Saturday, October 28, 2023

ECG Blog #401 — What Kind of Block?

The ECG in Figure-1 was obtained from an elderly woman — who presented to the ED (Emergency Department) for dyspnea on exertion over recent weeks
  • What are YOUR "Quick Thoughts" about this case?

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

MY "Quick Thoughts" on Today's CASE:
The ECG in Figure-1 is highly concerning — so it is indeed fortunate that this elderly woman came to the ED when she did!
  • The rhythm in Figure-1 is complex — and defies precise interpretation without careful study. That said — obvious findings include: i) Marked bradycardia!ii) Tiny-but-definitely present P waves in the long lead V1 rhythm strip — which at 1st glance look like they may (?) be regular! — iii) Non-conduction of a number of these regular P waves — suggesting at least some form of significant AV block; — and, iv) At least 3 different QRS morphologies (if not more) — which considering that the lead monitored is lead V1, may represent variations of normal, RBBB and LBBB conduction! (Right and Left Bundle Branch Block conduction).

  • PEARL #1: The goal of clinical ECG interpretation of a tracing such as this one is to expedite interpretation of "the essentials" — and to leave details of the ECG and rhythm strip shown in Figure-1 until later, when time is available. I therefore intentionally did not dive deeper than the  4 general conclusions noted above in the 1st bullet — which took me no more than seconds to arrive at! My Immediate Impression — was that this elderly woman with a several week history of symptoms would most likely leave the hospital with a pacemaker.

 Interpretation of the 12-lead ECG in Figure-1 is no easy task! This is because there are multiple QRS morphologies — and we do not yet know which are supraventricular (nor with what kind of conduction propoerties).  That said — LOOK to see if there is an underlying rhythm!

  • Beats #5 and #7 look to be narrow and are both preceded by P waves with a constant and normal PR interval. This suggests that beats #5 and #7 are probably normal sinus-conducted beats. This means that we can assess ST-T wave morphology for ischemic changes in simultaneously-recorded leads V1,V2,V3 for beat #5 — and in leads V4,V5,V6 for beat #7.

  • There is deep, symmetric T wave inversion with a prolonged QTc interval in anterior leads V1,V2,V3. This suggests ischemia of uncertain duration.
  • The ST-T wave appearance in leads V4,V5,V6 is less worrisome — with shallow T inversion in V4 — and ST segment flattening with slight depression in leads V5,V6 — but which does not look acute.

  • Beyond-the-Core: Advanced interpreters may already suspect that beat #2 in the long lead V1 rhythm strip is sinus-conducted with RBBB (given its rSR' morphology in lead V1 — and being preceded by the same PR interval before this beat as was seen for sinus beats #5 and 7)
  • Similarly — Advanced interpreters may also suspect that beat #4 in the long lead V1 is sinus-conducted with LBBB (given its all negative QRS in lead V1, and its monophasic positive morphology in lead aVL — also preceded by the same PR interval as for the other sinus-conducted beats).
  • The "good news" — is that ST-T wave appearance in simultaneously-recorded leads I,II,III for beat #2 — and in leads aVR,aVL,aVF for beat #4 — does not look acute.

IMPRESSION of Today’s Tracing:
The main problem in today's case of this elderly woman with a several week history of dyspnea on exertion — is the markedly bradycardic rhythm with some form of AV block
  • Given this patient's older age — if nothing "fixable" is found, she most likely has SSS (Sick Sinus Syndrome) and will need a pacemaker (See ECG Blog #342 for more on SSS).
  • Given the history of dyspnea on exertion over a several week period (but no mention of chest pain) and — the finding of deep, symmetric T wave inversion in the anterior leads (as per Pearl #2) — it is possible that the onset of her symptoms is the result of a "Silent MI" (See ECG Blog #228 for more on "Silent" MI)
  • KEY Point: As fascinating as today’s rhythm disorder is — a detailed explanation for the mechanism of this rhythm is not needed for optimal clinical management. Instead — the clinical points summarized in the above 2 bullets suffice! That said — I believe appreciation of the probable mechanism for today's rhythm is instructive, and reinforces our interpretation. For those with an interest in learning more — Follow along with me below!


Looking Closer at Today's Rhythm:
Regardless of whether you recognized the advanced points I raised above under "Beyond-the-Core" the KEY is to recognize the marked bradycardia with some form of significant AV block, with need for referral for possible (probable) pacemaker implantation.
  • CREDIT if you also recognized the deep, symmetric anterior T wave inversion — suggestive of possible "silent MI" several weeks earlier at the time this patient's symptoms began.

Next Steps for Determination of the Rhythm:
  • The easiest next step in interpretation — is to label P waves in the long lead V1 rhythm strip. It is because of the small amplitude of P wave deflections in this lead — that calipers so greatly facilitate (and speed up) detection of atrial activity.

  • PEARL #3: I've labeled with RED arrows in Figure-2 — the P waves in the long lead V1 rhythm strip. Some of these P waves are partially hidden within some of the T waves. This is precisely where calipers assist: — Select 2 P waves in a row that you definitely see. Then "walk out" this caliper setting throughout the entire lead V1 rhythm strip.

  • PEARL #4: Take another LOOK at the long lead V1 rhythm strip in Figure-2. Now that all P waves are labeled — Isn't it much easier to appreciate that the PR intervals before beats #1,2; 4; 5; 6; 7; and 8 are all the same! This tells us that despite the different QRS morphologies — each of these beats is sinus-conducted!

Figure-2: I've labeled all P waves in today's rhythm with RED arrows.

WHY so many QRS Morphologies?
I've already alluded to why there are multiple QRS morphologies. LOOK at Figure-3 — in which I've added colored labels to facilitate discussion.
  • RED arrows in Figure-3 highlight sinus-conducted P waves — because each of the QRS complexes that follow these P waves (ie, beats #1,2,4,5,6,7 and 8) is preceded by a constant and normal PR interval.

  • YELLOW arrow P waves are not conducted. It should be apparent that there is "high-grade" 2nd-degree AV block — because in the presence of a regular atrial rhythm, we see several instances in which consecutive YELLOW arrow P waves do not conduct despite adequate opportunity to do so (See ECG Blog #399 — for more on "high-grade" AV block).

  • I distinguish the remaining P wave with a BLUE arrow — because this P wave has a longer PR interval than all of the RED arrow P waves — and is followed by a non-conducted (ie, YELLOW arrow) P wave after beat #3. This suggests that beats #2 and #3 form a 3:2 cycle of AV Wenckebach (ie, Mobitz I 2nd-degree AV block).
I have also labeled the different QRS morphologies in Figure-3:
  • PEARL #5: The beauty of having a 12-lead ECG with a simultaneously-recorded long lead rhythm strip below it — is that this provides us with "4 looks" at QRS morphology for each of the 8 beats in today's rhythm.

  • Beats #1,4,6 and 8 — all look similar in the long lead V1 rhythm strip (ie, they all manifest a wide negative QRS complex). The reason that I know this is consistent with LBBB conduction — is that we see the typical all-positive, wide upright QRS for beat #1 in simultaneously-recorded lead I — for beat #4 in lead aVL — and for beat #8 in lead V6. QRS morphology for beat #6 is also consistent with LBBB conduction — because the QRS is predominantly negative in each of the anterior leads.
  • Beat #2 is consistent with RBBB conduction — because it manifests an rSR' in the long lead V1 — with a wide terminal S wave in simultaneously-recorded lateral lead I.
  • I also labeled beat #3 as consistent with RBBB conduction — because of its similarity to the QRS appearance of beat #2 in the long lead V1 rhythm strip.
  • Beat #5 is not wide, but manifests a small r' deflection in the long lead V1 — so this beat most probably reflects incomplete RBBB conduction.

  • PEARL #6: Indication for permanent pacing is justified in today's case on multiple grounds, including: i) This elderly patient with marked bradycardia has been symptomatic for weeks; ii) Her rhythm is high-grade 2nd-degree AV block; and, iii) There is alternating BBB (Bundle Branch Block) — which of itself is indication of severe conduction system disease at risk of developing ventricular standstill. 

Figure-3: I've added colored labels of P waves and QRS complexes to facilitate discussion of conduction properties (See text).

Laddergram Illustration:
At this point — I needed to work out, and then draw a laddergram that I could then verify to ensure a plausible mechanism for today's arrhythmia.
  • Sequential legends over the next 4 Figures illustrate my thought process. (See ECG Blog #188 for review on how to read and/or draw Laddergrams).

  • To EMPHASIZE: Today's laddergram was challenging. I fully acknowledge needing several attempts until I could finally derive a plausible mechanism involving dual-level block out of the AV node. That said — my hope is that even readers with limited experience with laddergrams will be able to follow the mechanism I propose in my final Figure-7.

Beginning the Laddergram:

Figure-4: It is usually easiest to begin a laddergram by marking the path of sinus P waves through the Atrial Tier (as per the RED lines drawn directly below the onset of each of the P waves — as shown here by the large GREEN arrows). Note that these RED lines in the Atrial Tier are nearly vertical — since conduction of sinus P waves through the atria is rapid. Note also that the P-P interval between successive P waves (vertical RED lines) is similar, albeit not quite equal (ie,There is slight sinus arrhythmia).

Figure-5: The most challenging part of most laddergrams is construction of the AV Nodal Tier — so I typically save that for last. Therefore, after drawing in all P waves into the Atrial Tier — It's easiest to next add in the Ventricular Tier the indication of all QRS complexes that are conducted. Perhaps the most complex aspect of today's rhythm — is realization that despite the changing QRS morphologies — each of the 8 beats in the long lead V1 rhythm strip are sinus-conducted beats! The large GREEN arrows show that I use the onset of each QRS complex as my landmark for entering beats #1-thru-8 into the Ventricular Tier.

Figure-6: As noted — each of the 8 beats in today's rhythm are sinus-conducted beats, albeit with different conduction properties! To better illustrate normal, RBBB or LBBB conduction — I've added light BLUE and PINK butt ends into the Ventricular Tier to schematically show the conduction defects. With completion of the Atrial and Ventricular Tiers — I was ready to begin solving the laddergram — which entailed postulating which of the P waves from the Atrial Tier would be able to make it through the AV Nodal Tier to be conducted to the ventricles. 

PEARL #7: Because of the complexity of today's rhythm — I went through some trail-and-error before arriving at the laddergram I propose below in Figure-7. Two KEY principles figured in my arriving at this laddergram:
  • Principle #1: It is extremely unusual for a patient to alternate between Mobitz I and Mobitz II. As a result — IF there is clear evidence of 2nd-degree AV block, Mobitz Type I somewhere on the tracing you are interpreting (or somewhere in other recently-obtained telemetry monitoring rhythm strips) — then it becomes highly likely that some form of Wenckebach conduction is responsible for other unknown forms of AV block that you see on that patient's ECG. 
  • As noted earlier — the increasing PR interval from beat #2-to-beat #3, followed by the non-conducted (YELLOW arrow) P wave after beat #3 — is consistent with a 3:2 cycle of AV Wenckebach (ie, Mobitz I 2nd-degree AV block). This makes it highly likely that the 2:1 block of beats #1,4,5,6,7 and 8 are also a manifestation of Wenckebach conduction.

  • Principle #2: Simple AV Wenckebach results in non-conduction of a single on-time P wave. But as per the YELLOW arrow P waves in Figure-7 — we see consecutive on-time, non-conducted P waves within several of the R-R intervals — which strongly suggests there is dual-level block out of the AV node! (See ECG Blog #347 for more on dual-level AV Wenckebach).

Putting It All Together:
  • As discussed in ECG Blog #347 — the DOTTED line in the AV Nodal Tier in Figure-7 schematically illustrates the 2 levels of exit block out of the AV Node.
  • We know that beats #2 and 3 are conducted to the ventricles in a 3:2 AV Wenckebach cycle.
  • We know that beats #1,4,5,6,7 and 8 are also all conducted beats, albeit with alternating bundle branch block.
  • This leaves us with having to postulate a path of transmission for each of the non-conducted (YELLOW arrow) P waves — in which the 3 R-R intervals that contain consecutive YELLOW arrow P waves — must manifest block of 1 of these P waves at each of the 2 levels within the AV Nodal Tier (which I schematically show in Figure-7).

Figure-7: My proposed laddergram for today's complex rhythm.


CASE Follow-Up:
Following assessment of this patient's initial rhythm — she was admitted to a monitored floor with plans for pacemaker placement. Unfortunately, before this could be accomplished — the patient went into cardiac arrest. She was successfully resuscitated — with a post-arrest rhythm similar to that seen in Figure-1.
  • Cardiac cath did not reveal significant coronary disease! So although I initially suspected that the deep anterior T wave inversion in the 12-lead tracing shown in Figure-1 (in association with the several week history of dyspnea) might reflect the occurence of a "silent" infarction at the time this patient's symptoms began — the negative cath argues against this. Instead — the negative cath favors more of a pure history of SSS (Sick Sinus Syndrome) in this elderly woman (See ECG Blog #342 for more on SSS — and ECG Blog #228 for more on "Silent" MI).

  • A permanent pacemaker was placed.

As always — welcome questions and/or comments on today's ECG Blog post! THANK YOU for your interest! 

Acknowledgment: My appreciation to Hans Helseth  (from Minnesota, USA) for the case and this tracing (and CREDIT to Hans for his well-drawn laddergram that I have slightly modified).

Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #188 — Reviews how to read and draw Laddegrams (with LINKS to more than 90 laddergram cases — many with step-by-step sequential illustration).

  • ECG Blog #192 — The Causes of AV Dissociation.
  • ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.

  • ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".

  • ECG Blog #259 — Reviews the concept of Dual-Level ABlock.
  • The October 25, 2021 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews my approach to another case of a Dual-Level Wenckebach block. 
  • ECG Blog #226 — Works through a complex Case Study (including an 11:00 minute ECG Video Pearl that walks you through step-by-step in the construction of a laddergram with Wenckebach conduction and dual-level block within the AV node).
  • ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.

ADDENDUM (10/28/2023):

This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.
  • Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks.
  • Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT thAV Blocks are — and what they are not!

ECG Media PEARL #71 (5:45 minutes Audio) — Reviews the phenomenon of Dual-Level Wenckebach out of the AV Node (HOW to recognize this phenomenon — and how to distinguish it from Mobitz II).


Saturday, October 21, 2023

ECG Blog #400 — Is this a NSTEMI?

The ECG in Figure-1 is from an older man with known coronary disease — who presents to the ED (Emergency Department) with new CP (Chest Pain) over the past several days. Troponin is pending.

  • In view of this history — How would you interpret the ECG in Figure-1?
  • Should the cath lab be activated?

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

MY Thoughts on the ECG in Figure-1:
Unfortunately — there is significant baseline artifact in today’s initial ECG (especially in the limb leads). That said — this artifact does not prevent accurate assessment because despite the thick, limb lead baseline undulations — overall QRST wave morphology remains consistent throughout the tracing.
  • The rhythm is sinus at ~75/minute. Intervals (PR, QRS, QTc) and the frontal plane axis are normal (about 0 degrees, given the isoelectric QRS in lead aVF). There is no chamber enlargement.

  • Regarding Q-R-S-T Wave Changes: There are no Q waves — and R wave progression is normal (with appropriate R wave amplitude in the anterior leads — and appropriate transition, in that the R wave becomes taller than the S wave is deep by lead V4).

Assessment of ST-T Waves in Figure-1:

In a patient with new CP — this is an extremely worrisome ECG!

  • There is J-point ST depression — with sharply angled downsloping ST segments in multiple leads. These depressed ST segments end with terminal T wave positivity in leads II,aVF; and in leads V2-thru-V6.

  • There is ST elevation in lead aVR > V1 (dotted RED lines in leads in Figure-2). The ST segment is flat in lead III.

  • IMPRESSION: Even without the benefit of a prior ECG for comparison in this patient with known coronary disease — the above noted ST-T wave changes in Figure-2 look acute. In this patient with new CP — the cath lab should be activated!

PEARL #1: Although seeing an elevated Troponin would provide additional support for immediate cardiac catheterization — the clinical reality is that the initial Troponin reading will not always be elevated in patients with acute coronary occlusion (See March 24, 2023 post in Dr. Smith's ECG Blog).

  • Since the initial Troponin will not always be elevated in patients with acute OMI ( = acute Occlusion-based MI) — an initial normal high-sensitivity Troponin should not be used to rule out acute OMI in patients with new CP and an abnormal ECG
  • Therefore — waiting until Troponin becomes elevated wastes precious time (and risks loss of valuable myocardium). Given the history in today's case and the ECG shown in Figure-2 — The cath lab should be immediately activated!

Figure-2: I've labeled some findings from Figure-1.

PEARL #2: As noted above — ECG #1 is remarkable for the presence of diffuse ST depression (in more than 7 leads!) — with ST elevation in lead aVR (as well as in lead V1). This ECG pattern suggests Diffuse Subendocardial Ischemia (DSI) — and should immediately prompt the following differential Diagnosis:
  • 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 another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient", etc.).

To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI). Instead — it suggests ischemia due to the above differential diagnosis!
  • That said, in today's patient, who presents with new CP and the ECG shown in Figure-2 — severe coronary disease with potential need for acute reperfusion should be assumed until proven otherwise.

PEARL #3: In today's initial ECG — Did YOU notice the negative U waves in leads V3 and V4? (BLUE arrows in Figure-2)
  • Having looked for negative U waves in patients with chest pain over a period of decades — I'll emphasize that this is not a common finding. That said, when you do see inverted U waves (as we do in ECG #1) — this is a significant marker of severe ischemia (Duque-Gonzálex et al — Cardiovascular Metal Sci 32(4), 2021).

Today's CASE Continues:
The worrisome findings in ECG #1 were recognized.
  • The initial Troponin came back significantly elevated. However while waiting for this initial Troponin value to come back — the patient reported that his CP had greatly decreased, and was almost gone. A repeat ECG (shown in Figure-3) was obtained at this time.

  • Based on near resolution of the patient's CP and the improvement on the repeat ECG (as seen in Figure-3— the diagnosis of NSTEMI (Non-ST-Elevation MI) was made. The call for immediate cath lab activation was cancelled.

  • Do YOU agree with the above management decisions?
  • Why or why not?

Figure-3: Comparison of the repeat and initial ECGs in today's case.

MY Thoughts on Seeing the Repeat ECG:
Lead-to-lead comparison in Figure-3 of the initial ECG in today's case — with the repeat ECG (done after the patient's CP had almost resolved) — shows marked improvement.
  • ST-T waves in ECG #2 are now uniformly flat — with virtually no ST elevation or depression.

  • IMPRESSION: The fact that the patient's CP has virtually resolved in association with the ECG "improvements" shown in Figure-3 — does not mean that this was a "NSTEMI". Instead, this change in ECG appearance (in this patient who presented with new CP that has now almost completely resolved) — is indication of "dynamic" ST-T wave changes!

When the 
ECG changes evolve in a way that corresponds to the coming and going of chest pain symptoms — this is important information. It tells us there is an active, ongoing process — and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter-definition of a STEMI has been satisfied.
  • The problem is — that the "culprit" artery may spontaneously open and close more than once during its process of arriving at a final result — so that even if ST elevation resolves in association with resolution of chest pain — this spontaneous reopening of the vessel, may just-as-easily be followed by spontaneous closure again — and this time, perhaps without spontaneous reopening.
  • It is this active evolution of ST-T wave changes that may occur with the coming and going of symptoms that we define as "dynamic" ECG changes. ST segments elevate with the onset of chest pain (signaling acute coronary occlusion) — and ST segments return toward their baseline, often followed by "reperfusion" changes of T wave inversion that signal reopening of the "culprit" vessel. The importance of recognizing these "dynamic" ECG changes — is that this indicates an unstable situation at risk of evolving further to permanent coronary occlusion.

  • Today's case differs from the above description — in that other than reciprocal leads aVR and V1 — there was no ST elevation on the initial ECG. This is not to say that there never was a period of ST elevation — but rather that no ST elevation was captured on the one ECG that was recorded during the time that the patient had CP.
  • That said, today's patient with known coronary disease — presented with new CP and a worrisome ECG picture of diffuse subendocardial ischemia — with "dynamic" ST-T wave changes in association with relief of CP. 

  • BOTTOM Line: Because the situation described above in today's case is clearly unstable — prompt cardiac cath was immediately indicated (and given the history — prompt cath was indicated as soon as the initial ECG was recorded). Given this situation — the anatomy needs to be defined to determine if acute reperfusion with PCI will be needed to prevent imminent coronary occlusion. 

  • Unfortunately, when cardiac cath is only performed days later — OMI confirmation is not always possible (as was the case for today's patient — such that the "final diagnosis" of NSTEMI is questionable, as is probably the case for many patients said to have had "NSTEMI" ...)


Acknowledgment: My appreciation to 張三毛 = JJ (from Taiwan) 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 #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript). 
  • ECG Blog #222 — Reviews the concept of Dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • ECG Blog #260 — Reviews another case that illustrates the concept of "dynamic" ST-T wave changes.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

  • ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes.

  • The January 9, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case is remarkable for the dynamic ST-T wave changes that are seen. It's helpful to appreciate: i) That acute ischemia/infarction is not the only potential cause of such changes (cardiac cath was normal); ii) That changes in heart rate, frontal plane axis and/or patient positioning can not always explain such changes; andiii) That entities such as repolariztion variants, LVH and/or acute myopericarditis may all contribute on occasion to produce an evolution of challenging dynamic ST-T wave changes on serial ECGs.

  • The August 22, 2020 post in Dr. Smith's ECG Blog — which illustrates another case of dynamic ST-T wave changes that resulted from a repolarization variant

  • The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.


ADDENDUM (10/21/2023):

ECG Media PEARL #39a (4:50 minutes Audio) — Reviews the concept of Dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).

ECG Media PEARL #46a (6:35 minutes Audio) — Reviews HOW to compare Serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).