ECG Blog #461 — STEMI, LV Aneurysm or Neither?

I was sent the ECG shown in Figure-1 — initially without the benefit of any history.

• How would you interpret this tracing?
•    — What is YOUR differential diagnosis of this tracing?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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The Obvious Concern:

• I immediately realized the reason that I was sent this tracing: ==> there is ST elevation in the anterior chest leads!

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MY Initial Thoughts on Figure-1:

Looking systematically:

• There is a regular sinus rhythm at ~85/minute (upright P waves in lead II — with a constant and normal PR interval).
• The QRS is narrow (ie, not more than 1/2 a large box in duration).
• The QTc is at most borderline prolonged.
• The Axis is markedly leftward, as per a predominantly negative QRS complex in lead aVF. Criteria for LAHB (Left Anterior HemiBlock) are fulfilled — given the predominantly negative QRS in lead II (ie, indicating a frontal plane axis more negative than -30 degrees).

Regarding Chamber Enlargement:

• Criteria for atrial enlargement are absent (Reviewed in ECG Blog #75). So, although there is a negative component to the terminal P wave in lead V1 — I favor undercalling LAA because of limited specificity for this amount of P wave negativity in V1 as an indication of LAA.
• That said — voltage for LVH is markedly increased!

There is marked LVH:

• I've reviewed criteria for LVH on many occasions (See ADDENDUM below — for review of LVH criteria that I favor — as well as ECG Blog #73 for full discussion).
• As per Figure-5 (in the Addendum below) — S wave amplitude is markedly increased in today's ECG (attaining an S wave depth = 28 mm in lead V2 — and an S wave depth = 28 mm in lead V4 — as shown in Figure-2).
• 
  
• PEARL #1: Sometimes with LVH — instead of seeing tall R waves with LV "Strain" in the lateral chest leads — we see the "mirror-image" opposite picture in right-sided leads V1,V2 (ie, LVH may be manifested by deep anterior S waves — with ST elevation in leads V1,V2 and/or V3). This is precisely what we see in today's case!

Figure-2: Assessment of R wave and S wave amplitude in the chest leads is rendered difficult by marked overlap of complexes in several leads. To facilitate assessment — I've colored in selected R waves and S waves.

Completing our Systematic Approach (with Q-R-S-T Changes):

• Q Waves — There is a tiny septal q wave in lead aVL — which is unlikely to be important. But there are large QS waves in anterior leads V1,V2,V3.
• R Wave Progression — Because of these large QS waves in the anterior leads, there is poor R wave progression (with Transition delayed until between leads V5-to-V6).
• ST-T Waves — I've drawn in the PR segment baseline in leads V1,V2,V3 of today's ECG to highlight the amount of ST elevation (RED arrows in Figure-3 indicating the J-point as the marker for judging the amont of ST elevation).
• Elsewhere, the 3 inferior leads and lead V6 show nonspecific ST-T wave flattening. Finally, lateral leads I and aVL show subtle, shallow T wave inversion — which is consistent with a "strain equivalent" pattern (as I highlight in Panel B of Figure-6 in today's Addendum).

Figure-3: I've labeled the PR segment baseline and J-points in selected chest leads to highlight the amount of ST elevation.

Putting It All Together:

Today's ECG shows a sinus rhythm at ~85/minute — a borderline QTc — LAHB — marked LVH — and — QS waves in leads V1,V2,V3, with no more than a tiny r wave in lead V4 — plus, ST elevation that begins in lead V1 and extends through to lead V5. Clinically — this may indicate any of the following (See Figure-4):

• i) Antero-Septal MI may have occurred at some point in time — as suggesed by QS waves in leads V1,V2,V3.
• 
  
• ii) That there is marked LVH is strongly suggested by the greatly increased chest lead QRS amplitudes (with S waves = 28 mm in leads V2 and V4 — as shown in Figure-4) — with a "strain equivalent" pattern in lateral leads I and aVL (BLUE arrows in these leads).
• The anterior lead ST elevation may simply reflect LV "strain" in a patient with marked LVH, which when manifest by deep anterior S waves (rather than tall lateral R waves) — may produce a vector in which the hypertrophied, posterior-lying left ventricle opposes normal anterior forces, thereby reducing (and sometimes eliminating) anterior r waves.
• PEARL #2: As shown within the RED insert in Figure-4 — In such cases, the ST-T wave changes of LV "strain" (that are usually seen in lateral leads) — may present a mirror-image opposite ST-T wave picture of "strain" in anterior leads. This may account for the anterior ST elevation seen in today's case (BLUE arrows in leads V1,V2,V3).
• 
  
• iii) There could be acute LAD (Left Anterior Descending) coronary Occlusion that is now superimposed on the ECG of a patient with longstanding LVH, perhaps with also previous anterior infarction.
• 
  
• iv) The findings in Figure-4 could reflect LV aneurysm.

Conclusion: As I contemplated today's tracing that I initially interpreted without the benefit of any history — I thought any of the above diagnostic possibilities might be present. Although I suspected that the ECG findings in Figure-4 were not acute — I was not at all certain of that suspicion from this single ECG.

• Clearly — a detailed history would be needed for adequate clinical assessment. Does this patient have a history of cardiac disease? Did the patient have CP? (Chest Pain). If so — When did the CP begin? Was CP still present at the time that the ECG in Figure-4 was taken?
• Can we find a previous ECG on this patient (looking to determine if the QS waves and ST elevation is new or old).
• Especially if CP was ongoing — a repeat ECG is needed (looking for signs of acute evolution) — in addition to Troponins, Echo and further assessment until we can determine if an acute process is in progress. 

Figure-4: I've labeled KEY findings in today's ECG.

CASE Follow-Up:

I later learned the history in today's case — which was that a middle-aged man with diabetes and hypertension — who presented to the ED (Emergency Department) for abdominal pain that had awakened him from sleep.

• The patient was markedly hypertensive in the ED — but he did not have CP.
• Chest X-Ray was normal. 
• Troponins were negative.
• Echo showed significant LVH with normal LV function and no wall motion abnormality.
• Radionuclide scan was negative for ischemia.
• Previous ECGs were found in the patient's chart — which showed similar findings of marked LVH with anterior ST elevation attributed to LV "strain".
• 
  
• In Summary: The patient's abdominal pain was treated. An acute cardiac event was ruled out. Cardiac cath was not done.

"Take Home" Message: Anterior lead ST elevation does not necessarily indicate acute infarction when the patient has LVH that is manifest by deep anterior S waves. In such cases — the anterior ST elevation may simply reflect LV "strain" (as per the "Mirror Test" that is shown within the RED insert in Figure-4).

• Further evaluation may be needed in such cases to clarify what may be "new" vs "old" (ie, To rule out a new acute event that could be superimposed on longstanding LVH).
• KEY Point: Anterior ST elevation is unlikely to represent LV "strain" if anterior S waves are not larger than is usually expected (ie, if there is no LVH). 

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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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 #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
• ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
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• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
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• 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?"). 

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ADDENDUM (12/21/2024): I've added below in Figure-5 and Figure-6 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

Figure-5: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-6: Illustration and description of LV “strain” and a “strain equivalent” pattern (See text).

ECG Blog #460 — A Wide Tachycardia ...

I was sent the ECG in Figure-1 — initially told only that it was obtained from an older man with “palpitations”.

• The cardiology team thought the rhythm was an SVT (SupraVentricular Tachycardia) — with QRS widening as a result of aberrant conduction.

QUESTION:

• Do YOU agree that the rhythm is consistent with an SVT, in which there is QRS widening because of aberrancy?
• How would you treat this patient?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 — shows a regular WCT ( = Wide-Complex Tachycardia) at ~160/minute, without clear sign of atrial activity.

• Clinically — The 1st priority in assessing this patient would be to determine hemodynamic status! (because IF this patient was unstable with this ECG — then regardless of what the rhythm happens to be — synchronized cardioversion would become immediately indicated).
• On the other hand — IF the patient is completely stable with this rhythm, then by definition — You have at least a “moment of time” to more thoroughly contemplate the etiology of this rhythm.

PEARL #1: As emphasized in many other blog posts (ie, ECG Blog #220 and Blog #196, to name just two) — the differential diagnosis of a regular WCT rhythm without clear sign of atrial activity should be assumed to be VT (Ventricular Tachycardia) until proven otherwise.

• Taking all comers in an unselected adult population — statistical likelihood that a regular WCT without atrial activity will be VT is at least 80%.
• If the patient is at least middle-aged, and especially if there is a history of underlying heart disease — then statistical likelihood that a regular WCT without atrial activity will be VT increases to ~90%. To Emphasize — This is a 90% likelihood of VT even before you look at the ECG!
• 
  
• In Today's CASE — All that we initially knew was that the patient was an "older adult" — but we were not told if he had underlying heart disease. So before looking at QRS morphology — statistical odds were ~80% likelihood of VT.

PEARL #2: Assessment of the frontal plane axis and consideration of QRS morphology in the 12-lead tracing during the WCT rhythm can increase (or decrease) statistical likelihood of VT from our initial estimate of ~80% (See ADDENDUM below for user-friendly criteria I favor for this purpose).

• Finding extreme axis deviation in the frontal plane during the WCT would strongly favor VT. 
• To Emphasize: By “extreme” axis deviation — the QRS must be entirely negative in either lead I or lead aVF. Even a small positive deflection in either of these leads negates the reliability of this criterion. 
• In Today's CASE — The 12-lead tracing in Figure-1 does not satisfy this “extreme” axis deviation criterion — because the axis is normal (ie, The net QRS deflection is positive in both leads I and aVF — therefore the axis lies between the normal range of 0-to-90 degrees). 

Perhaps the most helpful criterion for assessing QRS morphology during a regular WCT rhythm — is whether QRS morphology resembles a typical conduction block? (ie, typical RBBB; typical LBBB — or bifascicular block with either RBBB/LAHB or RBBB/LPHB).

• As emphasized in ECG Blog #204 — Focus on the 3 KEY leads ( = leads I,V1,V6) facilitates recognition of RBBB and LBBB within seconds. That said — whereas somewhat atypical QRS morphology does not necessarily indicate VT  — the finding of a completely typical QRS morphology for RBBB or LBBB may greatly increase the likelihood of a supraventricular rhythm.

In Today's CASE — QRS morphology is very atypical for either RBBB or LBBB. As a result — the WCT rhythm in Figure-1 has to be assumed VT until proven otherwise!

• ECG #1 is not consistent with LBBB — because while the QRS is all positive in lead V6, there is no predominant negativity in the anterior leads.
• ECG #1 is not consistent with RBBB — because: i) Lead V1 lacks a triphasic morphology; — ii) Lateral leads I and V6 lack any terminal S wave; — and, especially because: iii) The QRS is almost all positive in all 6 chest leads (there is no more than a tiny initial q wave in leads V3,V4,V5).

PEARL #3: If ever there is concordance of QRS complexes in all 6 chest leads (ie, all 6 chest leads are either entirely positive or entirely negative) — this is virtually diagnostic of VT.

• The sensitivity of this criterion not good — such that it will be rare that you will see positive or negative QRS concordance in all 6 chest leads during a regular WCT rhythm. That said, if ever you do — then you have essentially made the diagnosis of VT. 
• 
  
• In Today's CASE — Those tiny initial q waves in leads V3,V4,V5 mean that positive concordance is not strictly present. That said — given how tiny these 3 precordial q waves are, I interpreted the almost all positive QRS in leads V1-thru-V6 as supportive of presumed VT (albeit not diagnostic).
• The only exceptions that I'm aware of to the above-cited morphologic criteria for VT are: i) IF the rhythm is antidromic AVRT — in which case the impulse travels forward over an AP (Accessory Pathway) in a patient with WPW, therefore resulting in a regular WCT rhythm that resembles VT (For more on the various arrhythmias in patients with WPW — See ECG Blog #18); — ii) If the baseline ECG during sinus rhythm manifests a widened and very abnormal QRS morphology as a result of prior infarction, cardiomyopathy and/or preexisting bundle branch block; — and, iii) If there is some toxicity (such as hyperkalemia) which widens and distorts QRS morphology.
• Conclusion: Assuming none of the above exceptions exist — the ECG in Figure-1 has to be presumed VT until proven otherwise. 

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CASE Conclusion:

Today's patient was hemodynamically stable in association with the ECG in Figure-1.

• In view of this patient's hemodynamic stability — medical therapy was initially tried. There was no response to vagal maneuvers, nor to 3 doses of Adenosine. This was followed with several Amiodarone boluses — again with no response.
• Some clinical history was obtained — which revealed that the patient has known coronary disease (S/P CABG — with ejection fraction of ~35%).

At this point — the cardiology team still suspected a supraventricular etiology for today's rhythm. That said, plans were made for synchronized cardioversion given lack of response to medical treatment. Before this could be done — the patient spontaneously converted to sinus rhythm.

Final Reflections on Today's CASE:

• The ECG in Figure-1 strongly suggests VT. That said — clinicians often need to begin treatment before they are 100% certain of the rhythm diagnosis. In today's case — a trial of medical therapy was reasonable since the patient was hemodynamically stable.
• It's important to appreciate that the odds that today's rhythm was VT immediately increased as soon as it was learned that the patient has significant underlying heart disease.
• Given that multiple doses of antiarrhythmic medication were given — there should have been adequate time in this patient with known significant coronary disease — to obtain a prior ECG. This could have been insightful if a prior tracing were to show a preexisting conduction defect in sinus rhythm with the same QRS morphology as seen in Figure-1. 
• 
  
• While nothing is 100% — the sequence and choice of treatment options should be influenced by relative probability of the differential diagnosis.
• Several doses of Adenosine were given in today's case. This drug is extremely effective for converting reentry SVT rhythms. It may also convert a certain number of patients with idiopathic VT. That said, by definition — today's patient does not have idiopathic VT, because he has known coronary disease. (See ECG Blog #197 — for review of idiopathic VT).
• Although the effects of Adenosine wear off within 30-90 seconds, and most patients tolerate this drug surprisingly well — Adenosine is not benign (See ECG Blog #402). As a result — I would not have risked using Adenosine in today's case ( = my opinion) given virtual nil chance of it working.
• That said — the fact that both vagal maneuvers and 3 doses of Adenosine failed to convert today's rhythm is yet more evidence in favor of VT.
• 
  
• IV Amiodarone (bolus and drip) — is an appropriate medication to try in today's case, given that this patient was hemodynamically stable. An advantage of this medication — is that it may be effective for both VT and SVT rhythms. As I lack full details from today's case — I do not know if it ultimately was the Amiodarone that converted today's WCT to sinus rhythm.
• IF the decision is made for a trial of medical therapy — the provider should stay at the bedside, ready to immediately cardiovert if at any time during the treatment process the patient's hemodynamic status deteriorates.
• Alternatively — a decision could have been made to sedate the patient and immediately cardiovert, given the 90+% likelihood of VT in this patient with known coronary disease.
• While important to engage in thoughtful discussion about cases like this — ultimately, "Ya gotta be there" to know which therapeutic option(s) might be best, given the particulars of any given case. I offer the above as retrospective reflection to stimulate discussion on actions to consider.
• My understanding is that the decision was made for today's patient to be formally evaluated by EP cardiology — with consideration given to ablation and/or insertion of an ICD (Implantable Cardioverter Defibrillator).
•  
• For more on evaluation and management of the regular WCT — See the ADDENDUM below.

 

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Acknowledgment: My appreciation for the anonymous submission of this case.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
• 
  
• ECG Blog #422 and Blog #425 — Cases with Congenital Heart Disease in Adults.
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
• 
  
• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• 
  
• ECG Blog #211 — WHY does Aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 and Blog #361 — Another regular WCT rhythm ...
• 
  
• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
• 
  
• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

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ADDENDUM (12/13/2024):

• I've reproduced below from ECG Blog #361 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

 

ECG Blog #459 — What did the Paramedics See?

I was sent the ECG shown in Figure-1 — told that the patient was a previously healthy 30-ish year old man who was seen by paramedics in the field for nausea and vomiting, which a little bit later was followed by CP (Chest Pain). 

• NOTE: This tracing does not satisfy STEMI criteria (ie, Sufficient ST elevation in at least 2 contiguous leads is lacking — which to qualify as a STEMI, would require ≥2 mm for leads V2,V3 in men and/or ≥1 mm for other leads).

QUESTION:

• Despite not satisfying STEMI criteria — Were the paramedics correct to request activating the cath lab given ECG #1?

Figure-1: The initial ECG in today’s case.

MY Thoughts on the ECG in Figure-1:

In a patient with new CP — ECG #1 is a worrisome tracing. The rhythm is sinus tachycardia at ~100/minute — with normal intervals, normal axis, and no chamber enlargement. I’ve highlighted the worrisome ECG findings in Figure-2:

• My “eye” was immediately captured by the 3 leads within the RED rectangle. As highlighted by the RED arrows — the T waves in leads V1,V2,V3 are all peaked and disproportionately taller-than-they-should-be in these anterior leads (in comparison with modest size of each QRS complex).
• Normally the T wave in lead V1 is either negative, or no more than minimally positive without noticeable ST elevation (which is very different than what we see in Figure-2).
• The hyperacute T waves in leads V2 and V3 — dwarf the QRS in these leads, with there being inappropriate (albeit <2 mm) ST elevation in lead V2. Ignoring the 3rd QRST complex in lead V3 (that is distorted by artifact) — the ST segment in lead V3 is inappropriately flat, if not slightly depressed.
• In the context of obviously hyperacute T waves in leads V1,V2,V3 — neighboring chest leads V4,V5 also manifest taller and more-peaked-than-they-should-be T waves that are hyperacute (BLUE arrows in these leads).

In addition — the limb leads in Figure-2 are abnormal:

• As is so often the case with acute proximal LAD OMI — lead aVL manifests ST elevation (RED arrow in this lead).
• Reciprocal ST depression is seen in each of the inferior leads (BLUE arrows in leads II,III,aVF).

IMPRESSION: Regardless of whether or not the “millimeter-definition” for a STEMI is satisfied — in this patient with new CP — this initial ECG in today's case is diagnostic of acute proximal LAD OMI.

• The cath lab should be immediately activated.

Figure-2: I've labeled the initial ECG in today's case.

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30 Seconds Later ...

• In Figure-3 — What do we now see in lead V3 in this repeat ECG, done just 30 seconds later? 

Figure-3: Comparison between ECG #1 — and the repeat ECG done just 30 seconds later. What do we now see in lead V3?

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ANSWER: 

• In Figure-3 — there is now T-QRS-D (Terminal QRS Distortion) — which is defined as the absence of both a J-wave and an S-wave in either lead V2, lead V3, and/or lead V4 (as discussed in ECG Blog #318).
• The clinical significance of T-QRS-D — is that it is virtually diagnostic of acute OMI (ie, of acute coronary Occlusion).
• In Figure-4 — Compare the QRST complex in lead V3 for both ECG #1 and ECG #2. Ignoring the 3rd QRS in lead V3 of ECG #1 (which is distorted by artifact) — Note that the S wave has been "lifted" above the baseline in ECG #2, which qualifies as T-QRS-D.
• To Emphasize: Clearly, T-QRS-D is not needed in today's case to make the diagnosis of acute LAD OMI — since multiple findings described above more than suffice to justify immediate cath lab activation. But there are occasions in which ST-T wave findings may be far more subtle, for which recognition of T-QRS-D may prove to be the decisive diagnostic feature.
• 
  
• Additional NOTE: 3 ECG findings combine to suggest a proximal location for today’s acute LAD occlusion. These are i) Hyperacute T waves in the chest leads that begin in lead V1; — ii) ST elevation is seen in lead aVL; — and, iii) There is reciprocal ST depression in all 3 inferior leads.

Figure-4: T-QRS-D is now seen in ECG #2.

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4 Minutes after ECG #2 ...

• What do we now see in Figure-5 — which compares the next serial tracing that was recorded 4 minutes after ECG #2?

Figure-5: Comparison between ECG #2 — and the next tracing recorded 4 minutes later. Has there been much change?

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ANSWER: 

In just 4 minutes — there have been a number of dynamic ST-T wave changes that we now see in Figure-5. These changes are best appreciated by lead-to-lead comparison, and include the following:

• The most remarkable ST-T wave changes have been in the chest leads — which now show obvious ST elevation (most marked in leads V2,V3 — but also in neighboring leads V1 and V4).
• Note further “lifting” of the J-point in lead V3 — resulting in more pronounced T-QRS-D compared to ECG #2.
• ST-T wave changes in ECG #3 (compared to ECG #2) are more subtle in the limb leads — but clearly show a more acute appearance to the inferior lead reciprocal depression and to the hyperacute T wave in lead aVL.

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2 Minutes after ECG #3 ...

• What do we now see in Figure-6 — which compares the next tracing ( = ECG #4) recorded 2 minutes after ECG #3? 

Figure-6: Comparison between the chest leads from ECG #3 — and the next 12-lead ECG, that was recorded 2 minutes later. What do we now see?

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ANSWER: 

In Figure-6 — We now see a run of ventricular beats.

• The first 3 beats in the limb leads from ECG #4 are sinus-conducted (with the RED arrow in lead II highlighting that there are upright sinus P waves with a constant and normal PR interval in this lead). Of note in ECG #4 — although the QRS complex “looks” wide in a number of leads for sinus-conducted beats — the QRS does not measure more than 0.10 second for these sinus-conducted beats (therefore not qualifying as wide).
• Beginning with beat #4 in the limb leads of ECG #4, and continuing through to beat #8 — P waves are lost and the QRS widens, with a constantly changing QRS morphology. I interpreted beats #4-thru-8 as a 5-beat run of PMVT (PolyMorphic Ventricular Tachycardia) — which presumably was precipitated by acute ischemia from the ongoing extensive MI.
• Ironically — there is less ST elevation in the chest leads of ECG #4 compared to ECG #3 — despite the fact that we now see a run of PMVT.

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CASE Follow-Up:

Shortly after ECG #4 was obtained — the patient developed VFib. Prolonged resuscitation, including numerous defibrillation attempts failed to convert the patient to a sustainable sinus rhythm. Unfortunately — the patient could not be resuscitated, as persistent VFib ultimately deteriorated to asystole.

• Presumably the patient died of cardiogenic shock from extensive anterior infarction.

Ischemic PMVT with Acute MI:

• Recent decades have seen a dramatic decrease in the incidence of sustained VT deteriorating to VFib as the ultimate lethal event in patients with acute MI. Prompt treatment with reperfusion of the "culprit" artery is largely responsible for the improved prognosis with these patients.
• That said — despite prompt treatment by paramedics on the scene in today's case — refractory VFib developed, and the patient could not be resuscitated.
• Clues to this patient's ultimate demise include: i) Extensive myocardial damage from acute proximal LAD occlusion (presumably resulting in cardiogenic shock with asystole as the terminal rhythm); — and ii) The run of PMVT seen in Figure-4 — with occurrence of this arrhythmia in the setting of acute infarction portending an extremely poor prognosis (Bhar-Amato — Arrhythmia Electrophysio Rev 6(3): 134-139, 2017 — and — Viskin S et al — Circulation 144(10): 823-839, 2021).

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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.

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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 #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = an acute coronary Occlusion MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• 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 ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
• 
  
• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• 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 #400 — Reviews the concept of "dynamic" ST-T wave changes.
• 
  
• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

ECG Blog #458 — Complete Heart Block?

I was sent this tracing — and told that providers thought that the rhythm was 3rd-degree (ie, complete) AV block.

• Do YOU agree?

Figure-1: The initial ECG in today’s case.

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NOTE: The tracing in Figure-1 is an 8-lead rhythm strip (and not a complete 12-lead ECG). This offers the advantage of providing 8 leads with simultaneously-recorded viewpoints of the same 7 beats that we see in this tracing. 

• Note also that the 3rd lead from the top is lead -aVR (and not +aVR) — with this negative perspective of lead aVR providing an electrical viewpoint of +30 degrees (which corresponds to an electrical viewpoint located between leads I and II ). 
• The reason we see lead -aVR in today's tracing, is that this ECG is provided by Dr. Magnus Nossen — who is from Norway, where the Cabrera Format is the standard for ECG recordings (Please check out ECG Blog #365 for potential advantages of the Cabrera Format).

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MY Thoughts on the Rhythm in Figure-1:

Regarding the clinical question posed by today's case — I immediately recognized that ECG #1 was unlikely to represent complete AV block — simply because the ventricular response is not regular.

• PEARL #1: While exceptions exist, most of the time when the rhythm is complete AV block — the escape rhythm will be regular (or at least fairly regular). This truism generally holds regardless of whether the escape rhythm originates from the AV Node — from the His — or from the ventricles.
• PEARL #2: My favorite follow-up to PEARL #1 — is that the best clue in a tracing with AV block that at least some on-time P waves are being conducted — is if one or more of the otherwise regular QRS complexes occur earlier-than-expected (which strongly suggests that the reason this QRS occurs earlier-than-expected — is that this QRS is being conducted to the ventricles). As a result, rather than "complete" AV block — this tells us that some form of 2nd-degree AV block is almost certain to be present.

The “Quick Answer” to Today’s Rhythm:

Even without calipers, as we look at the rhythm in Figure-1 — it should take no more than seconds to recognize that there are P waves that look to be too far away from neighboring QRS complexes to conduct — BUT — that at least beat #4 occurs a little bit earlier than expected. This suggests that beat #4 is probably conducted (albeit with a long PR interval) — such that this rhythm is unlikely to be complete AV block.

• To Emphasize: Regardless of whether the rhythm in Figure-1 represents 2nd- or 3rd-degree AV block — the overall ventricular rate is slow (in the 40s/minute) — so that IF this patient is symptomatic and no “fixable” cause of the bradycardia is found — pacing might still be needed. 

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The "Longer" Answer: = What then is going on?

As always — I favor systematic assessment of the cardiac rhythm by the Ps, Qs, 3R Approach (See ECG Blog #185 for review).

Returning to Figure-1 — I look for the Ps, Qs and 3Rs:

• P waves are clearly present in today's rhythm. Although small in amplitude — these P waves are fairly well seen in lead II. 
• In Figure-2 — I've highlighted with RED arrows those sinus P waves that we definitely see.

PEARL #3: One of the KEY features of 2nd- or 3rd- degree AV block — is that the atrial rhythm will usually be regular (or at least almost regular — if there is an underlying sinus arrhythmia).

• Awareness of this feature helps to exclude potential mimics of AV block, such as non-conducted PACs (in which case the atrial rhythm will clearly be “off” — much more obviously than by the limited irregularity of a ventriculophasic sinus arrhythmia).
• HINT: Using calipers facilitates (and expedites) the search to determine if an underlying regular atrial rhythm is present.

LOOK again at Figure-2. Considering the RED arrow sinus P waves in this tracing that we know are definitely present:

• Don’t the small extra deflections under the 2 PINK arrows (occurring just after the QRS complex of beats #5 and #7) correspond to a location where you’d expect to see P waves if there was an underlying regular sinus rhythm?
• Isn’t the T wave of beat #2 slightly more peaked than all other T waves in the long lead II rhythm strip (under the WHITE arrow)?
• Therefore — Haven’t we just established that it is almost certain that an underlying regular sinus rhythm is present in Figure-2?

Figure-2: Identifying the partially hidden P waves.

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Continuing with the Ps, Qs, 3Rs ... ( = Looking at the QRS):

• PEARL #4: "More leads are better than one!"

Although I generally favor starting with lead II in rhythm analysis — the QRS complex does not look much different from one beat-to-the-next in this lead.

• Confession: I was in fact initially misled in my interpretation of today's rhythm — beause I forgot to apply PEARL #4 ...
• Then I looked more closely at lead V5. 

In Figure-3 — I highlight the most helpful CLUE for solving today's complex arrhythmia — which is the changing QRS morphology for the 7 beats in Figure-3:

• Overall — The QRS complex is clearly wide (at least 3 little boxes, or ≥0.12 second in duration).
• The most logical reason for the changing QRS morphology that is best seen in lead V5 — is that some beats are conducted (albeit with some form of conduction defect) — while other beats arise from a ventricular "escape" focus.

Figure-3: The KEY to solving today’s arrhythmia — is to appreciate that the changing QRS morphology is most easily seen in lead V5. I’ve added RED arrows in both leads II and V5 to highlight the underlying regular sinus rhythm in both of these leads.

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The Next STEPS …

From this point on — I focus on the long lead V5 rhythm strip that I’ve labeled in Figure-4:

• RED arrows show the fairly regular underlying sinus rhythm (albeit with some ventriculophasic sinus arrhythmia) — that we worked out above in Figure-2.
• 3 different QRS shapes are seen in Figure-4: i) Beats #1,3,5,7 look similar (with a widened RSr’ complex); — ii) Beats #2 and 4 look similar (each with a fragmented RR’ complex); — and, iii) Beat #6 resembles beats #2 and 4 — but lacks the distinct, wide terminal S wave that the other 2 beats have.
• The last KEY finding results from application of PEARLS #1 and 2 — for which we need to carefully measure all R-R intervals (as I’ve done in msec. in Figure-4).

QUESTION:

• Which QRS complexes in Figure-4 are most likely to represent escape beats?

Figure-4: Focusing on the lead V5 rhythm strip — RED arrows highlight the underlying sinus arrhythmia — with R-R intervals measured in msec.

Which Beats in Figure-4 represent Ventricular Escape?

Ventricular escape beats are most easily recognized by the presence of: i) A different QRS morphology compared to sinus-conducted beats; — ii) A longer preceding R-R interval; — and, iii) The absence of a preceding P wave with a PR interval that is likely to conduct.

• The 3 QRS complexes in Figure-4 with the longest preceding R-R intervals are beats #3, 5 and 7 (with preceding R-R intervals of 1400 msec. — 1410 msec. — and 1400 msec., respectively).
• Beat #3 is preceded by a P wave with a PR interval that looks too short to conduct. Beats #5 and 7 are both preceded by P waves with PR intervals that look too long to conduct.
• QRS morphology of each of these 3 beats is the same (an RSr’ complex) — which suggests that beats #3,5,7 are all ventricular escape beats with a preceding R-R interval of ~7 large boxes (corresponding to a ventricular escape rate of ~43/minute).
• Beat #1 is also most probably a ventricular  escape beat — because it manifests the same RSr’ morphology as do beats #3,5,7. 
• Advanced Point: Even though beat #1 in Figure-4 is preceded by a P wave with a seemingly reasonable PR interval (of ~0.18 second) — this PR interval is probably still too short to conduct because of the degree of underlying AV block in today’s tracing.

Which Beats in Figure-4 are probably Conducted?

Applying PEARL #2 — beats #2 and 4 both occur significantly earlier-than-expected (ie, with preceding R-R intervals of 1340 msec. and 1280 msec., respectively). This suggests that both of these beats are conducted.

• PEARL #5: Knowing that beats #2 and 4 are conducted allows us to deduce 2 more important points: i) That the QRS morphology of conducted beats looks like the RSr’ complex of beats #2 and 4; — and, ii) That despite their markedly prolonged PR intervals — the P waves preceding beats #2 and 4 are conducting because of how early these beats occur — which implies a significant degree of AV block is present.

This leaves us with beat #6 as the only unaccounted QRS complex:

• Note that QRS morphology of beat #6 is intermediate between the QRS morphology of escape beats #1,3,5,7 — and sinus-conducted beats #2 and 4. This suggests that beat #6 is a Fusion beat (See ECG Blog #128 — for more on fusion beats).
• Support that beat #6 truly is a fusion beat — is forthcoming from the finding of its relatively longer preceding R-R interval (of 1380 msec.) — and — a preceding P wave with a PR interval that would seem likely to be able to conduct.

Putting Together the “Longer” Answer:

By the Ps, Qs, 3R Approach — the rhythm in Figure-4 is slow (average rate ~40/minute) — slightly irregular — with an underlying sinus arrhythmia and several different widened QRS morphologies — for which some P waves are conducting, but others are not.

• The rhythm in Figure-4 — therefore represents some form of 2nd-degree AV block, with significant bradycardia.

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What about the Other Leads?

As noted earlier — today's tracing is not a 12-lead ECG. That said, this rhythm recording shows all 6 limb leads and 2 of the chest leads — such that enough leads are present to provide insight to the clinical situation.

• It's important to rule out an acute event.

In Figure-5 — I focus on QRST morphology of the 2 conducted beats in this tracing ( = beats #2 and #4) — since it is much more difficult to assess for acute changes with escape or fusion beats.

• The rsR' complex in lead V1 — in association with wide terminal S wave in lead I, and to a lesser extent in lead V5 — is consistent with underlying RBBB (Right Bundle Branch Block).
• The predominantly negative QRS complex in lead I — in association with the presence of a qR pattern in inferior leads II,III,aVF — is consistent with LPHB (Left Posterior HemiBlock) — so that there is bifascicular block (RBBB/LPHB).
• Extra notching in multiple leads (ie, especially in leads I,II,V5) indicates fragmentation, which is often a sign of previous scarring with significant underlying heart disease.
• The above said — assessment of ST-T wave changes in the 8 leads shown in Figure-5 does not suggest acute changes.

Figure-5: Assessing today's tracing for ECG findings (including whether or not there was recent infarction). To facilitate assessment — I focus on the 8 leads that we see in the 2 sinus-conducted beats ( = beats #2 and #4). Doing so suggests there is RBBB/LPHB — but there are no acute ST-T wave changes.

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The LADDERGRAM: 

For clarity over the next 5 Figures — I work out what I believe is the most plausible mechanism for today's complex arrhythmia:

Figure-6: It is usually easiest to begin a laddergram by filling in the Atrial Tier — which I've done with near-vertical lines for the 10 P waves in this tracing. I have also filled in the information we derived regarding the Ventricular Tier — in that beats #2 and #4 are conducted — beats #1,3,5,7 are ventricular escape beats — and beat #6 is a fusion beat.
= = = = = = = = = = = = =
Now the challenge begins — as we try to "solve" the laddergram by figuring out which of the P waves in the Atrial Tier are being conducted to the ventricles.

Figure-7: Since beats #2 and 4 are conducted — I've drawn in slanted BLUE lines connecting those P waves presumed to be conducting to the ventricles (albeit these P waves are conducting with very prolonged PR intervals). Since beat #6 is a fusion beat — I've also connected the P wave before it to represent the supraventricular component of this fusion.

Figure-8: This leaves us with a series of P waves about which we don't know if AV block prevents conduction to the ventricles — or — if those P waves would have conducted had there not been escape beats blocking their path of conduction.

Figure-9: I thought it most logical to postulate that the RED butt ends in the AV Nodal Tier were the result of AV block preventing conduction — whereas the BLUE butt ends indicate P waves that probably would have conducted, had it not been for escape beats #1,3,5,7 blocking their path to the ventricles.

Figure-10: Finishing my proposed laddergram (and color-coding the P waves in the lead V5 rhythm strip) — RED arrow P waves represent sinus conduction — YELLOW arrow P waves are non-conducted because of AV block — and PINK arrow P waves are accompanied by a question mark because I can not prove these P waves would have been able to conduct had it not been for the ventricular escape beats.
= = = = = = = = = = = = =
BOTTOM Line: This patient with bifascicular block (RBBB/LPHB) — has some form of 2nd-degree AV block, in which there is marked bradycardia (effective rate in the 40s) — and for which those P waves that do conduct, do so with marked 1st-degree AV block. Unless some "fixable" cause of this conduction disturbance can be found — the patient will probably need a pacemaker.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #164 and ECG Blog #251 —Review of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
• 
  
• ECG Blog #404 — Walks you through a step-by-step approach to this AV block case (with links to a VIDEO of this case, and to Blog #344 for more details).
• 
  
• ECG Blog #352 — emphasizes that 1st-degree AV block with a very long PR interval may have hemodynamic consequences.

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ADDENDUM (12/1/2024) — RP/PR Reciprocity ... 

I received a comment today on this tracing from David Richley, who is well known to most ECG enthusiasts who frequent any of the many ECG internet forums. Dave always offers the most astute commentary on complex arrhythmia interpretation. 

• NOTE: What follows below goes beyond-the-core! But for those readers who love complex arrhythmia diagnosis — I think you'll find what follows is both fascinating and extremely useful in complex tracings such as the one in today's case!

Dave writes the following:

• Dear Ken — I enjoyed your latest ECG blog and I fully agree with your analysis. In addition to all the points you make, I think this is a great example of RP/PR Reciprocity — in which the PR interval of the conducted beats is inversely proportional to the preceding RP interval (Please see Figure-11 below).
• 
  
• When I have presented similar ECGs in class, the question that is occasionally asked is: If these are conducted beats — How come the PR intervals are all different? 
• The answer is RP/PR Reciprocity: The ventricular escape beats conduct retrogradely into (but not through) the AV node, and render it refractory to stimulation. When subsequently a sinus impulse arrives at the AV node — the speed with which it conducts depends on the relative refractoriness of the node. 
• 
  
• PEARL #6: The longer the RP interval — the more time the AV node has to recover, and the shorter the PR interval will be. Obviously, if the sinus impulse is very early (very short RP interval) — the AV node will be in its ARP (Absolute Refractory Period), and the impulse will fail to conduct at all. 

Figure-11: Submitted by David Richley — in which he calculates the RP and PR intervals for the 3 conducted beats in today's tracing. Note that there is RP/PR Reciprocity — in that the shortest RP interval ( = 720 msec.) results in the longest PR interval ( = 640 msec.).
And, the longest RP interval ( = 960 msec.) results in the shortest PR interval ( = 400 msec.).

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PEARL #7: = the "Footprints" of Wenckebach:

David Richley's astute observation regarding today's case brings up a KEY concept known as the "Footprints" of Wenckebach — that I've discussed in many prior ECG Blog posts (You'll find many of these Wenckebach tracings with illustrative laddergrams in my ECG Blog #188).

• In addition to group beating (that many readers are familiar with) — there are a number of other characteristics that suggest a periodicity consistent with some form of Wenckebach conduction. Marriott has colorfuly labeled these characteristics as the "Footprints" of Wenckebach.
• To Emphasize: Wenckebach conduction does not always manifest each of these findings. That said — the recognition that several of these characteristics are present goes a long way toward suggesting the diagnosis! (and this is the reason I suspected within seconds — that some form of Wenckebach conduction was present in today's case). 

These are the "Footprints" to look for:

• Group beating.
• Lengthening of the PR interval until a beat is dropped — after which the cycle resumes and the PR interval shortens.
• A regular atrial rhythm (ie, a regular, or at least fairly regular P-P interval).
• The pause that contains the dropped beat is less than twice the shortest R-R interval.
• Progressive shortening of the R-R interval within groups of beats, until a beat is dropped.
• RP/PR Reciprocity (as explained above by David Richley).

Today's case is extremely challenging — because none of the PR intervals of the conducting beats are the same. There is however group beating — a fairly regular atrial rhythm — and (as per Figure-11) — RP/PR Reciprocity!

• As always — My appreciation to David Richley for reminding me of the importance of RP/PR Reciprocity that Dr. Barney Marriott first taught me decades ago!

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Additional LINKS of Interest:

• ECG Blog #164 — the "Footprints" of Wenckebach.
• ECG Blog #236 — has a 15-minute ECG Video Pearl on the 2nd-degree AV blocks (I begin talking about the "Footprints" at ~1:20 in this video).
• ECG Blog #235 — in the ADDENDUM to this Blog #235 (at the bottom of the page) — David Richley adds more Pearls regarding advanced AV block diagnosis.
• 
  
• ECG Blog #188 — in which I provide LINKS to over 115 laddergrams (many showing step-by-step analysis) — of which there are many examples of Wenckebach conduction.
• NOTE: I have added a LINK to facilitate finding this Laddergram page (See the TOP bar of the MENU just below my Blog name at the top of every page in my Blog! ).