COPY of Blog #504- AMELIA's CASE — COPY

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 — Today's case is an ECG Video!

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The 3 successive lead II rhythm strips shown in Figure-1 — are from a 10-year old child with palpitations.

QUESTIONS:

• What is the rhythm? 
• What to consider clinically?

Figure-1: Succesive rhythm strips from a 10-year old child with palpitations.

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Below is the Video presentation of today's case (9 minutes):

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Acknowledgment: My appreciation for today's case — sent to me from an anonymous follower.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #188 — Reviews how to read and draw Laddergram (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
• ECG Blog #192 — AV Dissociation by Usurpation — Default — or by AV Block?

 

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ADDENDUM (11/XXXX/2025): 

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The 2:30 minute ECG Video below reviews:

• The Ps,Qs,3R Approach — for systematic rhythm interpretation.
• Some additional general tips on rhythm interpretation.

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.

 

 

Hello everyone!

Today's ECG Video — is from a 10-year old child with palpitations.

The case consists of 3 successive lead II rhythm strips — that I wanted to present — because they illustrate a series of important concepts regarding arrhythmia interpretation.

Here are the 3 rhythm strips. What's going on?

So — LET's GET to today's case.

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Amelia — VERY interesting tracings — and I DO plan to make an ECG Blog of this. I will definitely draw a laddergram — but I haven't yet decided if I'll be doing an audio recording blog or a written one. And to keep it fairly simply (and more easy to understand) — I think I wil just use the lead II record from 3 of the 4 tracings that you sent me (similar to the attached figure).

The lead II from ECG #1 — There is an underlying junctional rhythm that is almost but not quite regular. Now, whereas the usual normal junctional escape rate in adults = 40-60/minute — it is FASTER in children (and the general rate range that I use in kids = 50-80/minute — which means that in your 10yo child, most of this tracing is NOT an "accelerated" junctional rhythm — but instead, a junctional escape rhythm that is unusual in not being as regular as junctional escape rhythms usually are. And, it is in ECG #3 that we an accelerated junctional rhythm (at least for the first 5 beats!).

 

We know all 7 beats in ECG #1 are junctional because of the AV dissociation that we see with P waves too near the QRS for the last 4 beats to conduct. So we can only guess why we don't see any sinus P waves in the beginning of ECG #1.

 

I suspect ECG #2 gives us the answer. First 2 beats are sinus — and then no sinus P wave until beat #3 — therefore, most probably there is an underlying sinus arrhythmia that on occasion slows down enough that junctional escape beats occur ( = beat #3 in ECG #2). The the junctional rhythm speeds up — and for beats #5,6,7 we now see retrograde P waves (GREEN arrows). What I will guess (and illustrate in my laddergram) — is that conduction from the AV node to the atria takes the SAME amount of time as does conduction from the AV node to the ventricles for beats #3 and 4 — but when the junctional rhythm speeds up (for beats #5,6,7 and for beats #1-thru-5 in ECG #3) — the AV node is not able to conduct as well, such that conduction back to the atria now takes longer and we then see retrograde (GREEN arrow) P waves!

 

But in ECG #3 — beat #6 is a PVC which does not conduct retrograde — such that the SA node has a little more time to recover, and sinus rhythm returns at a fast enough rate to maintain control of the rhythm.

 

BOTTOM LINE — We have a combination of things = Sinus brady with arrhythmia + an irregular junctional escape rhythm that at times becomes accelerated. This is not a "normal" response — so we need to look for potential factors that might be causing intermittent accelerated junctional escape (ie, illicit drugs? alcohol? stress? anxiety? fear? who knows? — but perhaps there is some clue in the history?).

 

So — IF you figure anything potential causative factors — let me know so I can include it in my write-up. If not, it's OK — as the rhythm strips alone are of value for a blog post.

Amelia — I will be happy to acknowledge you. Please tell me the city and country you'd like me to list after your name — OR — if you prefer, I can keep this case as being sent by an anonymous source.

 

It may be a little while before I publish this — but in any case, I'll let you know. In the meantime — I hope the above helps you in the management of this patient! 

 

From Amelia:

Thank you very much for the explanations!! Actually this case is of my boss, and the colleague who works with my boss was so interested about it and she asked me to share it with you. She is much interested in ECG. I forwarded her all the explanations. We thank you very much! Unfortunately because it is not my personal case, you can publish it with anonymous, it will be perfect like this. We found no causative factors in the patien’s history, no illicit substances, no alcohol but she is indeed more anxious because she lives with the idea that she has a heart problem. We tried to calm her down but her mother doesn’t help her at all.

COPY of Blog #503 — Cause of a Pause- EXTRA COPY

 

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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 #14 — first published in 2011).

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QUESTION: Interpret the Lead MCL-1 rhythm strip that is shown below in Figure-1.

• What is the cause of the pauses in this tracing?  Is there AV block?
• Why is the PR interval preceding beat #7 shorter than the PR for other sinus beats?

Figure-1: What is the cause of the pauses? (between beats #2-3 and between #6-7).

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INTERPRETATION: The rhythm in Figure-1 is irregular in a pattern of group beating (with short pauses between beats #2-3 and #6-7). The QRS complex is narrow (ie, not more than half a large box in duration). The underlying rhythm appears to be sinus, with similar-looking P waves showing a fixed PR interval preceding beats #1, 2, 3, 4, 5, 6, 8, and 9 in this right-sided Lead MCL-1 rhythm strip.

• Despite the presence of group beating — there is no evidence of Wenckebach or other form of AV block on this tracing.  Instead, the "cause" of the pause lies within the T waves of beats #2 and 6.

The Most Common Cause of a Pause: 

Although most premature supraventricular beats (PACs or PJCs) are conducted normally to the ventricles (ie, with a narrow QRS complex) — this is not always the case.  Instead, PACs (or PJCs) may sometimes occur so early in the cycle as to be "blocked" (non-conducted) — because the conduction system is still in an absolute refractory state.

• This is the situation for premature impulse A in schematic Figure-2 (which shows A occurring during the ARP = Absolute Refractory Period).

Figure-2: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

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• At other times — premature (early) beats may occur during the RRP (Relative Refractory Period) — in which case aberrantconduction (with a wide and different-looking QRS) occurs.  This is the situation for premature impulse B in Figure 2.  Because impulse B occurs during the RRP — part (but not all) of the ventricular conduction system has recovered. Most often PACs occurring at Point B will conduct with some form of bundle branch block and/or hemiblock (reflecting that part of the conduction system which has not yet recovered).

• Premature impulse C in Figure 2 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).

KEY Clinical Point: 

The most common cause of a pause is a blocked PAC (corresponding to a PAC occurring at Point A in Figure 2). Blocked PACs occur much more often than any form of AV block.

• Blocked PACs are often subtle and difficult to detect. That said — they will be found IF looked for (they'll often be hiding/notching a part of the preceding T wave).

Returning to the Questions in this Case: 

We illustrate our Answers in Figure 3:

• The cause of the pause in this case is a blocked PAC (arrow in the T wave of beat #6 highlights the "telltale notching" of a PAC buried in this T wave).  A similar very early-occurring PAC (corresponding to a PAC at point B in Figure 2 can be seen notching the T wave of beat #2).
• The occurrence of a PAC resets the sinus cycle, usually with a brief pause after the early beat. The reason the PR interval preceding beat #7 is shorter - is that beat #7 is a junctional escape beat that occurs just before before the P wave that precedes it is able to conduct to the ventricles. Normal sinus rhythm then resumes with beat #8.
• Finally - is the subtle finding that the escape interval preceding beat #3 (ie, the distance between beats #2-3) is slight longer than the distance between beats #6-7. This accounts for why beat #3 is sinus-conducted (with a normal PR interval) — whereas slightly earlier occurring beat #7 is a junctional escape beat (that occurs just before the P wave preceding it is able to conduct to the ventricles).

Figure-3: Answer to Figure-1.

BOTTOM Line: 

The commonest cause of a pause is a blocked PAC. Remembering this truism will hopefully remind you to always look carefully in the T wave at the onset of all pauses to see if the "telltale" notching of a blocked PAC is in hiding. 

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From ECG Blog #57

https://ecg-interpretation.blogspot.com/2012/12/ecg-interpretation-review-57-mobitz-i.html

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Interpret the lead MCL-1 rhythm strip shown in Figure 1.

• Does this rhythm represent Mobitz I (Wenckebach) or Mobitz II AV block?
• Is a pacemaker likely to be needed? 

Figure 1: Lead MCL-1 rhythm strip. Is this Mobitz I or Mobitz II? 

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INTERPRETATION:  Neither Mobitz I nor Mobitz II is present. Rather than AV block – the rhythm in Figure 1 is an insightful example of the “mischief” that blocked PACs (Premature Atrial Contractions) can cause, especially when PACs are frequent.

     We have previously reviewed the basics of the 2nd degree AV blocks (See ECG Blog #19 – Blog #20 – Blog #21 – and Blog #22). Essential to the diagnosis that some type of AV block is present are 2 ECG findings:

• Finding #1: A consistent underlying atrial rhythm (usually sinus) – which is established by similar morphology of P waves on the tracing. Occasional PACs or junctional beats may be seen – but constantly changing P wave morphology is much more suggestive of other phenomena (wandering pacemaker; sinus pauses or arrest; multifocal atrial tachycardia) than of “AV block”.
• Finding #2: A regular (or at least fairly regular) atrial rhythm should be seen when some form of AV block is present. Clearly – there may be underlying sinus arrhythmia. In addition – slight variation in regularity of the underlying sinus rhythm may be the result of the AV block itself (known as “ventriculophasic sinus arrhythmia”) – in which the P‑P interval tends to shorten for P waves that sandwich a QRS complex (thought to be due to transiently increased perfusion immediately following ventricular contraction). However, gross variation in the P‑P interval is usually not seen when the primary problem is AV block.

WHY FIGURE 1 is Not AV BLOCK: AV block is not present in Figure 1 – because the above 2 ECG findings are absent. This becomes obvious in Figure 2, in which red arrows highlight each P wave:

Figure 2: Red arrows highlight each P wave in Figure 1.

• P wave morphology changes in Figure 1 (and in Figure 2). Sinus P waves are seen as a biphasic (small pointed positive followed by rounded negative) deflection preceding beats #1, 2, 3, 4, 5 and 6. In contrast – P waves buried within the ST-T wave of beats #1-thru-6 are triphasic (small negative-then positive-then narrow negative) deflections that clearly look different in morphology than the sinus P waves. These triphasic-deflection P waves arise from an atrial site other than the sinus node.
• Red arrows in Figure 2 make it obvious that the P-P interval varies. In fact there is a pattern to this P‑P variation (alternating short-long cycles) produced by the fact that every-other-P wave is early (premature). The underlying rhythm is atrial bigeminy (every other beat is a PAC).

PEARL: The Commonest Cause of a Pause is a Blocked PAC

     We introduced the concept of “blocked” PACs in ECG Blog #14. Depending at what point within the refractory period a premature beat occurs – a PAC may conduct: i) Normally; ii) With aberrant conduction (if part of the ventricular conduction system is still refractory); or iii) The PAC may occur so early as to fall within the absolute refractory period when no conduction is possible. This is what is occurring in Figure 2 – in which every-other-P-wave is blocked (non-conducted)!

• The commonest cause of a pause is a blocked PAC!  Blocked PACs are far more common than any form of heart block. Although sometimes subtle – blocked PACs can be identified if looked for. Close inspection of T waves at the beginning of a relative pause will usually reveal a notch or other small deformity not evident in the T waves of normally conducted sinus beats.

BEYOND-the-CORE: What is Happening with Beat #7?

     Unlike the PACs occurring within the T waves of beats #1-thru-5 (which are non-conducted) – the PAC that notches the T wave of beat #6 is conducted (ie, beat #7)!

• The reason for QRS widening and the different QRS morphology of beat #7 – is that this PAC conducts with LBBB (Left Bundle Branch Block) aberration. It presumably occurs during the RRP (Relative Refractory Period) – as illustrated in Figure 2 of ECG Blog #14.
• The reason for the longer-than-anticipated PR interval preceding beat #7 – is that the PAC that occurs within the T wave of beat #6 encounters a still partially refractory AV node, resulting in delay of conduction to the ventricles.

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BOTTOM LINE: The commonest cause of a pause is a blocked PAC. Remembering to think of this truism whenever you assess a tracing for possible AV block will prove invaluable in uncovering the real reason for the rhythm disturbance in a surprising number of cases. Blocked PACs occur far more often than any form of AV block.

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COPY of Blog #502 (Video) - Wellens' Syndrome?- COPY

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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 being awakened by very severe CP that morning.

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 being 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:

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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).
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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.
• ECG Blog #350 — another case of Wellens' Syndrome.
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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).

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ADDENDUM (10/XXX/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-3 — 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-3:

• 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-3: 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-4 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose ECGs are shown in Figure-4 — 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-4 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-4). 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-4: 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-3 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.
• Finally, a word about the 2 ECG Patterns in Figure-3. 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 the example in Figure-3 — Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. Deep, symmetric T wave inversion per se is seen in a number of other conditions, and is 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.

 

COPY of ECG Blog #500 — Can You Solve this CASE?- EXTRA

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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 he/she 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 may 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.

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!

=================================

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 slight 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 this truism holds the key for determining which of the 2 remaining beats (#7 or #8) is sinus-conducted.

I illustrate this concept in Figure-4 — in which I show my measurements of 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.). This tells us that beat #7 is sinus-conducted — whereas beat #8 (which manifests a slightly shorter PR interval) is another junctional escape beat.

I illustrate the above findings schematically in Figure-5 — in which RED arrow P waves indicate 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 normally conducted to the ventricles.

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

=================================

Laddergram Illustration:

For clarity of the above relationships — I add in Figure-6 my proposed laddergrams for today's tracing:

• XXXX

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

XXXXXXXXX

So the reason that the P-P interval is not as regular as a "normal sinus rhythm" would be — is that we have sinus bradycardia and arrhythmia. Clinically — your patient is on 2 medications (ß-block and verapamil or diltiazem) that may each cause sinus brady and arrhythmia. Since your patient is 70 years old — we need to assess for SSS ( = Sick Sinus Syndrome) — but in order to diagnose SSS — we need to RULE OUT that the brady rhythm is being causes by rate-slowing medications — so we need to see the effect of tapering and stopping these to meds. You can only diagnose SSS after you rule out potentially other "fixable" causes of bradycardia — so rule out recent ischemia/infarction — hypothyroidism — sleep apnea — electrolyte disturbance — and rate-slowing medication. And if this degree of symptomatic bradycardia (Your patient is having syncopal episodes) — then a permanent pacemaker is needed. But it is possible that if you stop ß-blockers and Ca-blockers — that he will resume having a normal heart rate.

Now the "incubation period" for SSS is often very long (up to a decade or more! ) — and your patient might have subtle (preclinical) SSS that is being exacerbated by the drugs. So we would just have to see what happens when the drugs are slowly withdrawn (whether this may or may not be safe to do as an out-patient vs as an in-patient).

So the above is the clinical part of this case. The rhythm is VERY interesting — and a GREAT teaching case! 

To facilitate seeing the P waves — My Figure-5 magnifies leads I and II (the 2 lines here are continuous — as I broke them up to be able to magnify what we are looking at). Once you know where the P waves are — We can measure the preceding R-R intervals — which I have done in milliseconds. We know beats #1,2,3,4,9 and 10 are not conducted — because the P wave does not occur at a point where it can possibly conduct. Note that the R-R interval preceding all of these beats (except beat #9) by the identical preceding R-R interval of 1480 msec. — so this is the R-R interval of junctional escape beats. The R-R preceding beat #9 is close to this (1460 msec.) — and you can have slight variation in the junctional escape rate — but beat #7 is sinus-conducted (as the preceding R-R is less = 1430 msec. and the PR interval is longer than for all other beats except for the PR interval before beat #6.

But in my Figure-7 (which is the laddergram) — We can see that the reason the PR interval preceding beat #6 is longer than the PR interval before beat #7 is that junctional escape beat #5 exerts some degree of retrograde conduction, which delays sinus-conducted beat #6 a little (thereby resulting in a slightly longer PR interval by "concealed" conduction). 

BOTTOM LINE — The this rhythm is marked sinus bradycardia and arrhythmia — with resultant appropriate junctional escape. This is an "escape-capture" rhythm (with beats #6 and 7 being "captured" sinus conduction). And again — given symptoms of syncopal episodes — if discontinuing the ß-blocker and Ca-blocker does not result in normalization of the rate — then the patient will need a pacemaker.

XXXXXXXXX

=======================

abdallah sbai sassi <dr.abdallahsbaisassi@gmail.com>

Thanks for your insights regarding this EKG. Of course, you can use it for your blog — it would be my pleasure. My full name is Abdallah Sbai Sassi, from Rabat, Morocco — thank u again for your time.

Non-dihydropyridine (non-DHP) calcium channel blockers, specifically verapamil and diltiazem, are the primary calcium blockers that cause bradycardia by slowing the heart rate. While some dihydropyridine CCBs like amlodipine have been linked to bradycardia in rare cases, they are more often associated with reflex sinus tachycardia because they are more vascular-selective than dihydropyridines.

MY REPLY:

The reason this case is so challenging — is that the P waves are tiny. But if you use all 12 leads (as I show here in my Figure-2) — you can figure out where all of the P waves are (ie, the BLUE vertical lines show that in leads V3,V4 — there are in fact P waves in lead II at this precise moment). So if you look at lead II in this figure — you can see there is a fairly regular atrial rate — except for the early beat #6 (which as you correctly say is a "capture" beat = that is sinus-conducted).

So the reason that the P-P interval is not as regular as a "normal sinus rhythm" would be — is that we have sinus bradycardia and arrhythmia. Clinically — your patient is on 2 medications (ß-block and verapamil or diltiazem) that may each cause sinus brady and arrhythmia. Since your patient is 70 years old — we need to assess for SSS ( = Sick Sinus Syndrome) — but in order to diagnose SSS — we need to RULE OUT that the brady rhythm is being causes by rate-slowing medications — so we need to see the effect of tapering and stopping these to meds. You can only diagnose SSS after you rule out potentially other "fixable" causes of bradycardia — so rule out recent ischemia/infarction — hypothyroidism — sleep apnea — electrolyte disturbance — and rate-slowing medication. And if this degree of symptomatic bradycardia (Your patient is having syncopal episodes) — then a permanent pacemaker is needed. But it is possible that if you stop ß-blockers and Ca-blockers — that he will resume having a normal heart rate.

Now the "incubation period" for SSS is often very long (up to a decade or more! ) — and your patient might have subtle (preclinical) SSS that is being exacerbated by the drugs. So we would just have to see what happens when the drugs are slowly withdrawn (whether this may or may not be safe to do as an out-patient vs as an in-patient).

So the above is the clinical part of this case. The rhythm is VERY interesting — and a GREAT teaching case! 

To facilitate seeing the P waves — My Figure-5 magnifies leads I and II (the 2 lines here are continuous — as I broke them up to be able to magnify what we are looking at). Once you know where the P waves are — We can measure the preceding R-R intervals — which I have done in milliseconds. We know beats #1,2,3,4,9 and 10 are not conducted — because the P wave does not occur at a point where it can possibly conduct. Note that the R-R interval preceding all of these beats (except beat #9) by the identical preceding R-R interval of 1480 msec. — so this is the R-R interval of junctional escape beats. The R-R preceding beat #9 is close to this (1460 msec.) — and you can have slight variation in the junctional escape rate — but beat #7 is sinus-conducted (as the preceding R-R is less = 1430 msec. and the PR interval is longer than for all other beats except for the PR interval before beat #6.

But in my Figure-7 (which is the laddergram) — We can see that the reason the PR interval preceding beat #6 is longer than the PR interval before beat #7 is that junctional escape beat #5 exerts some degree of retrograde conduction, which delays sinus-conducted beat #6 a little (thereby resulting in a slightly longer PR interval by "concealed" conduction). 

BOTTOM LINE — The this rhythm is marked sinus bradycardia and arrhythmia — with resultant appropriate junctional escape. This is an "escape-capture" rhythm (with beats #6 and 7 being "captured" sinus conduction). And again — given symptoms of syncopal episodes — if discontinuing the ß-blocker and Ca-blocker does not result in normalization of the rate — then the patient will need a pacemaker.

==================================

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

==================================

 

==============================

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 rhythm).

—  —

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).