Sunday, May 10, 2015

ECG Blog #111 (Addendum to ECG Video-9) - How to Distinguish between Escape vs Conduction?

NOTE: This is an advanced ECG post that supplements my ECG Video-9. The essential concepts to master were presented in the Video. But for those who want more — this post looks closer at how to tell which beats in a tracing with 2nd-dgree (but not complete) AV block are likely to be conducted vs which beats represent a non-conducting escape focus. Spoiler Alert: What follows assumes you have already seen our ECG Video-9. We start with the Answer to that case — and then explore in more detail how we got there ...
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In ECG Blog #110 ( = ECG Video-9) We presented the case of a 75-year old woman with syncope and dyspnea who presented to the ED (Emergency Department) with the simultaneously-recorded 3-lead rhythm strip shown in Figure-1. Although health care providers on the scene initially diagnosed this rhythm as complete AV block — there is ample evidence against this diagnosis!
  • QUESTION: Can you think of at least 3 reasons why we know that beats #1-thru-5 represent an escape focus, and — that beats #6-thru-9 in Figure-1 are being conducted?
Figure-1: Simultaneously-recorded 3-lead rhythm strip from a 75-year old woman with syncope. Red arrows in lead II highlight regular atrial activity. Although there is AV dissociation early on — this rhythm is not complete AV block. Can you think of at least 3 reasons why we know that beats #1-thru-5 represent an escape focus, and  that beats #6-thru-9 are being conducted? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
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ANSWER: The KEY to interpreting this rhythm strip (and to developing the complex laddergram that we work through in ECG Video-9) — lies with recognizing that the QRS complexes for beats #1-thru-5 represent a ventricular escape focus. To arrive at this conclusion — We approach this arrhythmia in the same way we approach any complex rhythm = Begin with what you know!
  • NOTE: Use of calipers is of invaluable assistance for interpreting this rhythm strip! To facilitate discussion — We substitute Figure-2 for Figure-1, in which we add in our caliper measurements of critical intervals.
Figure-2: Our caliper measurements of key intervals have been added. How do these numbers support our contention that beats #1-thru-5 represent an escape focus? (See text).
Why then do we say that beats #1-thru-5 represent a ventricular escape focus?
  • Starting with what we know the constant PR interval (of 195 msec.) for the last 4 beats on this tracing confirms sinus conduction. It should be emphasized that there is 2:1 AV block during these last 4 beats — but the fact that the previously variable PR interval suddenly becomes constant ( = 0.195 second) tells us beyond doubt that sinus conduction is at least intermittently occurring.
  • Note that the QRS complex manifests an rS configuration in lead V1 (small initial positive r wave; deep negative S wave) for these 4 sinus-conducted beats. In contrast — each of the preceding 5 beats manifest a multiphasic (rsR’s’) complex in lead V1. Since there is no apparent reason for aberrant conduction during beats #1-thru-5 (since the ventricular rate isn’t overly fast) — the most logical reason for this change in QRS morphology is the presence of an escape focus for beats #1-thru-5 (especially since QRS morphology changes beginning with beat #6, which is the first of 4 consecutive beats to conduct with the constant PR interval of 195 msec.).
  • Finally — the R-R interval shortens prior to beat #6. In our experience, in the presence of AV dissociation — one of the most helpful clues that intermittent conduction is occurring — is recognition of unexpected shortening in the R-R interval. This is admittedly subtle in Figure-2. Nevertheless, preceding R-R intervals for the first 5 beats on the tracing are between 1.22-to-1.24 second — whereas the R-R interval preceding the change in QRS morphology (that begins with beat #6) = 1.20 second. Additional slight shortening of the R-R interval is seen preceding the next 3 sinus-conducted beats. Admittedly, underlying subtle variation in the rate of both the escape rhythm and the sinus rate complicate assessment of R-R interval duration — but the fact that all sinus-conducted beats (#6-thru-9) manifest a shorter R-R interval than all non-conducted beats clearly supports our contention that beats #1-thru-5 represent an escape focus.
  • We surmise that the escape focus is below the AV node — because QRS morphology of beats #1-thru-5 significantly differs from QRS morphology for the 4 conducted beats (#6-thru-9). That said — the fact that QRS duration of these 5 escape beats (#1-thru-5) is no more than minimally widened suggests that the site of escape is still within the conduction system — probably within the bundle branch sysem.
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CONCLUSION: Full discussion of this case (with illustrative laddergram) is presented in our ECG Video-9. While recognition of all subtleties described above is clearly not needed to correctly interpret this rhythm — Our hope is that these more advanced concepts provide additional insight for optimal assessment of the AV blocks.
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  • NOTE: For full review on the Basics of AV Blocks  Please check out our 58-minute ECG Video-8 .
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Acknowledgment — My appreciation to the following individual:
  • Dr. Jenda Stros (Liberec, Czech Republic) — for providing me with the case for my ECG Blogs #110, 111, and for  Video-Blog #9.
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Thursday, May 7, 2015

ECG Blog #110 (ECG Video-Blog-9) - Is AV Block Complete? / Laddergram Primer

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     This is the 9th installment of my ECG Video Blog. This 23-minute video features a case for distinguishing between Complete AV Block vs AV Dissociation. Our discussion features how to draw the laddergram for this case. Your Feedback is welcome on these ECG Video-Blogs!
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NOTE: There are advantages to using a video format format. These include:
  • Ability to illustrate concepts not done full justice by the written word.
  • Greater dispersion of my content through Google & YouTube. This material is free for anyone to use.
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LINKS to my ECG Video-Blog installments:
  • ECG Video-Blog #1-Revised (= Blog #95) — Is there AV Block?
  • ECG Video-Blog #2 (= Blog #96) — Bundle Branch Blocks
  • ECG Video-Blog #3 (Blog #97— SVT with marked ST Depression
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  • ECG Video-Blog #4 (= Blog #98) — Clinical Arrhythmia Mgmt (Part I )
  • ECG Video-Blog #5 (Blog #99) — Clinical Arrhythmia Mgmt (Part 2 )
  • ECG Video-Blog #6 (Blog #100) — Clinical Arrhythmia Mgmt (Part 3 )
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  • ECG Video-Blog #7 (= Blog #101) — Wide Tachycardia + Chest Pain
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  • ECG Video-Blog #8 ( = Blog #105) — Basics of AV Block
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  •    ECG Video-Blog #9 ( = Blog #110) — Complete AV Block? / Laddergrams
  •     Addendum to Video-9 ( ECG Blog #111) — Review of Key Concepts
  •     Click Here for Timed Contents to Video-Blog #9!
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    Acknowledgment — My appreciation to the following individual:
    • Dr. Jenda Stros (Liberec, Czech Republic) — for providing me with the case for ECG Video-Blog #9.
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    The patient is a 75-year old woman who presented to the Emergency Department with syncope and shortness of breath. A diagnosis of Complete (3rd-Degree) AV Block was made from the ECG shown in Figure-1. The patient was hemodynamically stable at the time this tracing was recorded.
    • Is the rhythm in Figure-1 complete AV Block?
    • Explain your answer ...
    Figure-1: Simultaneously-recorded 3-lead rhythm strip obtained from a 75 year old woman with syncope and shortness of breath. Is this complete AV Block? Explain WHY this is (or might not be) complete AV Block. NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
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    GT– https://youtu.be/WJWotBhmirM  on YouTube to view this ECG Video (23 minutes).
    • Click Here  — for a Timed CONTENTS of Video-Blog #9.
    • Please check out our ECG Blog-111 for an Addendum to ECG Video #9.
    • Please also check out my ECG Video Blog page on Google. The link is easy to remember = www.videoecg.com -
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    NOTE: For a Power Point Show (.ppsx) version of my Video Blogs - CLICK HERE. This folder will contain links to download a .ppsx version that allows faster viewing:
      • Download the .ppsx to your computer desktop.
      • The PPT show is without automatic sound. YOU activate only the Audio clips you want.
      • Hover your mouse over the highlighted Audio. You may play and/or pause if/as you like.
      • Feel free to use this .ppsx for teaching with my blessings!
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      Sunday, April 19, 2015

      ECG Blog #109 (Interesting Tachycardia - Video)

      As a novel concept — I thought I would post this short (1.5 minute) video I edited from material provided to me by Alex Kroeze. The patient was hemodynamically stable
      Figure-1: Freeze-frame of the interesting SVT rhythm in this video. See YouTube link for additional monitoring. NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
      MORAL of this Video: — that artifact unfortunately often precludes accurate determination of atrial activity (therefore disguising the mechanism of tachycardias such as this one ...).
      • PACs seem to occur at the onset of the SVT (SupraVentricular Tachycardia) runs — but underlying artifact makes discerning what happens a bit elusive ...
      That said — fun to look at (to the music of Vivaldi's 4 Seasons).


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      ACKNOWLEDGMENT: My appreciation goes to Alex Kroeze for allowing me to edit and post his tracings.
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      Saturday, April 11, 2015

      ECG Blog #108 (Ventricular Rhythms - AIVR - VT)

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      NOTE: This is the "short version" of my ECG Blog #107 — in that I only address the 3-lead rhythm strip shown below (which was Figure-3 in Blog #107)
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      The simultaneously-recorded 3-lead rhythm strip shown in the Figure was obtained from a 69-year old woman with a longterm history of palpitations. Her symptoms had been increasing over recent weeks, in association with "chest tightness" and dizziness. Her prior medical history was benign  and she was hemodynamically stable at the time this tracing was recorded.
      • How would you interpret the rhythm shown in the Figure?
      • What are clinical implications of this rhythm
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      Figure: Simultaneously-recorded 3-lead Rhythm Strip, obtained from a 69-year old woman with palpitations. She was hemodynamically stable at the time of this tracing. What is the rhythm? What clinical implications are associated with this rhythm? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
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      InterpretationThe rhythm is fairly regular — albeit with slight variation in rate.
      • The QRS complex is wide (at least 3 little boxes = ≥0.12 second in duration).
      • Normal sinus P waves are missing in lead II. Instead, there are retrograde (negative) P waves that are clearly seen to occur after the QRS in lead II (red arrows).
      • The rhythm is AIVR (Accelerated IdioVentricular Rhythm) — which is a slower form of ventricular tachycardia.
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      Discussion: AIVR is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate (which is ~20-40/minute— and slower than hemodynamically significant Ventricular Tachycardia (ie, VT at rates >130-140/minute).
      • The usual rate of AIVR is therefore between ~60-110/minute (with an area of "overlap" between AIVR and fast VT at ~110-130/minute).
      • AIVR generally occurs in one of the following clinical settingsi) as a rhythm during cardiac arrest; ii) in the monitoring phase of acute MI (especially with inferior MI); or iii) as a reperfusion arrhythmia (following thrombolysis, acute angioplasty, or spontaneous reperfusion). It may also occur in patients with underlying coronary disease, cardiomyopathy, with digoxin toxicity — and rarely in otherwise healthy subjects without underlying heart disease.
      • AIVR is often an "escape rhythm" — in that it arises because both the SA and AV nodes are not functioning. IF treatment is needed (because loss of the atrial "kick" results in hypotension) — Atropine is the drug of choice (in hope of speeding up the SA node to resume its pacemaking function). AIVR should not be shocked nor treated with antiarrhythmic medication such as Amiodarone/Procainamide — since doing so might result in asystole ...
      We do NOT know why the patient in this case presented with runs of AIVR (possibly for a period of years ... ). Recent or remote ischemia/infarction and cardiomyopathy should be ruled out. The possibility of SSS (Sick Sinus Syndrome) — with emergence of AIVR as an escape rhythm should also be considered as part of the work-up. Unfortunately — We have no follow-up ...

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      ACKNOWLEDGMENT: My appreciation goes to Sam Walker (from Auckland, New Zealand) for allowing me to use this case and these tracings. 
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      - For more information  GO TO:
      • For a review pdf of basic Rhythm Interpretation ( = Section 02.0 from my ECG-2014-ePub) — GO TO http://tinyurl.com/ECG-2-Rhythm — AIVR is reviewed in Section 02.38.
      • For full review of additional more complex tracings obtained on this patient — Please see our ECG Blog #107.
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      Monday, April 6, 2015

      ECG Blog #107 (PVCs - Couplets - Echo Beats - AIVR - Retrograde Conduction)

      The tracings shown in Figure-1, Figure-2, and Figure-3 — were obtained in short succession from a 69-year old woman with a history of intermittent, brief duration palpitations over the past few years. Palpitations had been increasing over the past 2 weeks. On the day of admission, she developed chest tightness with "dizziness". On hearing this story and noting the irregularity in her rhythm  her primary care physician referred the patient for admission to the hospital.
      • Past Medical History — fairly benign. No significant cardiac history. NO medications!
      • NOTE: At no time during transport to the hospital was the patient unstable. That said, her BP decreased from 130/75 mmHg to 105 mmHg systolic at the time the rhythm strip in Figure-3 was recorded.
      How would you interpret this series of tracings?
      • Is there evidence of atrial activity? If so — Is there any normal atrial activity?
      • Can you explain the reason for the change in rhythm seen in Figure-1 compared to the rhythm seen in Figure-3?
      • Can you explain why her BP decreased at the time the rhythm in Figure-3 was recorded?
      • Does the patient's 12-lead ECG explain the longterm history of palpitations?
      • Clinically — How would you proceed? Is immediate treatment indicated?
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      Figure-1: Initial 3-lead Rhythm Strip, obtained from a 69-year old woman with a longterm history of palpitations. She was hemodynamically stable at the time of this tracing. What is the rhythm? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
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      Figure-2: 12-lead ECG obtained shortly after the rhythm strip in Figure-1 was recorded. Is there evidence of normal atrial activity? Does this 12-lead ECG explain the reason for this patient's longterm palpitations?
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      Figure-3: Subsequent 3-lead Rhythm Strip. Of note, the patient's BP decreased from 130/75 mmHg to 105 mmHg systolic at the time this tracing was recorded. What might explain this decrease in blood pressure?
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      MY Interpretation and ANSWERS to this Case:
      • NOTE: My colleagues on the EKG Club are still actively debating the mechanism of this arrhythmia. As the esteemed cardiologist Rosenbaum once said, "Every self-respecting arrhythmia has at least 3 possible interpretations". BELOW is "My Take" on the mechanism and the most important teaching points to take away from this interesting case: 
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      The "SHORT" Answer: We see no evidence of sinus rhythm — since an upright conducting P wave is never seen in lead II on any of these 3 tracings. Regardless of whether one postulates an ectopic low atrial rhythm (negative conducting P waves are intermittently seen in lead II vs a complex mechanism of retrograde atrial conduction from ventricular beats that intermittently capture the ventricles (via echo beats— there is an absence of normal sinus P wave conduction.
      • There are frequent ventricular beats occurring at a relatively slow rate. These occur in couplets in Figure-4 (beats #2,3; 5,6; 8,9; and 11,12). In Figure-3 — they occurred as a run of AIVR (Accelerated IdioVentricular Rhythm), as we'll discuss more in Figure-6.
      • So the "SHORT Answer"  — is that this previously thought-to-be healthy 69-year old woman has been having runs of AIVR for no apparent reason. Given her history of palpitations over a period of years — for all we know, she may have intermittently been having this arrhythmia over that period of time ... 
      Figure-4: I have labeled Figure-1. RED arrows indicate negative P waves in lead II. Beats #1,4,7,10 and 13 are narrow and are supraventricular. Pairs of ventricular beats are seen for beats #2,3; 5,6; 8,9; and 11,12 (See text).
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      Completion of the "SHORT" Answer: AIVR is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate (which is ~20-40/minute— and slower than hemodynamically significant Ventricular Tachycardia (ie, VT at rates >130-140/minute).
      • The usual rate of AIVR is therefore between ~60-110/minute (with an area of "overlap" between AIVR and fast VT at ~120-130/minute).
      • AIVR generally occurs in one of the following clinical settings: i) as a rhythm during cardiac arrest; ii) in the monitoring phase of acute MI (especially with inferior MI); or iii) as a reperfusion arrhythmia (following thrombolytics, angioplasty, or spontaneous reperfusion). It may also occur in patients with underlying coronary disease, cardiomyopathy, with digoxin toxicity — and rarely in otherwise healthy subjects without underlying heart disease.
      • AIVR is often an "escape rhythm" — in that it arises because both the SA and AV nodes are not functioning. IF treatment is needed (because loss of the atrial "kick" results in hypotension) — Atropine is the drug of choice (in hope of speeding up the SA node to resume its pacemaking function). AIVR should not be shocked nor treated with Amiodarone/Procainamide — since doing so might result in asystole ...
      • We do NOT know why the patient in this case presented with runs of AIVR (possibly for a period of years ... ). Recent or remote ischemia/infarction and cardiomyopathy should be ruled out. The possibility of SSS (Sick Sinus Syndrome) — with emergence of AIVR as an escape rhythm should also be considered. We can only speculate on potential management if this 69-year old woman turns out to have no underlying cardiac disease and her bouts of AIVR continue ...
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      TIME for the FASCINATING ANSWER: Despite seeming regularity of the negative P waves in lead II of Figure-4 (red arrows— We do not think this represents an ectopic low atrial rhythm. This is because in Figure-3 there is 1:1 V:A ( = retrograde) conduction (See Figure-7 belowand, morphology of the negative P waves in Figure-3 is identical to P wave morphology in Figure-4. Therefore it is most likely that all negative P waves in lead II are retrograde! 
      • The Laddergram in Figure-5 illustrates the mechanism we propose. Just like forward-conducting reentry SVT (SupraVentricular Tachycardia) rhythms have option to conduct down either the "fast" or "slow" AV nodal pathway — ventricular beats that conduct retrograde have similar option to utilize either the "fast" or "slow" pathway when they conduct back to the atria. Most of the time such retrograde ventricular conduction utilizes the "fast" pathway.
      • In this case — We suspect retrograde conduction from ventricular beats #3,6,9 and 12 in Figure-5 are conducted back to the atria using the slow pathway! (red dotted lines in the laddergram). This is the most logical reason to explain the dramatic increase in retrograde RP' conduction between beats #2,5,8,11 vs the much longer RP' interval for beats #3,6,9 and 12.
      • Because of this slow retrograde conduction from beats #3,6,9 and 12 — there is time for the fast pathway to recover, which allows forward conduction of an "echo beat" to the ventricles (beats #4,7,10 and 13 in Figure-5).
      Figure-5: Laddergram depiction of the Lead II rhythm strip in Figure-4 . Of interest  the RP' interval is short for beats #2,5,8, and 11 — but increases markedly for beats #3,6,9 and 12. We suspect that the preceding shorter R-R interval (corresponding to an AIVR rate of ~100/minute) leads to refractoriness of the retrograde fast pathway — with resultant retrograde conduction over the unblocked slow pathway (dotted lines), producing a longer RP' interval and, thereby allowing enough time for echo beats to form (beats #4,7,10,13) that conduct to the ventricles (See text). NOTE: I revised this laddergram on 4/7/2015 in attempt to better reflect that the fast pathway is preferentially used for retrograde conduction for beats #2,5,8 and 11  and, that the reason the slow pathway (dotted lines) is used on alternate beats for retrograde conduction through the AV Node, is that the fast pathway is blocked on these alternate beats ...
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      There remains the question of WHY retrograde conduction from ventricular beats #3,6,9 and 12 in Figure-5 utilized the slow pathway — but uniformly uses the fast pathway for retrograde conduction for all of the beats in Figure-3 (shown below in Figure-6).
      • Note that the rate of AIVR in Figure-6 is slower (~85/minute) than it was for beats #3,6,9 and 12 in Figure-5 (where the shorter preceding R-R interval of ~600 msec corresponds to an AIVR rate of ~100/minute). Therefore — there is more time with this slower AIVR rate in Figure-6 for fast pathway recovery, allowing 1:1 V:A retrograde conduction in Figure-6 with a short RP' interval. 
      • You'll recall mention that the patient's BP decreased from 130/75 mmHg in Figure-5 — to 100 mmHg systolic in Figure-6. Perhaps this was because there is at least some "atrial kick" occurring in Figure-5 (albeit by non-sinus-initiated echo beats) — vs complete loss of the atrial kick in Figure-6, in which all beats originate from the ventricles.
      Figure-6: I have labeled Figure-3. RED arrows indicate retrograde atrial activity. At the slower AIVR rate seen here (~85/minute— there is enough time for the fast pathway to recover and allow 1:1 retrograde conduction with a short RP' interval.
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      FINALLY — There remains this patient's 12-lead ECG (reproduced below in Figure-7).
      Figure-7: I have labeled the 12-lead ECG that was shown in Figure-2. RED arrows indicate atrial activity in lead II. Note that the rhythm changes with beat #5 in lead aVF! (See text).
      There are several interesting features on this 12-lead:
      • The rhythm begins for beats #1-thru-4 as was illustrated on our laddergram in Figure-5. But then the rhythm changes with beat #5! Even though we do not have a simultaneously-recorded long lead II — We know the rhythm changes, because there is no negative P wave preceding beats #5 and 6 in lead aVF (green arrows). It is difficult to tell if there is any P wave at all preceding beats #5 and 6 — but we certainly do not see the negative P waves we saw earlier in lead aVF in Figure-4.
      • There may be a sinus P wave preceding QRS complexes in lead V1 (blue arrow with question mark). Against this theory is the very short PR interval .... but there certainly does appear to be an upright deflection preceding both QRS complexes seen in lead V1.
      • While not certain of the mechanism for narrow beats #5-thru-10 in Figure-7 — at least the rhythm is supraventricular and the runs of AIVR have at least temporarily stopped.
      • There may be a QS complex in lead III of this 12-lead tracing. That said — there is no Q wave in either lead II or lead aVF, so there is not clear evidence of prior infarction. ST-T wave changes of supraventricular beats show nonspecific ST-T wave flattening — but really no indication on this 12-lead ECG as to why this 69-year old woman was having persistent runs of AIVR ...
      Hopefully we will have a chance to get follow-up on this case ...

      • P.S. Now return to Figure-6 and measure with calipers the R-R interval for each beat in this rhythm strip. Note that there is subtle-but-real variation in the R-R interval! Thus, this patient's underlying AIVR rhythm shows variation in rate — which sets up conditions for the alternating differing availability for retrograde conduction in fast and slow pathways that we saw in the laddergram in Figure-5.

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      ACKNOWLEDGMENT: My appreciation goes to Sam Walker (from Auckland, New Zealand) for allowing me to use this case and these tracings. 
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      - For more information  GO TO:
      • For a review pdf of basic Rhythm Interpretation ( = Section 02.0 from my ECG-2014-ePub) — GO TO http://tinyurl.com/ECG-2-Rhythm — AIVR is reviewed in Section 02.38.
      • For review on How to Draw a Laddergram — Please checkout ECG Blog #69 
      • NOTE: For a simpler version of this blog post that just reviews the rhythm strip of AIVR — Please check out ECG Blog 108 
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