ECG Blog #350 — Severe CP; Not Much on ECG

The patient whose ECG is shown in Figure-1 — was seen in a rural office (not near to any hospital) — for chest pain.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Is this tracing benign?

Figure-1: The initial ECG in today's case — which was obtained during severe chest pain! (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

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

Regarding Q-R-S-T Changes:

• Considering the small size of the QRS complex in lead III — the Q wave in this lead is wide and relatively large. No other Q waves are seen. 
• R wave progression — is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

The most remarkable findings in Figure-1 relate to ST-T wave Changes:

• In the Limb Leads — there is nonspecific ST-T wave flattening in high-lateral leads I and aVL.
• Although there may be a tiny amount of ST elevation in lead III — the T wave is upright, and the ST-T waves in leads II and aVF look normal. Overall — ST-T wave changes in the limb leads do not look to be acute.

In the Chest Leads:

• There is slight, upward-sloping ST elevation in lead V2 and V3 — which of itself is not an abnormal finding (ie, Slight, upward-sloping ST elevation in these 2 anterior leads is a common and normal finding).
• That said — there is more than the minimal amount of ST elevation that may normally be seen in lead V1. Raising suspicion that the ST-T wave in lead V1 is significant — are the findings in lead V6 of: i) ST depression; and, ii) T wave "imbalance", with the positive T wave in lead V6 beings smaller than the upright T wave in lead V1 (as highlighted within the dotted BLUE rectangles in Figure-2 — discussed in detail below).
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• Finally — Although there is no ST segment elevation in leads V3 and V4 — the T waves in these leads are biphasic (initially positive — then terminally negative, as per the double RED arrows in Figure-2).

Figure-2: I've labeled KEY findings in the initial ECG (See text).

PEARL #1: When T waves in each of the chest leads are upright (as they are in Figure-2) — the T wave in lead V1 is usually not taller than the T wave in lead V6. This "Imbalance" of precordial T-waves is not seen very often — and in the “right” clinical setting, has been associated with recent OMI (Occlusion-based MI) from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).

• NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized (See ECG Blog #182 and My Comment at the bottom of the page in the June 1, 2022 post in Dr. Smith's ECG Blog — for an additional examples of this finding).
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• To Emphasize: As an isolated finding — I would not be certain of the significance of the ST-T wave appearance in lead V1. BUT in the clinical setting of this patient presenting to the office for chest pain with: i) ST depression and the smaller upright T wave in lead V6 — and — ii) Terminal negativity of the T waves in leads V3,V4 — my index of suspicion for a recent event was raised.

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The CASE Continues:

Given the patient's chest pain — and the above ECG findings in Figure-2 — the patient was immediately referred to cardiology. But because all symptoms soon resolved, and the patient lived far away — he decided to return home.

• The patient returned to the office the next day feeling "absolutely fine" — and requesting another ECG in hope of being given "a clean bill of health".

The repeat ECG (which was recorded ~17 hours after ECG #1) — is shown together with the initial ECG in Figure-3.

QUESTIONS:

• Given the above clinical context — How would YOU interpret the repeat ECG #2 that is shown in Figure-3?
• Can you explain WHY the ST-T wave findings in ECG #1 were so subtle — despite the presence of 8/10 chest pain?

Figure-3: Comparison between the initial ECG — and the repeat ECG obtained when the patient was pain-free. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECGs in Figure-3:

There has been a dramatic change in the appearance of ECG #2 — compared to ECG #1 that was obtained the day before!

• Other than minimal shallow T wave inversion in lead aVL of ECG #2 — there has been essentially no change in the limb leads. The relatively large Q wave in lead III is unchanged.
• In contrast — ST segments are now coved in all Chest Leads — with persistent ST elevation in leads V1,V2 — increased J-point ST depression in leads V4,V5,V6 — and new deep, symmetric T wave inversion in all chest leads.
• 
  
• In addition — it is important to NOTE: i) Lead V2 shows slight ST elevation with sharp descent of an initially upright T wave that evolves into terminal negativity; and, ii) Anterior R waves are preserved! — and, iii) The patient was without chest pain at the time ECG #2 was recorded!
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• IMPRESSION: The clinical picture and serial ECGs of this patient are diagnostic of Wellens' Syndrome! The deep T wave inversion across the chest leads represent reperfusion T waves from spontaneous reopening of a proximal LAD occlusion. That the LAD is now most probably still "open" — is supported by the fact that this patient's chest pain has not returned since the previous day. The additional fact that chest lead R wave amplitude has been preserved — is encouraging, and suggests that the amount of myocardial damage may be limited!

What is Wellens' Syndrome?

The clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD (Left Anterior Descending) coronary artery narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). That said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. For clarity — Consider the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• 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). NOTE: This characteristic T wave picture is seen in lead V2 of ECG #2 (in Figure-3).

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 LAD 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" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending 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 not be new infarction Q (or QS) waves.
• 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 of the LAD, which 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).
• 
  
• Clinically — the risk posed by Wellens' Syndrome — is that it is proof that there has already been acute thrombotic occlusion of the LAD, 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 (with no guarantee that there will again be spontaneous reopening the next time the vessel occludes).
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• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" Wellens' appearance).
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• Please see the Audio Pearl and Figures-5 and -6 below in the ADDENDUM for more on Wellens' Syndrome

WHY then Were ST-T Findings so Subtle in ECG #1?

I initially found it surprising that despite the history of severe new chest pain (subjective severity score by the patient = 8/10) — the ECG findings in the initial tracing were relatively modest.

• The probable reason for the relatively modest ST-T wave findings in the initial tracing — is that ECG #1 presumably reflects a state of "pseudo-normalization". It is likely that minutes before ECG #1 was recorded — there was marked precordial lead ST elevation. IF the stenotic LAD had just spontaneously reopened near the time that ECG #1 was recorded — then elevated ST segments "on their way" toward developing deep T wave inversion might be nearly isoelectric, as they are in ECG #1.
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• PEARL #2: Development of subtle-but-real biphasic (up-down) T waves, as are seen in leads V4,V5 in ECG #1 (double RED arrows in Figure-2) — in a patient whose severe chest pain is rapidly resolving, may be the earliest sign of the characteristic T wave appearance seen in Wellens' Syndrome.
• 
  
• PEARL #3: As emphasized above — an essential criterion for the diagnosis of Wellens' Syndrome, is that the patient must be pain-free at the time that the defining ECG is recorded. But catching this "pain-free" state on ECG depends on when and how many ECGs are obtained! Although the patient in today's case was still having severe chest pain at the time ECG #1 was recorded — by the history provided above, this patient's chest pain resolved soon after ECG #1 was obtained — and the patient remained pain-free (at least until the time he returned to the office the next day to record ECG #2).
• 
  
• PEARL #4: The importance of promptly recognizing Wellens' Syndrome — is that this identifies a high-grade proximal LAD stenosis that has already undergone brief occlusion (with fortunate spontaneous reopening of the "culprit" LAD lesion). The problem is that the LAD may spontaneously reocclude — with no guarantee that it will spontaneously reopen again. Therefore — recognition of Wellens' Syndrome is indication for timely cath in the hope of preventing a longer-lasting occlusion that causes significant myocardial damage.

What did this Patient's Baseline ECG Show?

Support that the subtle ECG findings in the initial tracing were truly acute — was forthcoming once this patient's prior ECG became available.

• Compare the patient's baseline ECG (obtained several years earlier — at a time when he was asymptomatic) — with the initial ECG in today's case (Figure-4). WHAT do you see?

Figure-4: Comparison between the initial ECG — and the patient's baseline ECG obtained several years earlier. (To improve visualization — I've digitized the original ECG using PMcardio).

Comparison of the Baseline ECG with ECG #1:

• The inferior leads in the baseline ECG are virtually identical to the inferior leads in today's initial tracing. Note in Figure-4 — that the relatively large and wide Q wave in lead III is essentially unchanged. This confirms that this Q wave is not a new finding. Whether this Q wave in lead III represents an old inferior infarction vs an incidental insignificant finding is uncertain (ie, an isolated Q wave in lead III or lead aVF is not necessarily an abnormal finding).
• In high-lateral leads I and aVL — there is nonspecific ST-T wave flattening in ECG #1 that was not seen in the baseline tracing. 
• 
  
• In the Chest Leads — the T waves in leads V1-thru-V6 are all upright and normal in appearance. Note especially that the amplitude of the upright T wave in lead V6 of ECG #3 is clearly greater than that of the T wave in lead V1 (ie, There is no precordial lead T wave "imbalance" in the baseline tracing). 
• The amount of J-point ST elevation in lead V1 is more in ECG #1 — than it was in the baseline tracing.
• 
  
• BOTTOM Line: Availability of this patient's baseline ECG confirms that the above described subtle ECG findings in leads I,aVL; V1; V3,V4; and V6 in today's initial tracing — are all acute findings!

FINAL Follow-Up:

I unfortunately do not know details of the longterm course for today's patient. But the final diagnosis from this patient's hospital admission was "NSTEMI" (ie, Non-ST Elevation Myocardial Infarction) — so it is clear that recognition of Wellens' Syndrome was missed.

• Even without troponin confirmation — the clinical history in today's case, when correlated to this patient's serial ECGs is diagnostic of OMI (ie, of brief coronary occlusion from Wellens' Syndrome — followed by spontaneous reopening of the "culprit" LAD lesion).
• Optimal therapy would have included cardiac cath with PCI.

PEARL #5: A KEY "Take-Home" Point from today's case — is appreciation of the importance of correlating the specific timing of serial ECGs to symptom severity. It is because the course of an acute evolving cardiac event may be stuttering (ie, with spontaneous reperfusion — and then reclosure of the "culprit" artery — sometimes repeated multiple times until the eventual "final state" of the culprit vessel is reached) — that the true story may only be learned by this detailed correlation. For example:

• The relatively modest ST-T wave changes that are seen in ECG #1 of today's case (despite the presence of severe chest pain at that time) — make sense when this initial tracing is interpreted in light of the completely normal ST-T wave appearance in the baseline tracing — and — the subsequent deep, symmetric T wave inversion seen in ECG #2 at a time when the patient was pain-free. It is this correlation of symptoms and serial ECGs that allows definitive diagnosis of Wellens' Syndrome (with the occurrence of a transient OMI — instead of the "default" diagnosis of NSTEMI that was made by the hospital team).
• 
  
• For another example of this step-by-step correlation of serial ECGs with symptom severity — Check out ECG Blog #337.

PEARL #6: I close today's case with brief reference to a new concept known as "Precordial Swirl". This unique ECG pattern strongly suggests a very proximal site of LAD occlusion (usually proximal to the 1st septal perforator branch) — with resultant septal ischemia, in addition to anterior wall and apical involvement (Details in the October 15, 2022 post in Dr. Smith's ECG Blog).

• In the setting of acute LAD OMI — the finding of Precordial "Swirl" is recognized by ST elevation in leads V1 and aVR — and reciprocal ST depression in leads V5 and V6. I like to focus on the ST-T wave appearance in leads V1 and V6.
• Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "precordial swirl" whenever there is suggestion of LAD OMI — and — in addition lead V1 looks different than expected!
• 
  
• NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.

Rather than "precordial swirl" — today's initial tracing represents part of the evolution of Wellens' Syndrome. But note that there is abnormal ST elevation in lead V1 (which is clearly new compared to baseline ECG #3) — and — there is ST depression in lead V6 of ECG #1 (which also was not present in the baseline tracing) — and — we know from the history in today's case that transient LAD occlusion did occur.

• I suspect that IF we could have obtained an ECG a little bit before ECG #1 — that we would have seen anterior ST elevation with definitive ST-T wave findings consistent with "precordial swirl". 

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ADDENDUM (10/1/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-5 and Figure-6.

 

 

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

Figure-6: Wellens’ Syndrome (Continued). 

—  — 

Today's ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not.

 

 

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Acknowledgment: My appreciation to Kianseng Ng and Chris Chow (from Malaysia) for the case and this tracing. 

• Credit to Kianseng Ng for coining the following quote: If the history is classical and the ECG is "normal" — then you probably missed something in the ECG.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
•  
• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
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• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
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• ECG Blog #326 — Reviews a case of Wellens' Syndrome that was missed.
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• ECG Blog #182 — and My Comment at the bottom of the page in the June 1, 2022 post in Dr. Smith's ECG Blog — show examples of T Wave Imbalance (ie, When the upright T in lead V1 is taller than the T in lead V6).
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• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
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• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).

ECG Blog #349 — Is there Capture?

The Lead II rhythm strip shown in Figure-1 — was obtained from a 60-year old man who was admitted to the hospital for an orthopedic injury. No chest pain. Hemodynamically stable with this rhythm. No acute injury was seen on his 12-lead tracing. The patient does give a history of "one or two episodes of fainting".

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• Is there capture?

Figure-1: Lead II rhythm strip obtained from a 60-year old man admitted for an orthopedic injury. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Approach to the ECG in Figure-1:

As always — My approach to rhythm diagnosis is encompassed by the memory aid, "Watch Your Ps, Qs and the 3Rs" (See ECG Blog #185):

• The overall Rate of today's rhythm is slow (ie, ~40-50/minute). Although the rhythm is not Regular — there is a "pattern" in the form of a bigeminal rhythm (ie, There are coupled beats that are spaced at a similar distance to the preceding QRS complex).

 

In Figure-2 — I schematically show that there are alternating longer-with-shorter R-R intervals (with BLUE and RED lines in Figure-2 showing very similar R-R intervals that alternate in "bigeminal" fashion).

• NOTE: The relationship between alternating R-R intervals is admittedly not perfect (ie, The R-R interval between beats #5-6 appears to be slightly longer than the other BLUE line R-R intervals). But overall — the fact that so many of the alternating R-R intervals repeat — suggests that this is not due to chance (and that some form of conduction is present)!

Figure-2: Schematic representation in which the RED and BLUE lines that I have drawn are constant in length. Note alternating longer-then-shorter R-R intervals — in which the longer R-R intervals (BLUE lines) are of similar (albeit not exact) length — and shorter R-R intervals (RED lines) are equal in length. This is not due to chance!

Continuing with the Ps, Qs & 3Rs:

• All 8 beats in today's rhythm have a narrow QRS complex. That said — odd-numbered beats look slightly different than the even-numbered beats. Realizing that we are only looking at a single lead — the fact that the QRS complex looks so narrow in this lead II suggests that all beats in today's tracing are supraventricular!
• 
  
• PEARL #1: Although possible that the reason for the slightly different QRS appearance of odd- vs even-numbered beats is due to aberrant conduction — it is more likely that the reason for this slight difference in QRS morphology is that beats #1,3,5,7 arise from a different site than beats #2,4,6,8.

I next looked for P waves:

• This is most easily done by use of calipers. Set your calipers to a P-P interval suggested by the distance between any 2 P waves that you can clearly see. Doing so allows you to "walk out" a fairly regular atrial rhythm (with slight variation in the P-P interval, consistent with sinus arrhythmia — as suggested by the RED arrows in Figure-3).

Figure-3: I've added RED arrows to highlight sinus P waves that "walk out" throughout the entire rhythm strip. There is slight sinus arrhythmia.

Finally — the last of the 5 KEY parameters: 

• The last parameter to rhythm assessment is the 3rd R = Related. We are looking to see if P waves are at all related to neighboring QRS complexes.
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• Figure-4 — shows that there is a "relationship" of P waves to neighboring QRS complexes — in the form of a constant (and normal) PR interval preceding beats #3,5,7 (ie, short horizontal RED lines of equal duration in Figure-4). This confirms that these beats are sinus-conducted.
• 
  
• NOTE: I was uncertain in Figure-4 — about the relationship (if any) between P waves highlighted by the YELLOW arrows — and their neighboring QRS complexes ( = beats #2,4,6,8) — because there is variation in the distance from these P waves to the next QRS (as suggested by the BLUE lines in Figure-4). 

Figure-4: Beats #3,5,7 are sinus-conducted, because the PR interval preceding these beats is constant. In contrast — beats #2,4,6,8 are unlikely to be conducted, because the PR interval preceding these beats is not constant.

IMPRESSION: The "Short" Answer

Take another LOOK at today's tracing (Figure-5 — reproduced from Figure-1). Thus far — We have established the following:

• Today's rhythm is supraventricular — and there is "group beating" in a bigeminal pattern (ie, alternating longer-then-shorter R-R intervals). 
• An underlying sinus rhythm is present (As shown in Figure-3 — fairly regular P waves are seen throughout the lead II rhythm strip = sinus arrhythmia).
• Odd-numbered beats are sinus-conducted.
• Even-numbered beats appear to represent junctional escape beats — since the PR interval preceding these beats is very long and not constant. In addition — the QRS complex is slightly different (less negative) than the narrow QRS of sinus-conducted beats. This pattern is consistent with "Escape-Capture" Bigeminy — in which the initial beat in each pair (ie, beats #2,4,6,8) is a junctional "escape" beat — and the 2nd beat in each pair represents "capture" (ie, sinus conduction) of an on-time sinus P wave (as seen for beats #3,5,7).
• There is also some form of 2nd-Degree AV Block — because a number of on-time P waves do not conduct despite having adequate opportunity to do so. 

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Beyond-the-Core: Some of you may have noticed that the PR interval preceding beat #1 looks to be slightly longer than the PR interval preceding the other odd-numbered beats in today’s tracing. As noted in the legend to Figure-1 — I've digitized today's tracing to improve visualization using PMcardio. Unfortunately, the original tracing that I received was folded — therefore slightly distorted. Although I suspect that the PR interval before beat #1 is the same as that of the other odd-numbered beats — I admittedly cannot prove this. 

• This is the “reality” of our current world, in which transmission of smart phone photos via the internet offers the amazing advantage of near-instant consultation with experts all over the world — but which unfortunately may lead to suboptimal resolution due to the need for a “quick” smart phone photo (without the time for precise ECG scanning). 
• That said — Regardless of whether the PR interval preceding beat #1 is (or is not) the same duration of the PR interval preceding beats #3,5,7 — We know that the identical PR interval preceding beats #3,5,7 is not due to chance (and that at least these 3 beats are conducted!). Therefore — my “Bottom Line” interpretation of today's tracing is the same!

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BOTTOM LINE for the “Short” Answer: 

The “group beating” pattern in today’s rhythm is consistent with “Escape-Capture” Bigeminy — due to some form of 2nd-degree AV block. 

• We can not determine from this single tracing if this represents a “high-grade” form of AV block (because we never see 2 P waves in a row that fail to conduct despite being given an adequate chance to do so). 
• That said — the overall ventricular rate of today’s rhythm is slow (ie, between 40-50/minute) — in this 60-year old man who presented with an orthopedic injury and “1 or 2 episodes of syncope”. 
• Further evaluation of this patient is clearly indicated — but considering the presence of symptoms + the overall slow ventricular rate — unless a "fixable" cause is found (ie, drug-induced bradycardia, recent ischemia/infarction, sleep apnea, hypothyroidism, etc.) — a pacemaker may be needed.
• 
  
• To EMPHASIZE: Although the above written “breakdown” of today’s case is long — an experienced interpreter using calipers should be able to arrive at my “Bottom Line” conclusion in no more than 1-2 minutes!

Figure-5: Taking another LOOK at today's rhythm.

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The LADDERGRAM:

For those who want to know more regarding my thoughts on the likely mechanism of today’s complex rhythm — A picture is worth 1,000 words! It's easiest to illustrate the mechanism I favor with step-by-step construction of a laddergram — which I do in Figures-6 through -12.

• NOTE: The clinical reality — is that complex arrhythmias sometimes have more than a single possible explanation. We simply can not always be 100% certain of the mechanism of an arrhythmia from the surface ECG. That said — IF we are able to construct a laddergram that demonstrates a physiologicallly sound supporting explanation — then we have established at least one plausible solution.

Figure-6: It is usually easiest to begin a laddergram by marking out the path of sinus P waves (vertical RED lines that are parallel to the onset of each P wave — which I show in the Atrial Tier). I’ve drawn these lines vertical — because speed of conduction through the atria is rapid.

Figure-7: Since all QRS complexes in this tracing are narrow — all beats are supravenricular! The large BLUE arrows show my landmark for entering QRS complexes — which is to drop a vertical line from the onset of each QRS down to the Ventricular Tier. Note that the RED lines that I've drawn in the Ventricular Tier are nearly vertical — since conduction of these supraventricular impulses through the ventricles is rapid. Note the pattern (ie, “group” beating) of the near-vertical arrows in this Ventricular Tier (ie, alternating longer-then-shorter R-R intervals, consistent with today’s bigeminal rhythm).

Figure-8: Now that I’ve filled in the Atrial Tier (with each of the RED-arrow sinus P waves) — and the Ventricular Tier (with each of the narrow QRS complexes in today’s tracing) — it’s time to begin “solving” the laddergram, which is done by filling in the middle (AV Nodal) Tier. I begin with those beats that I am virtually certain are sinus-conducted (ie, beats #1,3,5,7).

Figure-9: As previously discussed — I believe beats #2,4,6 and 8 represent junctional escape beats — because: i) These beats occur at the end of longer R-R intervals which are of similar duration; ii) The PR intervals preceding these beats are extremely long; iii) As per Figure-4 — the PR intervals preceding these beats are not constant; and, iv) While all QRS complexes in today’s tracing are narrow — QRS morphology of these even-numbered beats is slightly different (ie, less negative) compared to the QRS morphology of odd-numbered beats. As noted above in PEARL #1 — this difference in QRS morphology is often an important clue suggesting a different site of origin. In the laddergram — I illustrate my theory that beats #2,4,6,8 are junctional escape beats with small BLUE circles that originate from within the AV Nodal Tier.

Figure-10: I’ve added BLUE butt-ends to show that those P waves that occur in the middle of the longer R-R intervals — are prevented from conducting to the ventricles by the junctional escape beats.

Figure-11: In addition to preventing conduction of those P waves that occur in the middle of the longer R-R intervals — retrograde conduction arising from these junctional escape beats (dotted BLUE butt-ends) — also prevents conduction of the next on-time P waves.

Figure-12: Final laddergram. The mechanism for the bigeminal group beating in today's case is the result of an "Escape-Capture" rhythm. The first beat in each pair represents a junctional "escape" beat. Retrograde conduction from junctional beats #2,4,6,8 prevents conduction of the next on-time P waves (explaining why P waves c,f,i, and l don't conduct). The on-time P waves that follow ( = d, g, j) are able to conduct normally (ie, P waves d,g,j “capture” the ventricles) to produce beats #3,5,7.

P.S.: There are a number of potential mechanisms that may produce an "escape-capture" rhythm. Today's rhythm just shows one of these. Links to related Blog Posts below show others.

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Acknowledgment: My appreciation to Praneet Manekar and Bharat Rewaria (from Amritsar, India) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 50 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #256 — Escape-Capture Bigeminy (with junctional escape and "capture" from retrograde conduction — with AUDIO Pearls on "Escape-Capture" and on "Sick Sinus Syndrome" plus Step-by-Step Laddergram).

• ECG Blog #163 — Escape-Capture Bigeminy (with sinus bradycardia and resultant junctional escape — and possibly also with SA block).
• ECG Blog #315 — Escape-Capture Bigeminy (from marked sinus bradycardia).
• ECG Blog #144 — Escape-Capture Bigeminy (from 2nd-degree AV block of uncertain severity).

ECG Blog #348 — A 14yo with Palpitations

The 3 non-consecutive rhythm strips shown in Figure-1 — were obtained from a 24-hour Holter monitor, that was done on an athletic young teenage boy. The patient had a history of palpitations occurring both at rest and with activity. These 3 rhythm strips were representative of frequent arrhythmic activity that was seen during the course of 24-hour monitoring. An Echo on this patient was normal.

• How would YOU interpret these rhythm strips? Do the widened beats in A and C represent short runs of NSVT (Non-Sustained Ventricular Tachycardia)?
• Given the above history — What is the likely diagnosis? 
• What treatment options should be considered?  

Figure-1: Non-consecutive rhythm strips obtained from a 24-hour Holter monitor — done on a young teenage boy with palpitations. (NOTE: — I do not have information on which leads were monitored in these tracings.) 

MY Thoughts on the ECG in Figure-1:

As per ECG Blog #185 — I favor the Ps, Qs, 3R Approach for interpretation of the cardiac rhythm — beginning with whichever of these 5 parameters is easiest to assess for the tracing in front of me:

• PEARL #1: The 3 rhythm strips in Figure-1 show obvious variation with clear irregularity. Whenever I see a complex arrhythmia that contains different elements (some of which appear to be easier than others to interpret) — I always begin with the easier parts of the rhythm to interpret. Doing so often reveals the underlying rhythm — which then often facilitates interpreting the more difficult parts of the tracing.

The “EASIEST” Place to Start in Figure-1:

The closest thing to an underlying sinus rhythm appears in Rhythm B. I suspect that the upper rhythm strip in each of the 3 tracings in Figure-1 (which is in RED) — is a standard lead II. If this is the case — then we are seeing normal-looking and upright P waves with a normal PR interval in front of beats #1, 4 and 5 — which means that the underlying rhythm is sinus (RED arrows in Rhythm B — as shown in Figure-2).

• Still looking at Rhythm B — The shape of the P waves in front of beats #3, 6, 7 and 8 looks slightly different than the shape of the P waves in front of beats #1,4,5 (PINK arrows highlighting slightly smaller P waves). The challenge is trying to determine if some (or all) of these PINK-arrow P waves represent sinus P waves (with some of the normal variation in sinus P wave morphology that is commonly seen due to artifact, movement, or random variation) — vs — P waves arising from another atrial focus.
• 
  
• Looking next at Rhythm C in Figure-2: The difference in P wave size and shape between the RED-arrow P wave (before beat #9 in C) — vs the PINK-arrow P waves (before beats #1,8,11) — looks to be real! So at this point — I was thinking that the underlying rhythm in today’s tracing was sinus — and that there was ectopic atrial activity.
• 
  
• Rhythm A in Figure-2 further supports this impression — with greatest difference in P wave size between the PINK-arrow P wave (before beat #16) — and the RED-arrow P waves (before beats #1,6,11 — which look to be larger in both monitoring leads of Rhythm A).

Figure-2: I’ve labeled definite atrial activity with PINK and RED arrows. At this point in my interpretation — I suspected that the underlying rhythm was sinus — with lots of ectopic atrial activity (See text).

The BLUE Arrows in Figure-3:

Keeping the important concept from PEARL #1 in mind (ie, To save interpretation of the more difficult parts of the tracing for last) — I now focused my attention on beat #2 in Rhythm B.

• Now looking at Figure-3 — In Rhythm B, beat #2 is seen to occur earlier than one would expect. The QRS complex of this beat looks identical to each of the 7 other beats in Rhythm B — and — the BLUE arrow preceding beat #2 highlights a premature P wave. Therefore — beat #2 in Rhythm B is a PAC (Premature Atrial Contraction).

PEARL #2: I find the saying, "Birds of a Feather Flock Together" — to be an extremely helpful reminder of an important concept in arrhythmia interpretation. 

• The meaning of this English proverb, "Birds of a Feather ..." — is that people of similar type, interest or character tend to mutually associate.
• 
  
• The relationship to cardiac arrhythmias of the saying, "Birds of a Feather" — is that IF we see other clear evidence on an arrhythmia of a frequent-occurring phenomenon — then additional less evident findings in that same patient probably reflect the same phenomenon.
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• For Example: Since we know that the BLUE arrow preceding beat #2 in B highlights a PAC — and, since other PINK arrows in Figure-3 all appear to represent some form of ectopic atrial activity — it is likely that the deflections highlighted by the 4 other BLUE arrows in this figure (seen over the small deflections between the run of rapid beats in Rhythm A) — also represent ectopic atrial activity. Therefore — beats #11-thru-15 in Rhythm A almost certainly represent a 5-beat run ATach! (Atrial Tachycardia).

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NOTE: Although we might expect that a run of ectopic ATach should manifest similar beat-to-beat P wave morphology — it turns out that P wave morphology (as well as the P-P interval) may vary with ATach. This is especially true at the onset of ATach episodes, when additional ectopic atrial sites may initially be participating.

• We have already seen some variation in P wave shape for a number of the PINK arrows in today's tracing. 

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The YELLOW Arrow in Figure-3:

Let's complete our study of Figure-3 — with a look at the deflection highlighted by the YELLOW arrow in Rhythm C.

• Beat #10 in Rhythm C is clearly early (ie, premature) — and, beat #10 is preceded by a premature P wave (ie, under the YELLOW arrow). Therefore — beat #10 in Rhythm C is a PAC.
• Note that the QRS complex of beat #10 in C looks different compared to each of the other QRS complexes preceded by a colored arrow in Figure-3. The reason for this — is that beat #10 in C is aberrantly conducted. As per the Ashman Phenomenon — the fact that beat #9 in C is preceded by a relatively long R-R interval, sets up conditions for aberrant conduction by prolonging the subsequent relative refractory period (See ECG Blog #70 — for full discussion of the Ashman Phenomenon).
• IF I am correct that the upper recording in rhythm strips A, B and C represents a standard lead II — then predominant negativity of the slightly widened QRS preceded by the YELLOW arrow for beat #10 in Rhythm C is consistent with LAHB (Left Anterior HemiBlock) aberration.

Figure-3: Blue arrows highlight ectopic atrial activity (including a 5-beat run of ectopic ATach in Rhythm A). The YELLOW arrow in C highlights that beat #10 is an aberrantly conducted PAC (See text).

QUESTION:

• What then are the WHITE arrows in Figure-4 pointing to?

ANSWER:

Note that a subtle (very-small-but-definitely-present) deflection appears under each of the WHITE arrows that I have added in Figure-4.

• No QRS complex follows these WHITE arrows.
• By the "Birds of a Feather" concept — since colored arrows provide ample evidence of ectopic atrial activity (including PACs) throughout today's tracing — these WHITE arrows in Figure-4 almost certainly highlight non-conducted (ie, "blocked") PACs, that are occurring during the absolute refractory period.

Figure-4: WHITE arrows highlight blocked PACs.

The Last 2 YELLOW Arrows in Figure-5:

It's finally time to address the more difficult part of today's tracing — which is to determine the etiology of the two 4-beat runs of widened and different-looking QRS complexes (ie, beats #7-thru-10 in Rhythm A — and beats #2-thru-5 in Rhythm C).

• PEARL #3: As emphasized in ECG Blog #211 — the most definitive criterion for diagnosing aberrant conduction, is to identify a premature P wave before the abnormal-looking beat or beats. This is precisely what each of the YELLOW arrows in Figure-5 do!

BOTTOM Line: The short runs of wide and different-looking beats in today's tracing do not represent runs of non-sustained VT. Instead — today's tracing shows an underlying sinus rhythm with multiple ectopic P waves.

• Many of these ectopic P waves occur early (ie, as PACs). Some of these PACs are conducted normally — while others are aberrantly conducted (ie, those that follow the YELLOW arrows). Other PACs are blocked (ie, those highlighted by WHITE arrows).
• Some ectopic P waves do not occur early (ie, the PINK arrows before beats #3, 6 and 7 in Rhythm B — and the PINK arrow before beats #8 and 11 in Rhythm C).
• Finally — there are 3 runs of ATach, each consisting of 4-5 beats. Two of these runs manifest QRS widening as a result of aberrant conduction (ie, beats #7-thru-10 in Rhythm A — and beats #2-thru-5 in Rhythm C). The remaining run of ATach manifests normal conduction (ie, beats #11-thru-15 in Rhythm A).

Figure-5: YELLOW arrows highlight PACs that precede abnormal-looking beats in today's tracing. This confirms that the different-looking beats that follow these YELLOW arrows are all aberrantly conducted!

Putting It All Together:

Reviewing the details of today's case — The patient is an athletic teenager who presents with a history of palpitations occurring both at rest and with activity. An Echo was unremarkable. Holter monitoring over 24 hours revealed frequent episodes similar to those seen in rhythm strips A, B and C.

• As emphasized above — this patient does not have ventricular tachycardia. Instead — the rhythm is sinus with multiple ectopic atrial activity, including frequent short runs of Atrial Tachycardia.
• 
  
• PEARL #4: Before accepting a primary arrhythmia diagnosis for the ECG findings in today's case — one needs to rule out underlying "fixable" causes of excess ectopic atrial activity. This might include some basic lab tests (to ensure a normal blood count, serum electrolyte and thyroid studies) — and ruling out extra-cardiac factors such as alcohol or stimulant drug use (ie, sympathomimetics, amphetamines, cocaine) — as well as factors such as excess anxiety, dehydration, sleep deprivation. In today's case — None of these potentially "fixable" factors were operative.

EAT (Ectopic Atrial Tachycardia):

The above evaluation leaves EAT as the most likely diagnosis for the teenage patient in today's case. (Although P wave morphology does show some variation in today's rhythm — MAT is exceedingly rare in children — so EAT is the most likely diagnosis).

• Although overall, EAT is not often seen in children — it nevertheless is the most common cause of "incessant" SVT in the pediatric age group. In children, this rhythm is usually "idiopathic" (ie, without known cause).
• An important complication of EAT to be aware of — is tachycardia-induced cardiomyopathy. It is for this reason that early recognition of EAT is especially important — since depending on the duration of this condition until diagnosis, the cardiomyopathy may or may not be reversible.
• The "good news" regarding today's case — is that this patient's Echo was normal (such that there was no indication of a developing cardiomyopathy!).
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• In the ED (Emergency Department) — Adenosine can be diagnostic of EAT, because it produces transient AV block that may clearly show the underlying atrial tachycardia. That said — Adenosine doesn't convert EAT. An additional problem — is that EAT does not always respond to other antiarrhythmic drugs, or even to cardioversion.
• EAT may respond differently in younger vs older children (Michel et al — Front. Pediatr: Vol. 8; Article 313 — June, 2020 — and Kang et al — Circulation: Arrhythmia and Electrophysiol 7:664-670, 2014). In children less than 3 years of age — EAT is more likely to spontaneously resolve. It is also more likely to respond to medication (ie, with a ß-blocker and/or IC agent).
• In contrast — EAT is less likely to respond to medication, and less likely to spontaneously resolve in older children.
• Definitive therapy of EAT is with RF (RadioFrequency) Ablation. Because of the better response to medical therapy, and the much greater chance of spontaneous remission — RF ablation is often delayed in younger children.
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• Regarding Today's Case: I do not have specific follow-up in today's case. That said — given the relatively older age of this pediatric patient, and the very frequent episodes of ATach (ie, producing an apparent "incessant" tachycardia) — referral to EP cardiology for ablation may ultimately be needed. 

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Acknowledgment: My appreciation to Najlae Kourireche (from Marrakech, Morocco) for the case and this tracing.

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Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
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• ECG Blog #140 — Example of alternating Bifascicular Block Aberration.
• ECG Blog #14 — Example of Blocked PACs.
• ECG Blog #15 — Example of an aberrantly conducted WCT rhythm.
• ECG Blog #33 — Example of PACs with varying degrees of Aberrant Conduction.
• ECG Blog #263 — Differentiation of WCT rhythms (ie, deciding between VT vs Aberrancy?).
• ECG Blog #211 — WHY does Aberrancy occur? (And why the most common form of aberrant conduction manifests RBBB morphology).
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• ECG Blog #70 — Reviews the Ashman Phenomenon (re aberrant conduction).
• ECG Blog #71 — Regarding the Ashman Phenomenon with Atrial Fibrillation.
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• 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 ECG Video Pearl #21 in this blog post. 
• ECG Blog #220 — Reviews My List for the Causes of a Regular WCT Rhythm (with Audio Pearl on assessing for hemodynamic stability). 
• ECG Blog #240 — Reviews the Case of a Regular SVT (SupraVentricular Tachycardia) Rhythm — with emphasis on how Rate of the rhythm may help in SVT diagnosis.

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ADDENDUM (12/3/2022):

I have added supplementary material below regarding the ECG diagnosis of Aberrant Conduction.

ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction so often manifests RBBB morphology).

• NOTE: I have excerpted a 6-page written summary regarding Aberrant Conduction from my ACLS-2013-ePub. This appears below in Figures-6, -7, and -8).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction.

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Figure-6: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-7: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-8: Aberrant Conduction (Continued) — Example/Summary.