Friday, May 31, 2024

ECG Blog #432 — "Should I Shock this Patient?"

I was sent the ECG in Figure-1 — without the benefit of any history.
  • Is this VT?
  • What is the 1st thing — that YOU would do?

Figure-1: I was sent this ECG without any history. Is this VT?

MY Thoughts on Today’s CASE:
As tempting as it might be to reach for the defibrillator on seeing the ECG shown in Figure-1 — My initial reaction was different.
  • At 1st glance, my impression from seeing ECG #1 — was that the rhythm is very fast and irregular — with a highly variable QRS morphology — and, without atrial activity. These initial observations clearly suggested that the rhythm was either a coarse VFib (perhaps with the gain of the monitor turned way up) — or — PMVT (PolyMorphic Ventricular Tachycardia) vs Torsades de Pointes (depending on whether the baseline QTc was normal or wide). 

I then saw the additional deflections that I highlight
 in Figure-2 with RED arrows.
  • What to do next?

Figure-2: I've labeled the initial ECG in today's case.

The 1st Thing to Do . . . ?

RED arrows in Figure-2 highlight the surprisingly regular occurrence of what appears to be vertical lines that suggest possible QRS complexes ...
  • The 1st Thing to Do: — Check the patient! Is there a pulse?

The patient had a regular pulse and was stable. No shock was needed. RED arrows represent QRS complexes.
  • While true that there are some additional deflections in the limb leads that may be confused for QRS complexes (PINK arrows) — the perfect regularity of the deflections above the RED arrows in the chest leads is the "tip-off" that the rhythm in Figure-2 is not some form of PMVT — but rather artifact distortion.


Another Example:
I never learned about artifact in medical school. But considering that patients have been shocked for tracings resembling the ECG shown in Figure-1 — it may be worthwhile to present another example.
  • If you only looked at leads III, aVR, aVL and aVF — Wouldn't you think that the rhythm in Figure-3 was VFib?

  • PEARL #1: As I emphasize in ECG Blog #148 (from where I took the tracing I show in Figure-3) — the BEST way to prove artifact — is to recognize persistence of an underlying spontaneous rhythm that is unaffected by any erratic or suspicious deflections that are seen. Therefore, despite close resemblance to VFib in leads III, aVR, aVL and aVF in this ECG — an underlying regular supraventricular (that is, narrow QRS) rhythm at a rate just under 100/minute can still be seen in other leads!
  • The vertical BLUE lines in the lower part of Figure-3 show that even in those leads that simulate VFib — we can still see indication of deflections that reveal the underlying supraventricular rhythm at ~100/minute!
  • PEARL #2: The simple step of going to the bedside to LOOK at the patient will often be revealing. Doing so will commonly show one or more electrode leads to be loose — OR — the patient to be shaking, trembling, shivering, having a seizure, scratching or other obvious cause of the bizarre deflections seen.

Figure-3: I've reproduced this tracing from ECG Blog #148 (See text).

Acknowledgment: My appreciation to Andreas Röschl (from Neumarkt, Germany) for the case and this tracing.

Related ECG Blog Posts to Today’s Case:

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the PsQs & 3R Approach.
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
Links to Examples of ARTIFACT:
What follows below is an expanding list of technical "misadventures" — many from Dr. Smith's ECG Blog (See My Comment at the bottom of these pages) — some from my ECG Blog and/or from other sources.

Tuesday, May 28, 2024

ECG Blog #431 — My New ECG-Rhythm Podcasts!

  • I recently recorded a series of 4 podcasts regarding KEY concepts in ECG interpretation.
  • Easy LINKS —   
  •                            —

  • Other ECG Audio PEARLS I previously made for my ECG Blog can be found in the right column of each page on this blog just below this icon — under, "ECG Audio PEARLS"

My New ECG Podcasts (5/28/2024): 
  • These podcasts are part of the Mayo Clinic Cardiovascular CME Podcasts Series ("Making Waves") — hosted by Dr. Anthony Kashou. They are found on the Mayo Clinic Cardiovasciular CME site. 
  • You can adjust the speed of the recording (If the speed is "slow" for you — increasing to 1.25 speed should be optimal for you! ).
  • Note the Timed Contents that I detail below facilitate finding specific material.

ECG Podcast #1 — Common Errors in ECG Interpretation (And How to Easily Correct these Errors!) — published by Mayo Clinic CV Podcast Series on 12/19/2023 (30 minutes).
  • 0:00 — Intro by Dr. Anthony Kashou: Welcome to Mayo Clinic’s ECG Segment: “Making Waves” (Today's discussion — About today’s speaker = Ken Grauer, MD).
  • 2:00 — Dr. Grauer: “How did you get so skilled at ECGs?” 
  • 3:30 — Me introducing today’s topic ( = “Common Errors in ECG Interpretation”) — and why I chose this topic.
  • 4:35 — I’m sent a tracing. The 1st “Error” is either no History (or a History that does not tell me what I need to know).
  • 6:40 — The need for a relevant History (Clinical examples!).
KEY POINT: Be sure to list all antiarrhythmic drugs (Note rate-slowing meds — Herbal products! — and ask about beta-blocker eye drops! ).
  • 13:10 — Next Error = NOT forcing yourself to commit to a diagnosis!
  • 14:10 — Next category of Errors = The need for a Systematic Approach (This will not slow you down! Instead — it speeds you up, improves your accuracy and makes you sound smarter!).
  • 15:50 — My System for Rhythm Interpretation ( = First, look at the patient! — then, “Watch your Ps, Qs & 3Rs” ).
  • 18:15 — The error of premature closure (Thinking there are only 2 answers = “VT or SVT” — because you forget the 3rd Answer = a relative probability statement!).
  • 19:50 — Not appreciating statistical odds! (ie, What are the odds that a regular WCT without P waves will be VT?).
  • 22:25 — What if you have a regular SVT ( = narrow-complex tachycardiawithout obvious P waves? (The 4 common causes? — The most commonly overlooked cause?) 
25:10 —  My System for 12-Lead ECG Interpretation: (What are the 6 KEY parameters to look for?)
  • The 6 KEY Parameters I favor for my Systematic Approach ( = Rate - Rhythm - Intervals [PR-QRS-QTc] - Axis - Chamber Enlargement & QRST Changes).
  • Be sure to look at Intervals at an early point in the process!

  • 27:50 — SUMMARY by Dr. Anthony Kashou. 

NOTE: For more on "My Take" regarding the ECG diagnosis of acute OMI — Please see my ECG Podcast #2 (LINK and detailed Contents below!) 
  • Please also Check Out my new ECG Videos #406, 407 and 408 on this topic (CLICK HERE)

  • For links to ECG cases of artifact and other "technical misadventures" — Please Check Out my ECG Blog #432 (to be published 1st week in June ...).
And regarding arrhythmias:

ECG Podcast #2 — ECG Errors that Lead to Missing Acute Coronary Occlusion (Reviewing the concept of OMI — and why the "STEMI Paradigm" is outdated and misses too many acute coronary occlusions!) — published by Mayo Clinic CV Podcast Series on 1/16/2024 (33 minutes).
  • 0:00 — Intro by Dr. Anthony Kashou: Welcome to Mayo Clinic’s ECG Segment: “Making Waves” (Today's discussion — About today’s speaker = Ken Grauer, MD).
  • 2:25 — Dr. Grauer: The 1st Error: Too many clinicians in 2024 are still stuck in the outdated millimeter-based STEMI Paradigm”. (What do we really care about in the patient with new CP [Chest Pain]? ).
  • 6:15 — Error #2: Overuse of the term, “NSTEMI — which practically speaking is a useless term. Many (if not most) NSTEMIs are actually OMIs ( = acute coronary Occlusion MIs).
  • 7:42 — Error #3: The ECG criteria for diagnosing an OMI?
  • 9:25 — Are there hyperacute T waves?
  • 11:37 — Can you find a prior tracing on the patient?
  • 12:20 — Look carefully at neighboring leads!
  • 13:10 — The “magical” mirror-image opposite relation! (Use of my Mirror Test to instantly identify posterior OMIs — and inferior OMIs by comparing leads III and aVL).
  • 15:35 — Why posterior leads are not needed!
  • 18:58 — Look for dynamic ST-T wave changes! (How often to repeat the ECG?)
  • 20:25 — The 1st high-sensitivity Troponin may be normal.
  • 21:00 — What to know about the prior tracing?
  • 21:50 — The Biggest Error —  is not correlating the History to each ECG that is done! (Because the provider does not appreciate the concept of spontaneous reperfusion!).
  • 29:00 — Today's Final Erroris not learning from our cases!

  • 31:28 — SUMMARY by Dr. Anthony Kashou.  

ECG Podcast #3 — Computerized ECG Interpretation and AI in 2024 (Is there any computerized ECG program that can reliably help clinicians to better interpret ECGs?) — published by Mayo Clinic CV Podcast Series on 3/19/2024 (28 minutes).
  • 0:00 — Intro by Dr. Anthony Kashou: Welcome to Mayo Clinic’s ECG Segment: “Making Waves” (Today's discussion — About today’s speaker = Ken Grauer, MD).
  • 2:00 — Dr. Kashou to Dr. Grauer: "In 2024 — Where do you see computerized ECG interpretations and AI?" 
Please NOTE: I divided my comments into 2 "Eras, regarding the use of computerized ECG interpretations: i) The initial Era (ie, from the mid-1980s until very recently); — andii) The new QOH (Queen OHearts) Era — in which the QOH application for assessment of acute OMI is so quickly becoming widely available! 

General Overview of this Podcast:
  • From 0:00-to-5:54 = Introductory material.
  • From 5:54-to-16:13 = Review of my experience with computerized ECG interpretation from the mid-1980s until very recently ( = the initial Era).
  • From 16:13-to-27:00 = How the new QOH application may dramatically improve rapid recognition of acute OMI(For listeners primarily interested in QOH — Feel free to jump to 16:13 in this 28 minute podcast).
  • From 27:00-to-END  SUMMARY by Dr. Anthony Kashou.

More Specific Breakdown of Contents:
  • 2:20 — My "Disclaimer": What follows today reflects my opinion, based on my experienceI have no financial interest in any commercial product related to my comments.
  • I begin by offering some Pros & Cons of AI in our Life "outside" of the ECG World ...
  • 5:54 — So how in 2024, do I think AI is impacting on ECG interpretation? How much "human oversight" is needed? 

  • 7:15 — A number of fundamental errors continue to be made! So — Where are we going with use of AI for ECG interpretations?
  • 8:00 — To answer, it's worth looking at where have we come from? I trace my experience with computerized ECG interpretation, which literally began decades ago, in the 1980s! During these decades (and up to the present) — there continues the tendency for too-many-clinicians to accept without question what the computer says. This needs to change.

  • 10:20 — How the computer can best assist clinicians with ECG interpretation? Realize that clinicians with different levels of experience and different training have different needs (ie, The needs of an experienced cardiologist or emergency physician are different than the needs of clinicians with far less training and experience in ECG interpretation).

  • 11:35 — My views on: Will the computer ever be able to interpret complex arrhythmias?

  • 12:15 — Regarding my experience from the 1980s until ~2010: How I went from hating computer interpretations to loving them (after I finally understood what the computer can and can not do).

  • 14:45 — Using my definition — Are YOU an “expert” ECG interpreter? The computer saves experts time. 
  • For non-experts" ( = 90-95% of clinicians, even though many such clinicians may still be very good interpreters) — the computer provides a 2nd opinion.

  • 16:13 — That was then ... What about now? (ie, What can AI offer us in 2024 as a way to improve our ECG interpretation?)

I emphasize these 4 concepts in these last 11 minutes (16:13-27:00)
  • — i) All ECG programs that I am aware of prior to development of QOH — are out-of-date, and of little-to-no use in emergency care! 
  • — ii) Computerized interpretations are not helpful for arrhythmia assessment (The simpler arrhythmias are obvious to capable clinicians — and the computer makes too many mistakes for complex tracings)
  • — iii) The new QOH application is already amazingly accurate in recognizing acute coronary Occlusion in cases when outdated STEMI criteria are not fulfilled (with rapid recognition of acute OMI that prompts early reperfusion saving valuable myocardium!). Future generations of QOH will continue to improve (See Dr. Stephen Smith's ECG Blog for numerous clinical cases illustrating features of this QOH application for OMI diagnosis); — and
  • — iv) Optimal clinical diagnosis of acute OMI at an early point in the process is best attained by the combination of a capable ECG interpreter who is open to receiving QOH input.

  • 27:00 — SUMMARY by Dr. Anthony Kashou. 
NOTE: For more on "My Take" regarding the ECG diagnosis of acute OMI — Please see my ECG Podcast #2 (LINK and detailed Contents below!) 
  • Please also Check Out my new ECG Videos #406, 407 and 408 on this topic (CLICK HERE)

  • For links to ECG cases of artifact and other "technical misadventures" — Please Check Out my ECG Blog #432 (to be published 1st week in June ...).
And regarding arrhythmias:

ECG Podcast #4 — All About Comparison ECGs for 12-Leads and Arrhythmias (Comparing ECGs seems so "easy" to do — but so often is not done correctly!) — published by Mayo Clinic CV Podcast Series on 5/21/2024 (35 minutes).
  • 0:00 — Intro by Dr. Anthony Kashou: Welcome to Mayo Clinic’s ECG Segment: “Making Waves” (Today's discussion — About today’s speaker = Ken Grauer, MD).
  • 1:50 — Dr. Kashou to Dr. Grauer: “What can we learn from ECG comparisons?” — and — “How best to compare tracings in time-efficient fashion?” 
  • 2:15 — ME introducing today’s topic — and WHY I chose to speak about this often-neglected but important clinical issue.
Please NOTE: I divided my comments into 2 "parts" regarding the use of comparison tracings: i) Comparison of one 12-lead ECG with another (ie, including use of serial ECGs in a patient with chest pain — and how BEST to use a prior "baseline" tracing); — and — ii) Optimal use of comparison tracing with cardiac arrhythmias! 
  • 2:50 — Let’s start with comparison of 12-Lead ECGsWhat are the problems? How to optimize the technique for comparison in time-efficient fashion?
  • 3:20 — First determine, "What are you comparing?" (ie, WHAT was going on at the time that the "prior" 12-lead ECG was done? — that is, Was the patient asymptomatic? — or — Was your "baseline" tracing recorded at the time of a previous infarction?) = WHAT are you comparing?

  • 5:25 — Moving on to serial ECGs. By correlating each ECG with whether CP (Chest Pain) was present (and if so — how severe?) — you can often tell IF the “culprit” vessel is now open or closed! 
  • KEY Point: It's essential to correlate each ECG with the status of CP at the time each tracing is recorded! (Write this on the actual ECG and in the chart – or else it will not be remembered).
  • 8:35 — Illustrating how correlating serial ECGs and the presence and severity of symptoms can diagnose an acute OMI (with need for prompt cath) — even when the initial ECG was “only" nonspecific.

  • 9:50 — How often to repeat the ECG in a patient with CP? (Answer: As often as is needed until you become certain about acute OMI or no OMI!).
  • NOTE: — Do not give morphine until you know what you will do with your patient! (ie, until you know if the cath lab needs to be activated!).

  • 10:50 — An acute evolving OMI may sometimes change in less than 5-to-10 minutes. As a result — ECGs may need to be repeated within a period of minutes! (especially IF there is a change in the presence or severity of CP).

  • 11:45 — Look for dynamic ST-T wave changes on serial tracings! These may be subtle — but when they occur in a patient presenting with CP, it is often (usually) an indication for prompt cath!

12:15 —
 My "Take" on the “optimal” time-efficient and accurate technique for comparing 12-lead ECGs? 
  • KEY Point: You have to go Lead-by-Lead from 1 tracing-to-the-2nd tracing! (because if you don’t — you will overlook subtle-but-important changes!)
  • NOTE: Careful lead-by lead comparison actually takes less time than the random way most clinicians compare 1 ECG with another. (Confession: I miss subtle "dynamic" changes when I do not do meticulous lead-by-lead comparison).
  • 14:05 — With serial 12-lead ECGs — “Be sure you are comparing apples with apples, and not with oranges”. That is — IF the frontal plane axis and/or precordial lead placement is not the same for the 2 tracings that we are comparing — this needs to be taken into account when we do serial comparison!

  • 16:50 — IF you see excessive artifact and/or other "technical misadventure" in a patient with new CP for whom you need to determine IF an acute OMI is ongoing — Repeat the ECG immediately! (ie, Don't wait to repeat the ECG ...).
  • 18:15 — Examples of technical “misadventures” (ie, Lead I should never normally show global negativity).
  • 18:40 — Regarding technical “misadventures” (ie, “Things that I wish I knew last year"— Be aware of PTA (Pulse-Tap Artifact) — which once you have seen it — can be instantly recognized! (to the amazement of your colleagues who are not aware of PTA!).

22:25 —
 Using serial tracings for optimal Rhythm interpretation!  
  • KEY Point: Look for additional simultaneously-recorded leads = “12 Leads are Better than One!” (ie, For example with tachycardias — the QRS may look narrow if all you have is 1 or 2 leads — whereas if part of the QRS lies on the baseline in the single lead you are looking at, this might be VT!).
  • 24:10 — The 5 BEST leads (in my opinion) for looking for atrial activity in a tachycardia are lead II (ie, The P must be upright in lead II if there is sinus rhythm — unless dextrocardia or lead misplacement) — and then leads V1III,aVF; and lead aVR (these 5 leads being my “Go-To-Leads” for finding subtle flutter waves — as well as for finding subtle retrograde activity and subtle AV dissociation).
  • 25:00 — The advantage of getting a 12-lead in an unknown tachycardia = “12 Leads are Better than One” ( = You have 12 leads to tell if the QRS is wide or narrow!).

  • 26:10 — Even though initial emergency treatment of a regular SVT rhythm will be similar (if not identicalregardless of what type of SVT the rhythm is — ultimate management will be better IF at some point you can determine for certain what type of SVT rhythm this was! — Get a post-conversion 12-lead ECG — and compare this to the initial 12-lead ECG obtained during the tachycardia!
  • Doing so helps to distinguish between the 4 most Common Causes of a regular SVT at ~150/minute, but without sinus P waves = i) Sinus tach; ii) Atrial tach; iii) Reentry SVT ( = AVNRT vs orthodromic AVRT)or iv) AFlutter (which is by far, the most commonly overlooked arrhythmia!).

  • 29:20 — And my last few minutes on, "HOW does a comparison ECG help you when interpreting a regular WCT (Wide-Complex Tachycardia) rhythm?
NOTE: Because of time restrictions in this podcast, I did not expand on the differential diagnosis of a regular WCT rhythm — which for practical purposes is: i) VT, VT, VT until proven otherwise!; ii) SVT with either rate-related aberrant conduction or a preexisting BBB (which is where a prior tracing can be so helpful!); — or — iii) Something else! (ie, a WPW-related tachyarrhythmia — Hyperkalemia! — some toxicity …)
  • See ECG Podcast #1 below for more 12-lead and problematic arrhythmia interpretation ...

  • 33:30 — SUMMARY by Dr. Anthony Kashou. 

Thursday, May 16, 2024

ECG Blog #430 — Just a Regular LBBB ECG?

The ECG in Figure-1 — was obtained from an older man who had just completed dialysis — and, is now complaining of abdominal discomfort that radiates to his chest.
  • The consultant interpreted this tracing as “LBBB” (Left Bundle Branch Block) — but not indicative of anything acute.

  • Do you agree with the consultant’s interpretation?
  • How would YOU approach this case?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio)

MY Initial Thoughts on Today’s CASE:
Given the older age of the patient in today’s case — and, the fact that he just completed dialysis — the chance of having underlying coronary disease is clearly increased. This patient's new complaint of pain that radiates to his chest therefore immediately places him in a higher-prevalence” group for having an acute event (especially since hemodialysis is a procedure in which transient hypotension is not uncommon).
  • For clarity in Figure-2 — I’ve labeled today’s initial ECG. The rhythm is sinus at ~85/minute (the RED arrow highlighing the upright P wave in lead II). The QRS complex is wide — with a morphology most consistent with LBBB ( = predominantly upright in left-sided leads I and aVL — and predominantly negative in the anterior leads).
  • Serum K+ was normal. 

  • NOTE: By my observation over the years — the experts do not agree on the classification of LBBB vs IVCD (IntraVentricular Conduction Defect). As I review in ECG Blog #204 “typical” LBBB is characterized by a supraventricular rhythm with QRS widening, in which there is a monophasic R wave in left-sided leads I and V6 — and an all-negative (or almost all negative) QRS in right-sided lead V1
  • The above said — many patients with LBBB also have marked LVH. Given the leftward and posterior orientation of a markedly enlarged LV (Left Ventricle) — the presence of an all-upright R wave may not be seen in left-sided lead V6. Instead, the all-positive R wave with LBBB may sometimes only appear in more lateral and posteriorly-oriented chest leads, such as V7,V8 or V9.
  • As a result — I would accept either LBBB or IVCD as a “correct” classification of the widened QRS morphology seen in Figure-2. Personally, I favor LBBB in view of the suggestive appearance of LBBB in the limb leads, with fairly deep anterior S waves — but my comments below are consistent with either LBBB or IVCD.

PEARL #1: Regardless of whether you interpreted the widened QRS morphology in today’s ECG as “LBBB” or “IVCD” — there are a number of ECG findings of increased concern beyond that of the conduction defect. Among them: 
  • There should never normally be a Q wave in a lateral lead with simple LBBB. As discussed in ECG Blog #204 — this is because by definition, the conduction defect with LBBB prevents normal left-to-right septal depolarization. The same is true for an IVCD pattern that mimics LBBB in the limb leads (as is seen in today’s ECG). Therefore — the Q waves in Figure-2 (BLUE arrows in leads I and aVL) suggest that in addition to the conduction defect — there is also scar” (usually from infarction at some point in time).

In addition to the abnormal Q waves — ST-T wave morphology is distinctly abnormal in almost every lead!
  • While more difficult to assess because of the lack of an all-upright R wave in lateral lead V6 — the shape of the ST-T waves in multiple leads is just not normal.
  • BLUE lines in leads V2,V3 show abnormal ST segment straightening (instead of the expected upsloping ST segment in these leads).
  • PURPLE lines in leads V4,V5,V6 show abnormal downsloping ST segments (with marked abnormal ST depression in leads V5,V6). In addition — the biphasic T wave with marked terminal positivity in leads V5,V6 looks distinctly acute (ie, T waves are not normally upright in lateral chest leads with LBBB).
  • Similar downsloping with marked, abnormal ST depression and abnormal biphasic T wave with marked terminal positivity — is seen in lead II.
  • While ST segments in leads III and aVF are not nearly as depressed or downsloping (as they are in lead II) — the ST segment straightening that we see in leads III and aVF, with marked angulation at the point where the ST segment meet the beginning of the T wave — is clearly not normal.
  • Finally — note how marked the ST elevation is in lead aVR (within the RED box in this lead).

Putting It All Together:
The older man in today’s case was clearly in a higher-prevalence group for an acute event — even before we looked at his initial ECG. As a result — there was need to assume that any potentially abnormal ECG findings that might be seen are acute until proven otherwise.
  • In summary, the ECG in Figure-2 shows sinus rhythm with LBBB — and diffusely abnormal ST-T wave depression with ST elevation in lead aVR. At the least — this pattern is consistent with DSI (Diffuse Subendocardial IschemiaSee ECG Blog #271 for more on DSI).
  • More than this — the Q waves in leads I and aVL — and the acute appearance of the downsloping ST depression with terminal T wave positivity — might reflect multi-vessel disease with recent and/or ongoing acute infarction.

  • Finding a prior tracing on this patient would be extremely helpful — as it would tell us what is "new" vs old.
  • Obtaining serial ECGs should prove insightful. Especially when correlated to the presence and relative severity of symptoms — serial tracings will convey if acute injury is ongoing. For example — a reduction in symptoms in association with improvement in ST-T wave changes, would suggest that the "culprit" vessel is spontaneously opening!
  • PEARL #2: In patients with ongoing symptoms — ST-T wave elevation and reciprocal ST depression may evolve over a period of minutes. As a result — Consider a repeat ECG as often as every 10-to-20 minutes in a patient with ongoing CP (Chest Pain)  until a definitive diagnosis can be made.

  • BOTTOM Line: On seeing today's ECG — prompt cath was clearly indicated.

Figure-2: I've labeled the initial ECG in today's case. 


Acknowledgment: My appreciation to Mayan Kain (from Tel Aviv, Israel) for the case and this tracing.




Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).
  • CLICK HERE  for my new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
  • CLICK HERE  for my new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
    • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
    • Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators— See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 

    • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
    • ECG Blog #230 — Reviews how to compare serial ECGs
    • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
    • ECG Blog #268 — Shows an example of reperfusion T waves.
    • ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.

    • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

    • ECG Blog #282 and ECG Blog #204 — review a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks (RBBB, LBBB and IVCD).

    • ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.


    Saturday, May 11, 2024

    ECG Blog #429 — Mobitz I or Mobitz II?

    The 12-lead ECG and long lead II rhythms shown in Figure-1 — was obtained from an older man with a recent history of “easy fatiguability” and a presyncopal episode.

    • How would YOU interpret the ECG in Figure-1?
    • Is the group beating due to the Mobitz I or Mobitz II type of 2nd-degree AV block?

    Figure-1: The initial ECG in today’s case. 

    MY Initial Thoughts on Today’s CASE:
    For clarity, given the above clinical history — I present my initial thoughts regarding clinical interpretation of today’s initial ECG in the sequence I used for assessment of this case. 
    • To EMPHASIZE: One of my goals in developing this ECG Blog — is to help clinicians to optimize their time efficiency. For example, in today's case — I completed my initial assessment of the tracing in Figure-1 in less than 1 minute. I outline my approach for doing so below. 

    MY Approach:
    When presented with a 12-lead ECG and accompanying long-lead rhythm strip — I favor spending a few quick seconds first taking a look at the long lead rhythm strip — before I look at the 12-lead. This is especially relevant when either the QRS is wide and/or the rhythm is not regular (and in today’s case — both of these conditions are present!).
    • By the Ps, Qs, 3R Approach (See ECG Blog #185) — the rhythm in the long-lead II of Figure-1 is not Regular. Instead — there is a pattern consistent with group beating” (ie, groups of 2 beats — each with similar spacing between these 2 beats — and — similar spacing during the slight pause between groups).
    • The QRS complex in the long lead II appears to be wide (ie, more than half a large box on ECG grid paper — and in Figure-1, at least 0.12 second).
    • P waves are present in front of each of the 13 beats in the long-lead II rhythm strip (RED arrows in Figure-2). These P waves are all upright in this lead II — with a constant and normal PR interval (ie, all P waves are Related to the QRS closest to them — in that the PR interval remains the same before all beats). There is therefore an underlying sinus rhythm in today's tracing.
    • The 5th parameter in the Ps,Qs,3R Approach is the 3rd R = Rate — which is difficult to determine because of the irregularity in the rhythm. That said — we can say that the rate is not overly fast.

    • To EMPHASIZE: Assessment of today’s rhythm by the approach outlined in the above bullets should take less than 30 seconds! The conclusion I came to (within these 30 seconds) — was that today’s rhythm manifests conduction of sinus beats at a reasonable heart rate — with a wide QRS and with group beating.

    Figure-2: I've labeled sinus P waves with RED arrows.

    PEARL #1: For as interesting as the rhythm in today’s case looks to be (ie, with group beating and a wide QRS) — I’ll suggest that optimal time efficiency for clinical assessment and management — would be to next figure out WHY the QRS complex is wide!
    • As noted above — there is sinus conduction in today's rhythm, with a constant and normal PR interval. As a result — there is no WPW. This means the cause of the wide QRS in today's rhythm is due to some type of conduction defect.

    • As reviewed below in today's ADDENDUM — attention to 3 KEY leads ( = right-sided lead V1 — and left-sided leads I and V6) — allows you to distinguish between the 3 principal types of conduction defects within seconds!
    • Normally — the QRS is predominantly negative in right-sided lead V1. Therefore — the combination of the widened RR' complex seen in lead V1 of Figure-2 — in association with the wide terminal S waves seen in left-sided leads I and V6 — is diagnostic of RBBB (Right Bundle Branch Block) as the explanation for QRS widening in today's case (See ECG Blog #282 for review on ECG diagnosis of the BBBs).

    PEARL #2: The ECG Video in today's ADDENDUM also reviews quick assessment of ST-T wave changes in bundle branch block. The simple rule that can be assessed within seconds, is that with either RBBB or LBBB — the ST-T wave in the 3 KEY leads (leads I, V1, V6) will be oppositely directed to the last QRS deflection in these 3 leads.
    • Since the last QRS deflection in lead V1 of Figure-2 is positive (ie, the R' ) — the ST-T wave in this lead should be negative. It is.
    • Since the last QRS deflection in lateral leads I and V6 is the negative S wave — the T wave in these leads should be positive. It is.

    • Looking next at neighboring leads in Figure-2 — there appear to be no acute ST-T wave changes.

    Next — A closer look at the Rhythm ... 


    PEARL #3: Despite the title of today’s blog post (which is, "Mobitz I or Mobitz II?" ) — We can tell at a glance that today’s rhythm does not represent any form of AV block — because the atrial rate is not regular!
    • Using calipers tremendously expedites the process. With 2nd- or 3rd-degree AV block — the atrial rate should be regular (or at least almost regular — if there is an underlying sinus arrhythmia) — but it should be clear from the timing of the RED arrows in Figure-2 — that no on-time P wave occurs between beats #1-2; #3-4; #5-6; #7-8; #9-10; #11-12.

    • For completeness, I'll note that SA Block can produce the bigeminal pattern of beats that we see in Figure-2 . That said, as emphasized in ECG Blog #312 — SA block is rare! I count on my fingers and toes the number of times I've seen true SA block over my decades of diligently looking for this rhythm disorder. 

    • Instead, as suggested in PEARL #4 — there is a much more common explanation for today's arrhythmia that we should look for first!

    PEARL #4: Perhaps my favorite mantra in arrhythmia interpretation is the following statement that I learned from Marriott: "The most common cause of a pause is a blocked PAC."
    • In clinical practice, when confronted with a "pause" in the rhythm — the finding of blocked PACs is far more common than any form of AV block
    • To emphasize, that by a "pause" — I mean any even slightly longer-than-expected interval, which clearly is present in Figure-2 — because the interval between the 2-beat groups is much longer than anticipated given the P-P interval between the RED arrow sinus P waves in this tracing.
    • As a result, as soon as I saw the bigeminal rhythm in today's case (ie, with brief pauses between each of the 2-beat groups) — I considered the possibility of blocked PACs.

    Now — Take another LOOK at Figure-2.
    • Carefully examine the ST-T wave of every odd-numbered beat in Figure-2 — and compare these ST-T waves with the the ST-T waves of each even-numbered beat. 

    • Is there any difference?

    I illustrate my ANSWER in Figure-3:

    Figure-3: Is there any difference in the ST-T waves?

    Figure-3 Explained:
    The challenge in looking for blocked PACs — is distinguishing between subtle differences in ST-T waves that are "real" vs artifact vs slight variations that can normally be seen in parts of the tracing.
    • Isn't the ST-T wave of every even-numbered beat in Figure-3 straighter (above the slanted BLUE lines) — than the ST-T wave of every odd-numbered beat (above the slanted RED lines)? That's because there is a non-conducted PAC that is hidden within the ST-T waves of every odd-numbered beat — and this is what causes this slight-but-real distortion of the ST segment! These blocked PACs serve to "reset" the SA node — and thereby produce the slight pause that we see between each of the 2-beat groups!

    • PEARL #5: It's important to appreciate that PACs that arise from a site close to the SA node may look similar in morphology to sinus P waves. For this reason — I always look at simultaneously-recorded leads for subtle differences in P wave morphology that might not be readily apparent on a single long lead rhythm strip. NOTE: YELLOW arrows in Figure-3 show that the difference in ST-T wave morphology between sinus-conducted beats and the beats with blocked PACs is most easily seen in leads V2 and V3.


    The Lesson I Learned a Long Time Ago ...
    • As emphasized earlier in PEARL #4: The most common cause of a pause is a blocked PAC. Blocked PACs are much common than any form of AV block.
    • Until I became aware of the fact that blocked PACs are the most common cause of a pause — I never saw blocked PACs.
    • Once I began to look for blocked PACs — I found them everywhere!

    • Remember that the biggest challenge in accurately diagnosing blocked PACs — is distinguishing between differences in ST-T waves that are "real" vs artifact vs slight variations that can normally be seen in parts of the tracing. 
    • KEY Point: In today's case — the reason I know that the differences in ST-T wave morphology between odd- and even-numbered beats is real — is because it is seen with every beat in the long lead rhythm strip in Figure-3.

    Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

     Related ECG Blog Posts to Today’s Case: 

    • ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.

    • ECG Blog #232 — Reviews the causes of Bigeminy.

    • ECG Blog #164 — Reviews a case of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
    • ECG Blog #252for a similar case as today (with LINKS to more examples of blocked PACs).



    ADDENDUM (5/11/2024): I've added below material regarding a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks


    ECG Media Pearl #22 (13:15 minutes Video) — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds. 


    • CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).