ECG Blog #502 (Video): Is this Wellens' Syndrome?

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 — Today's case is an ECG Video!

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The ECG in Figure-1 is from an older patient who was awakened by severe CP (Chest Pain) in the middle of the night. The CP was intermittent throughout the night — with her again awakened by very severe CP that morning.

• The patient called EMS that morning — but her CP had almost disappeared by the time the paramedics arrived (which is when the ECG in Figure-1 was recorded).

QUESTIONS:

• Is this Wellens' Syndrome? 
• — or — Is it something else?

Figure-1: The ECG in today's Case.

Below is the Video presentation of today's case (6 minutes):

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

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• 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).
• 
  
• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
• 
  
• ECG Blog #350 — another case of Wellens' Syndrome.
• ECG Blog #326 — Reviews a case that was missed.
• 
  
• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
• 
  
• 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).

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ADDENDUM (10/25/2025): I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog).

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The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published over 40 years ago! I thought it insightful to return to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):

• The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
• I've reproduced (and adapted) in Figure-2 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
• Most patients also showed characteristic changes in lead V4.
• Most patients showed some (but less) ST-T wave change in lead V1.
• In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.
• 
  
• Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after hospital admission.
• Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:

The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-2:

• Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
• Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep.

Figure-2: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:

I've reproduced (and adapted) in Figure-3 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose serial ECGs are shown in Figure-3 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
•  
• Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-3 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
• 
  
• Not shown in Figure-3 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-3). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
• 
  
• Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-3: Representative sequential ECGs from one of the patients in the original 1982 article. 
— Panel A: The initial ECG on admission to the hospital; 
— Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing). 
— Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

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Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described over 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.

• One of the 2 ECG Patterns shown in Figure-3, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
• Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remained normal, or were no more than minimally elevated.
• Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.

• We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.
•  The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).
• BUT: What spontaneously occludes, and then spontaneously reopens — may continue with this cycle of occlusion — reopening — reocclusion — reopening — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
• 
  
• Clinically: We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example — resolution of chest pain in association with reduction of ST elevation suggests that the "culprit" vessel has spontaneously reopened. And, if this is followed by return of chest pain in association with renewed ST elevation — the "culprit" artery has probably reclosed.
• The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
• Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
• It is not "Wellens' Syndrome" — IF the patient is having CP (Chest Pain) at the time one of the ECG patterns in Figure-2 are seen. Active CP suggests that the "culprit" artery is still occluded.
• Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.

A final word about the 2 ECG Patterns in Figure-2. 

• As suggested from data in the original 1982 manuscript, Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
• Unlike Pattern A in Figure-2 — Pattern B may be limited to symmetric T wave inversion in a number of chest leads without an initially positive T wave, that then steeply descends into terminal negativity. The diagnostic problem — is that deep, symmetric T wave inversion may be seen in a number of other conditions, and is therefore much less specific for Wellens' Syndrome.

In Conclusion: The 145 patients studied by de Zwaan, Bär & Wellens in 1982 continue to this day to provide clinical insight into the nature of Wellens' Syndrome.

 

ECG Blog #501 (15) — Is this a Run of VT?

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NOTE: I’ve decided to update and republish several of my favorite cases from years past. (Today's post is an improved version of ECG Blog #15 — first published in 2011).

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The rhythm in Figure-1 — is from a right-sided MCL-1 monitoring lead.

• Does a run of VT (Ventricular Tachycardia) begin with beat #6?
• How certain are you of your diagnosis?

Figure-1: Does a run of VT begin with beat #6?

MY Thoughts on the Rhythm in Figure-1:

The underlying rhythm (as suggested by the first 5 beats) — is sinus tachycardia at ~105/minute (ie, The QRS is narrow and regular, with an R-R interval for the first 5 beats of just under 3 large boxes — and with P waves showing a fixed PR interval before each QRS for beats #1-5). 

• After beat #5 — Sinus rhythm is interrupted by a run of a regular WCT rhythm (Wide-ComplexTachycardia).  
• The rate of this regular WCT rhythm is ~200/minute (the R-R interval of every-other-beat for the WCT run is ~3 large boxes — so half the rate = 300÷3 =100 X 2 ~200/minute).
• We don't know for how long this run lasts — since it is still ongoing as the rhythm strip ends after beat #14.
• Sinus P waves are absent during the WCT, but — Doesn't it look like some form of atrial activity is present?

PEARL #1: The finding of atrial activity during a run of a regular WCT rhythm does not necessarily mean that the rhythm is supraventricular. This is because both reentry SVT rhythms, as well as VT may conduct retrograde with 1:1 VA conduction.

• Whereas retrograde P waves are generally negative in the inferior leads — they are usually positive in a right-sided lead such as aVR, V1 or MCL-1. Therefore — the small, upright pointed deflections that we seem to see occurring in the middle of the R-R interval during the WCT (ie, starting after beat #6) — do not tell us the answer.

PEARL #2: The width of QRS complexes during the tachycardia that begins with beat #6 clearly looks wider than it is for the first 5 sinus-conducted beats. That said — it does not look "very" wide.

• That said — We only see 1/12 of the ECG in Figure-1. Part of the QRS may lie on the baseline. When it does — then the QRS may "look" narrow in some leads, whereas in reality — the QRS may be very wide in other leads. 
• "12 leads are better than one!" (ie, When possible, if your patient is hemodynamically stable — Try to get a 12-lead ECG during the tachycardia! ).
• The above said, we might suspect that the rhythm in Figure-1 is supraventricular — because the initial deflection of QRS complexes during the WCT run is upright and narrow (very much like it is for the first 5 sinus-conducted beats). 
• In addition — S waves of the QRS during the run are steeply (rapidly) descending. This suggests supraventricular conduction — whereas with VT, the initial QRS deflection tends to be wider (because the impulse is not arising from within the ventricular conduction system — and is therefore is slower to depolarize the ventricles). 
• The above said — exceptions exist — and "12 leads are better than one" for determining IF the QRS is (or is not) truly wide during a tachycardia.

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KEY Point: How does the WCT run begin in Figure-1? 

(ie, What do we see just before beat #6?).

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ANSWER:

Note the RED arrow that I've added in Figure-2!

• This red arrow notches the T wave that precedes the run of widened beats ( = the T wave of beat #5). This is the "tell-tale" notching of a PAC (Premature Atrial Contraction) — that in Figure-2, precipitates a reentry SVT ( = AVNRT or AVRT).
• In contrast — the onset of VT is not preceded by a PAC.

Figure-2: Answer to Figure-1.

PEARL #3: To Emphasize: The most common cause of a regular WCT rhythm is ventricular tachycardia! That said — there are times when we can definitely exclude VT from consideration.  The rhythm in Figure-2 is one of those times. 

• QRS widening during a tachycardia may occur because of rate-related aberrant conduction (See below). The best way to diagnose aberrant conduction — is by identifying a premature P wave at the onset of the tachycardia. The RED arrow in Figure-2 does just that.
• PACs are sometimes difficult to identify — because they may be partially (or totally) hidden within the preceding T wave. But not in Figure-2. The way that we can be sure that the notching highlighted by the RED arrow is "real" (and not the result of artifact) — is that none of the 4 preceding T waves of the sinus-conducted beats show any hint of notching.
• And, as previously noted — 2 additional findings consistent (albeit not diagnostic) of a supraventricular etiology for beats #6-thru-#14 are: i) that the amount of QRS widening during the run appears to be minimal — and, ii) that the initial deflection (both the small, slender r wave and the steep downslope of the S wave) is similar in morphology to the initial part of the QRS of sinus beats.

Laddergram Illustration:

Appreciation of the mechanism of a reentry SVT is best conveyed by laddergram (as shown in Figure-3):

• Beats #1-thru-5 are sinus conducted.
• Beat #6 is a PAC. This starts the sequence — with retrograde conduction back to the atria (dotted lines that arise from within the AV nodal tier). 
• When "the timing is just right" — the mechanism by which a PAC may initiate a run of a reentry SVT — is if this early beat arrives at the AV node and finds the fast pathway still to be refractory, such that conduction to the ventricles occurs over the slow pathway — whereby a self-sustaining reentry loop is potentially established.

Figure-3: Laddergram illustration of a reentry SVT — in which a PAC precipitates establishment of a self-sustaining reentry loop.

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NOTE: Please check out my ADDENDUM #2 below regarding the insightful comment that I have just received from WB Ren.

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So Why is the QRS Wide in Figure-2?

The reason QRS complexes are wide in the run of SVT that begins with beat #6 — is that the fast heart rate precipitates a run of rate-related aberrant conduction. As shown in Figure-4 — Depending on when during the period of repolarization a PAC occurs — there are 3 possibilities for conduction:

• Possibility #1: Premature Impulse A — occurs so early as to fall within the ARP (Absolute Refractory Period). Because the entire conduction system is still in an abolute refractory state — premature impulse A is "blocked" (ie, non-conducted to the ventricles).
• Possibility #2: Premature Impulse C — occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (with a narrow QRS that looks identical to other sinus beats on the tracing).
• Possibility #3: Premature Impulse B occurs at an intermediate point during the RRP (Relative Refractory Period). A PAC occurring at Point B will therefore conduct aberrantly (ie, with QRS widening) — because only part (but not all) of the ventricular conduction system has recovered.
• 
  
• PEARL #4: Most often PACs that occur during the RRP will conduct with some form of bundle branch block and/or hemiblock pattern (reflecting that part of the cnduction system which has not yet recovered).

Figure-4: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

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Putting It All Together:

The MCL-1 rhythm in today's case begins with 5 sinus-conducted beats. This is followed by a regular WCT run of at least 9 beats, until the rhythm strip ends.

• The WCT manifests a rate of ~200/minute. This rate is faster than usual for sinus tachycardia in an adult — and "off" for untreated AFlutter with 2:1 AV conduction (untreated AFlutter most often manifesting a ventricular rate close to 150/minute). This strongly suggests that the differential diagnosis is between a reentry SVT rhythm (ie, AVNRT or orthodromic AVRT) with QRS widening as a result of rate-related aberrant conudction — vs — VT.
• As shown by the RED arrow in Figure-2 — a "tell-tale" PAC initiates the run of wide beats. This virtually confirms that the WCT is supraventricular due to a reentry SVT (as per the laddergram in Figure-3).

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ADDENDUM #1 (10/19/2025):

• Included below is more on 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 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-5, -6, and -7).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

Figure-5: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-6: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-7: Aberrant Conduction (Continued) — Example/Summary.

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ADDENDUM #2 (10/21/2025):

My appreciation goes out to WB Ren, an EP cardiologist — who has just left me the following comment on the CCRG (Critical Care Recent Guidelines) Facebook ECG forum:

Dr. Ren wrote the following: "Thank you for this case. It is very interesting. As I agree with everything you say, may I point you to a subtlety that caught my eye… During the “WCT” (which as you pointed out, is not that wide) — there is a recurring pattern. 

• P waves 7,9,11,13 are preceded by QRS with slightly different slurring of the end of the S wave. As well as these P waves have a lower amplitude. If this was a classic typical AVNRT, everything would be uniform. 
• As there is beat-to-beat variation in the end-upstroke of the S and P waves — this makes me consider an orthodromic-conducting AP (Accessory Pathway) concomitant to dual AV nodal physiology. 
• Now this can only be proven on an EP study but this is not out of the realm of possibility, as I have seen 2 in the past month or so."

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On review of today's tracing — I completely agree with Dr. Ren!

• What I had initially taken as random variation — is very clearly a recurring pattern — as I show in my amended Figure-2a. This is too consistent to be by chance.

Figure-2a: As per WB Ren — there clearly is a recurring pattern of alternating retrograde P wave morphology (alternating RED and YELLOW ovals). There is also some alternation of S wave morphology.

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I've also amended my laddergram in Figure 3a: 

• As per Dr. Ren — specifics of the reentry circuit in today's case can only be proven via EP study — but I greatly appreciate his observation that makes perfect sense.
• Final thought: RP' intervals of both retrograde P wave morphologies manifest a fairly long RP' interval, which is consistent with conduction over an AP.

Figure-3a: My amended laddergram — in which RED and YELLOW dotted lines show alternating pathways for the retrograde limb of the reentry circuit.

ECG Blog #500 — Can You Solve this CASE?

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NOTE: I started my ECG Blog in 2010 — and this is my 500th ECG Blog case! The reason I saved this case for #500 — is that it is challenging — but in the spirit of the great fictional detective Sherlock Holmes — logical deduction (which is what we often need to apply when solving a complex arrhythmia) allows us to arrive at the most plausible answer. Are YOU up for the challenge?

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The ECG in Figure-1 is from an older patient who reports 2 syncopal episodes, but no chest pain. He is on a ß-blocker and a calcium-channel blocking agent.

QUESTIONS:

• What is the rhythm in Figure-1?
• What is the cause of this rhythm?
• What is the recommended treatment?

• Extra Credit: Can you explain each of the 10 beats?

Figure-1: The initial ECG in today's case — from an older patient with syncope, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

My Initial Thoughts:

The history — and a 2-second look at this tracing gets us started!

• The patient is "older" — he/she presents with an obviously slow and not completely regular rhythm (overall heart rate under 50/minute) — and, is on rate-slowing medication ( = the ß-blocker — and perhaps also verapamil or diltiazem, which are the main rate-slowing calcium blocker medications).
• 
  
• PEARL #1: Given this history — if the very slow heart rate is not the result of rate-slowing medication — and, acute ischemia/infarction, hypothyroidism and sleep apnea are not factors — then a component of SSS (Sick Sinus Syndrome) is probably operative (See ECG Video below in the ADDENDUM for review of the features of SSS). 

As to the Rhythm ...

The reason this case is so challenging — is that the P waves are tiny!

Take Another LOOK at the ECG in Figure-1:

• Focus on lead II — because this is the best lead to use when searching for sinus P waves (ie, If we see an upright P wave in lead II with similar P wave morphology in a number of beats — this probably reflects an underlying sinus rhythm).
• Are there any of the 10 beats in this tracing that we know are preceded by upright P waves in this lead II?
• Are there any P waves that we think may be conducting?
• Are there any P waves that we know are not conducting?
• 
  
• PEARL #2: The Sherlock Holmes principle that we apply for complex arrhythmia interpretation is simple: Start with what you know to be true. After this is established — we can work our way toward assessing those aspects of this complex tracing that we are not yet certain about.

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What I Immediately Knew to be True:

Although tiny — I was quickly able in Figure-1 to identify a number of P waves. I have labeled what I quickly saw in Figure-2:

• The last 4 RED arrows in lead II are clearly highlighting sinus P waves (ie, Despite being of extremely low amplitude — all 4 of these P waves are upright and manifest the same P wave morphology).
• The PR interval preceding beats #7,8,9 is decreasing and different for each of these beats. We know the PR interval preceding beat #9 is too short to conduct.
• In addition — it is clear that the last RED arrow P wave in lead II can not be conducting, because it occurs after beat #10.
• Given that the PR interval preceding beats #7 and 8 is different (ie, The PR interval before beat #8 being a little bit shorter than the PR interval before beat #7) — this means that at most — only one of these P waves can be conducting (depending on what the “normal” PR interval for conduction is for this patient).

Armed with the knowledge that today’s ECG ends with 4 fairly regular sinus P waves ( = the last 4 RED arrows) — it seems logical to suspect that underlying sinus P waves might be present throughout this tracing. This puts us to the task of testing this hypothesis, keeping in mind how small sinus P waves are in this tracing.

• KEY Point: There is virtually no artifact on this tracing. As a result — even minor differences in morphology are most probably "real" — and likely to represent hidden atrial activity.
• With this in mind, as we look at the beginning of ECG #1 — it should be clear that the 1st RED arrow in lead II highlights a sinus P wave, albeit with a PR interval too short to conduct.
• 
  
• PEARL #3: Knowing what the P-P interval is from the last 4 RED arrow P waves in lead II — tells us approximately where to look for additional sinus P waves in the beginning of the lead II rhythm strip.
• For this reason — I thought the tiny distortion in the baseline seen immediately after beat #2 in lead II (ie, between the 2 RED arrows right after beat #2) most probably represents the 2nd sinus P wave in this tracing (albeit this P wave is partially hidden within the last part of the QRS complex before it).
• 
  
• PEARL #4: This is where the use of simultaneously-recorded leads is so useful for confirming our suspicion of additional atrial activity. Use of this concept allows me to confirm that the small upright deflection seen right after the QRS of beat #3 in lead II ( = the 3rd RED arrow in this lead) is real — because the vertical BLUE timeline below it highlights comparable small deflections at the same point in the cycle just after beat #3 in simultaneously-recorded leads V4,V5,V6.
• 
  
• An especially subtle distortion then appears near the beginning of the T wave of beat #4 in lead II (ie, between the 2 light BLUE arrows in this lead). Referral to the 2nd vertical BLUE timeline confirms that this subtle distortion of the T wave of beat #4 in lead II is indeed the 4th sinus P wave (because a comparable subtle distortion of the T wave of beat #4 occurs at the same point in lead V4).
• All that remains for us to do at this point — is to confirm where the 5th sinus P wave in lead II occurs (and the vertical RED timeline does this by highlighting a similar T wave distortion at the same point after beat #5 in lead V3).

Figure-2: I have labeled the sinus P waves that we have identified with colored arrows in lead II.

Which Beat in Figure-2 Occurs Earlier than Expected?

Now STEP BACK for a moment. Take a look at what we've established in Figure-2?

• We know that the rhythm is supraventricular (because the QRS is narrow in all leads throughout this tracing).
• There is a fairly regular atrial rhythm ( = the colored P waves in the lead II rhythm strip).
• Most of the 10 beats in this rhythm are not sinus-conducted. They can't be — because the PR intervals before beats #1 and #9 are too short to conduct — and the P waves closest to beats #2,3,4,5 and #10 all occur after the QRS. 
• This tells us: i) That there is AV dissociation for at least part of this tracing — because the P waves nearest to beats #1,2,3,4,5 and #9,10 are not related to their neighboring QRS complex; — and, ii) That these 7 beats (#1,2,3,4,5; and #9,10) — are all junctional escape beats occurring at an appropriate junctional escape rate of between 40-50/minute.
• Finally (as we step back a bit from this tracing) — We can see that the ventricular rhythm in Figure-2 is almost regular — with the exception of one beat.

QUESTION:

• Which beat in Figure-2 occurs earlier-than-expected?
• Why does this beat occur early?

ANSWER:

• Beat #6 in lead II clearly occurs earlier-than-expected. 
• 
  
• PEARL #5: When there is an underlying regular (or at least fairly regular) sinus rhythm, such that all sinus P waves are "on time" (as shown by the colored P wave arrows in Figure-2) — the finding of a beat that occurs earlier-than-expected strongly suggests that this beat is conducted. This tells us that beat #6 in Figure-2 is a "capture" beat that is being conducted by the "on time" sinus P wave in front of it!

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Let's Magnify the Lead II Rhythm Strip:

At this point in our analysis — I'm going to magnify the lead II rhythm strip that we have been focusing on, as this will greatly facilitate our observations.

• I have done this in Figure-3 — in which I break up the 10-beat tracing from Figure-2 into 2 parts.

Figure-3: I've magnified the lead II rhythm strip from Figure-2.

Orient yourself to the rhythm in Figure-3:

• RED arrows highlight the underlying sinus bradycardia, with a component of sinus arrhythmia.
• As described earlier — beats #1,2,3,4,5 are all junctional escape beats at a rate in the 40s — and, beat #6 represents a sinus-capture beat.
• The rhythm strip ends with 2 additional junctional escape beats ( = beats #9,10).
• This leaves us with beats #7,8 that we have not yet defined.

PEARL #6: If your goal is to confidently interpret complex arrhythmias — then the use of calipers is essential!

• Escape rhythms are usually regular (or at least almost regular). Awareness of the wisdom in this statement holds the KEY for determining which of the 2 remaining beats (#7 or #8) is sinus-conducted.

I illustrate the above concept in Figure-4 — in which I show my measurements for each of the R-R intervals in today's tracing.

• QUESTION: What do these R-R interval measurements tell you about beats #7 and 8?

Figure-4: I've measured R-R intervals from Figure-3.

ANSWER:

• Note that the R-R interval preceding each of the junctional escape beats in Figure-4 is constant at 1480 milliseconds, with the exception of the slight variation (to 1460 msec.) preceding junctional beat #9.
• KEY Point: The R-R interval preceding beat #7 is shorter-than-expected ( = 1430 msec. — instead of 1480 msec.). As per PEARL #5, this tells us that beat #7 is sinus-conducted — whereas beat #8 (which manifests a slightly shorter PR interval) must be another junctional escape beat.

I illustrate the above findings in Figure-5 — in which the RED arrow P waves in lead II indicate the 2 sinus-conducted beats.

• YELLOW arrow P waves highlight "on-time" P waves that are not conducting.
• Note in Figure-5 that the PR interval preceding beat #7 is slightly more than 1 large box in duration — which tells us that there is 1st-degree AV block for this one "on-time" sinus P wave that is conducted normally to the ventricles.

Figure-5: RED arrows indicate sinus-conducted beats. YELLOW arrows highlight "on-time" P waves that are not conducting.

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Laddergram Illustration:

To clarify of the above relationships — I add in Figure-6 my proposed laddergram for today's tracing:

• As noted above — it is the RED arrow P waves that are sinus-conducted. All other beats on this tracing are junctional escape beats. The reason junctional beats are able to occur — is that for most of this tracing, the junctional escape rate is slightly faster than the rate of the sinus bradycardia.
• Junctional impulses in Figure-6 are seen to conduct retrograde for a short distance (dotted butt ends within the AV Nodal Tier).
• The reason the "capture" beat ( = beat #6) is preceded by a longer PR interval than the PR interval for sinus-conducted beat #7 — is that retrograde conduction from junctional beat #5 delays conduction of the next sinus P wave.
• The 2nd RED arrow P wave is right "on-time" — and able to conduct to the ventricles, albeit with 1st-degree AV block. Thereafter, the rate of sinus P waves slows — with the result being that the slightly faster junctional escape rate once again takes over the rhythm to produce junctional beats #8,9,10.

Figure-6: My proposed laddergrams for today's case.

Putting It All Together:

• The underlying rhythm in today's case is sinus bradycardia and arrhythmia. This probably is being exacerbated by use of rate-slowing medication (ie, the ß-blocker and the calcium blocker, if the specific drug used is verapamil or diltiazem).
• There is a tendency to interpret today's rhythm as junctional escape. That said — this is not an optimal interpretation of today's rhythm. Instead, it would be better to describe today's rhythm as underlying sinus bradycardia with sinus arrhythmia — that results in AV dissociation and an escape junctional rhythm with occasional "capture" beats.
• Given that today's patient is an older adult with 2 syncopal episodes — he/she may have SSS (Sick Sinus Syndrome). In this case, even after stopping cardioactive medications and ruling out ischemia/infarction — hypothyroidism — medication effect — and sleep apnea — IF the rhythm in Figure-6 persists — the patient will need a pacemaker as treatment for SSS.
• 
  
• PEARL #7: Perhaps the most concise way to describe today's rhythm — is by saying this is an "escape-capture" rhythm as a result of sinus bradycardia with junctional escape (See LINKS below for other examples of "escape-capture" rhythms).
• 
  
• PEARL #8: AV dissociation is not a diagnosis. Instead, it is merely a description of the lack of relationship between "on-time" sinus P waves and neighboring QRS complexes. AV dissociation may be transient (lasting for as little as a single beat) — or — it may persist throughout the entire rhythm strip. But even though there is AV dissociation for most of the beats in today's ECG — neither 2nd-degree nor 3rd-degree AV block is present. Instead — there is AV dissociation by "default" of the sinus node pacemaker that slows below the rate of the junctional escape rhythm (See the 3rd ECG Video in the ADDENDUM below for more on the 3 Causes of AV Dissociation).

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Acknowledgment: My appreciation to Abdallah Sbai Sassi (from Rabat, Morocco) for the case and this tracing.

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Additional Relevant 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 100 laddergram cases — many with step-by-step sequential illustration) — See the quick access LINK in the upper Menu on top of every page in this Blog!
• 
  
• 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).

Other Post with "Escape-Capture" Rhythms: 

• ECG Blog #349 — another example of Escape-Capture with Step-by-Step Laddergrams.

• 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).

ADDENDUM:

• These 2 ECG Videos cover KEY concepts in today's case:

—  —

ECG Media PEARL #68 (6:15 minutes Audio) — Reviews the meaning of the term, "Escape-Capture" (this being a special form of bigeminal rhyhm).

—  —

ECG Media PEARL #69 (2:45 minutes Audio) — Reviews the ECG findings of SSS = Sick Sinus Syndrome (excerpted from the Audio Pearl presented in Blog #252).

ECG Media PEARL #9 (4:45 minutes) — reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block.