Friday, June 14, 2024

ECG Blog #434 — WHY Did this Patient Arrest?


The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED (Emergency Department) in cardiac arrest. ROSC (Return Of Spontaneous Circulation) was obtained — and ECG #1 was recorded.
  • In view of this history — How would YOU interpret the ECG in Figure-1? Should you activate the cath lab?

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

MY Initial Thoughts:
Although there are different approaches regarding decision-making as to which patients with ROSC following OHCA (Out-of-Hospital Cardiac Arrest) should undergo prompt cardiac catheterization — what does appear to be clear, is that the post-ROSC ECG helps to identify patients at highest risk who may benefit from coronary reperfusion (Gentile et al — JAHA 12:3027923, 2023 — and — Baldi et al — JAMA Netw Open 4(1): e2032875, 2021).
  • Prompt cath is therefore advised if the post-ROSC shows an acute STEMI.
  • The decision of whether to cath patients with a less definitive post-ROSC ECG is less clear. Waiting a few extra minutes to repeat the ECG in such patients may help reduce false positive results when there are equivocal findings on the initial post-ROSC tracing.

The Post-ROSC ECG in Today’s CASE:
The initial ECG following ROSC in today’s case is clearly abnormal. I’ve highlighted KEY findings in Figure-2.
  • Although there is significant baseline artifact in the limb leads of ECG #1 — the underlying rhythm is sinus — as conveyed by the presence of upright P waves with a constant and normal PR interval in lead II (BLUE arrows in lead II of Figure-2). The rhythm is regular — at a rate just over 100/minute = sinus tachycardia (ie, the R-R interval is just under 3 large boxes in duration).

  • PEARL #1: In general — lead II is the best lead for assessment of P waves to determine if sinus rhythm is present. Sinus rhythm is defined by the presence of upright conducting P waves in this lead. 
  • The above said, when for whatever reason sinus P waves are not well seen in lead II — the 2nd-best lead when looking to determine if sinus rhythm is present, is lead V1. Recognition of a negative P wave deflection with fixed PR interval before the next QRS (similar to that highlighted by BLUE arrows in lead V1 of Figure-1) — confirms that the rhythm in today's ECG is sinus.

PEARL #2:
 We can tell at a glance in Figure-1 — that the "culprit" causing the artifact in today's ECG is the RA (Right Arm) extremity. The cause of the abnormal baseline deflections seen in Figure-2 is most likely muscle tremor artifact (See Bouthillet T — ACLS Med Training, Dec, 2015). A quick LOOK at the patient would confirm this — but unfortunately, there is no information about the patient's appearance.
  • NOTE: Abnormal baseline deflections in Figure-2 are maximal in leads I,II and aVRAs discussed in ECG Blog #255 — the extremity primarily responsible for a certain type of artifact — can be quickly recognized by the finding of greatest artifact amplitude in 2 of the 3 standard limb leads (ie, in leads I and II for Figure-2) — and, minimally or not seen at all in the 3rd standard limb lead (ie, artifact is minimal in lead III). By Einthoven's Triangle — this localizes the "culprit" extremity to the RA electrode.

  • SHORTCUT (To find the "culprit" extremity within seconds! ): When 2 of the standard limb leads clearly show greater artifact amplitude than the 3rd standard limb lead — then whichever augmented lead shows maximal amplitude indicates the "culprit" extremity (which is lead aVR in Figure-2 = which means that the RA is the "culprit" extremity).
  • Clinically — Rapid determination of the "culprit" extremity may facilitate quick correction (ie, If you could quickly know to look if the RA electrode had become loose — this may be easy to rectify).

Figure-2: I've labeled the initial ECG.

Continuing with assessment of ECG #1 in Figure-2:
  • The rhythm is sinus tachycardia at ~110/minute. The QRS complex is obviously wide. QRS morphology is consistent with RBBB (ie, all positive QRS in right-sided lead V1 — with wide terminal S wave in left-sided leads I and V6).
  • The all negative QRS complexes in each of the inferior leads indicate marked LAD (Left Axis Deviation). That said, rather than LAHB (Left Anterior HemiBlock) — the all-negative QRS in leads II,III,aVF is really a “QS” wave — which therefore suggests inferior MI at some point in time (possibly with or without associated LAHB).

  • The most worrisome part of this tracing is in the chest leads. RED arrows in leads V2,V3,V4 mark the J-point, which defines the end of the QRS complex in these leads. Everything to the right of these arrows entails the ST segment. As can be seen when compared to the dotted RED lines that mark the baseline in these leads — there is marked ST segment elevation, which is most dramatic in leads V3 and V4. This is followed by especially “bulky” (hyperacute) T waves in leads V5,V6, that are clearly taller, “fatter”-at their peak and wider-at-their base than expected given amplitude of the QRS complex in these leads.
  • Adding support to the occurrence of proximal LAD OMI — is the ST elevation that is clearly seen in lead aVL. Although harder to appreciate because of the variable baseline — there is also a hyperacute T wave in lead I.

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

PEARL #3: Today’s ECG provides an excellent example of T-QRS-D (Terminal QRS Distortion)When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction)

I illustrate the ECG finding of T-QRS-D below in Figure-3, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. To review:
  • T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3 (and/or probably also in lead V4). Although simple to define — this finding may be subtle! It takes a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words. I’ve taken thlead V3 examples in Figure-3 from previous cases posted on Dr. Smith’s ECG Blog:
  • TOP in Figure-3 — Despite marked ST elevation in lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
  • BOTTOM in Figure-3 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Figure-3: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).


To Emphasize: The phenomenon of T-QRS-D is not needed in today's case to recognize the acute STEMI. Once the J-point is recognized in the chest leads (RED arrows in leads V2,V3,V4 of Figure-2) — the marked ST elevation becomes obvious.
  • In my experience — T-QRS-D is not a common finding among patients with acute coronary occlusion. That said, the importance of being aware of this phenomenon — is that on occasion other signs of acute OMI may not be obvious, such that seeing T-QRS-D may be a KEY finding in support of acute infarction (See ECG Blog #318).
  • Today's case is also noteworthy in that T-QRS-D is seen in association with RBBB — which has only been described on rare occasions (See the March 28, 2021 post in Dr. Smith's ECG Blog).
=================================

CASE Conclusion:
As noted above — the middle-aged man in today's case presented to the ED in cardiac arrest. Retrospective questioning of the driver who brought this patient to the hospital revealed that he was having chest pain as the reason for presenting to the ED. He became unconscious on arrival.
  • A series of VFib episodes followed — each time with successful defibrillation. ROSC (Return Of Spontaneous Circulation).
  • Cardiac cath was not performed — because the interventionist did not recognize the ECG signs of acute MI.


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

Acknowledgment: My appreciation to Nirdosh Ashok Kumar (from Karachi, Pakistan) 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 — reviews 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.

    • ECG Blog #318 — reviews the concept of T-QRS-D (Terminal-QRS-Distortion).


     



    Friday, June 7, 2024

    ECG #433 — Which Lead Convinced Me?


    The ECG in Figure-1 was obtained from a previously healthy older man — who presented to the ED (Emergency Department) with new but atypical CP (Chest Pain) for several hours.


    QUESTIONS:
    • Given this history — How would YOU interpret this ECG?
    • Which lead is the most concerning?

    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 ECG:
    The older age of today’s patient — and the fact that he presents to the ED for new CP immediately places this patient in a higher-prevalence risk category (albeit there is some reduction in risk — given the “atypical” nature of his CP). Clearly, more information (ie, assessment of his initial ECG) will be needed for optimal decision-making.
    • The initial ECG that is shown in Figure-1 is not normal! That said — the abnormal findings are subtle.

    Looking Systematically (as per ECG Blog #205):
    • The rhythm is sinus. All intervals (PR, QRS, QTc) are normal. The axis is vertical — but still within normal limits (ie, the QRS is slightly more positive than negative in lead I — so the frontal plane axis is +75-80 degrees). There is no chamber enlargement.

    Regarding Q-R-S-T Changes:
    • Small and narrow Q waves are seen in the inferior and lateral chest leads (ie, in leads II,III,aVF; and in V5,V6).
    • R Wave Progression — is normal, with transition (where the R wave becomes taller than the S wave is deep) taking place normally (seen here in ECG #1 — to be between leads V3-to-V4).

    Regarding ST-T Wave Changes:
    • PEARL #1: The one lead that immediately "caught my eye" in today's tracing — is lead I (within the RED rectangle in Figure-2). There simply is no way that the ST-T wave in lead I is normal because: i) The ST segment is straightened in lead I (as per the horizontal RED line that I drew over the ST segment in this lead); and, ii) The J-point of this straightened ST segment is depressed (and considering the tiny size of the QRS in lead I — this ST depression is significant!).

    • There is subtle-but-real J-point ST elevation in lead III and lead aVF (BLUE arrows in these leads). I was not initially certain of what (if anything) to make of this slight J-point ST elevation in these inferior leads, given the gentle upsloping (ie, "smiley"-configuration) shape and the lack of any J-point ST elevation in the 3rd inferior lead ( = lead II).
    • I considered that the symmetric T wave inversion in lead aVL might represent a reciprocal change (BLUE question mark in this lead) — BUT — PEARL #2: The T wave may normally be inverted in lead aVL when the frontal plane axis is vertical, as it is in Figure-2.

    • PEARL #3: I considered that the small q waves seen in leads II,III,aVF might represent the injury marker of inferior infarction — but in addition to normal septal q waves being commonly seen in one or more lateral leads (as they are here in leads V5,V6)normal septal q waves may also normally be seen in the inferior leads when the frontal plane axis is vertical, as it is in Figure-2.

    • BOTTOM Line: Were it not for the ST-T wave appearance in lead I — I would not have been at all certain that the above described changes in leads II,III,aVF and aVL were acute, and not simply a manifestation of a repolarization variant in a patient with a vertical frontal plane axis. BUT — Given that I knew that the ST-T wave appearance in lead I was definitely abnormal — My "working diagnosis" was acute inferior OMI until proven otherwise.

    PEARL #4: Because of the common blood supply to the inferior and posterior walls of the LV (Left Ventricle) — I always look for subtle signs of acute posterior OMI when I am looking for a way to support my suspicion of acute inferior OMI. Normally — leads V2 and V3 manifest slight-but-real, gently upsloping ST elevation. The fact that if anything — the J-point in lead V3 of ECG #1 is slightly depressed (BLUE arrow in this lead) — strongly suggests that there is an acute posterior OMI in Figure-2.
    • NOTE: The more leads that manifest ST-T wave abnormalities — the greater the support that there is an ongoing acute process. My "eye" was next captured by the ST-T wave appearance in leads V4,V5,V6 (within the BLUE rectangle in Figure-2). As per the BLUE lines I've drawn over the ST segments in these leads — there is flattening and slight J-point depression.

    • Putting This All Together: Given the history that the older man in today's case presented with new symptoms — and, has ST depression in lead V3 suggestive of posterior OMI — which lends further support to the limb lead changes suggesting inferior OMI — plus also manifesting ST flattening with ST depression in lateral chest leads (V4,V5,V6) — my "working diagnosis" expanded to an acute infero-postero OMI (plus my suspicion that this older patient may well have multivessel disease).

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


    ==============================
    QUESTION:
    • Is there misplacement of any electrode leads?
    • IF so — WHY is this relevant?



    ANSWER:
    The only 3 leads that I've not yet mentioned in today's tracing are leads aVR, V1 and V2. 
    • Lead aVR in Figure-2 — shows slight ST elevation. I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease (ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400).

    • I strongly suspect that the electrode leads for V1 and V2 may be placed too high on the chest. As discussed in ECG Blog #274 — the clues that suggest there is too-high placement of leads V1,V2 include: i) The negative P wave in leads V1 and V2 of Figure-2; ii) The subtle r' that we see in lead V2; and, iii) How similar the QRST complex in leads V1 and V2 look to the QRST in lead aVR! It is especially this last clue that makes me so suspicious of V1,V2 misplacement — because the symmetric T wave inversion we see in lead V2 looks totally "out-of-place", compared to the ST-T wave appearance in neighboring lead V3 (the BLUE question mark over the T wave in lead V2).

    PEARL #5:
     The clinical importance of recognizing lead V1,V2 misplacement — is that this potentially negates the diagnostic value of assessing leads V1,V2 in this patient for whom we are trying to diagnose acute posterior OMI.
    • ST depression with posterior OMI tends to be maximal in leads V2, V3 and/or V4 (with ST depression often beginning in lead V1). Losing the diagnostic utility of leads V1 and V2 in Figure-2 — therefore hinders our ability to recognize posterior OMI in today's patient. 

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

    The CASE Continues:
    The clues to acute infero-postero OMI that I discussed above were not recognized.
    • Even when several initial high-sensitivity troponin values came back with definite (albeit modest) elevation — the possibility of acute OMI was not recognized.
    • The initial ECG was not repeated for several hours ...
    • Troponin values continued to rise — and frank ST elevation was finally seen on repeat ECGs.


    Additional LESSONS To Be Learned:
    ECG findings in Figure-1 are subtle — but they are definitely present. At the least — these ECG changes should have raised concern for a potential acute event.
    • When in doubt about an acute event — Repeat the ECG! In acutely evolving coronary occlusion — "dynamic" ST-T wave changes may occur in as short of a time period as several minutes. As a result — I favor repeating ECGs every ~10-20 minutes until you are comfortable that acute OMI is or is not occurring.
    • In a patient with new symptoms and subtle ECG changes — the finding of even modest troponin elevation tells us to accept this as evidence of acute OMI until we prove otherwise. Prompt cath is indicated.
    • Correlate each serial ECG with notation of the presence and relative severity of symptoms. Improvement of symptoms that correlates with improvement in ECG findings does not mean "all is well". Instead, it most probably indicates "dynamic" ST-T wave changes in a patient with an evolving OMI. Prompt cath and PCI are likely to be needed.
    • Even without ECG changes — persistent ischemic-sounding chest pain is indication for prompt cath.
    • Finally — the EASIEST way to ensure that you will be able to tell a complete "story" as to the presence and relative severity of symptoms at the time that each ECG was recorded — is if written notation is made on each ECG as it is done on a scale from 0-to-10 of the patient's chest pain at that time.


    ==================================
    Acknowledgment: My appreciation to Giuseppe Trainito (from Butera, Italy) 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 (and also Diffuse Subendocardial Ischemia).

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

      • ECG Blog #274 — How to tell if leads V1,V2 are misplaced.





      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 ANSWER:
      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 — tinyurl.com/KG-ECG-Podcasts   
      •                            —  https://tinyurl.com/KG-Blog-431

      • 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 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.