead II rhythm strip in Figure-2 are probably not being conducted to the ventricles!




NOTE: I've devoted ECG Media Pearl #61 (above) to addressing the challenge for determining IF a given on-time P wave is (or is not) being conducted to the ventricles.



PEARL #3: One of the BEST clues that one-or-more on-time sinus P waves is being conducted to the ventricles — is IF you see one-or-more QRS complexes occurring earlier-than-expected considering regularity of the R-R interval for other beats in the tracing.

  • To better assess which beat(s) in Figure-2 are likely to be conducted — I carefully measured all R-R intervals in the long lead II rhythm strip (Figure-3).


Figure-3: I have measured all R-R intervals (in milliseconds) in Figure-2. Note that all but 2 of these R-R intervals are identical (See text).


MY Thoughts on the Rhythm in Figure-3:

As I've already alluded to — the rhythm in today's case is more complex than I initially thought. Precise measurement of all R-R intervals in the long lead II rhythm strip suggests the following:

  • All R-R intervals are identical (ie, measuring 720 msec.)  except for the 2 R-R intervals between beats #8-9 and 9-10 (which measure 600 and 700 msec., respectively).
  • The PR interval preceding each of the 14 beats on this tracing is continually changing. But rather than progressive increase in the PR interval (until a beat is dropped) — the PR interval is decreasing as one moves from beat #2 until beat #6 — and then again as one moves from beat #9 until beat #14. This tells us that P waves are not related to neighboring QRS complexes for those beats in which the R-R interval is regular (ie, there is AV dissociation for all beats preceded by a PR interval = 720 msec.).
  • Since the QRS complex is narrow and the R-R interval is perfectly regular for all but 2 beats on this tracing, during which time there is AV dissociation — this means that the rhythm for most of this tracing is junctional! It also means that there is AV dissociation for most of this tracing!
  • An R-R interval of 720 msec. (ie, 3.6 large boxes) corresponds to a ventricular rate of ~85/minute. Since the usual rate of an AV nodal escape pacemaker in adults is between 40-60/minute — this defines the underlying rhythm in Figure-3 as an accelerated junctional rhythm. 




  • WHY is the R-R interval between beats #8-9 so much shorter than all other R-R intervals in this tracing?




The only logical conclusion to draw from the finding that the R-R interval between beats #8-9 is so much shorter than all other R-R intervals — is that beat #9 must be conducted!

  • This means that the on-time P wave that is hiding within the T wave of beat #8 must be conducting to the ventricles with a long PR interval.
  • I strongly suspect that the reason the R-R interval between beats #9-10 is also shorter (at 700 msec.) than all other R-R intervals (which are all 720 msec.) — is that beat #10 is probably also being conducted to the ventricles.



PEARL #4: Support that not only beat #9 — but also beat #10 are both conducted to the ventricles is forthcoming from a look at simultaneously-recorded leads V2 and V3. Note that although the QRS complex for beats #8, 9 and 10 in these 2 leads is narrow — QRS morphology for the 2 beats that occur earlier-than-expected (ie, beats #9 and 10) is different than for beat #8 which is on-time (ie, preceded by an R-R interval = 720 msec.).

  • Because the site within the AV node from which a junctional escape beat may arise can be slightly different than the site in the AV node that a normal, sinus-conducted beat passes through — sometimes (not always!) you may see slightly different QRS morphology for junctional beats compared to sinus-conducted beats. When this finding occurs (as it does for beats #8, 9 and 10 in leads V2 and V3) — it can be very helpful in telling you whether a certain beat is or is not conducted.


PEARL #5: Despite the fact that there is AV dissociation for most of today's tracing — there is no evidence of 2nd or 3rd-degree AV block! This is because we have not proven that P waves (RED arrows) in Figure-3 had an adequate chance to conduct, but still failed to do so.

  • On the contrary — 2 QRS complexes in Figure-3 are conducted (ie, beats #9 and 10) — and beat #10 is conducted with no more than minimal prolongation of the PR interval.




SUMMARY Thus Far of Today's Rhythm: This leaves us with the following conclusions about the rhythm in today's case:

  • There is an underlying sinus arrhythmia (RED arrows) — with AV dissociation for most of the long lead II rhythm strip in Figure-3.
  • An accelerated junctional rhythm at ~85/minute is present for most of this tracing.
  • The accelerated junctional rhythm is interrupted by sinus capture of beats #9 and 10.



PEARL #6: As emphasized in ECG Blog #192 (and also in ECG Blog #191) — AV dissociation is not a diagnosis. Instead — ADissociation is an ECG finding that is the result of one of Causes. These are: i) 2nd- or 3rd-degree AV Block (in which one or more P waves that should conduct do not conduct because of AV block)ii) AV dissociation by "Usurpation" (in which an accelerated junctional rhythm takesover the pacemaking function)and/oriii) AV dissociation by "Default" (in which slowing = "default" of the SA nodal pacemaker allows a junctional escape pacemaker to emerge).

  • As stated in Pearl #5 — there is no evidence of 2nd or 3rd-degree AV block in today's tracing. Instead — when given a "chance" to conduct — beat #10 is conducted with an almost normal PR interval.
  • The cause of AV dissociation in Figure-3 is also not the result of "default" — since although the rate of sinus P waves is slower than the junctional rate — the sinus rate does not drop below 60/minute.
  • By the process of elimination — the cause of AV dissociation in Figure-3 is "Usurpation" of the underlying sinus arrhythmia by an accelerated junctional rhythm, which at ~85/minute is clearly faster than the usual 40-60/minute AV nodal escape rate.
  • Technically — I would interpret the ECG in Figure-3 as showing: i) An accelerated junctional rhythm at ~85/minute — which results in AV dissociation by "usurpation" over the underlying slower sinus arrhythmia; and, ii) An otherwise unremarkable 12-lead ECG with an isolated Q wave in lead III (with a tiny q in aVF) — but no acute ST-T wave changes.


PEARL #7: Did YOU notice that there is a technical mishap with lead V5, which is clearly misplaced (ie, It makes no physiologic for the QRS complex to be predominantly negative in lead V5 — when it is entirely positive in neighboring leads V4 and V6). That said — this technical mishap does not negate our overall interpretation of an unremarkable ECG except for the rhythm.



CLINICALLY: What To Do? We are told that the ECG in Figure-3 was obtained as part of a routine exam of an otherwise healthy and asymptomatic 30-year old man.

  • Intermittent appearance in an otherwise healthy, young adult of a junctional escape rhythm that falls within the usual "escape range" for adults (of between ~40-60/minute) — is not unusual, and often reflects a normal variant rhythm.
  • In contrast — an accelerated junctional rhythm (or junctional tachycardiais not a common rhythm, and especially in older adults is likely the result of some underlying pathology. Among common causes of an accelerated junctional rhythm include acute ischemia/infarction — myocarditis — post-operative state — digoxin toxicity — sympathomimetic medication — shock — among other causes.
  • That said — IF the patient in today's case is truly an otherwise healthy adult who is completely asymptomatic, is not abusing medication, and who has no evidence of underlying heart disease (ie, if his Echo is normal) — then it is likely that the accelerated junctional rhythm and resultant AV dissociation in Figure-3 is benign.



LADDERGRAM: For clarity of my above discussion — I propose the laddergram shown in Figure-4.

  • I welcome other proposals for the mechanism of today's interesting rhythm!

Figure-4: My proposed laddergram for the rhythm in today's case. Fortuitous occurrence of the on-time P wave that peaks the T wave of beat #8 allows conduction to the ventricles of beat #9, albeit with a prolonged PR interval. 

— The following P wave is also "on time", and occurs at a point in the cardiac cycle in which it is able to capture the ventricles (because it is not inhibited by retrograde conduction from the AV node) — and is therefore conducted with an almost normal PR interval to produce beat #10

Thereafter, the accelerated junctional focus (which is faster than the underlying sinus rhythm) once again takes over (ie, "usurps") the rhythm for the remaining 4 beats on the tracing.



Acknowledgment: My appreciation to Muhammad Zeb (from Karachi, Pakistan) for allowing me to use this case and these tracings.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation
  • ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation.
  • ECG Blog #192 — Reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block. 
  • ECG Blog #191 — Emphasizes the difference between AV Dissociation vs Complete AV Block.

ADDENDUM (8/28/2021) I asked for other "proposals" for the mechanism in today's rhythm — and David Richley (who is well known to many readers of this blog) has promptly responded. BELOW is Dave's comment to me. To facilitate visualizing the scenario that Dave describes — I made Figure-5.
  • I believe Dave's scenario is valid. I had made similar observations that he describes — but I had decided not to mention these for 3 reasons: i) I didn't want to further complicate my already complicated explanation; ii) We can not fully see the T wave that precedes beat #1 (so hard to tell if a P wave is hidden within); and, iii) In the other simultaneously-obtained 11 leads (above the long lead II rhythm strip) — I thought there was some variation in QRST morphology that was not totally consistent ...
  • BOTTOM LINE: Dave's theory is equally valid as mine. I believe we both agree that there is AV dissociation by "usurpation", resulting from an accelerated lower pacemaker (which could indeed cause "fusion" beats if originating from within the conduction system [ie, the His] but below the AV Node). I do not think it possible to know for certain what the true mechanism of this arrhythmia is from this single tracing. We both agree that the mechanism is more complex than one might initially think. Regardless of the fascinating details of whatever the true mechanism is — I think the cliical approach I suggested above remains valid.

HERE is Dave's Comment:

Hi Ken. I enjoyed reading your latest ECG blog and wondered if I might make an additional observation and deduction.

You rightly point out that beats 9 and 10 have a slightly different QRS shape from that of the rest of the beats because they are conducted beats. This is evident not only from the QRS shape in leads V2 and V3, but also from a slightly narrower QRS in lead II. Technically the QRS width is similar at the base of the complex, but the R wave narrows as it rises in the conducted beats, resulting in them occupying a smaller area. However, although beat 10 has a narrower-than-usual QRS, it’s not as narrow as that of beat 9. In V2 and V3 beat 10 also has an S wave depth and T wave height that are intermediate between those of beats 8 and 9. Therefore, I think beat 10 may be a fusion beat – partly conducted via the normal AV-node-His pathway, and partly via the slightly different conduction route of the junctional escape beats. I admit that I don’t what the anatomical basis of this slightly different conduction route might be.

Knowing that the conducted beats have a slightly different QRS morphology from the escape beats in lead II — I re-examined the rest of the ECG to see if there might be evidence of additional conducted or fusion beats. It appears that beats 1 and 2 also have slightly narrower complexes in lead II, and a deeper S wave in lead I — so perhaps they too are conducted or, perhaps more likely, fusion beats, with each showing a different degree of fusion as evidenced by the different S wave depths in lead I. Certainly, there is no reason to think that the P wave before beat 2 should not be able to conduct and its PR interval is very similar to that of beat 10.

This ECG may be even more complex than it first appears! — Dave

Figure-5: I've added YELLOW arrows to today's tracing to highlight those P waves that David Richley feels may be conducting (I drew this figure to illustrate Dave's comment above).

Monday, August 23, 2021

ECG Blog #246 (60) — What is the Mirror Test?

Imagine that the ECG in Figure-1 was obtained from an older patient with epigastric discomfort and "heartburn". No prior tracing is available for comparison.



  • How would you interpret the ECG in Figure-1?
  • Where is the problem?


Figure-1: ECG obtained from an older patient with epigastric discomfort and "heartburn". WHERE is the problem?



NOTE: Some readers may prefer at this point to listen to the 8:30-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 this tracing (that appear below ECG MP-60).



Today's ECG Media PEARL #60 (8:30 minutes Audio) — Reviews use of the "Mirror Test" to facilitate recognition of: i) Acute Posterior MI; ii) Acute High-Lateral or Inferior MI (ie, the "magical" reciprocal relationship between leads III and aVL)andiii) Anterior ST elevation due to LVH (that is not indicative of anterior MI).

  • NOTE: I've added LINKS to related ECG blog posts to better illustrate the concepts put forth in today's Audio Pearl (These LINKS are shown below at the end of this blog post).




MY Sequential Thoughts on the ECG in Figure-1:

As always — I favor the use of a Systematic Approach (which I review in ECG Blog #205):

  • Rate & Rhythm: The P wave is upright in lead II — so the rhythm in Figure-1 is sinus tachycardia at ~105/minute. 
  • Intervals (PR/QRS/QTc): The PR interval is normal — the QRS complex is narrow — and, the QTc appears slightly prolonged (albeit difficult to assess the QTc interval when the heart rate is faster than 90-100/minute).
  • Axis: There is a leftward axis — as determined by almost complete negativity of the QRS in lead aVF. I'd estimate the frontal plane axis at -30 degrees, as the QRS complex in lead II is approximately equiphasic (ie, equal parts positive and negative).
  • Chamber Enlargement: None. Instead — there is low voltage in the limb leads (ie, none of the 6 limb leads measure more than 5 mm).


Regarding Q-R-S-T Changes:

  • Q Waves — There are large Q waves in each of the inferior leads (ie, in leads II, III and aVF). There are also deeper-than-expected Q waves in leads V4, V5 and V6. And, there is a tiny-but-present initial q wave in lead V3 that simply should not be there (ie, normal septal q waves are uncommon in lead V4, and they should not be seen in lead V3).
  • R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) occurs early, between leads V1-to-V2 (Transition normally occurs between leads V2-to-V4).
  • ST-T Wave Changes — There is slight-but-real ST elevation in each of the inferior leads. There is also very subtle ST elevation in lead V6. ST segments are flat (if not, slightly depressed) in leads I, aVL and V5. There is ST depression in leads V1-thru-V4, with maximal ST depression in leads V2 and V3.


Putting It All Together: The ECG in Figure-1 strongly suggests there has been recent (if not acute) infero-postero-lateral OMI ( = Occlusion-based Myocardial Infarction). I'll add the following important points:

  • It's impossible to date the MI in today's case. The fact that Q waves in each of the inferior leads are deep would seem to favor a less acute onset. No R wave at all is seen in lead III — and no more than the tiniest of r waves is seen in lead aVF. That said — on occasion, significant Q waves have been known to form in as little as 1-to-2 hours. In addition — it is entirely possible that this older patient had a previous inferior infarction — and is now having acute reinfarction of the inferior wall. Bottom Line: We can not rule out the possibility of a very recent, or even acute ongoing infarction simply on the basis of the large size of inferior Q waves.
  • In favor of a more recent onset for the inferior lead changes is the fact that coved ST elevation persists in each of the 3 inferior leads. While the shape and amount of ST elevation in leads III and aVF looks to be less acute (and is more consistent with an older event) — the shape and amount of ST elevation in lead II is clearly of more concern (especially considering modest amplitude of the R wave in this lead). Although minimal in amount — the shape of the scooped ST segment in lead aVL is potentially consistent with a reciprocalchange with respect to the ST segment shape in lead III.
  • In lead V6 — there is a relatively large Q wave — a slightly coved, and perhaps ever-so-slightly elevated ST segment — with beginning T wave inversion. Given the ECG changes just described in the limb leads, this suggests there has been lateral infarction, albeit of an indeterminate age.
  • We are not told when symptoms began for the patient in today's case. This is yet another factor that makes determination of the "age" of infarction difficult.

  • PEARL #1: It is the ST depression in leads V1-thru-V4 (which is maximal in leads V2 and V3) that raises greatest concern for a posterior infarction in today's case that must be assumed acute and ongoing until proven otherwise. 


  • Did YOU notice the positive "Mirror" Test? (See Figure-2).

Figure-2: Illustration of a positive Mirror Test for the ECG that was shown in Figure-1 (See text).

The Positive Mirror Test in Figure-2:

As discussed in detail in Audio Pearl #60 (above) — the Mirror Test is used as a visual aid to facilitate recognition of acute posterior MI. The principle of this test is simple: It is based on the fact that the mirror-image view of anterior leads provides insight to the nature of electrical activity as viewed by the posterior wall of the left ventricle.

  • Note that I have vertically flipped anterior leads V1, V2 and V3 in the far right portion of Figure-2 (the mirror-image view of these 3 leads is outlined in RED). The shape of the ST depression seen in leads V1V2 and V3 of Figure-2, when vertically flipped (as viewed in the Mirror Test) suggests deepening Q waves — worrisome shape and amount of ST elevation — and already deep T wave inversion.
  • PEARL #2: The finding of ST depression that localizes to the anterior leads, and which is maximal in leads V2 and/or V3 — strongly suggests posterior infarction that may be acute. Many providers equate the picture of ST-T wave changes that we see in the anterior leads of Figure-2 as a "STEMI-equivalent" — since this ECG pattern is equally indicative of acute OMI in need prompt reperfusion, as is an acute MI in which there is ST elevation (Please see ECG Blog #193including Audio Pearl #10 in that blog post — for detailed discussion on the concept and clinical implications of diagnosing acute OMI).
  • NOTE: Early transition (ie, development of an R wave taller than the S wave is deep already by lead V2supports the diagnosis of posterior infarction in Figure-2. In the Mirror Test — the taller R waves become in anterior leads V1, V2 and V3 — the deeper the Q waves these R waves become when these anterior leads are vertically flipped.

PEARL #3: Did YOU notice the fragmented QRS complexes in leads III and aVF of Figure-2? Although obvious that there has been inferior infarction at some point (ie, from the depth of the inferior Q waves — and the loss of R wave amplitude in these leads) — fragmentation of the inferior Q waves in leads III and aVF is yet one more indication of "scar" (and in this case, of prior infarction)



Conclusion to Today's Case:

The patient in today's case presented with epigarstric discomfort and "heartburn". Especially in an older patient — this history certainly could be consistent with symptoms of an acute cardiac event. ECG findings of concern include sinus tachycardia — infero-lateral infarction of uncertain age (with residual ST elevation) — andposterior infarction marked by a positive Mirror Test with localized anterior ST depression that is maximal in leads V2 and V3. 

  • An acute ongoing event should be assumed until proven otherwise. Ideally — prompt cath for diagnosis and potential reperfusion should be performed.




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: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI.
  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
  • ECG Blog #245 — Reviews the ECG diagnosis of LVH, including CAVEATS that may complicate assessment of associated acute ischemia.
  • 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
  • The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia.
  • The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH, by cutting off S wave voltage in the anterior leads.
  • The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction. 

  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).


ADDENDUM (8/23/2021): I've added below in Figure-3 review of a case in which there is an isolated posterior MI (ie, without accompanying inferor lead ST elevation).



Figure-3: KEY points in the recognition of isolated posterior MI (This figure is taken from ECG Blog #193 — in which I review the "Basics" for predicting the "culprit" artery).