Wednesday, July 29, 2015

ECG BLOG #115 (Early Repolarization — Peaked T Waves — Anterior STEMI — DeWinter)

The 12-lead ECG shown in Figure-1 was obtained from a 50-year old man with chest discomfort.
  • How would you interpret this ECG?
  • Are the findings seen suggestive of Early Repolarization — or something else?
  • Clinically — What would you do?
Figure-1: 12-lead ECG obtained from a 50-year old man with chest discomfort. NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
ANSWERS: Assessment of the ECG shown in Figure-1 in view of the limited history provided (ie, a middle-aged man with chest discomfort) — is indeed a challenging task. Practically speaking — a definitive answer to the question of whether the ECG picture in Figure-1 represents a normal repolarization variant vs early anterior STEMI (ST Elevation Myocardial Infarction) is not forthcoming from interpretation of this single tracing.
Our Interpretation of Figure-1: The rhythm is sinus — with slight variability in rate (sinus arrhythmia). All intervals and the mean QRS axis are normal. Although QRS amplitudes are somewhat difficult to discern in some of the chest leads (due to overlap of complexes) — there does not appear to be ECG evidence for chamber enlargement (the R wave amplitude in V5 = 21mm + the 9mm S wave in V2 fall shy of the required 35mm threshold for LVH).
  • Superficial Assessment of Q-R-S-T Changes: There are no Q waves. Transition occurs normally between V3-to-V4. There is no more than minimal ST elevation in leads I and V2. All T waves are upright (except in aVR) — and there appears to be no obvious ST depression. The shape of the upsloping segment of T waves in leads V2-thru-V6 is concave up (ie, “smiley”-configuration).
  • More Discriminating Assessment of Q-R-S-T Changes: The patient is a 50-year old man with chest discomfort. This fact alone calls for far greater scrutiny in assessing Q-R-S-T changes than would be the case if the patient was asymptomatic. Although Q waves are absent and transition occurs normally between V3-to-V4 (since the R wave in V4 appears slightly taller than the S wave is deep) — r wave amplitude is decidedly reduced in V1,V2,V3. In this context — the T waves seen in leads V2,V3 appear to be disproportionately tall and peaked, with a rounder (fatter) T wave peak in V2 than should-be-expected given the relatively low amplitude rS complex in this lead. Closer scrutiny of the limb leads reveals that they are not completely “normal” as was initially suggested by superficial assessment. Instead, the ST segments in leads III and aVF appear flattened (despite the presence of upright T waves in these leads) — and the subtle-but-real 0.5mm J-point ST elevation in lead I might in fact be relevant.
BOTTOM LINE: All of these findings are extremely subtle. They may mean nothing. But in a 50-year old man with new chest discomfort — they could also be harbingers of an important acute event about to evolve …
  • KEY POINTS: It is OK not to be certain about the clinical significance of a single ECG. This happens often. Awareness that early on, an acute STEMI (especially when anterior in location) — may be difficult to recognize is essential. More discriminating ECG assessment is needed in such cases. Reduced anterior r wave amplitude with taller-than-expected anterior T waves (especially if peaked T waves look broader than-they-should-be) should prompt more careful assessment of limb leads for subtle abnormalities. The finding of a longer-than-expected (albeit not necessarily prolonged) QT interval would add support to the possibility of an acute event. But even if meticulous ECG assessment does not suggest clear abnormalities — a patient with potentially worrisome symptoms of new cardiac onset should not be sent home until the provider can attain a comfort level that nothing acute is evolving.
  • WHAT To DO: In addition to obtaining a more complete history and performing a careful physical exam — 3 interventions may be extremely helpful: i) Looking to see if prior ECGs are available for comparison (transmission from a distance being expedited if necessary by smart phone messaging); ii) Repeating the ECG as needed (since an acute evolving event may produce significant ECG changes in a surprisingly short period of time); and iii) Performing ECHO at the bedside (normal LV function in a patient with chest pain is reassuring — whereas localized wall motion abnormality suggests an acute event).
WHAT Happened: The ECG in Figure-2 was obtained just 8 minutes after the Figure-1 ECG. Is the diagnosis now more clear?
Figure-2: Follow-up ECG obtained 8 minutes after the ECG shown in Figure-1.
Interpretation of Figure-2: We doubt anyone would have predicted how emphatically the original ECG from Figure-1 has changed in as short a time period as 8 minutes!
  • Sinus rhythm persists in Figure-2. There is now dramatic (>5mm) ST elevation in leads V2,V3 — with a lesser (but still very significant) degree of ST elevation in leads I,aVL and V4,5,6. Increased T wave amplitude and peaking is evident in leads V2-thru-V6, with hyperacute ST-T waves in virtually all of the leads with ST elevation. Small-but-real q waves now appear to be present at least in leads I, aVL and V6. In addition — there is now marked reciprocal ST depression in leads III and aVF. The combination of findings are strongly suggestive of acute LAD (Left Anterior Descending coronary artery) occlusion.
Comparing the ECG picture of the original tracing (Figure-1) with the follow-up ECG obtained just 8 minutes later (Figure-2) — We note the following:
  • There are now small-but-real new lateral q waves. In addition — the rSR’ complex seen in leads V2,V3 (just before onset of the marked J-point ST elevation in these leads) — probably serves as a “Q-wave equivalent” given slight-but-real loss of r wave from V1-to-V2 and obvious large ongoing acute anterior infarction.
  • The subtle ST elevation in lead I and ST flattening in leads III,aVF from Figure-1 were indeed real findings that came before the obvious evolution of ST-T wave changes that are seen in these same leads in Figure-2.
  • Finally — Figure-2 adds support that the chest lead T wave peaking with disproportionately tall T waves (and fatter-than-expected T wave peak) in leads V1,V2 of Figure-1 was indeed a subtle harbinger of the dramatic ST-T wave changes that followed just 8 minutes later …
P.S. — While one may debate the pros and cons of routine high-sensitivity troponin assessment for all comers with chest discomfort — dependence on a first early troponin assay (with the term “early” referring to the time of the blood draw with respect to the time of symptom onset) — regardless of what the troponin result turns out to be (positive or negative) is unlikely to: i) Completely rule out the possibility of an early acute event (since early on, there may be false negatives … ); or ii) Be the deciding factor for determining whether or not the interventionist should perform immediate cardiac catheterization. Our bias is therefore that other factors (ie, clinical history and exam; initial and serial ECGs; stat Echo) are more important than the initial troponin value for determining whether a patient like the one in this case has an acute coronary occlusion likely to benefit from acute reperfusion therapy.
ACKNOWLEDGMENT: My thanks to Haris Skrbo (of Capjlina in Bosnia & Herzegovina) for allowing me to reproduce this tracing and clinical case.

Monday, July 27, 2015

ECG Blog #114 (Standard Recording — Cabrera Format — Recording Speed)

How would you interpret the 12-lead ECG in Figure-1? This tracing was obtained from a previously healthy middle-aged woman who presented with back pain over the previous month.
  • Does her ECG provide any clue to the etiology of her symptoms?
HINT: Can you explain why the QRS complex in lead aVR shows global positivity (ie, positive P wave, QRS complex and T wave)?
Figure-1: 12-lead ECG obtained from a middle-aged woman with back pain over the past month. NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
ANSWER: The ECG in Figure-1 provides no clue to the etiology of this patient’s symptoms. The reason the P wave, QRS complex and T wave are all positive in aVR, is that instead of the usual 12-lead format (that interpreters in the United States are accustomed to) — the Cabrera format has been used instead.
  • 12-lead ECGs that are recorded in the United States typically display simultaneous recording of 4 sets of 3 leads (leads I,II,III; aVR,aVL,aVF; V1,2,3; and V4,5,6). One or more long lead rhythm strips are typically displayed immediately below the 12-lead. In contrast — Note that a simultaneously-recorded long lead rhythm strip for each of the 12-leads is displayed in Figure-1 — and, that the vertical sequence used for the limb leads is markedly different from the usual format. That is, rather than lead I — the first lead displayed is lead aVL.
  • Note that a minus sign appears before the designation aVR (ie, -aVR). The reason for global positivity is that the polarity of lead aVR has been reversed. As a result — the mirror image picture (ie, global positivity rather than negativity) is displayed for –aVR.
Our Interpretation of Figure-1: Unfortunately, there is some distortion of this 12-lead tracing, arising from the fact that this figure represents a smart phone photograph rather than a flat scan of the ECG. In addition, there is some baseline drift movement; interference artifact (the thick, vertical geometric lines most prominently seen in lead V1, with finer baseline undulations perhaps due to muscle contraction in several other leads); and other motion or improper skin-electrode contact artifact (seen best at various points in the long lead V2 rhythm strip). That said — the overall quality of this tracing is sufficient for appropriate interpretation.
  • The rhythm is sinus at about 80/minute. The PR, QRS and QT intervals are normal. The axis is leftward, but not enough to qualify as LAHB (Left Anterior HemiBlock) — since the QRS complex in the long lead II is not consistently more negative than positive. There is no chamber enlargement.
  • Regarding Q-R-S-T Changes — a small q wave is seen in lead aVL; Transition may be slightly delayed (the R wave only becomes consistently more positive than the S wave is deep between V3-to-V5) — but there are no more than minimal nonspecific ST-T wave abnormalities (slight flattening in several leads) that do not at all appear acute. Thus, we find no explanation for this patient’s symptoms from her ECG that is shown in Figure-1.
The Cabrera Format:  Used in Other Countries
Electrocardiography has long been recognized as an essential diagnostic tool used across the world. While a similar display format (with no more than minor variation) is used for ECG recording throughout the United States — variations in format are used in many countries. Since many U.S. clinicians only rarely (if ever) see ECG recording formats that differ significantly from their own — these clinicians may fail to recognize other formats. Given the exponentially increasing use of the internet for international medical correspondence (with now literally scores of international Facebook ECG forums) — plus ever expanding daily use of smart phone photographs for rapid remote consultation with experts regarding problematic ECGs  the clinical reality is that virtually all clinicians will from time-to-time encounter ECG formats that differ from the format they are most accustomed to. This clinical reality is my purpose for presenting this ECG Blog post.
  • Illustration of the principal features of the Cabrera format is seen in Figure-2 — in which we highlight the vertical lead orientation (with blue and red rectangles) — and insert the Cabrera axis system in the upper righthand corner of the tracing. Note that vertical limb lead display begins with lead aVL — employs reversed polarity for aVR (within the blue rectangle) — and that each of the 6 limb leads are separated by the equal increment of 30 degrees in the frontal plane. Thus, lead –aVR is situated at a frontal plane angle corresponding to +30 degrees (in between lead I at 0 degrees and lead II at +60 degrees).
Figure-2: The 12-lead ECG from Figure-1 has been labeled, highlighting features of the Cabrera format. Note vertical limb lead sequencing begins with lead aVL — and that reversed polarity is used for aVR, with lead –aVR being situated in between leads I and II at +30 degrees (within the blue rectangle).
Although first description of the sequential limb lead format shown in Figure-2 was made by Fumagalli (in 1949) — development of this format is attributed to Cabrera. The Cabrera sequential lead system for ECG recording has been in general use in Sweden since 1977, with current use in several other countries. 
  • In many ways, the Cabrera format offers a much more logical display of limb lead sequencing. As opposed to the traditional U.S. format (in which limb leads are grouped into standard leads I,II,III and augmented leads aVR,L,F) — there is gradually progressive (equally spaced) sequencing with the Cabrera format from lead aVL (at -30 degrees) to lead III (at +120 degrees). 
  • Using the Cabrera format enhances the clinical utility of aVR by effectively adding lead –aVR as a transition lead between lateral and inferior frontal plane location. This allows greater specificity of the extent of high lateral and inferior ischemia or infarction. It also simplifies both axis and ST-T wave vector calculation in the frontal plane — since no more than a glance at the 6 sequential Cabrera leads is now needed for instant determination of which lead(s) manifests greatest net QRS and/or ST-T wave deflection. 
  • Finally, comparison with serial tracings in a given patient is easier — because sequential limb lead display makes serial variation in Q wave presence, QRS amplitude, and ST-T wave displacements much more evident as to what represents probable “real change” in patient status vs serial alteration in ECG waveforms primarily due to a difference in lead placement.
Despite the above potential advantages of more logical sequential lead placement — the Cabrera format seems unlikely to replace the non-sequential traditional U.S. format, at least for the immediate future. Old established habits are difficult to break ... — even when a newer approach seems technically easy to implement and clinically advantageous. 
  • As a result — it is important for clinicians to be aware that their particular system of lead system recording is not universally used across the globe.
P.S. Another variation in format to be aware of is the recording speed of the ECG. Whereas most of the world employs a standard recording speed of 25mm/second (which is the recording speed used in Figure-1) — some countries favor ECG recording at twice this speed ( = 50mm/second). Awareness of this variation is essential when interpreting tracings submitted from other parts of the world, especially since notation of the recording speed used may be unintentionally deleted from that part of the ECG within the photograph being sent. At double the recording speed (ie, 50mm/second) — the QRS complex appears twice as wide, and the R-R interval appears twice as long as these parameters appear when the recording speed is 25mm/second. In addition  ST-T wave appearance looks markedly different at twice the recording speed, such that familiar patterns of ST-T wave abnormalities may no longer be recognized ...
ACKNOWLEDGMENT: My thanks to Alexandru Radulian (of Bucharest, Romania) for allowing me to reproduce this tracing and use this clinical case.

Sunday, June 7, 2015

ECG Blog #113 (ECG Video-Blogs-10,11,12) - Rhythm Diagnosis-Basics (Parts I,II,III)

     This 3-part Video Series (under the umbrella of my ECG Blog #113) contains the 10th, 11th and 12th installments of my ECG Video Blog. My collective GOAL for this 3-part Series — is to address the Basics of ECG Rhythm Diagnosis, starting from the VERY beginning. My hope is that by doing so — clinicians desirous of a step-by-step approach could quickly learn to apply the essentials of Arrhythmia Diagnosis, even if they previously had little or no formal training in this area. Plenty of PEARLS for more advanced interpreters are sprinkled in along the way.
     This Video Series took me several hundred hours to make. I hope you enjoy the fruit of my efforts! For convenience — these are the Direct Links to these 3 YouTube Videos (and to a Link-Timed Contents for each of them):

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.
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
  • ------------------------------------------------------------
  • ECG Video-Blog #4 (= Blog #98) — Clinical Arrhythmia Mgmt (Part I )
  •    Please check out our Cardiac Arrhythmia page = - 
  •    Click Here for Timed Contents to Video-Blogs #4,5,6!
  • ECG Video-Blog #5 (Blog #99) — Clinical Arrhythmia Mgmt (Part 2 )
  • ECG Video-Blog #6 (Blog #100) — Clinical Arrhythmia Mgmt (Part 3 )
  • ------------------------------------------------------------
  • ECG Video-Blog #7 (= Blog #101) — Wide Tachycardia + Chest Pain
  • ECG Video-Blog #8 ( = Blog #105) — Basics of AV Block
  • ------------------------------------------------------------
  • ECG Video-Blog #9 ( = Blog #110) — Complete AV Block? / Laddergrams
  • ECG Video-Blogs #10,11,12 ( = Blog #113) — Rhythm Diagnosis Basics
  •    Click Here for a Link-Timed Contents to Video-Blogs #10,11,12!

     This 3-part Video Series addresses the Basics of ECG Rhythm Diagnosis, starting from the very beginning ... but also with plenty of PEARLS along the way for more experienced interpreters.
  • Below in Figure 1 — an example of some issues discussed. I believe this 3-part Video Series brings the topic to life!
Figure-1: Slide showing part of the discussion on ECG diagnosis of Atrial Flutter. NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
Direct Links to these YouTube Videos are the following:
  • ECG Video Blog-10 — Rhythm Basics: Part 1 (28 minutes)
  • ECG Video Blog-11 — Rhythm Basics: Part 2 (48 minutes)
  • ECG Video Blog-12 — Rhythm Basics: Part 3 (coming soon! )
  • Click Here  — for a Timed CONTENTS of Video-Blogs #10,11,12.
  • Please also check out my ECG Video Blog page on Google. The link is easy to remember = -
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!

    Saturday, May 23, 2015

    ECG Blog #112 (Sinus Rhythm – Lead II – Nonspecific ST-T Wave Abnormalities

    The ECG in Figure-1 was obtained from a 43-year old man who presented to his primary care clinician because he “wasn’t feeling well”. His symptoms suggested an influenza-like syndrome. The ECG was ordered because of some associated and atypical chest discomfort.
    • Are you concerned about the ST-T wave changes on this tracing?
    • Any other findings of note?
    Figure-1: 12-lead ECG and lead II rhythm strip obtained from a 43-year old man with influenza-like illness and atypical chest pain. Are you concerned about ST-T wave changes on this tracing? Other findings of note? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
    ANSWER: The reason we selected this tracing was not because of the ST-T wave changes. Instead, our focus was on the cardiac rhythm. If you did not appreciate anything unusual about the rhythm Take a 2nd look ... 
    The rhythm is fairly regular at a rate slightly less than 100/minute. There is no P wave visible in lead II. We say this based not only on the 3 beats shown for lead II within the 12-lead ECG, but also on complete lack of atrial activity on any of the 15 beats seen in the long lead II rhythm strip at the bottom of the tracing. Therefore — this is not a sinus rhythm.
    • Atrial activity is seen in several other limb leads. That is, small-but-definitely-present upright P waves with a fixed PR interval are seen preceding each QRS in leads I and aVL — and, a small negative P wave precedes each QRS in lead III. Thus, this is a low atrial rhythm.
    • Tiny upright P waves are also seen in lead V1 and V2. These would be easy to overlook were it not for the presence of definite atrial activity in leads I,III and aVL.
    Regarding the other findings on this tracing:
    Intervals: Both QRS duration and the QT interval are normal. Since the rhythm is not sinus — we cannot assess the PR interval (other than to say that it does not appear to be prolonged).
    • Axis: Normal (approximately +50 degrees).
    • Chamber Enlargement: None.
    • Q-R-S-T Changes: No consistent Q waves are seen. Transition may occur slightly early (the QRS complex is equiphasic by lead V2 — and definitely positive by lead V3). There is nonspecific ST-T wave flattening in multiple leads — but nothing that appears to be acute.
    IMPRESSION: As stated — the reason this ECG was obtained was the patient’s description of atypical chest discomfort. While ultimate decision-making depends on full clinical assessment of the patient — this ECG should be reassuring in that at least there are no acute changes. The presence of nonspecific ST-T wave abnormalities and a non-sinus (low atrial) rhythm are not pathologic per se — and may simply reflect that the patient was not feeling well with an influenza-like illness. Whether or not to repeat the ECG if the patient’s clinical course is otherwise uneventful — is a determination that can be decided in follow-up.
    KEY Point: Assuming there is no dextrocardia or lead misplacement — IF there is no upright P wave in lead II — then the rhythm is not sinus! For this reason, the very 1st Thing To Do when assessing any 12-lead ECG or rhythm strip — is to look at lead II to see if an upright P wave is (or is not) present. In our experience, failure to do so accounts for the main reason that non-sinus rhythms are sometimes overlooked ...
    • Although lead II is typically the best lead for visualizing P waves there are times when other leads may visualize atrial activity not seen in lead II. In general anatomic proximity of lead V1 (overlying the atria) makes this lead the 2nd-best for visualizing atrial activity. This is especially true when the rhythm is non-sinus. Leads III and aVR are other leads on a 12-lead tracing that often pick up non-sinus activity that might not be seen in lead II. Bottom Line: If no atrial activity is seen in lead II Be sure to survey each of the other 11 leads before concluding that no atrial activity is present.

    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 ...
    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.
    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.
    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.
    • NOTE: For full review on the Basics of AV Blocks  Please check out our 58-minute ECG Video-8 .
    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.