ECG Blog #440 — What is the "PVC Clue"?

The patient in today's case is an older man who called EMS for new CP (Chest Pain) — only to suffer witnessed cardiac arrest as the paramedics arrived on the scene. The patient was successfully resuscitated, and his initial ECG (shown in Figure-1) — was transmitted to the nearest cath-capable facility.

Treating clinicians (including the on-call cardiologist) refused to activate the cath lab on the basis of ECG #1 — saying, "There is no evidence of an acute STEMI, therefore no need for prompt cath with PCI".

QUESTIONS:

• Do YOU Agree with the above interpretation of ECG #1?
•   Should the cath lab have been immediately activated?

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

Need for Prompt Cath and PCI after Cardiac Arrest?

Because of how often the question arises as to the need for prompt cath with PCI following successful OHCA (Out-of-Hospital Cardiac Arrest) — I've copied my initial comments from ECG Blog #434: 

• There are different approaches regarding decision-making as to which patients with ROSC (Return Of Spontaneous Circulation) following OHCA should undergo prompt cardiac catheterization. What does appear to be clear — is that the post-ROSC ECG helps to identify which patients are at highest risk, and who therefore 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 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.
• 
  
•    — "MY Take" — It seems to be common sense that even if millimeter-based criteria for a STEMI are not present — that IF there are other ECG criteria indicative of acute coronary occlusion as the cause of OHCA — that prompt cath is not only reasonable, but should be advised.

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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. The rhythm is regular at ~100/minute ( = sinus tachycardia).
• The QTc appears to be slightly prolonged (although more difficult to assess given the rapid heart rate). The frontal plane axis is normal (+70 degrees). There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are tiny Q waves in leads III and aVF — which is not necessarily abnormal given the vertical axis.
• R wave progression is slightly delayed — with transition (where the R wave becomes taller than the S wave is deep) only occurring between lead V4-to-V5. That said, a definite initial positive deflection (r wave) is present in leads V2 and V3, with slight increase in size in lead V4 — so the significance of this finding is uncertain from this single ECG.

Figure-2: I've labeled key findings in today's initial ECG.

The KEY to assessment of ECG #1 regards ST-T Waves:

• The most striking findings are in lead aVL (within the RED rectangle in Figure-2) — in which there is coved ST elevation with straightening of the ST segment takeoff, followed by terminal T wave inversion. 
• 
  
• PEARL #1: Because of the small size of the QRS complex in lead aVL — the above noted abnormal ST-T wave findings are admittedly subtle. That said — the height of the hyperacute T wave in lead aVL matches the height of the r wave in this lead — and there is no denying the subtle-but-real terminal T wave inversion in aVL, which is never normal when following a hyperacute T wave.
• PEARL #2: Any doubt about the validity of the ST-T wave picture in lead aVL should be immediately resolved on seeing the abnormally straightened and depressed ST segments in each of the inferior leads (within the BLUE rectangles). In view of the terminal T wave positivity in leads II,III,aVF — these inferior leads manifest the mirror-image opposite picture of the elevated ST segment with terminal negativity seen in lead aVL ( = true reciprocal changes).
• 
  
• PEARL #3: It's important to appreciate in this older man with new CP, that IF we stopped here — the subtle-but-real ST elevation in lead aVL with indisputable reciprocal ST-T wave changes in each of the inferior leads is already diagnostic of an acute OMI until proven otherwise. That said, the fact that these limb lead ST-T wave changes are so suggestive — needs to increase our scrutiny of chest lead findings!
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• PEARL #4: Aren't the T waves in leads V2,V3,V4 (and probably also in lead V5) a bit "bulkier" than expected? By this I mean that the T waves in these leads look "fatter"-at-their-peak and wider-at-their-base than expected given modest amplitude of the QRS complex in these leads (BLUE arrows in Figure-2). Although admittedly subtle — in the context of this older patient with new CP and indisputable acute findings of ST elevation in aVL (with reciprocal ST depression in the inferior leads) — I interpreted these chest lead findings as suggestive of hyperacute T waves in multiple chest leads, consistent with acute LAD (Left Anterior Descending) OMI until proven otherwise.
• 
  
• To Emphasize — It can be challenging to determine what does and does not constitute a "hyperacute" T wave. Admittedly, this assessment is at times subjective (See ECG Blog #183 and ECG Blog #218 for more on this topic). The "good news" — is that practice increases one's comfort with recognizing when a given T wave is hyperacute. Ultimately — You can check yourself to see if what you thought was a "hyperacute" T wave, went on to evolve frank ST elevation in subsequent serial tracings.

PEARL #5 (Beyond-the-Core): As a more advanced point, having arrived at the presumptive diagnosis of acute LAD OMI in this older patient with new CP, who experienced out-of-hospital Cardiac Arrest, witnessed by EMS — I looked closer at the neighboring leads "sandwiching" the hyperacute T waves in leads V2-thru-V5.

• The ST segment in lead V1 is coved, and ever-so-slightly elevated. Considering small size of the QRS in this lead — this is not a normal appearance for the ST-T wave in V1.
• In lead V6 — the ST segment is straight and appears to be slightly depressed. This differs from the appearance of the ST-T wave in neighboring lead V5. 
• As discussed in ECG Blog #380 — in the setting of acute LAD OMI, the finding of ST elevation in lead V1 (especially when V1 manifests a different ST segment shape than the shape of the ST segment in other anterior leads) — plus — ST depression beginning in lead V5 or V6 — suggests the presence of precordial "Swirl" in Figure-2 (ie, in which the site of LAD occlusion is so proximal as to result in ischemia of the septum).

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To Emphasize: It only took seconds for me to arrive at my presumptive diagnosis of an acute OMI — simply by: i) Knowing that this older patient had new CP severe enough to call EMS; and, ii) Recognizing the presence of clearly acute ST-T wave changes within the 2 colored rectangles in Figure-2 (ie, in leads II,III,aVF and aVL).

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Today's CASE Continues:

Given the ECG findings in Figure-2 and the witnessed cardiac arrest — the EMS team felt justification of prompt cath with PCI was established.

• Unfortunately — it would take more convincing of the emergency physician and consulting cardiologist that cardiac cath was needed, because "ECG #1 did not satisfy criteria for a STEMI".

For clarity in Figure-2 — I've put the repeat ECG together with the initial ECG done 36 minutes earlier.

QUESTIONS:

• In light of the initial ECG — How would YOU interpret the repeat ECG done 36 minutes later?
• Was I correct in my suspicion that the T waves in the initial ECG were hyperacute?
• Do the PVCs in ECG #2 provide additional information?

Figure-3: Comparison between the 2 ECGs in today's case.

ANSWERS:

The underlying rhythm in today's repeat ECG is sinus. There are frequent PVCs — which appear to have a fixed coupling interval. Focusing on the sinus-conducted beats — there appears to be somewhat less ST depression in the inferior leads of ECG #2, as well as a less hyperacute appearance to the ST segment in lead aVL. But a very different impression is provided by what occurs in the chest leads!

• RED arrows in Figure-4 highlight ongoing evolution of the proximal LAD OMI. Thus, there is more ST elevation in lead V1 of the repeat ECG — new straightening of the ST segment takeoff in leads V2,V3,V4 — definite ST elevation now in leads V2,V3 — and clear increase in the hyperacute appearance of the more "voluminous" ST-T waves in leads V2-thru-V6.
• PEARL #6: Lead-by-lead comparison of the ST-T waves in the 2 ECGs in Figure-4 confirms my earlier suspicion that T waves in the chest leads of ECG #1 were indeed hyperacute!
• 
  
• PEARL #7: As I illustrated in ECG Blog #340 (See Figure-3 in that post) — PVCs may sometimes show clearly abnormal ST elevation that is diagnostic of an acute MI. This is seen for the PVCs within the dotted RED ovals below in Figure-4. 
• While not needed for diagnostic purposes in today's case (because the OMI is readily apparent from ST-T wave changes in sinus-conducted beats alone in Figure-4) — Awareness of PEARL #7 may prove invaluable for diagnosing acute OMI when no clear ST elevation is seen in sinus-conducted beats.

Figure-4: I've labeled key findings in the repeat ECG.

CASE Conclusion:

• Cardiac cath was performed — and confirmed 100% LAD occlusion at a point just distal to the 1st Diagonal. The patient was doing well in follow-up.

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Acknowledgment: My appreciation to Edward Brunacci (from Sydney, Australia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #228 — Reviews the concept of acute STEMI changes being seen in a PVC.
• ECG Blog #434 — Reviews a case involving assessment of the post-resuscitation ECG (ie, Which post-arrest patients need prompt cath?).
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" should be replaced by "OMI" — which stands for an MI caused by acute coronary Occlusion).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• 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 ECG Blog #380 — as well as My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• 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.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

 

ECG Blog #439 — How Many Possibilities?

How would YOU interpret the rhythm in Figure-1 — if you were sent this tracing without the benefit of any history? 

Figure-1: How would YOU interpret this rhythm?

The "Quick" Answer:

My initial thoughts on the rhythm in Figure-1:

• The rhythm in Figure-1 is not completely regular. That said — the R-R interval for the first 5 beats looks regular. The R-R interval for the last few beats is shorter than this — but also regular. Thus, there is "group beating", in that there are 2 parts ( = 2 groups of beats) in today's tracing (ie, beats #1-thru-5 — and then beats #6-thru-8).
• The QRS complex does not look wide in this single lead rhythm strip. That said — since we only see a single lead, we have no idea if the QRS might look wider if viewed from the perspective of a different lead.
• P waves are present in Figure-1. There appears to be more P waves than QRS complexes — which means that not all P waves are conducting.
• On the other hand — IF we look in front of each of the 8 QRS complexes in this tracing — each of these 8 beats is preceded by a P wave, with what appears to be a constant PR interval. Therefore, each of these 8 beats is conducted. That said, since the P waves occurring near the mid-point of the R-R interval for the first 5 beats are not conducted — some form of AV block is present.
• 
  
• PEARL #1: Of the 3 degrees of AV block — the fact that at least some P waves are conducted tells us that the rhythm is not complete AV block. And, since this is not a simple 1st-degree AV block — it must be some form of 2nd-degree AV block ( = the "Quick" Answer).

Additional "Quick" Thoughts:

There are many reasons why today's tracing is challenging to interpret. These include the following:

• From the long lead II rhythm strip that we see in Figure-1 — We do not know if the QRS complex is wide or narrow. Although it does not look as if the QRS in this rhythm strip exceeds 0.10 second in duration — it is possible that a part of the QRS may lie on the baseline, thereby leading to a false impression that the QRS is narrow when in fact it is wide. The wide terminal S wave that we see in Figure-1 suggests there may be RBBB (Right Bundle Branch Block) — although we cannot tell for certain without a 12-lead tracing.
• The T waves in this long lead II rhythm strip look to be extra "peaked". This peaking is so pronounced — that it looks like it would still be present regardless of whether additional P waves might be hidden within these T waves. These T waves are also preceded by a surprisingly flat ST segment — which raises 2 possibilities: i) That the patient may have hyperkalemia (and possibly also hypocalcemia given the flat ST segments preceding these peaked T waves); and, ii) There may be recent and/or ongoing infarction — as these may represent either hyperacute T waves or reperfusion T waves that are commonly seen after acute MI.

PEARL #2: No definite conclusions can be reached regarding ST-T wave appearance from a single-lead rhythm strip. For this — a 12-lead tracing is needed. 

• The reason determining if either hyperkalemia or recent infarction have occurred is important — is that optimal management of AV block may depend on the answer (ie, Correction of hyperkalemia or reperfusion of acute coronary occlusion may be essential components of initial treatment).
• PEARL #3: A brief relevant History — is an important component for optimal management of complex rhythm disorders. A brief relevant history may also provide an important clue to etiology (ie, AV Wenckebach = Mobitz I 2nd-degree AV block — most commonly occurs in association with recent or acute inferior MI — which is why I'd want to know IF the ST-T wave appearance in this lead II rhythm strip is the result of inferior MI). 

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QUESTION: Are P Waves Regular?

Most of the time with AV block — the atrial rhythm will be regular (or at least almost regular — if there is an underlying sinus arrhythmia).

• The EASIEST way to determine if the underlying atrial rhythm is regular — is to find 2 P wave deflections in a row — and then to see IF you can "walk out" this P-P interval throughout the entire rhythm strip. 
• RED arrows in Figure-2 show the 2 P waves I've selected.

Figure-2: RED arrows highlight 2 P wave deflections in a row.

ANSWER: P waves are Regular!

The FASTEST way to establish that the underlying atrial rhythm in Figure-2 is regular — is by use of calipers. 

• RED arrows in Figure-3 highlight these regular P waves. I was able to easily "walk out" a regular P-P interval throughout this rhythm strip.

Figure-3: The atrial rhythm is regular.

PEARL #4: The combination of group beating — with an underlying regular atrial rhythm in which some (but not all) P waves are conducting — should immediately suggest the possibility of AV Wenckebach (especially IF the 12-lead ECG suggests recent or acute inferior and/or infero-postero infarction).

• That said — the fact the more than a single RED arrow P wave in a row is not conducted in Figure-3 — indicates a more complex mechanism than simple Mobitz I.

PEARL #5: As noted above — today's arrhythmia appears to represent some form of 2nd-degree AV block. It's important to appreciate that we can not rule out the possibility that this rhythm represents Mobitz II 2nd-degree AV block, in which case the patient will need a pacemaker (See ECG Blog #236 — for review on the ECG diagnosis of the 2nd-degree AV Blocks).

• KEY criteria for Mobitz II are: i) That we see at least 2 consecutive on-time but non-conducted P waves; and, ii) That the PR interval remains constant in front of all conducted beats. Both of these criteria are fulfilled in Figure-3.
• Most (albeit not all) of the time — the QRS complex will be wide with Mobitz II (because the level of this AV block originates below the AV Node). And although the QRS complex does not look wide in Figure-3 — we are only looking at a single lead, and it is possible that a part of the QRS lies on the baseline (ie, giving the false impression that the QRS is narrow when in fact it is wide).

PEARL #6: The above said — I suspect today's rhythm is not Mobitz II, but instead represents a more complex form of Wenckebach conduction.

• Mobitz I is much more common than Mobitz II. In my experience — well over 95% of all the 2nd-degree AV blocks I have seen over my decades of studying this phenomena have been Mobitz I. Clinically, this is important — because pacing is much less likely to be needed with Mobitz I. In contrast — prompt pacing is essential for Mobitz II, because of the disturbing tendency for this conduction defect to suddenly progress to non-conduction of multiple consecutive beats (and even ventricular standstill).
• 
  
• Seeing the 12-lead ECG on this patient would be insightful! In addition to settling the issue regarding QRS width — it should provide insight as to whether we are dealing with hyperkalemia (diffuse T wave peaking in multiple leads?) — inferior MI (which would favor Mobitz I) — or anterior MI (which would favor Mobitz II).
• 
  
• Reviewing recent telemetry monitoring could provide the answer! It is because we do not see consecutively conducted QRS complexes in Figure-3 — that we are unable to determine if the PR interval is increasing before failed conduction. It is extremely unlikely for a patient to switch back-and-forth between Mobitz I and Mobitz II. Therefore — IF ongoing telemetry monitoring shows periods during which clear Mobitz I is present (ie, with progressive increase in the PR interval until a beat is dropped) — then it becomes very likely that all monitoring on this patient represents some variation of AV Wenckebach.

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The LADDERGRAM: 

At this point I needed a laddergram to help me work out my theory for what might represent a plausible mechanism other than Mobitz II for today's complex arrhythmia (Figure-4).

• NOTE: I fully acknowledge that more than a single solution may be plausible for today's arrhythmia (ie, As per PEARL #5 — I can not rule out the possibility that today's arrhythmia might represent Mobitz II 2nd-degree AV block).

Figure-4: I needed to draw a laddergram . . .

KEY Point: As I've commented in previous ECG Blog posts — Wenckebach conduction may occur at more than a single level within the AV Node. 

• When this happens — complex conduction relationships may be seen, including non-conduction of consecutive on-time P waves (See ECG Blog #259 and ECG Blog #416 — for more on Dual-Level AV Wenckebach — which is what I suspected in today's rhythm).

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STEP-by-STEP . . .

Figure-5: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. BLUE arrows show the onset of P waves as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I drew in near-vertical lines in the Atrial Tier.

Figure-6: Laddergram STEP-2. I next fill in the Ventricular Tier.
 BLUE arrows show the onset of each QRS complex as my reference point for each of the QRS complexes in this tracing.

Note that I drew in near-vertical lines for each of the 8 QRS beats in the Ventricular Tier. (If the 12-lead ECG were to show bundle branch block with a wide QRS complex — I would then draw more angled lines in the ventricular tier to reflect slower conduction as impulses passed through the ventricles).

KEY Point: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figure-5 and Figure-6). Now the challenge begins — for trying to "solve" the laddergram by figuring out which of the P waves in the Atrial Tier are being conducted to the ventricles.

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NOTE: Because I suspected dual-level AV block within the AV Node — from this point forth (beginning with Figure-7) — I divided the AV Nodal Tier into 2 parts (by drawing in a horizontal BLACK dotted line).

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Figure-7: Of the 8 beats in today's tracing — I decided to save the first 4 beats for last, since non-conduction of consecutive P waves portended a more complex mechanism. In contrast — there appeared to be a straight-forward 2:1 block for beats #5-thru-8. I've drawn in BLUE lines reflect this 2:1 conduction through the upper level within the AV Node.

Figure-8: BLUE lines reflect conduction of every-other-P-wave through the lower level within the AV Node, until finally reaching the ventricles.

Figure-9: Since we know that the P waves that occur just before beats #5-thru-8 are all conducting (because they all manifest the same PR interval) — the P wave before beat #1 must also be conducting, because this beat is preceded by the same PR interval!

Figure-10: Similarly — the P waves before beats #2,3 and 4 must also be conducting — because each of these beats is preceded by the same PR interval! This leaves us with having to postulate the path through the conduction system for the 2 unaccounted-for RED arrow P waves.

Figure-11: Looking first at the R-R interval between beats #1-to-2 — I thought the most logical theory is to postulate that the 1st atrial impulse makes it through the upper but not the lower AV Nodal level. The 2nd atrial impulse makes it through the Atrial Tier, but not through any part of the AV Node.

Figure-12: Once again — the "symmetry" in the relative intervals for each of the atrial impulses in the remaining 3 groups (BLUE lines within the AV Nodal Tier) — suggests a similar conduction pattern to the one I drew in Figure-11 for the atrial impulses between beats #1 and 2.

Figure-13: My completed laddergram. I explain the consecutive non-conducted P waves as the result of 2nd-degree AV block — in which there is dual-level block within the AV Node for the first 5 beats (ie, with 3:2 Wenckebach conduction through the upper AV Nodal level — and 2:1 conduction through the lower AV Nodal level).

In contrast — there is simple 2:1 AV block for the last few beats. Since it would be unlikely to switch back-and-forth between the Mobitz I and Mobitz II forms of 2nd-degree AV block — I thought it most likely that the conduction defect in today's case reflects 2nd-degree AV block, with AV Wenckebach occurring at 2 levels within the AV Node.

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FINAL Points Regarding Today's Rhythm:

• P waves are upright in lead II — and the atrial rate is ~100/minute. As a result, rather than atrial tachycardia — I suspect we are seeing a slightly increased sinus rate with the above described 2nd-degree dual-level AV block.
• As to the question of whether today's rhythm does or does not represent a "high-grade" form of AV block — I find the answer semantic, in that: i) The block could be considered "high-grade" — because more than 1 on-time P wave in a row is not conducted; — BUT — ii) The block occurs at 2 levels out of the AV Node — at each of these levels being a Mobitz I type block (with Mobitz I generally not considered as a "high-grade" conduction disturbance).
  
• That said — the overall ventricular rate in today's rhythm is slow (dropping down to the 40s). As a result, if significant bradycardia persists (especially if accompanied by symptoms) — then pacing may be needed.
• The "good news" — is that the cause of this bradycardia and conduction block may be the result of a "fixable" condition that if identified and successfully treated, might restore a normal rate and rhythm (ie, If the peaked T waves were due to hyperkalemia — or if there could be successful reperfusion of an acute infarction).
• Successful management of today's patient will depend on determining the cause of this rhythm.

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Acknowledgment: My appreciation to Sam Collis (from England) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #192 — The 3 Causes of AV Dissociation.

• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
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• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #251 — Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach.
• ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach). 
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• ECG Blog #63 — Mobitz I, 2nd-Degree AV Block with Junctional Escape Beats.
• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
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• ECG Blog #259 — Reviews step-by-step laddergram for a patient with Dual-Level AV Block.
• ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.
• 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 #416 — Case Study of acute OMI with step-by-step illustration of dual-level AV Wenckebach.
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• ECG Blog #405 — ECG Video presentation that reviews the distinction between AV Dissociation vs Complete (3rd-degree) AV Block (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).

 

ADDENDUM (7/18/2024):

—  —

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).

 

ECG Blog #438 — A Paramedic Diagnosis ...

The ECG in Figure-1 was obtained from a previously healthy middle-aged woman — who was awakened by new-onset CP (Chest Pain) that began ~3 hours before this ECG was obtained. She was stable hemodynamically — but still with CP at the time ECG #1 was recorded.

• The patient reports 3 shorter episodes of CP the day before.

QUESTIONS:

• Given this history — How would YOU interpret this ECG?
• Should the cath lab be activated?

Figure-1: The initial ECG in today's case (See text).

MY Thoughts on Today’s ECG:

In view of the above history — the initial ECG in today's case is clearly of concern. The rhythm is sinus at 70-75/minute — with normal intervals (PR,QRS, QTc) — normal axis — and no chamber enlargement.

• My "eye" was immediately attracted to leads V2 and V3 (within the RED rectangle in Figure-2). There is early transition in these chest leads (with surprisingly tall R waves in leads V1,V2 — and the R becoming taller than the S wave is deep by lead V3).
• The ST segment in leads V2 and V3 is inappropriately straightened (as often emphasized in this ECG Blog — there should normally be slight, gently upsloping ST elevation in these leads).
• Continuing wth neighboring leads V4, V5 and V6 — the T waves in these leads look hyperacute (BLUE arrows) — in that their ST segment takeoff is straightened, with these T waves being larger-than-expected in size with a widened base.
• PEARL #1: By itself — the appearance of the T wave in lead V4 does not necessarily look abnormal. However, in the context of the clearly abnormal ST-T wave findings in leads V2,V3 — and the more acute-looking appearance of the T waves in leads V5 and V6 — I interpreted the T wave in lead V4 as representing the beginning of this hyperacute change.

MY Impression of ECG #1: Given the history of new-onset CP in this middle-aged woman — this initial prehospital ECG in Figure-2 suggests posterior OMI beginning and/or ongoing over the past day that this patient has had symptoms.

• Given her new episode of CP that awakened her from sleep just 3 hours earlier (and which is still ongoing) — the cath lab should be activated! 
• 
  
• PEARL #2: Admittedly — the ECG findings in this initial ECG are subtle. But abnormalities are present in each of the chest leads in this patient with new CP. In this clinical context — this ECG is diagnostic of acute posterior OMI. 
• It should be appreciated that the reason for the lack of clear ST depression in leads V2,V3 — and the lack of ST elevation in leads V4,V5,V6 — may be the ongoing clinical course in this patient, that includes multiple CP episodes over the past day (ie, There could be spontaneous opening and reclosing of the "culprit" vessel over this period of time). It may be that the ECG in Figure-2 represents some pseudo-normalization of what might have be more prominent ST-T wave changes on an earlier ECG.
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• PEARL #3: In addition to posterior involvement — the hyperacute T waves in the lateral chest leads suggest there is acute postero-lateral OMI, which in the absence of obvious inferior lead changes — points to the LCx (Left Circumflex) as the most likely "culprit" artery.
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• PEARL #4: The unexpectedly tall R waves in leads V1,V2 lend support to concern that there may be completed posterior infarction (See ECG Blog #354) — as the mirror-image reflection of deepening Q waves is increasing amplitude of the R wave in anterior leads. Unexpectedly tall anterior R waves is especially likely to signal completed posterior infarction IF this finding is new compared to prior ECGs.

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

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The CASE Continues:

Serial ECGs were obtained by the prehospital team. Figure-3 offers a comparison between one of these repeat ECGs — and the original prehospital ECG (with ~30 minutes separating the time between the recording of these 2 tracings).

• WHAT do you learn from the repeat ECG in Figure-3?

Figure-3: Comparison of the initial ECG — with the repeat ECG done in the field ~30 minutes after the initial ECG.

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What We Learn from the Repeat ECG:

IF there was any doubt after seeing ECG #1 about the need for prompt cath lab activation — that doubt should be removed by the "dynamic" ST-T wave changes that are evident in virtually all leads in the repeat ECG.

• PEARL #5: The BEST way to compare one serial ECG with another — is to put both tracings side-by-side — and to then go lead-by-lead, always comparing one lead area to the corresponding lead area in the 2nd ECG.
• Instead — it is all-to-common for clinicians to ignore this important procedural point. Instead, the tendency is to try to "gain time" by looking at 1 tracing in its entirety — and then the 2nd tracing in its entirety without taking the time to directly compare each lead area with the corresponding lead area in the 2nd tracing. The reality is that unless you compare the 2 tracings by going lead-by-lead — it is all-too-easy to overlook subtle but important findings.
• Along the way — it is also important to ensure that our lead-by-lead comparison is "comparing apples with apples, and not with oranges". By this I mean — that we want to ensure that any changes in ST-T wave morphology are not the result of a significant frontal plane axis shift or due to a change in chest lead electrode placement.

Applying this Comparison Technique in Figure-4:

Although there is a slight frontal plane axis shift (from about +40 degrees in ECG #1 — to +60 degrees in ECG #2) — this small change is unlikely to alter our assessment of comparative limb lead ST-T wave appearance. Chest lead QRS morphology appearance is essentially the same in both tracings. Therefore — any ST-T wave changes that we note between these 2 ECGs are likely to be "real".

• In the Limb leads of ECG #2 — there now is subtle-but-real ST elevation in each of the inferior leads (as seen by respect to the dotted RED line baseline in each of these leads). 
• ST-T waves in these inferior leads have a more acute appearance than they did in ECG #1 (ie, there is more straightening of the elevated ST segment takeoff) — and we may be seeing the beginning of small inferior lead Q waves.
• The BLUE arrow in lead aVL — highlights ST segment straightening that was not present in ECG #1. I interpreted this as a reciprocal change to the new inferior lead ST elevation.

In Chest Leads:

• BLUE arrows in leads V2 and V3 — highlight an increase in ST depression.
• In leads V5 and V6 — there should be no doubt that there is a more acute appearance with straightening of the ST segment takeoff and increased ST elevation (with respect to the dotted RED lines in these leads).

MY Impression of ECG #2: In this patient with ongoing CP — the repeat ECG in Figure-4 confirms "dynamic" ST-T wave changes. 

• Prompt cath is indicated! — in this symptomatic patient with acute ongoing infero-postero-lateral OMI.

Figure-4: I've labeled findings in the repeat ECG.

CASE Follow-Up:

• Serial troponin values were markedly elevated.
• Cardiac cath revealed normal left main and LAD branches — and, a small but non-obstructed RCA. The main trunk of the LCx (Left Circumflex) showed a 50% lesion in the middle of this vessel — with severe narrowing proximally in the 1st Obtuse Marginal branch of the LCx, which was felt to be the "culprit" artery. Angioplasty was successfully performed.

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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = an acute coronary Occlusion MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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