Tuesday, August 30, 2022

ECG Blog #329 — Normal Variant in a Young Adult?

The ECG in Figure-1 — was obtained from an asymptomatic young adult as part of his pre-employment medical exam. The patient has been healthy, without medical complaints. On seeing this ECG — an Echo was obtained, which was reported as a normal study.
  • How would YOU interpret the ECG in Figure-1?
  • Is this a "normal variant"?

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:
This case was sent to me via the internet. I interpreted the ECG as follows:
  • The rhythm is sinus at ~80-85/minute. The PR and QRS intervals are normal. The QTc is at most borderline prolonged. The frontal plane axis is normal (ie, about +20 degrees).
  • There is no chamber enlargement (ie, Given that the patient is a young adult, and presumably less than 35 years old — QRS amplitude is not increased).

Regarding Q-R-S-T Changes:
  • Q waves — At most, there are tiny q waves in the high lateral leads (I,aVL) — which are "normal septal q waves".
  • R Wave Progression — There is early transition (with R=S already by lead V2).
  • ST-T Wave Changes — There is ST elevation in leads V1-V3 (attaining ~1.5 mm in lead V2) — with steep descent of the T wave in lead V2, that leads into terminal negativity of the T wave. But the most remarkable ECG finding — is the symmetric T wave inversion seen in multiple leads (which is surprisingly deep in leads V3-V5).

IMPRESSION: Although this young adult was asymptomatic at the time this ECG was recorded — the ST-T wave changes seen in Figure-1 are not consistent with a simple "normal variant" pattern.
  • There are many types of early repolarization and repolarization variant patterns (See My Comment at the bottom of the page in the May 23, 2022 post in Dr. Smith's ECG Blog).
  • Included among the more common of these variant patterns is anterior TWI (T Wave Inversion) — either as a "persistent juvenile T wave pattern"or — in association with a repolarization pattern characterized by coved ST elevation with terminal TWI. The problem is the difficulty that may sometimes arise when trying to distinguish between benign vs pathological patterns (especially between HCM [Hypertrophic CardioMyopathy]and ACM [Arrhythmogenic CardioMyopathy]).
  • Although previously referred to as ARVC (Arrhythmogenic Right Ventricular Cardiomyopathy) — variants that also involve the LV (Left Ventricle) or both ventricles have been increasingly described. The overall incidence of ACM is ~1/5,000 — with anterior TWI being a primary diagnostic criterion when there is predominant RV involvement — and lateral TWI when there is predominant LV involvement (Corrado et alCirculation Research 121:784-802, 2017).
  • Among the ECG criteria associated with HCManterior TWI may be seen in ~3% of cases (Other ECG criteria associated with HCM are described in ECG Blog #81). If there is doubt when considering the possibility of HCM — Echo is diagnostic.

Overall — the ECG may provide clues to whether a certain pattern of ST-T wave changes is likely to be benign or pathologic. That said — ECG screening is not a perfect tool. Although detailed discussion of this subject extends beyond the scope of this ECG Blog — I list below some generalities that may be helpful in assessment (D'Ascenzi et al — Clin Cardiol 43(8): 827-833, 2020) (Walsh, Smith et al — J Electrocardiog 56: 15-23, 2019) (Wilson et al Br J Sports Med 46(Suppl-1), 2012).
  • Clearly, in a patient with any suspicious ECG findings — the presence of any symptoms (ie, syncope-presyncope; concerning arrhythmias; chest pain)and/or — a positive family history (ie, for sudden death at any early age — or malignant arrhythmias) — immediately places that patient in a higher-risk category (for which more complete evaluation is indicated).

  • Anterior TWI when seen in asymptomatic subjects, is more likely to be benign (especially in black athletic individuals) when there is: i) J-point ST elevation; ii) J-point notching or slurring consistent with early repolarization; iii) Biphasic TWI; iv) When anterior TWI does not extend beyond lead V3 (although healthy black athletes occasionally manifest anterior TWI up to lead V4); and/or, v) When there are voltage criteria for LVH.
  • Anterior TWI is more likely to be associated with ACM (or other underlying structural cause) IF there is: i) Anterior TWI that is preceded by either an isoelectric or depressed ST segment; ii) Low voltage on ECG; iii) Q or QS waves; and/or, iv) PVCs.

  • Overall — the finding of Lateral TWI (with or without inferior TWI) — should increase suspicion for an underlying cardiomyopathy. To emphasize — that lateral TWI may be a benign finding. But there should be a very low threshold for additional evaluation when lateral TWI is seen in an asymptomatic subject.

What About Today's Case?
As noted above — the ECG in today's case is clearly abnormal. Although this younger adult is completely asymptomatic — the pattern of deep, diffuse T wave inversion (in no less than 8 leads — and including inferior and lateral lead distribution)is beyond that expected as a benign normal variant pattern.
  • It is good that an Echo was already ordered on today's patient. Although initial interpretation of this Echo was normal — further review of the Echo study raised the question (without definitive answer) of some apical abnormality.

  • NOTE #1: An underlying cardiomyopathy is not necessarily ruled out by a normal Echo. When suspicion of underlying pathology is higher — cardiac MRI (Magnetic Resonance Imaging) is definitely indicated, with special techniques including contrast enhancement to optimize detection of ACM and apical HCM (See Corrado et al Eur Heart J 41(14):1414-1429, 2020for more on MRI evaluation of ACM)

  • Results of cardiac MRI are pending in today's case.

  • NOTE #2: In a certain percentage of cases — abnormal TWI on ECG may predate anatomic evidence of an underlying cardiomyopathy by as much as a number of years. As a result — serial evaluations over time may be indicated in selected higher-risk patients (and/or those with especially abnormal ECG findings).

  • Additional components of full evaluation include a careful family history — and at times, exercise testing and 24-hour Holter monitoring
  • Use of genetic testing (with consideration of a familial channelopathy) extends beyond the scope of this blog post.

  • P.S.: Although the ECG appearance of the ST-T wave in lead V2 resembles that of a "Wellens'-like T wave"today's case is not consistent with Wellens' Syndrome! This is because a specific history (ie, of prior chest pain that has completely resolved at the time the ECG is recorded) — is essential for the diagnosis of Wellens' Syndrome. Instead — today's case is from an asymptomatic young adult who is in for his pre-employment exam. It's important to remember that other clinical entities (ie, completed infarction, LV aneurysm, LVH, repolarization variants, etc.) may manifest similar ST-T wave changes that are seen with true Wellens' Syndrome. (See ECG Blog #320for more on what Wellens' Syndrome is and is not).

Some Examples of Repolarization Patterns:
  • ECG Blog #60 — for an example coved ST segments with diffuse TWI as part of a pre-participation physical performed on a healthy 20-year old football player.
  • ECG Blog #254 — for an example of coved anterior ST Elevation with terminal T wave negativity resembling "Wellens-like" ST-T waves.
  • My Comment at the bottom of the page in the September 15, 2020 post of Dr. Smith's ECG Blog (for a middle-aged adult with ST elevation and peaked T waves that turned out to be a repolarization variant).


Acknowledgment: My appreciation to Mohamed Wafiq Shoukry (from Kuwait) for the case and this tracing. 


Related ECG Blog Posts to Today’s Case:

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

Thursday, August 25, 2022

ECG Blog #328 — What Happened After the Fall?

The ECG in Figure-1 — was obtained from a middle-aged man with a long history of alcoholic liver disease, who was admitted following a fall. He was acutely ill at the time this ECG was recorded.

  • How would YOU interpret the ECG in Figure-1?
  • ClinicallyWhat might account for the changes you see?

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

NOTE: There are a number of reasons why interpretation of today's rhythm turned out to be especially challenging. These include:
  • There is artifact.
  • P waves are small — and they are not seen in most leads.
  • The QRS complex in lead II is tiny — because QRS morphology in leads I and III is almost oppositely directed (This makes it difficult to distinguish between P waves vs QRS complexes vs T waves in the single long lead II rhythm strip).
  • The underlying rhythm is not obvious.
  • There is more than 1 QRS morphology.

MY Thoughts on the ECG in Figure-1:
I thought the KEY for interpreting today's rhythm was to first identify atrial activity. As I allude to above — this initial task was complicated by the small size of P waves — and the difficulty distinguishing between P waves vs QRS complexes vs T waves in the long lead II rhythm strip.
  • There are 2 QRS complexes that look different from the other 14 beats ( = beats #1 and 13). The QRS for these 2 beats appears to be very wide — is not preceded by a P wave — and at least for beat #13, this beat occurs early (See Figure-2which highlights these 2 beats that look different in all simultaneously-recorded leads). Presumably — beats #1 and 13 are PVCs (Premature Ventricular Contractions).

  • Because electrical activity for the PVC which is beat #1 is oppositely directed in lead I (which is predominantly negative) compared to lead III (which is all positive) — QRS morphology for this PVC in intervening lead II is almost a null vector. I have illustrated this "almost null-vector" for the QRS of these 2 PVCs in the long lead II rhythm strip by means of vertical BLUE timelines placed at the beginning and end of these 2 PVCs in Figure-2.

Figure-2: I've placed vertical BLUE timelines at the onset and offset of the QRS for beats #1 and 13, which are PVCs (See text).

Identifying the P Waves:
I count today's tracing as among the most difficult I have encountered for identifying atrial activity. I approached this task in steps:
  • STEP-1: I find it easiest to begin by quick overview of the entire long lead rhythm strip — with the goal of trying to identify at least 2 deflections in-a-row that look like sinus P waves
  • STEP-2: IF there is an underlying sinus rhythm — then once I identify 2 definite P waves (and determine the P-P interval between them) — it should become much easier to know where to look for additional sinus P waves.

  • PEARL #1: The use of calipers is essential for "solving" today's rhythm. It is simply impossible to accurately assess relative P-P and R-R intervals in a complex tracing like this one unless you use calipers.
  • PEARL #2: Contrary to what many clinician think — Using calipers speeds up your interpretation! This is because once you set your calipers to a given P-P or R-R interval — it takes no more than seconds to "walk through" that interval in other parts of the tracing.

  • Applying these principles in Figure-3 — I've highlighted with RED arrows the 2 deflections that I thought looked most like sinus P waves. NOTE: If these 2 RED arrows in Figure-3 are indeed sinus P waves — then the PR interval preceding beats #7 and 8 is not equal (which immediately suggests that there may be AV dissociation).

  • Realizing that the P-P interval of an underlying sinus rhythm will not always be exactly the same for every beat (ie, there may be a sinus arrhythmia) — I used the P-P interval suggested by the distance between these 2 RED arrows in Figure-3 — and thought the "extra" deflection seen at the onset of the preceding 2 QRS complexes (PINK arrows) most probably represented the 2 preceding sinus P waves.

Figure-3: Starting with the 2 consecutive deflections that I thought looked most like sinus P waves (RED arrows) — I used this P-P interval to look backward — which suggested that the "extra" deflection at the onset of the QRS of beats #5 and 6 (PINK arrows) represented the preceding 2 P waves.

Walking Out Additional P Waves:
Encouraged by what seems to truly be 4 sinus P waves in a row (with approximately the same P-P interval between these P waves) — I continued working my way backward with calipers set at this similar P-P interval (PINK arrows in Figure-4).
  • Although the deflections highlighted by PINK arrows in Figure-4 are admittedly not as definitive for pointing out P waves as they are for the RED arrows — there are subtle indications of an "extra something" that occurs with similar P-P interval spacing between deflections.

Figure-4: Working my way backward with calipers set at a similar P-P interval — I thought additional sinus P waves were probably present under the PINK arrows.

The Underlying Rhythm Is Sinus!
Although subtle — I felt that I was able to march out fairly regular sinus P waves throughout the entire long lead II rhythm strip (additional ARROWS that I added to the rhythm strip in Figure-5).
  • Obviously — No sign of atrial activity can be seen between the artifactual "dip" in the baseline between beats #8-9. But IF we continue advancing calipers from just before beat #8 onward (applying a similar P-P interval that I've used up until this point) — a slight "something" is seen under each of the next 8 PINK arrows in Figure-5. While fully acknowledging that this extra "something" is subtle (ie, no more than slight deformation of a T wave — or a "pseudo-r wave" at the onset of the QRS for beats #15,16) — I think it highly unlikely that these "extra" deflections are all due to chance.
  • NOTE: I used a WHITE arrow for the tiny deflection coinciding with the end of the QRS complex of the 1st PVC (which is beat #1) — because I can not prove this deflection is a P wave. But this extra little deflection does occur on time at a similar P-P interval spacing prior to the 1st RED arrow.

  • BOTTOM LINE: Nothing is perfect. That said — the colored arrows I have placed in Figure-5 are spaced at a similar (albeit not exactly equal) P-P interval duration from each other. I strongly suspect that these arrows represent an underlying sinus mechanism (ie, sinus arrhythmia) in today's tracing.

Figure-5: Working my way forward from where I left off in Figure-4 — I feel the colored arrows represent an underlying fairly regular sinus rhythm throughout the entire rhythm strip.

Are P Waves Related to Neighboring QRS Complexes?
Now that we have identified an underlying sinus rhythm in Figure-5 — We need to determine IF any of these P waves are related to neighboring QRS complexes?
  • We have already identified beats #1 and 13 as PVCs.

  • QRS morphology for the remaining 14 beats in the long lead II rhythm strip is very similar — and the R-R interval (except for the PVCs) is surprisingly regular. Thus, although QRS morphology changes with each 3-lead grouping — it appears that beats #2-thru-12; and #14-16 are all arising from the same site.
  • The QRS complex for these 14 beats is wide. While more difficult to appreciate this for beats #2,3,4 in lead III — and for beats #5-8 in lead aVF — there is no doubt that the QRS complex for beats #2-12; and #14-16 in the chest leads is wide.

  • FOCUS Attention on the QRS complex for each of these 14 beats (ie, beats #2-thru-12; and #14-16). Looking at the nearest colored arrow in Figure-5 to each of these 14 beats — Isn't the relationship between each QRS and each of these colored arrows constantly changing? This suggests there is complete AV dissociation! (ie, all P waves are unrelated to neighboring QRS complexes!).

  • Since the QRS complex of beats #2-12 and #14-16 is wide and completely dissociated from neighboring P waves — I suspect that these 14 beats  represent an accelerated ventricular rhythm. That said — I fully acknowledge that I can not rule out the possibility of an accelerated junctional rhythm with preexisting RBBB/LAHB (although judging by QRS morphology — I feel this would be less likely).

To clarify my proposed interpretation of the rhythm in today's case — I've drawn a Laddergram in Figure-6.

Figure-6: My laddergram illustration of today's rhythm. None of the regular sinus P waves in the Atrial Tier are able to be conducted to the ventricles. Thus, there is complete AV dissociation — which I propose is resulting from an accelerated ventricular rhythm (RED circles arising from the Ventricular Tier) — and from 2 PVCs (beats #1 and 13) arising from another site in the ventricles.

PEARL #3: Regardless of the site of the rhythm for beats #2-12 and #14-16 — the rate of the ventricular response in Figure-6 is almost the same as the rate of the sinus P waves (ie, the rate of both the ventricular response and the rate of sinus P waves is ~90-to-100/minute). This proximity of the rate for these 2 independent pacemakers qualifies the rhythm as isorhythmic AV dissociation
  • As discussed in ECG Blog #195 — the phenomenon of isorhythmic AV dissociation could account for the slight variation that we see in P-P and R-R intervals. With this phenomenon, despite independent beating of the SA node and escape pacemaker — there is often a "back-and-forth" relationship between P waves and neighboring QRS complexes. Although my reading of the literature fails to provide a definitive mechanism for this phenomenon — both pacemakers appear to be subject to slightly differing influences involving autonomic reflexes and vagal tone (with resultant slight ongoing variation in the P-P and R-R intervals).

PEARL #4: Although there is complete AV dissociation in today's rhythm (because none of the P waves in the long lead rhythm strip are conducted to the ventricles) — this rhythm does not qualify as complete AV block. As emphasized in ECG Blog #195 — this is because none of the P waves (RED arrows in Figure-6) have a chance to conduct.
  • The rate of the ventricular response (at ~90-100/minute) — is simply too fast to allow P waves the opportunity to occur during a time when the PR interval would be both long enough to allow conduction to the ventricles — and, at a time when P waves are not occurring simultaneous with the QRS complex or within the ST segment during the absolute refractory period.

  • BOTTOM LINE Regarding Today's Rhythm: There may or may not be some degree of AV block. We simply can not tell from the 16-beat rhythm strip provided in today's case. What we can say — is that there is a fairly rapid underlying sinus rhythm with complete AV dissociation due to near identical sinus and ventricular rates + 2 PVCs. The escape pacemaker — is most likely an accelerated ventricular rhythm.

FINAL Step: What About the Rest of Today's ECG?
Now that we've interpreted the rhythm in today's tracing — we need to return to the rest of the 12-lead ECG (which for clarity — I've reproduced in Figure-7). The remarkable findings are: i) ST segment coving in all 6 chest leads; ii) Marked J-point ST depression in these chest leads (that attains 2-3 mm in leads V3-thru-V5); and, iii) Deep, symmetric T wave inversion in all 6 chest leads — that is clearly beyond that expected with simple RBBB.
  • Regardless of whether beats #2-12 and #14-16 represent an accelerated ventricular escape focus or junctional tachycardia with RBBB/LAHB — these ST-T wave changes are markedly abnormal, and indicative of some acute process.

  • Regarding the Differential Diagnosis that immediately comes to mind considering today's abnormal rhythm and the dramatic ST-T wave changes seen in the chest leads — I think of: i) Acute ischemia/infarction; ii) Massic acute PE (Pulmonary Embolism); and, iii) Acute fat embolism

  • Given the History ( = an acutely-ill patient with alcoholic liver disease — admitted for a recent fall)I favored either acute PE or acute fat embolism as the more likely precipitating event.
Figure-7: I've reproduced Figure-2 — so that we can focus on assessment of the ST-T waves in today's tracing (See text).

CASE Follow-Up:
Our follow-up of today's case is unfortunately limited — but I learned that this patient died several hours later, after the ECG in Figure-7 was recorded. 
  • Although I know little of the specific nature of this patient's fall that prompted hospital admission — I thought his rapid demise in association with today's ECG was most consistent with either acute PE or fat embolism as the precipitating cause.

  • Increasing attention has focused on massive acute PE in recent years as a cause of sudden death or rapid patient demise in patient's presenting with shock or acute dyspnea. This diagnosis should especially be thought of when the initial ECG shows anterior (or diffuse) chest lead T wave inversion and/or ST depression similar to that seen in Figure-7. (See ECG Blog #313for more on the ECG diagnosis of acute PE).
  • Much less attention has focused on the entity of fat embolism — which may cause similar unexpected and rapid demise. This syndrome most often follows orthopedic trauma — and is characterized by systemic dissemination of fat emboli throughout the systemic circulation. In many instances — the diagnosis of fat embolism is only established during autopsy. (See Kwiatt & Seamon: Int J Crit Illn Inj Sci 3(1):64-68, 2013and — Adeyinka & Pierre: NIH StatPearls, 2022for more on fat embolism syndrome).


Acknowledgment: My appreciation to Bipin Kumar (from Koderma, India) for the case and this tracing.


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 Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #188 — for Review on how to read (and drawLaddergrams (with links to numerous illustrative laddergrams — with step-by-step explanation).

Saturday, August 20, 2022

ECG Blog #327 - Can You Explain this Rhythm?

The ECG in Figure-1 — is from a young woman with a several week history of intermittent “palpitations”.
  • How would YOU interpret this tracing?

Extra Credit”:
  • How would you describe atrial activity throughout the long lead II rhythm strip in Figure-1?
  • Can you explain why there are 2 different QRS morphologies in this tracing?

Figure-1: The initial ECG in today’s case — obtained from a young woman with intermittent “palpitations” in recent weeks.

MY Thoughts on the ECG in Figure-1:
There is a LOT going on in this tracing. My “thought process” for assessing the rhythm in this tracing was as follows:
  • PEARL #1: When there are multiple components to an arrhythmia (including both “easier” vs “harder”-to interpret parts)I favor beginning with those parts of the tracing that are easiest to interpret.
  • As part of this “process” — Look to see if there is an underlying rhythm? (ie, Are there any sinus-conducted beats?).

  • PEARL #2: The simple step of labeling sinus P waves can greatly facilitate determining the mechanism of the rhythm. Take another LOOK at today's tracing in Figure-2 — in which I have labeled all sinus P waves with RED arrows.

Figure-2: I’ve labeled all sinus P waves from Figure-1 with RED arrows.

Taking Another Look at ECG #1:
Now that I've labeled all P waves — Isn't it much easier to appreciate that beats #2-thru-6 in Figure-2 represent an underlying sinus rhythm? (ie, RED arrows showing fairly regular sinus P waves near the beginning of this tracing)
  • Of note — the underlying sinus rate is at least 90/minute, or a bit fast (which makes us wonder about what might be stimulating an "almost sinus tachycardia" in this patient).
  • After these first 5 sinus P waves (in front of beats #2-thru-6) — RED arrows highlight that there are 3 additional sinus P waves in the remainder of the tracing (ie, before beats #9, 15 and 16).

The 2nd QRS morphology seen in the long lead II rhythm strip — is an RS complex, in which the S wave is slightly deeper than the R wave is tall (seen for beats #1, 7-thru-15, and 17).
  • To figure out what these RS beats are — I looked first at beats #18, 12 and 14none of which are preceded by any P wave. These beats are not overly wide — BUT — If we focus our attention on simultaneously-recorded leads II and III for beat #1 — and simultaneously-recorded lead aVF for beat #7 — we see a LAHB (Left Anterior HemiBlock) morphology (within the dotted PINK rectangles for beats #1 and 7 in Figure-3).

  • IF we now look at simultaneously-recorded lead V1 for beats #10,11 — we see an all upright complex consistent with RBBB (Right Bundle Branch Block) morphology (within the dotted PINK rectangles for beats #10 and 11 in Figure-3).

  • And IF we put these findings together — RS complexes that are not overly wide and not preceded by P waves for beats #1,8,12,14 — but which manifest a RBBB/LAHB morphology — These are fascicular beats (arising from the Left Posterior HemiFascicle).

KEY Point: Although RS complexes for beats #9 and 15 are preceded by P waves — the PR interval preceding these beats is too short to conduct (ie, the PR interval preceding beats #9 and 15 is clearly shorter than the PR interval preceding sinus-conducted beats #2-thru-6). Therefore — beats #9 and 15 are also fascicular beats!
  • By extrapolation — all of the similar-looking RS complexes on this tracing ( = beats #1, 7-thru-15, and 17) must be fascicular beats. Some of these fascicular beats occur earlier-than-expected (ie, beat #7) — and some occur at a slower rate than sinus-conducted beats #2-thru-6. And then we see a salvo of 3 fascicular beats in a row (ie, beats #9,10,11) — and a couplet of 2 fascicular beats in a row (ie, beats #12,13).

  • NOTE: The hemifascicles are in the ventricles — so for practical purposes, these fascicular beats all behave functionally like ventricular beats. Those that occur earlier-than-expected act functionally like PVCs (ie, beat #7). Beats #12 and 13 are functionally like a ventricular couplet — and beats #9,10,11 like a ventricular salvo. And those fascicular beats preceded by a longer R-R interval represent fascicular "escape" beats (which considering the ventricular location of the hemifascicles — represents a slightly accelerated escape rate).

  • The final beat to mention — is beat #16. This is a normal, sinus-conducted beat — because both the preceding PR interval and QRS morphology of beat #16 is the same as the preceding PR interval and QRS morphology of sinus-conducted beats #2-thru-6.

Figure-3: Use of simultaneously-recorded leads to determine that all of the similar-looking RS complexes in the long lead II rhythm strip manifest an RBBB/LAHB morphology (albeit with minimal QRS widening). Beats #1,7-thru-15 and 17 are therefore fascicular beats arising from the left posterior hemifascicle (See text).

QUESTIONS Regarding Figure-3:

  • Did YOU see evidence of additional atrial activity?

  • IF not — Take a look at the YELLOW and WHITE arrows in Figure-4. What do these arrows that occur after the QRS of beats #7 and #9-thru-14 represent?

Figure-4: What do the YELLOW and WHITE arrows that occur after the QRS of beat #7 and beats #9-thru-14 represent? (See text).

The YELLOW and WHITE Arrows:
The YELLOW and WHITE arrows in Figure-4 represent retrograde conduction! The fascinating aspect of this retrograde conduction — is that the RP' interval is not the same for all of these arrows. Instead — the RP' interval (ie, the distance from the QRS until the point when you see the retrograde P wave) — is slightly longer for the YELLOW arrows.
  • It seems that when there is a longer preceding R-R interval before a fascicular beat (ie, as occurs before beats #12 and 14) — there is more time to “recover” — so retrograde conduction is faster (ie, producing a shorter RP’ interval = as seen by WHITE arrows).
  • In contrast — beats #7, 10, 11 and 13 occur much closer to the preceding QRS — therefore leaving less time to recover. The result is that retrograde conduction is not as efficient and takes longer (which results in the slightly longer RP' interval highlighted by the YELLOW arrows).
  • The reason there is no retrograde conduction after fascicular beats #9 and 15 — is that both of these fascicular beats are preceded by a sinus P wave with a PR interval that is too short to conduct — but which is able to render intervening AV nodal tissue refractory to retrograde conduction from a fascicular beat arising from below this level.

  • NOTE: The retrograde conduction that occurs in Figure-4 after beats #7,11,13 and 14 — presumably resets the SA Node. This results in a slight pause after these beats. The beats that follow (ie, beats #8,9,12,14 and 15) — are fascicular "escape" beats (and since the R-R interval before these beats is between 3-4 large boxes — the rate of "fascicular escape" is ~80/minute, which is accelerated).


LADDERGRAM of Today's Rhythm:

For clarity — I've drawn a laddergram to explain today's rhythm. Since fascicular beats originate from the ventricles — I've schematically drawn these beats as RED circles beginning at the bottom of the Ventricular Tier (Figure-5).

Figure-5: Laddergram illustration of today's rhythm. A fascicular beat starts the tracing ( = beat #1). We do not see how long the R-R interval preceding this 1st fascicular beat is. There follows 5 sinus-conducted beats ( = beats #2-thru-6) — after which occurs a premature fascicular beat ( = beat #7). There follows the sequence of fascicular beats we described above — with escape (beats #8,9) — the salvo (beats #9,10,11) — the couplet (beats #12,13) — more escape (beats #14,15 — with some fusion occurring for beat #15) — a normal sinus beat (beat #16) — with the rhythm strip ending with a final premature fascicular beat (beat #17).

Putting It All Together:
The young woman in today's case presented with a several week history of intermittent but symptomatic palpitations.
  • Clinically — We have an underlying "almost sinus tachycardia" — there is a somewhat accelerated fascicular escape focus, with premature fascicular beats (including a couplet and salvo). Taken together — these findings suggest something is stimulating the heart to produce this unusual rhythm.
  • Regarding the rest of the 12-lead tracing — the QTc is not prolonged — the frontal plane axis is normal — and there is no chamber enlargement by voltage criteria. That said — the one "normal beat" that we do see in leads V5,V6 (ie, beat #16) does show ST-T wave depression with a morphology consistent with LV "strain" — so despite this patient's young age and lack of voltage criteria — there may be true LVH.
  • There are no normally-conducted sinus beats in leads V1,V2,V3 — but looking at simultaneously-recorded ST-T waves in other limb leads (corresponding to sinus beats #2-thru-6) — there is some ST depression. Clearly a sustained tachycardia (or frequent premature beats) can alter ST-T waves — so we will not know the “true” ST-T wave morphology until the rate slows down and remains slow for a period of time.

  • IMPRESSION: The patient is symptomatic with an unusual arrhythmia that may explain her palpitations. Evaluation should focus on ruling out underlying heart disease (formal Echo) — complete blood count, thyroid function and electrolyte studies — chest X-ray — and a very careful History asking about anything (and everything!) that the patient ingests (ie, See ECG Blog #321 — in which a 17yo developed a sustained ventricular rhythm as a result of an unusual Chinese herb she was taking — that could have been easily overlooked if not for careful history-taking).
  • If careful evaluation and history did not reveal a cause of this patient's arrhythmia — then empiric use of a beta-blocker may help to control the ectopics. Surprisingly, especially in young adults — low doses of a beta-blocker are often all that is needed to control a symptomatic arrhythmia.

CASE Follow-Up:
This patient was initially treated with short-term Amiodarone — which controlled her arrhythmia. She was then switched over to a low-dose beta-blocker. Evaluation revealed she had primary hypothyroidism — and she was started on replacement therapy.
  • My review of literature suggested that unlike hyperthyroidism — hypothyroidism is usually not directly associated with an increase risk of tachyarrhythmias (Udovcic et alKlein & Danzi). Hypothyroidism may cause bradycardia. When severe — it may be associated with some QTc prolongation, AV conduction disturbances, reduced contractility and/or diastolic dysfunction — so arrhythmias might be seen as an indirect result of this endocrine disorder.


Acknowledgment: My appreciation to Bipin Kumar (from Koderma, India) for the case and this tracing.


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 Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #188 — for Review on how to read (and draw) Laddergrams (with links to numerous illustrative laddergrams — with step-by-step explanation).

Monday, August 15, 2022

ECG Blog #326 — This Case Was Missed ...

The ECG in Figure-1 was obtained from a man in his 60s with known coronary disease — who called EMS for an episode of more severe CP (Chest Pain) that day. The patient describes increasing angina over the previous ~2 months. ECG #1 was recorded when EMS arrived — at which time the patient's CP had totally resolved.
  • In light of this history — HOW would you interpret ECG #1?
  • Would you activate the cath lab?

Figure-1: The initial ECG in today's case. The patient's chest pain had totally resolved at the time this tracing was recorded.

MY Thoughts on ECG #1:
The underlying rhythm in ECG #1 is sinus. Although it is difficult to be certain of the reason for the irregularity without a long lead rhythm strip — it appears that the early beats are the result of PACs (Premature Atrial Contractions).
  • There is significant baseline artifact in the limb leads. That said — we still can interpret this tracing.
  • In addition to sinus rhythm with PACs — intervals (PR, QRS, QTc) and the frontal plane axis (about +30 degrees) are normal.

Regarding Chamber Enlargement:
  • There is LAA (Left Atrial Abnormality) — suggested by the deep negative component to the P wave in lead V1 (See ECG Blog #75for ECG diagnosis of LAA/RAA). The reason I do not suspect too-high placement of leads V1,V2 — is that the QRS complex in these leads looks so very different than the QRS in lead aVR (See ECG Blog #274for detection of when Leads V1,V2 are placed too high on the chest).

  • Criteria for LVH are satisfied. That is, the S wave for the 2 sinus-conducted beats in lead V2 + the R wave in lead V5 ≥35 mm. Voltage criteria for LVH may also be satisfied in lead V3 — as what appears to be a very deep S wave in this lead is "cut off" by the limits of the ECG paper (See ECG Blog #245 regarding ECG criteria for LVH).
  • The ST depression in leads V5,V6 may at least in part be the result of LV "strain".

Regarding Q-R-S-T Changes:
  • Large Q waves (relative to QRS amplitude in the same lead) are present in leads III and aVF. A small-but-definitely-present Q wave is also seen in the 3rd inferior lead ( = lead II).
  • R wave progression is normal — with Transition (where the R wave becomes larger than the S wave is deep) occurring appropriately between leads V3-to-V4.

The most concerning findings in ECG #1 relate to ST-T wave appearance in a number of leads:
  • The ST-T wave in lead III looks hyperacute! Specifically — there appears to be subtle-but-real ST elevation, with a straightened ST segment takeoff — that terminates in T wave negativity.
  • While lacking the suggestion of ST elevation — the ST segment in lead aVF also ends in T wave negativity.
  • Lead II (which is the 3rd inferior lead) — does not show these changes.

  • PEARL #1: In a patient with new chest pain — one KEY to interpretation of this tracing is the reciprocal change in lead aVL (ie, with respect to the hyperacute ST-T wave, with terminal T wave negativity in lead III). Specifically — the ST segment in lead aVL is straightened, angulates subtly downward — and ends with a surprisingly tall positive T wave (ie, resembling mirror-image opposite changes to what we see in lead III). This reciprocal appearance of lead aVL to lead III suggests recent (or acute) inferior OMI until proven otherwise! (See ECG Blog #184 re this "magical" reciprocal relationship with OMI between leads III and aVL).
  • To a lesser extent — reciprocal change is also seen in the other high-lateral lead ( = lead I), in the form of ST segment straightening, slight ST depression and terminal T wave positivity.

  • PEARL #2: The T waves are taller and more-peaked-than-expected in leads V2 and V3. This more-peaked-than-expected T wave appearance continues in leads V4 and V5. In a patient with suspected recent or acute inferior OMI — this is strongly suggestive of reperfusion T waves from associated posterior wall MI.

  • PEARL #3: There is ST depression in leads V4, V5 and V6. This may be multifactorial (ie, could be from LV "strain" — or — reflect reciprocal ST depression in a similar way as is seen in leads I and aVL — and/or — could reflect ischemia from multi-vessel disease).

  • NOTE: For more on concepts mentioned above — See ECG Blog #193 (regarding the concept of OMI = Occlusion-based MI) — and ECG Blog #258 (regarding how to "date" an MI — and appearance of peaked anterior T waves as indication of posterior wall reperfusion).

Putting It All Together:
The patient in today's case is a man in his 60s with known coronary disease. He reports recent anginal symptoms — with an episode of more severe chest pain on the day of admission. BUT — this chest pain has completely resolved by the time his initial ECG (shown in Figure-1) is obtained.
  • In view of this history — ECG #1 strongly suggests that infero-postero OMI (Occlusion-based MI) occurred at the time of this patient's episode of severe chest pain.
  • The terminal T wave negativity in leads III and aVF — as well as the more-peaked-than-expected anterior lead T waves both suggest that spontaneous reperfusion has occurred in these infero-postero leads.
  • The fact that this patient's chest pain is totally relieved in association with ECG #1 — strongly suggests that at this time, the "culprit" artery (almost certainly the RCA or LCx) is open!

  • PEARL #4: This sequence of events, in association with a pain-free state at the time reperfusion T waves are seen is consistent with Wellens' Syndrome. While the ST-T wave changes of Wellens' Syndrome are almost always associated with LAD (Left Anterior Descending) coronary artery occlusion — Wellens' Syndrome can also be seen in the inferior leads — and that appears to be what today's case represents!

  • PEARL #5: Recognition of Wellens' Syndrome tells us there has been recent coronary occlusion with at least momentary spontaneous reperfusion. BUT — What has spontaneously reopened — may just as easily spontaneously close again. BOTTOM Line: Timely cardiac cath is indicated — with the goal of preventing reocclusion of the "culprit" artery. KEY: The history in today's case — in association with the ECG findings in Figure-1 — indicate the need for prompt cath!

A Bit More on Wellens' Syndrome:
As emphasized above in Pearls #4 and #5 — the vast majority of Wellens' Syndrome cases are seen in the anterior leads, and are indicative of a high-grade proximal LAD stenosis. Lessons learned about this syndrome since its initial description by de Zwaan, Bär and Wellens in 1982 include the following:
  • There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
  • There should be no more than minimal (if any) troponin elevation
  • There are no new infarction Q waves.
  • There may be slight (but not marked) ST elevation in one or more of the chest leads.
  • There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4)

What Wellens' Syndrome is NOT:
Greatest misunderstanding relates to what Wellens' Syndrome is not! Avoidance of this misunderstanding is best accomplished by appreciating the pathophysiology of this syndrome. In essence — the characteristic biphasic T wave appearance with terminal negativity reflects a reperfusion T wave! The patient has recently had total coronary occlusion for a brief period of time — but has now spontaneously reperfused.
  • The chest pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. But the reason the definition of Wellens' Syndrome requires the patient to be pain-free at the time the defining ECG is done — is that the "culprit" lesion is now open. IF the "culprit" lesion was still occluded — then rather than a warning of an impending large infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
  • There is no more than minimal (if any) troponin elevation — because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. IF there is greater troponin elevation — this implies that significant myocardial damage has already occurred (which by definition means that you are dealing with a completed infarction — and not with Wellens' Syndrome).
  • For this same reason — there should ideally not be new infarction Q (or QS) waves. That said — I take this criterion as "relative" — because it has been shown that Q waves can sometimes form in as little as 1-2 hours — and that Q waves can resolve when reperfusion of the "culprit" artery occurs quickly.

  • NOTE: There is no more than slight ST elevation — because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
  • Instead — the characteristic biphasic T wave with rapid T wave descent into terminal negativity is an indication that there was brief total occlusion — but that the "culprit" artery has now reperfused. This ECG finding is a reperfusion T wave. It may look identical to the ST-T wave appearance after a STEMI with marked troponin elevation that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).

  • To Emphasize: The risk posed clinically by Wellens' Syndrome — is that it is proof there has already been acute thrombotic occlusion of the "culprit" artery (albeit brief in duration and followed by spontaneous reopening of the vessel). But what spontaneously occluded and then reopened — is at high-risk of spontaneously occluding again (witno guarantee that there will again be spontaneous reopening the next time the vessel occludes).

The CASE Continues:
The EMS team correctly interpreted the initial tracing in today's case as highly suggestive of a recent acute event. Twenty minutes later — the patient's chest pain returned, and ECG #2 was obtained.

  • In view of the above clinical scenario — HOW would you interpret the repeat ECG shown in Figure-2?

Figure-2: Comparion of the initial ECG — with the repeat ECG done ~20 minutes later when the patient's chest pain returned.

MY Thoughts on the Repeat ECG:
It looks like the rhythm in ECG #2 has changed from sinus — to a low atrial rhythm, because the P wave in lead II is now smaller than the P wave in lead I, and the P wave is entirely negative in lead III. Otherwise — the frontal plane axis and QRS morphology are very similar to ECG #1. The most remarkable change between these 2 tracings relates to subtle-but-real differences in the limb leads:
  • PEARL #6: Awareness that the initial ECG in today's case was obtained at the time the patient was pain-free and was highly suggestive of an inferior lead Wellens' Syndrome — greatly facilitates our interpretation of ECG #2, because we know what to look for!
  • The T wave in each of the inferior leads of ECG #2 all now look hyperacute! The terminal T wave negativity that was seen in leads III and aVF of ECG #1 is gone, and replaced by taller, more upright T waves. There is more ST elevation in lead III. The T wave in lead II has clearly become more positive than it was in ECG #1.
  • Confirmation that these inferior lead ST-T wave changes are real — is forthcoming from scrutiny of high-lateral leads I and aVL. Both of these leads clearly show more J-point ST depression — with decrease in the amplitude of the terminal T wave positivity that had been present in ECG #1. Increased angulation of ST segment descent in lead aVL makes for a perfect reciprocal pattern to the increased hyperacuity and ST elevation now seen in lead III.

  • PEARL #7: ECG #2 was obtained at the time this patient's chest pain returned. The above-described ST-T wave changes in association with this return of chest pain tell us that the "culprit" vessel (most probably the RCA) has once again occluded!

Unfortunately — the above ECG changes were not recognized by clinicians at the PCI receiving center. The patient was not accepted as a candidate for acute intervention.

The CASE Continues:
Five minutes later — the patient's chest pain suddenly resolved. Another ECG was obtained at this time (Figure-3).

  • Is the fact that ECG #3 was obtained at the time this patient's chest pain suddenly resolved — consistent with the interpretation of this case thus far?

Figure-3: Comparison of the 3 ECGs in today's case.

MY Thoughts on ECG #3:
It looks like sinus rhythm has returned in ECG #3, albeit with PACs (ie, the P wave for the 1st and 3rd beats in lead II are sinus-conducted — and once again show a larger P wave than is seen in lead I).
  • The "culprit" artery (most probably the RCA) — has once again reopened! We know this — because the patient's chest pain suddenly resolved corresponding to ECG #3, that shows resolution of inferior lead hyperacute T waves (that now show symmetric T wave inversion in leads III and aVF = reperfusion T waves!).
  • Lateral leads I and aVL now show resolution of ST depression, with return of marked terminal T wave positivity.
  • There is also less ST depression in lateral chest leads V4,5,6 than was present in ECG #2.

  • BOTTOM Line: Within the space of 25 minutes — the sequential ECGs in Figure-3 confirm that today's patient manifested an inferior lead version of Wellens' Syndrome, with "dynamic" ST-T wave changes indicative of repetitive reopening and reclosing of the "culprit" artery.

Lessons To Be Learned:
  • The importance of obtaining serial ECGs in patient with new symptoms can not be overstated.
  • Correlation of serial ECG findings with the coming and going (and with the relative severity) of patient symptoms can tell a "story" that may let you know when the "culprit" artery has reopened and/or is reoccluding.
  • Awareness that this course of changing symptoms, in association with "dynamic" ST-T wave changes is indication for prompt cath (because spontaneous reopening of the "culprit" vessel may be temporary — and the next time the vessel occludes it might not spontaneously reopen again).
  • The receiving provider team in today's case did not recognize the significance of ECG evolution correlated to changing symptom severity. As a result — acute intervention did not occur. The limited follow-up that I have of this case indicates that recognition of an acute event only occurred later when serum troponin returned elevated. There is much to be learned.


Acknowledgment: My appreciation to Sam Collis (from England) for the case and this tracing.


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.

  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
  • ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.

  • ECG Blog #254 — What Wellens' Syndrome is and is not.
  • ECG Blog #320 — Wellens' Syndrome with acute 1st Diagonal OMI.
  • For Review on the "History" of Wellens' Syndrome (from the original 1982 article) — Please SEE My Comment at the bottom of the page in the August 12, 2022 post in Dr. Smith's ECG Blog.

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • 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 #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T waves).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

ADDENDUM (August 15, 2022):

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


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

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

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

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

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

Audio PEARL #26a (7:40 minutes) — Reviews what Wellens' Syndrome is — and what it is not (from ECG Blog #254).

  • CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.



Figure-5: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-6: Wellens’ Syndrome (Continued).