What do you think of these 2 ECGs in patients with chest pain? How to approach these?

What do you think of these 2 ECGs in patients with chest pain?  How to approach these?

ECG 1 (sent to my by Sam Ghali @EM_resus)

ECG 2

ECG 1 

This was sent to me with no clinical information and the question "what do you think?"  

My answer was: "sinus rhythm with right atrial enlargement, probable right ventricular hypertrophy, and old inferior MI with inferior LV aneurysm."  The T-wave inversion in I and aVL is reciprocal to the Old inferior aneurysm.

After I sent my answer, I received this history:

66 yo man presented with chest pain

History of CAD [unclear details out of state, stent(s)?]

STEMI alerted pre-hospital

Found to have very elevated lactate

Significant AKI

Aortic thrombus (chronic) on CT

hS Trop T:   1609->2471->1929 ng/L

Cards was planning on  cath when metabolic situation settled

Angiogram: no culprit and all open arteries.

Final diagnosis: type II MI due to illness

The Queen of Hearts said "OMI with mid confidence."  Version 1 of the Queen does not do a good job of recognizing LV aneurysm morphology, whether it is anterior (which for an expert is not too difficult because they almost always have QS-waves) or inferior (which is even very difficult much of the time for me, because inferior aneurysm frequently has QR-waves)

How to approach?  --when the diagnosis could be "ST Elevation due to Old MI" or "LV Aneurysm Morphology", it is essential to look into the old charts and old ECGs, if available.  It is also essential to assess for other etiologies of the symptoms, and in this case the patient had physiological derangement, with elevated lactate and AKI.  This points to another inciting etiology rather than ACS as the primary mover.  

These physiological derangements do not rule out ACS, but make it much more likely that the patients illness was incited by another factor.

ECG 2

I was reading ECGs on the system and came across ECG 2 and said out loud: "This is a fake."  A colleague sitting next to me asked "why?", and I answered that there is a "saddleback" in lead III and well-formed Q-wave.  Saddleback ST elevation is rarely due to OMI. 

However, on very few occasions Saddleback STE actually is due to OMI.

The Queen of Hearts had stated "Not OMI with low confidence"

There was a previous ECG available:

This confirmed my opinion.

I found out later that the patient had gone to the cath lab.  And I found out that the cath lab activation was a result of this follow up ECG:

I find this to be a negative ECG, except that there is now new ST Depression in V4-V6.

However, there is new tachycardia, and that new ST depression could be a result of supply-demand ischemia from tachycardia.

This time, the Queen of Hearts diagnosed this as "OMI with High Confidence."

This Queen interpretation led to a false positive cath lab activation.

Alternative Management: Always look into the patient's chart!! (including the old ECG above, which was not seen)

In fact, I found that I had blogged this patient before (!!!) due to the ECG that looked like inferior aneurysm.  There were many previous similar ECGs.  Here is that post: 

A Patient with Vertigo

Angiogram 3 months ago:

Severe three vessel native CAD with occlusion of the mid-Cx, mid-LAD, and mid-RCA including several areas of in-stent stenosis or occlusion.  4/4 patent bypass grafts (RIMA > dLAD, LIMA > OM, SVG > rPDA, and free radial > rPLA1) with severe native vessel stenosis just beyond the anastomosis in the dLAD, OM, and rPDA

Previous coronary disease and h/o CABG tells you that there probably is an old infarct and that the baseline ECG is likely to be abnormal and that you should read the present ECG in that context.

Previous Echo:

Normal left ventricular cavity size, mildly increased wall thickness and moderate LV systolic dysfunction.

The estimated left ventricular ejection fraction is 35-40 %.

Regional wall motion abnormality- basal inferior akinetic.

Regional wall motion abnormality- basal inferolateral, akinetic.

Regional wall motion abnormality-apex small .

An Akinetic wall can have the same "LV aneurysm" Morphology as a Dyskinetic wall ("diastolic dyskinesis" is the echo definition of aneurysm.)

The cath lab was activated and there was no acute OMI.  False Positive.

Discussion:

These are very complex cases in which there could be OMI or there could be old MI.  These are the kind of cases in which you want to consult your friendly cardiologist and have a discussion.  But that is only if your cardiologists accept the idea of OMI (Acute Coronary Occlusion in the Absence of ST Elevation criteria).  To make such a consultation,  there must be mutual trust that the consultant will not dismiss your concerns or say "Nah, couldn't be."

It can take years to build such trust.

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

MY Comment, by KEN GRAUER, MD (7/30/2024):

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

The "theme" of My Comment in today's case is — Shape is KEY!

• For clarity and ease of comparison in Figure-1 — I've labeled and put together the initial 2 ECGs in today's case.

MY Thoughts on ECG #1:

This is a complex tracing. I saw the following:

• There is significant baseline artifact. This is relevant to our interpretation given the difficulty it poses for assessment of ST-T wave changes in multiple leads.
• That said — the rhythm is clearly sinus with a normal PR interval.
• QRS morphology is not normal. That said — the QRS is really not wide (ie, not more than 0.10 second). Given the all upright QRS complex in lead V1, with narrow but definite terminal S waves in lateral leads I and V6 — this QRS morphology is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• The QTc is prolonged (I measure the QT at ~0.44 second — which corrected for the rate of ~80/minute, comes out to a QTc ~0.49 second).
• There is marked LAD (Left Axis Deviation) — with entirely negative QRS complexes in each of the inferior leads. This is consistent with LAHB (Left Anterior HemiBlock).
• There is RAA (Right Atrial Abnormality) — as determined by the presence of tall, peaked and pointed P waves in the inferior leads (ie, P waves ≥2.5 mm in amplitude).
• There may be RVH (Right Ventricular Hypertrophy) — which always needs to be considered if there is true right atrial enlargement. Because of the artifiact — we can not tell if QRS morphology in lead V1 is triphasic (rsR') or represents a qR pattern, which could be consistent with pulmonary hypertension (for more on RAA, RVH — See My Comment in the February 12, 2023 post).
• There may be LVH by Peguero criteria (See My Comment in the June 20, 2020 post) — as suggested by the very deep S waves in leads V3 and V4 (with the PURPLE arrow in lead V3 showing that S wave amplitude is cut off in this lead).

Regarding Q-R-S-T Changes:

• More than inferior Q waves — there is marked fragmentation on each downslope of the S wave in the inferior leads (RED arrows in these leads). It is because of this marked fragmentation that the “attempt” to form a positive deflection in each inferior lead never makes it back to the baseline before being overtaken by resumption of S wave negativity. In my experience — this fragmented QRS shape in any one (let alone all 3) of the inferior leads strongly suggests inferior infarction at some point in time.
• Regarding R wave progression — I interpreted the seemingly multi-phasic upright complex in lead V1 as the result of IRBBB rather than RVH because: i) There is marked LAD with no more than modest depth of the S wave in lead I; and, ii) I thought the overall ECG picture more suggestive of coronary disease rather than RVH. Yet predominant positivity never occurs in the lateral chest leads — and I could not rule out the possibility of RVH on this ECG alone.
• The shape of the S-T segments in the inferior leads is coved, of relatively long duration, and shows slight ST elevation. This shape forms a “picture to remember” — that does not look acute. That this inferior lead ST-T wave appearance is unlikely to be acute — is further supported by a lack of reciprocal ST depression in high-lateral leads I and aVL. Instead (as per Dr. Smith) — this “picture” strongly suggests inferior wall aneurysm, especially given the inferior lead S wave fragmentation marker of prior inferior MI described above.
• Finally — there is ST segment straightening and depression beginning in lead V3 beyond that expected for simple IRBBB (BLUE arrows in the chest leads).

BOTTOM Line: Like Dr. Smith — as a single ECG that I interpreted knowing only that the patient had "chest pain" — I thought ECG #1 did not look acute. But there are multiple complexities that beg further explanation.

• I suspected prior inferior MI with IRBBB/LAHB — and now with inferior wall aneurysm. There is ST depression in leads V3-thru-V5 that I thought likely to reflect multi-vessel disease — but with need to explain the reason for RAA, probable LVH, and possible RVH. But – not an OMI.
• As per Dr. Smith — this patient turned out to have Troponin elevation due to Type-2 MI (clean coronaries on cath). Instead — his clinical presentation was dominated by acute renal failure with severe acidosis. We are left with more questions than answers (ie, How severe is his underlying coronary disease? Any RVH or pulmonary hypertension?) — but this is not the ECG of acute coronary conclusion.
• Personal NOTE: I have been fooled more than once by chest pain in the setting of severe underlying disease (ie, acidosis, sepsis). The KEY is to recognize that ECG #1 is unlikely to represent an acute OMI — with clinical priority to treat underlying conditions, and to then reassess symptoms and repeat ECGs as needed.

Figure-1: I've labeled the initial 2 ECGs in today's case.

MY Thoughts on ECG #2:

I found today’s 2nd tracing easier to interpret — in that there were far fewer complicating findings.

• The rhythm is sinus — with normal intervals (PR-QRS-QTc). There is LAD (negative QRS in lead aVF) — but an axis not leftward enough to qualify as LAHB (predominant positivity in lead II).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are very large and wide Q waves in leads III and aVF — with a small-but-present Q wave in lead II (RED arrows in these leads). This patient has had inferior infarction at some point in time.
• R wave progression shows slight delay in transition (the R wave only becomes taller than the S wave is deep between lead V4-to-V5).
• S-T elevation is seen in each of the inferior leads, followed by a prominent upright T wave. That said — the shape of the elevated inferior lead ST segments manifests an upward concavity (ie, "smiley" configuration). As per Dr. Smith — this shape is less likely to represent an acute cardiac event.
• Although both high-lateral leads ( = leads I and aVL) manifest ST depression — the precise mirror-image opposite ST-T wave picture from lead III — is seen in lead aVL (within the BLUE rectangle, in which I merely inverted one QRST complex from lead III). This to me suggested a similar acuity (or lack thereof) for both lead aVL and the inferior leads.
• There is slight, nonspecific ST-T wave flattening in leads V1,V2 and V6.

BOTTOM Line: Once again, as a single ECG that I interpreted knowing only that the patient had “chest pain” — I thought ECG #2 did not look acute. 

• The deep, wide Q waves in leads III and aVF (with small-but-present Q in lead II) — strongly suggest prior infarction. This patient almost certainly does have underlying coronary disease. Clinically, if I was managing this patient — more information would clearly be needed (ie, specifics of the history; repeat ECG; troponins; comparison with prior tracings, etc.). But as a single ECG without the benefit of more information — the shape of these inferior lead ST segments — and the lack in the chest leads of any suggestion of associated acute posterior involvement — suggest this is not the result of acute coronary conclusion.
• As per Dr. Smith — review of this patient's chart told the story. Not surprisingly — the patient had very severe underlying coronary disease — but no acute OMI.

 

What diagnosis might you strongly suspect from the ECG in this patient with chronic progressive shortness of breath?

Written by Magnus Nossen

ECG interpretation is largely based on pattern recognition. Today's case provides another example of an ECG pattern that you can put in your memory bank. There are numerous different patterns one needs to learn in order to master the art of ECG interpretation. 

The recording was obtained from a 20 something female complaining of chronic progressive shortness of breath. 

Can you make the diagnosis of the patient in today's case off of the ECG? 

What is on your list of differential diagnoses? 

The ECG in todays post shows normal sinus rhythm. The HR is about 80bpm. There is normal AV conduction. There is an incomplete RBBB with and rSr’ QRS morphology in the right precordial leads V1-V2. Borderline right axis deviation. The QRS duration is less 100ms. Incomplete RBBB can be a normal finding. There are T wave inversions extending to V3. There is fragmentation/notching of all three R waves in the inferior leads. 

The above constellation of findings, notching of the QRS in all three inferior leads accompanied by an incomplete or complete RBBB is quite specific for hemodynamically significant ASD.  

Above you can see the inferior leads beneath each other. One QRS complex has been magnified from each lead. The QRS notching is apparent. This is the Crochetage sign.

The patient in today's case was found to have both a large secundum type ASD as well as partial anomalous pulmonary venous return in which one of the pulmonary veins drained to the right atrium. Both the ASD and the anomalous pulmonary venous return will give volume overload of the right heart causing the ECG findings in today's case. 

The chief complaint in today's case was SOB. The symptoms had progressed over time. Had there been acute onset of symptoms a pulmonary embolus would have had to been ruled out. It is important to identify patients with large ASDs as these patients are at risk of paradoxical embolism and large ASD are also associated with right heart failure. Timely intervention is needed to prevent irreversible damage to the pulmonary vasculature and the right heart. The patient in todays case underwent surgical correction of her congenital heart defect. 

Learning points:

Crochetage sign is strongly associated with hemodynamically significant left to right shunts at the atrial level. 

(Most commonly caused by large ASD) 

Acute and chronic RV strain can have some similar ECG findings, but acute right heart strain is usually not associated with QRS fragmentation in the inferior leads. 

Crochetage sign is associated paradoxical embolism and can be a clue to the cause of cryptogenic stroke

A young woman with epigastric pain. ECG Crochetage sign? What is the significance?

Crochetage sign

Crochetage sign LITFL

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

MY Comment, by KEN GRAUER, MD (7/28/2024):

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

Nice case by Dr. Nossen that reviews the Crochetage Sign (which I discussed in My Comment from the January 8, 2020 post in Dr. Smith's ECG Blog). Depending on the clinical setting in which you practice — this may (or may not) be an ECG sign that you have encountered.

• That said — the combination of ECG findings described by Dr. Nossen in today's case, in association with the clinical history of a young woman complaining of progressive shortness of breath — should prompt immediate consideration of a potential hemodynamically significant ASD (Atrial Septal Defect).

ECG Findings in Today's Case:

As per Dr. Nossen — the ECG signs of a significant ASD in today's case include the following: i) Incomplete RBBB pattern (rSr' in lead V1 — with narrow terminal S waves in lateral leads I and V6); — ii) Vertical (nearly rightward) frontal plane axis (suggested by the nearly more-negative-than-positive S wave in lead I); iii) RV "strain" — suggested by deep and symmetric anterior T wave inversion; — and, iv) The Crochetage Sign.

• For clarity in Figure-1 — I've reproduced Dr. Nossen's magnified illustration of the crochetage sign in today's case.

Figure-1: I've added WHITE arrows to highlight the crochetage sign in each of the inferior leads.

Regarding the Crochetage Sign:

As I reviewed in the January 8, 2020 post — the term “crochetage” is French. The infinitive of the verb that means “to crochet” ( = crocheter in French) — and the initial literature on this subject came out of Paris in 1996 by Heller et al in JACC. 

• The study by Heller et al is noteworthy, because their conclusions hold true today, more than 20 years later. Their study was based on evaluation of 1,560 older children and adults — in which they searched for a Crochetage Pattern ( = a notch on the upstroke of the R wave in one or more of the inferior leads). Five different types of valvular heart disease were present among subjects in their study (about 1/3 had secundum atrial septal defect) — and about 1/3 of the patients were normal subjects.
• There was a high (but far-from-perfect) correlation between the presence of crochetage in the patients with ASD (Atrial Septal Defect). Specificity for ASD greatly increased (ie, ≥92% in their study) when crochetage was seen in all 3 of the inferior leads — and/or — when incomplete RBBB (IRBBB) was also present.
• I don’t believe the mechanism for the crochetage “notch” on ECG with ASD is known. What has been observed — is that presence of crochetage showed good correlation to shunt severity. Of interest — early disappearance of crochetage was observed in ~1/3 of patients following surgical correction (though the IRBBB pattern persisted).

NOTE: Although descriptions vary in the literature that I've seen — true crochetage is said to occur on the upstroke of the R wave in inferior leads, occurring within the first 80 msec. of the QRS. So in today's ECG — the notching (WHITE arrows in Figure-1) — simulates the triphasic pattern of rbbb conduction in lead III — occurs on the upstroke in lead aVF — but on the downstroke (instead of the upstroke) of the R wave in lead II. That said — many of the examples that I've seen posted on-line are not necessarily on the "upstroke" of the R wave. 

• Clinical Question: — What we should make of notching that we occasionally see in one or more of the inferior leads as a result of any of the following: i) Artifact; ii) A "rbbb equivalent" pattern (in which a triphasic complex may be seen in lead III and/or lead aVF — with similar implication as an incomplete RBBB pattern); — or — iii) As a result of scarring (fragmentation) in a patient with prior infarction and/or cardiomyopathy. That is — How to distinguish occasional inferior lead notching from crochetage that is likely to be a "true" marker of a significant ASD?
• Application of Bayes' Theorem may help in answering this clinical question (See My Comment in the April 19, 2024 post in Dr. Smith's ECG Blog) — in that the prevalence of an ASD in the population being looked at should prove insightful (ie, Notching in 1 or 2, but not 3 inferior leads — in an otherwise asymptomatic patient without IRBBB or RV "strain" — is unlikely to be a marker for ASD).
•  
• Final Clinical Point: Listen carefully for signs of ASD (ie, fixed split S2) when inferior lead notching is seen — especially if incomplete RBBB or RV "strain" is seen — and have a low threshold for getting an Echo if ASD is a consideration.

Resuscitated from ventricular fibrillation. Should the cath lab be activated?

This patient was witnessed by bystanders to collapse.  They started CPR.  EMS arrived and found him in Ventricular Fibrillation (VF).  He was defibrillated into VT.  He then underwent dual sequential defibrillation into asystole.  After 1 mg of epinephrine they achieved ROSC.  Total prehospital meds were epinephrine 1 mg x 3, amiodarone 300 mg and 100 mL of 8.4% sodium bicarbonate.

The patient was brought to the ED and had this ECG recorded:

What do you think?  And what do you want to do?

The ECG shows severe ischemia, possibly posterior OMI.   But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia.  It takes time for that ischemia to resolve.  After cardiac arrest, I ALWAYS wait 15 minutes after an ECG like this and record another.  The ST depression usually resolves, or is clearly resolving (getting much better).

Just as important is pretest probability: did the patient report chest pain prior to collapse?  Then assume there is ACS.  In this case, the patient was 30 years old and there was reportedly some drug paraphernalia in the area.  This may or may not be true, but it should give you pause.  On the other hand, cardiac arrest from opiates is respiratory arrest followed by cardiac arrest, and the rhythm is usually brady-asystole, not ventricular fibrillation.  VF should make you think of ischemia, cardiomyopathy (especially scar from old MI), or one many other cardiac but non-ischemic etiologies.

In this case, the cath lab was activated and the patient had a normal angiogram.

See these related cases:

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

Cardiac arrest #3: ST depression, Is it STEMI? or is he an ACCESS Trial Candidate?

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

MY Comment, by KEN GRAUER, MD (7/25/2024):

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

Clinical ECG interpretation is a 2-Step process.

• For clarity in Figure-1 — I've reproduced today's ECG — obtained following successful resuscitation of out-of-hospital cardiac arrest.

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

   — The 2 Steps in ECG Interpretation —

STEP #1: Describe what you see ....

• The rhythm in Figure-1 is rapid and supraventricular (the QRS is narrow in all leads). The rate is ~130/minute. Although not immediately apparent (because it is hard to distinguish the limits of a P wave in lead II) — the rhythm is Sinus Tachycardia, as other leads correspond to the timing of what seems to be an upright deflection that is subtly notching the end of the T wave in lead II (and which almost certainly represents the sinus P wave). Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit (as the patient's condition improves) — allowing clearer definition between the T and P waves.
• Otherwise — there is early transition (predominant R wave already by lead V2) — and what appears to be generous voltage (that is probably not abnormal given the young adult age of today's patient).
• 
  
• The most remarkable finding is in Figure-1 — is the diffuse and marked ST depression (most prominent in the chest leads) — with ST elevation in lead aVR > V1.

================================= 

STEP #2: Clinically apply to the case at hand ....

• The ECG "picture" that we see in Figure-1 of a supraventricular rhythm with diffuse ST depression, except for ST elevation in lead aVR (and to a lesser extent in lead V1) — defines the important clinical entity known as DSI (Diffuse Subendocardial Ischemia).

As we have often emphasized on Dr. Smith's ECG Blog (See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease. Many patients with DSI do have severe coronary disease — but many do not. Therefore — recognition of DSI on ECG should prompt consideration of 2 Categories of diagnostic entities:

• Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• 
  
• Subendocardial Ischemia from some other Cause (ie, sustained tachycardia — sinus or from some other arrhythmia; shock/profound hypotension; GI bleeding; anemia, etc.) — or, potentially as occurred in today's case — Cardiac arrest secondary to respiratory arrest from a non-cardiac cause.

In Summary: Today's case serves as a reminder of the 2-Step process in clinical ECG interpretation. Rather than slowing the interpretation down — ECG assessment is actually sped up.

• Description of today's ECG findings (Sinus tachycardia with diffuse ST depression and ST elevation in aVR) — is diagnostic of DSI. 
• As demonstrated by Dr. Smith in his above discussion — Application of the ECG findings in Figure-1 to today's clinical scenario (ie, marked sinus tachycardia in this younger adult with drug overdose and respiratory arrest) — provides an immediate and much more likely explanation for DSI than trying to postulate ACS.

ECG Podcasts on 12-Lead & Arrhythmias — Pearls, Pitfalls, OMI & AI and Lots More

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

• I recently recorded a series of 4 podcasts regarding KEY concepts in ECG interpretation.
•     Easy LINK —  https://tinyurl.com/KG-Blog-431 —

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

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

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 tachycardia) without 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 — 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 Comment at the bottom of the page of the February 18, 2024 post in Dr. Smith's ECG Blog.

And regarding arrhythmias:

• For more on the regular WCT — See My Comment in the May 5, 2020 post and in the April 15, 2020 post in Dr. Smith's ECG Blog. 
• For more on the regular SVT — See My Comment in the October 25, 2022 post and in the March 6, 2020 post in Dr. Smith's ECG Blog
• For more on recognizing AFlutter — See My Comment in the May 1, 2023 post in Dr. Smith's ECG Blog.

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

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 Error — is 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); — and, ii) The new QOH (Queen Of Hearts) 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 experience. I 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. 

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: My comments are divided 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 ECGs. What 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 V1; III, 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 identical) regardless 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 — 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.