ECG Blog #172 (ST Elevation – J-Point – Osborn – OMI vs Repolarization)

The ECG shown in Figure-1 was obtained from a 52-year old man. There was concern about acute infero-lateral MI vs acute pericarditis.

• WHICH of these conditions do you think is present? How certain are you about the diagnosis?
• What are we missing?

Figure-1: ECG obtained from a 52-year old man. The differential diagnosis was acute infero-lateral MI vs acute pericarditis (See text). NOTE — Enlarge by clicking on the Figure.

COMMENT: What we are missing — is a brief History about the circumstances surrounding this ECG. The patient was found outside during the winter months. His core temperature on arrival in the ED was 83 degrees Fahrenheit ( = 28 degrees Celsius).

Descriptive Analysis:

• Rate & Rhythm — The rhythm is sinus bradycardia at ~55/minute.
• Intervals — The PR interval is normal. The QRS complex is normal (ie, not more than half a large box in duration = ≤0.10 second). However, the QT interval is clearly prolonged; it is nearly 3 large boxes in duration (ie, ~560 msec).
• Axis — The mean QRS axis is normal (about +75 degrees).
• Chamber Enlargement — None.

Looking Next at Q-R-S-T Changes:

• Q Waves — There are very small and narrow q waves are seen in the infero-lateral leads (ie, leads II,III,aVF; and V5, V6).
• R Wave Progression — There is normal R wave progression, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V3.

Regarding ST-T Wave Changes:

• The most remarkable findings are: i) Prominent J-point notching (RED arrows in Figure-2) and/or J-point slurring (BLUE arrows) in multiple leads; and, ii) 1-1.5 mm of upward-sloping ST elevation in the inferior leads (II,III,aVF) — and in leads V2-thru-V6. Other leads show nonspecific ST-T wave flattening.

Figure-2: I’ve added to Figure-1 my measurement of the QT interval + ARROWS to highlight J-point notching/slurring (See text).

DISCUSSION: I intentionally omitted the history of cold exposure for several reasons. FIRST — Descriptive Analysis of this (or any other) ECG is the SAME regardless of the history.

• It is the Clinical Interpretation that will change, depending on clinical circumstances surrounding the case (See ECG Blog #93 — for “My Take” on use of a Systematic Approach to ECG Interpretation).

We have previously discussed the ECG findings of Hypothermia (See ECG Bog #149). Both that case and this one are similar in that: i) There is bradycardia; ii) There is QTc prolongation with associated ST elevation in multiple leads; iii) Other ECG findings of acute MI are lacking (ie, No Q waves, or no more than very small and narrow q waves; No reciprocal ST depression); and, iv) There are prominent Osborn waves ( = J-point notching) in multiple leads (RED arrows in Figure-2). The J-point slurring in this tracing (BLUE arrows) is also a temperature-related phenomenon.

• NOTE: Neither patient (ie, not the patient from ECG Blog #149, nor the patient in today’s case) had acute MI or pericarditis — despite the presence of significant ST elevation in multiple leads.
• PEARL #1 — While impossible to completely rule out the possibility of acute MI or pericarditis from the ECG shown in Figure-1 — it is good to remember that ST elevation in multiple leads is one of the ECG Findings of hypothermia.
• PEARL #2 — Even if this hypothermic patient was having an acute STEMI (ST-Elevation MI) — cardiac catheterization would best be deferred until core temperature was raised. At that point, the ECG can be repeated — and, if ST elevation has greatly resolved (and the patient is not having chest pain) — then low core temperature (and not ongoing infarction) was the likely cause of the ST elevation.

ECG Blog #171 (Culprit Artery - Repolarization Variant vs OMI - Mirror-Image)

The only information provided on the patient whose ECG is shown in Figure-1 — was that the patient was a 54-year old man. NO history was available.

• IF this tracing was in your “pile-of-ECGs-to-be-read” — What would you do?

Figure-1: 12-lead ECG obtained on a 54-year old man. NO history available. What are your thoughts? (See text). NOTE — Enlarge by clicking on the Figure.

Descriptive Analysis:

• Rate & Rhythm — The rhythm is sinus bradycardia at a rate between 55-60/minute.
• Intervals — The PR, QRS and QTc intervals are all normal. If anything, the QTc is relatively short (I measure ~380 msec).
• Axis — The mean QRS axis is normal (about +75 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — Small and narrow q waves are seen in the infero-lateral leads (ie, leads II,III,aVF; and V4-thru-V6).
• R Wave Progression — Transition occurs normally (here, between leads V2-to-V3) — albeit the R wave in lead V2 has already become relatively tall (~7 mm).

Regarding ST-T Wave Changes:

• There is 1-1.5 mm of concave-up ST elevation in each of the inferior leads (ie, leads II,III,aVF). The mirror-image opposite ST-T wave picture of what we see in lead III appears in lead aVL. In addition — there appears to be 1 mm of flat ST segment depression in lead I.
• In the chest leads — there is ~1.5 mm of J-point ST depression in lead V2. As has been previously mentioned — this occurs in association with an R wave in lead V2 that is already surprisingly tall (~7 mm).

Figure-2: Schematic representation of mirror-image relationships from Figure-1 (See text).

Putting It All Together: The KEYS to interpreting this tracing lie with appreciating several mirror-image relationships (Figure-2):

• When ST segment elevation in the inferior leads is acute — there is an almost “magic” mirror-image relationship between the way the ST-T wave looks in lead III, compared to lead aVL. These 2 leads are nearly 180 degrees opposed to one another — therefore they show reciprocal changes.
• Note in Figure-2 — how the mirror-image of the ST-T wave in lead aVL (within the light BLUE insert) — looks identical to the shape of the elevated ST-T wave in lead III (within the WHITE rectangle).
• Similarly, the mirror-image of the elevated ST-T wave in lead III (within the light BLUE insert) — looks identical to the shape of the inverted ST-T wave in lead aVL (within the WHITE rectangle).
• Confirmation that the above mirror-image relationships are real and represent an acute change consistent with acute inferior MI — is forthcoming from the clearly abnormal shelf-like ST depression we see in lead I.
• Further support of recent (if not ongoing acute) occlusion of the RCA (Right Coronary Artery) — is suggested by the positive Mirror Test we see for the QRST complex in lead V2 (For more on the Mirror Test — See ECG Blog #80). Anterior leads (ie, leads V1, V2 and/or V3) often manifest the mirror-image opposite picture of ongoing events in the left ventricular posterior wall — and the mirror-image of the QRST complex in lead V2 (within the light BLUE insert) shows a large Q wave + downward coved ST elevation, that leads to beginning T wave inversion.

BOTTOM Line: One has to interpret the ECG in Figure-1 as consistent with recent (if not ongoing acute) RCA occlusion until proven otherwise. Since this tracing was in your “pile-of-ECGs-to-be-read” — the responsibility falls on YOU to immediately look up the patient to find out WHAT is going on?

• In addition to acute infero-postero MI — there may also be acute RV involvement in Figure-1 — since rather than ST depression, the ST segment in lead V1 is not at all depressed as would be expected with acute posterior MI. That said — right-sided chest leads would be needed to know for certain if there is or is not associated acute RV involvement.

P.S. — Unfortunately — follow-up in this case is lacking. The patient was seen years ago — and I have no further information on the case. Nevertheless, I thought it worthwhile to discuss how even when no clinical information is available — how the mirror-image opposite relationships we see in this tracing tell us we have to assume these ECG changes are acute until we prove otherwise.

ECG Blog #170 (Atypical Chest Pain - Mirror Image - Troponin - Lcx - Lad)

The ECG in Figure-1 was obtained from a 30-year old man with an unusual story. He was admitted to the hospital to “Rule Out MI” — with what was described as “atypical” chest pain, that was not thought to be cardiac in etiology. Serial troponins were negative. His initial ECG (not shown) was interpreted by a capable emergency physician as “normal”. The patient had a normal Stress Echo, in which he attained his target heart rate and showed no wall motion abnormality. He was about to be discharged from the hospital with a diagnosis of atypical non-cardiac chest pain. His pre-discharge ECG ( = ECG #2) is shown in Figure-1. There were no new symptoms at the time ECG #2 was done. How would you interpret this pre-discharge ECG ( = ECG #2)?

• What would you do, given that all testing to this point had been normal?

Figure-1: This is the follow-up ECG, obtained on this 30-year old man who was about to be discharged from the hospital. His initial ECG (not shown) was interpreted as “normal”. Serial troponins, and Stress Echo were completely normal (See text). NOTE — Enlarge by clicking on the Figure.

COMMENT: We can’t comment on the initial ECG — since it is not shown. What we can say — is that ECG #2 is not a normal tracing! Presumably, had the initial ECG been as abnormal as this 2nd ECG — the capable clinician who interpreted that initial tracing would presumably have at least seen some of the abnormalities — BUT — We can’t comment on what we are not shown ...

Descriptive Analysis of ECG #2:

• Rate & Rhythm — It’s hard to be certain what the cardiac rhythm is! This is clearly a supraventricular rhythm — because the QRS complex is decidedly narrow. But there is no long lead rhythm strip. The R-R interval is not completely regular. It looks like there is atrial activity in front of some QRS complexes — but a clearly upright P wave is lacking in lead II. I’d guess this is an ectopic atrial rhythm, perhaps with some junctional escape beats — but I can’t rule out the possibility of a nearly regular AFib. A longer period of monitoring is clearly needed to determine for certain ... Bottom Line: The above said — Since the rhythm is supraventricular, we can assess ST-T waves in ECG #2 for potential ischemic changes!
• Intervals — The PR interval is irrelevant in this tracing — since we don’t see consistent atrial activity. As noted — the QRS complex is narrow. The QTc interval appears to be normal.
• Axis — The mean QRS axis is normal (about +25 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — Small and narrow q waves are seen in high lateral leads I and aVL.
• R Wave Progression — Transition occurs normally (here, between leads V2-to-V3) — albeit abruptly (ie, the QRS was almost all negative in lead V2 — and abruptly becomes almost all positive by lead V3).
• Regarding ST-T Wave Changes:
• There is 1-2mm of concave-up ST elevation in leads I and aVL. The mirror-image opposite ST-T wave picture of what we see in lead aVL appears in lead III. Of note — there is ~2mm of J-point ST depression in lead III — and 1-1.5mm of J-point ST depression in leads II and aVF.
• The ST-T wave in lead V2 is somewhat distorted by artifact (ie, the contour of the ST segment in V2 is not at all smooth). That said — the T wave looks disproportionately peaked in V2, with a disproportionately wide base — however, other than nonspecific ST-T wave flattening in leads V4-thru-V6, there do not appear to be acute changes in the remaining chest leads.

Putting It All Together: The limb leads in ECG #2 are clearly abnormal. ST elevation in high-lateral leads — with a mirror-image opposite appearance of the ST-T in lead aVL compared to lead III should suggest an acute cardiac event until you prove otherwise (For more on this point — Please see My Comment at the bottom of the page in the 10/6/2018 SSmith ECG Blog post).

Follow-Up on This Case: Based on the abnormal pre-discharge ECG in Figure-1 — the cardiologist took this patient to the cath lab. He was found to have a very tight stenosis of a dominant LCx (Left Circumflex) coronary artery — which was successfully stented.

• It is fortunate that this pre-discharge ECG was obtained and interpreted before sending this patient home.
• Learning Point: The initial ECG in a patient with significant coronary disease may not always be abnormal. Serial troponins and stress testing may also be normal. None of this rules out the possibility of severe underlying coronary disease.

ECG Blog #169 (Tachycardia - Regular SVT - Calipers)

The patient whose ECG is shown in Figure-1 was hemodynamically stable. There was debate among his providers as to what the rhythm in this ECG was.

• What do YOU think the rhythm is?
• What is the differential diagnosis?
• Why can you be virtually certain what this rhythm is even before treating and before any diagnostic maneuvers?

Figure-1: The initial ECG in this case (See text).

ANSWERS: Detailed discussion of this case and the differential diagnosis can be found in the November 12, 2019 post on Dr. Stephen Smith's ECG Blog!

ECG Blog #168 (STEMI - complex AV Block - Laddergram - Calipers)

The ECG in Figure-1 was obtained from a middle-aged woman who presented with a syncopal attack and hypotension. No chest pain.

• How would you interpret this ECG?
• What is the “culprit” artery?
• What is the rhythm?

Confession: I am still not completely certain about all that is going on with the cardiac rhythm in this tracing. That said — several statements about the rhythm can be made with certainty. And, I have a theory …

Figure-1: 12-Lead ECG and simultaneously-recorded long lead II rhythm strip, obtained from a middle-aged woman with syncope and hypotension. (See text). NOTE — Enlarge by clicking on the Figure.

COMMENT: This is a complex tracing! As I fully acknowledge above — I am still not certain of all aspects of the arrhythmia, details of which I’ll address a little bit later. For the moment — suffice it to say that: i) All beats on this tracing are supraventricular; ii) There are lots of P waves; iii) Some of these P waves look like they may be conducting; and, iv) There appears to be some form of AV block.

• PEARL: Although the arrhythmia in Figure-1 is fascinating (!) — Recognizing that more detailed analysis beyond what I state above in i), ii), iii) and iv) is not needed at this point in order to initiate the most important priorities in management!
• Therefore — it is BEST not to spend any more time trying to decipher this rhythm until you have completed your Systematic Approach for assessment of QRS and ST-T wave morphology!

Descriptive Analysis of the ECG in Figure-1: Focusing attention on QRS morphology in the 12-lead tracing — there is GOOD reason for this woman to have presented with syncope and hypotension!

• Rate & Rhythm — Sinus tachycardia with what appears to be some complex form of AV block (Details in a moment! ).
• Intervals — The PR interval varies (See below). The QRS complex for all beats on this tracing is narrow. The QTc interval appears to be normal.
• Axis — The mean QRS axis is normal (about +70 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — There is a small, but fairly wide Q wave in lead III. One of the 2 complexes in lead aVF appears to have a small Q wave.
• R Wave Progression — Transition occurs normally (here, between leads V3-to-V4).

Regarding ST-T Wave Changes:

• There is hyperacute ST elevation in each of the inferior leads! ST elevation is clearly more marked in lead III compared to lead II. There may be beginning T wave inversion in lead III, but not yet in other inferior leads.
• There is mirror-image (reciprocal) ST depression in lead aVL when one compares this to the shape of the ST elevation in lead III. To a lesser degree — there is also reciprocal ST-T wave depression in lead I. PEARL: As we have discussed in previous ECG Blogs (most recently in ECG Blog#167) — there is an almost “magic” mirror-image relationship between leads III and aVL in many (most) cases of acute inferior MI.
• Otherwise — there is marked ST depression, that rises to hyperacute T waves in leads V2, V3 and V4.
• Surprisingly — there is slight-but-real ST elevation in lead V1 (usually there is no ST elevation in lead V1).

Putting It All Together: QRS morphology for the ECG shown Figure-1 is diagnostic of acute infero-postero STEMI. Note the following:

• Acute posterior involvement is diagnosed by the presence of unexpected ST depression in anterior leads. Anterior leads show the “mirror-image” of what one expects to see in posterior leads (such as leads V7, V8, V9). Isn’t the “shelf-like” ST depression rising to prominent T wave in lead V2 virtually the mirror-image of the ST elevation + T wave inversion expected with acute MI? (See ECG Blog #80 for application of the “mirror test” for diagnosing posterior MI).
• The “culprit” artery (See ECG Blog #80) — is almost certain to be acute RCA (Right Coronary Artery) occlusion because: i) Statistics (~85% of patients have a dominant right system — so that acute RCA occlusion is much more likely than LCx [Left Circumflex] occlusion to be the cause of inferior MI); ii) ST elevation in lead III > lead II; iii) there is marked reciprocal ST depression in lead aVL; and, iv) there is no sign of associated lateral infarction (ie, no ST elevation in any of the lateral leads).
• NOTE: In addition to being an anterior lead — lead V1 is also a right-sided lead. The unexpected finding of ST elevation in lead V1 tells us that in addition to acute infero-postero STEMI — there is also acute RV (Right Ventricular) involvement. 
• PEARL: Most of the time, right-sided leads will be needed to diagnose acute RV MI. However, when there is definite ST elevation in lead V1 in a patient with acute inferior MI — this almost certainly indicates that ST elevation from acute RV MI has cancelled out the ST depression that you would otherwise have seen in lead V1 from ongoing posterior MI.
• Recognition of acute RV MI in association with acute infero-postero MI localizes the “culprit” artery to the RCA — because the LCx does not vascularize the right ventricle. This further establishes the proximal RCA as the “culprit” artery in Figure-1.
• FOLLOW-UP: Cardiac cath confirmed acute occlusion of the proximal RCA — and, reperfusion was achieved by stenting this vessel. Presumably, the degree of AV block improved as the patient recovered (although I’m not privileged to those details).

My Purpose — in presenting this case was 3-fold: i) This case provides an excellent example of how to recognize acute OMI (Occlusion-related Myocardial Infarction) in a patient without chest pain — despite distraction from the presence of a complex form of AV block; ii) How to assess a complex form of AV block, such as is evident in Figure-1; — and, iii) How use of a Laddergram can assist in this assessment.

• As I have already emphasized — detailed assessment of this rhythm is not essential for initiating the key priorities of management. I would be HAPPY — if you simply recognize the presence of a complex form of AV block — and, that the cause of this arrhythmia and the patient’s syncope/hypotension is acute OMI in need of immediate cath + reperfusion.
• PEARL: Don’t even bother trying to assess this rhythm unless you are using a pair of calipers. In my opinion — it is virtually impossible to assess a complex rhythm such as this one without calipers. The cardiologist who tries to assess complex arrhythmias without using calipers — is a cardiologist who will miss the diagnosis of many complex rhythms.

Looking Closer at the Rhythm: While admittedly not certain about all aspects of the rhythm in Figure-1 — there are a number of Observations that we can make:

• The rhythm is supraventricular — since all QRS complexes on this tracing are narrow.
• Using calipers — We can say that Sinus P waves are present (RED arrows in the long lead II rhythm strip in Figure-2). This sinus rhythm is fast (ie, sinus tachycardia) — and fairly (but not completely) regular. Since it would be unlikely to “miss” occasional P waves — I’ve added WHITE arrows in Figure-2 where I suspect additional sinus P waves are located (partially or totally hidden by simultaneously-occurring QRS complexes).
• In addition to sinus arrhythmia — there is a phenomenon known as ventriculophasic sinus arrhythmia — in which severe bradycardia from AV block may cause variation in the P-P interval. When this happens — the P-P interval that “sandwiches” a QRS complex tends to be shorter than P-P intervals without enclosed QRS complexes (thought to be due to better perfusion following cardiac contraction that occurs just after a QRS). Using calipers verifies the presence of ventriculophasic sinus arrhythmia in Figure-2.
• There are a number of consecutively-occurring P waves in Figure-2 that are not followed by QRS complexes. This suggests that at the least — there is high-grade AV block in this tracing (which I define as AV block in which more than one sinus P wave in a row fails to conduct despite having adequate opportunity to conduct).
• The ventricular rhythm is not regular! This suggests that complete (3rd-degree) AV block is not likely — since the ventricular escape rhythm is usually at least fairly regular when AV block is complete. This defines the rhythm in Figure-2 as high-grade 2nd-Degree AV block.

PEARL — Common things are common! In the presence of acute inferior MI (as this patient has) — AV Wenckebach is by far (!!!) the most common type of 2nd-Degree AV Block.

• Therefore — whenever I see acute inferior STEMI with a fast-but-irregular sinus rhythm in which there are intermittent pauses — I specifically look for Wenckebach conduction. In my experience — this almost always turns out to be the cause of the irregularity! (For an example of this — See ECG Blog #55).

Figure-2: I’ve added ARROWS to indicate definite (and probable) atrial activity. WHITE arrows indicate where I suspect there are P waves, albeit hidden by the QRS complex (See text).

Is there Any Conduction in Figure-2?

As I stated at the outset — this is a complex rhythm! We’ve already established that there is high-grade 2nd-degree AV block with numerous non-conducted P waves. The next step in determining specifics of this rhythm to establish IF there is any conduction? This is best accomplished by use of a Laddergram (Figure-3):

• NOTE: Although learning to draw laddergrams is challenging (it literally took me many years to become comfortable doing so! ) — learning to read laddergrams is easy and intuitive! (IF you would like Review on using Laddergrams — See ECG Blog #69 and Blog #164).
• The 1st Step in drawing a laddergram is filling in the Atrial Tier where you see P waves (Figure-3). Since conduction of the electrical impulse through the atria is fast (passing over specialized atrial conduction tracts) — we represent atrial conduction on a laddergram by a vertical line through the Atrial Tier.

Figure-3: Step #1 in drawing a laddergram = Filling in the Atrial Tier where you see P waves. Since conduction of impulse through the atria is fast — we represent atrial conduction by a vertical line through the Atrial Tier (See text).

PEARL: You’ll be amazed at how much EASIER it becomes to see relationships (or lack thereof) between P waves and neighboring QRS complexes the moment you highlight P waves (RED arrows in Figure-4).

• The EASIEST way to determine IF there is any conduction in the rhythm you are assessing — is to see IF there are any identical PR intervals?
• NOTE — The PR intervals preceding beats #1, 4, 6 and 9 are all identical. This tells us that these 4 beats must be conducting. Figure-4 shows how we represent conduction through the AV node and through the ventricles for these 4 beats. The reason there is a greater slant (ie, greater angulation) for conduction through the AV Nodal Tier compared to conduction through the Atria and through the Ventricles — is that conduction of the electrical impulse is slowest going through the AV node.

Figure-4: The PR intervals preceding beats #1, 4, 6 and 9 are identical. Therefore — these 4 beats must be conducting (See text).

Are Any Other Beats Conducted in Figure-4?

Following through with the KEY principle that identical PR intervals are unlikely to be due to chance — We look next at Figure-4 to see IF any other PR interval duration repeats.

• Caliper measurement of the PR interval preceding beats #5 and #7 is identical. This strongly suggests that these 2 beats are also conducted, albeit with a longer PR interval than for beats #1,4, 6 and 9. We illustrate this in Figure-5.
• This leaves us with uncertainty about beats #2, 3 and 8 (QUESTION MARKS in Figure-5).

Figure-5: Beats #5 and 7 also appear to be conducting, albeit with a longer PR interval than for beats #1, 4, 6 and 9 (See text).

PEARL: The longest R-R interval in this rhythm strip is between beats #2-3. When working with a complex conduction disturbance — unexpected shortening of the R-R interval often tells you that earlier-than-expected beats are being conducted!

• I do not know if beat #3 that terminates the longest R-R interval — is a junctional escape beat or a sinus-conducted beat. We cannot know this for certain without additional monitoring …
• However — Since beats #2 and #8 in Figure-5 are both preceded by an R-R interval that is shorter than the R-R interval between beats #2-3 — I suspect beats #2 and #8 are probably conducting!

What then is the Mechanism of the Rhythm?

At this point — I admittedly was not sure how to draw in lines representing conduction of beats #2 and 8 (and possibly also beat #3).

• After pondering this arrhythmia for longer than I care to admit … — I decided that I needed to think “out of the box”. (I said this rhythm was complex … ).
• NOTE — Some forms of AV Wenckebach may exhibit Wenckebach conduction at multiple levels within the AV Node.

What IF there were 2 Levels of Block within the AV Node?

The BEST way to illustrate the concept of a dual-level block within the AV Node — is by clicking successively on the magnified view of the next 5 Figures. The legends of these Figures describe my ladder problem-solving approach.

Figure-6: The horizontal black DOTTED line pictorially represents the initial (upper) level of block within the AV node. Imagine each of the sinus impulses reaches this level within the AV node. Our task in completing this laddergram — will be to connect impulses at this upper level within the AV node — with the 9 QRS complexes below that are conducted through the ventricles (which I’ve drawn in the Ventricular Tier). SUGGESTION: Click on THIS Figure-6 to enlarge this tracing. Then ADVANCE on your device through the next 4 Figures (ie, Figures 7-thru-10) to BEST appreciate my approach for laddergram problem-solving.

Figure-7: As we have previously deduced — since the PR intervals preceding beats #1, 4, 6 and 9 are all identical — these beats must be conducting. I’ve illustrated this by connecting these P waves preceding beats #1, 4, 6 and 9 — with their respective QRS complexes in the Ventricular Tier of Figure-7.

Figure-8: I’ve made an assumption that all 9 beats in Figure-8 are conducting. As stated earlier — I can’t rule out the possibility that beat #3, which is preceded by the longest R-R interval, might represent a junctional escape beat. But as we’ll see in a minute — a more logical rhythm mechanism can be postulated by assuming that beat #3 is also being conducted (albeit with a greatly prolonged PR interval). PEARL: Although admittedly not perfectly symmetric — Isn’t there a pattern of grouped beats with PR interval lengthening within the 2nd level of block within the AV Nodal Tier?

Figure-9: Let’s now make the assumption that there is also some form of Wenckebach conduction at the initial level of block within the AV node. IF this is so — then there will need to be non-conduction of 1 atrial impulse at the end of each group. I pictorially represent this by the BUTT ENDs that I have drawn in within the initial level of block in the AV Nodal Tier.

Figure-10: To complete the laddergram — Let’s make a final assumption that for those impulses that successfully get through the upper (initial) level of block in the AV node — that 4 of these impulses fail to make it through the 2nd (lower) level of block in the AV node (pictorially represented by the BUTT ENDs drawn within the lower level of block in the AV Nodal tier of Figure-10).

BOTTOM LINE: My favorite quote about complex arrhythmias is by Rosenbaum, who said: “Every self-respecting arrhythmia has at least 3 possible interpretations”. While I cannot prove that my interpretation of this complex arrhythmia is the only correct one — IF you are able to construct a laddergram that makes sense (as I have done in Figure-10) — then my theory qualifies as at least one possible mechanism for this complex rhythm. Other theories from anyone reading this blog are welcome!

• To Emphasize — Deriving a precise mechanism for this complex arrhythmia (as I propose in Figure-10) — is not nearly as important as the other TAKE-HOME Points from this case!
• TAKE-HOME Points from this Case: What is most important to appreciate from this case is the following: i) Although this patient did not have chest pain — she did have other symptoms (ie, syncope; hypotension) that could be consistent with acute MI; ii) The rhythm is supraventricular — with lots of sinus P waves, some of which are conducting — and others, which are not conducting. Therefore, the rhythm represents some form of 2nd-Degree AV Block; iii) QRS morphology is diagnostic for an acute STEMI. Management priorities include prompt activation of the cath lab with the goal of achieving timely coronary reperfusion; iv) Since this patient has an acute inferior MI — and, there is 2nd-Degree AV Block with group beating and a narrow QRS complex — the mechanism of this AV block statistically (ie, over 90% likelihood) is almost certain to represent some form of AV Wenckebach (Mobitz I); and, v) Chances are, that IF you are able to promptly achieve coronary reperfusion (which should be your highest priority) — that this very complex form of AV Wenckebach will improve, if not completely resolve.

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Acknowledgment: My appreciation to Wai Shein (from Myanmar) for the case and this tracing.

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