ECG Blog #418 — A Single Lead Tells the Tale ...

The ECG in Figure-1 was obtained from a previously healthy man in his 40s — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain) that awakened him from sleep.

• ECG #1 was recorded ~90 minutes after the patient was awakened from sleep. He was still having CP. 

QUESTIONS:

• In view of this history — How would YOU interpret the ECG in Figure-1?
• Does a single lead “tell the tale”?

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

MY Thoughts on the ECG in Figure-1:

The important points about today’s history are: i) That the patient is a previously healthy man in his 40s; — ii) That the patient was awakened from sleep by new CP; — and, iii) That his CP was still ongoing 90 minutes after it began, at the time ECG #1 was recorded in the ED.

• The ECG in Figure-1 shows normal sinus rhythm at ~75/minute — with normal intervals (PR-QRS-QTc) and axis — and no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q waves: There are no Q waves. There is a small-but-present initial positive deflection ( = r wave) in lead III (I don't count as "Q waves" the initial negative deflections we see in leads aVR and V1 — since it is normal to see Q waves in these leads).
• R wave progression: There are good-sized R waves beginning in lead V2 — albeit there is slight delay in transition (with the R wave becoming taller than the S wave is deep only between leads V4-to-V5).

What About ST-T Wave Changes?

As we assess today's initial ECG for ST-T wave changes — It is important to remember that this patient was previously healthy — and — he was awakened from sleep by CP that was still present 90 minutes later (ie, at the time this initial ECG was recorded!).

• As a result — We need to consider this patient to be in a higher-risk group for having an acute event. This point emphasizes that the burden of proof falls on us as medical providers to prove that this patient is not having an acute event, rather than the other way around!

We Need to Remember the Following:

• Even with an acute event — the initial ECG may not necessarily show remarkable changes — and/or — ECG changes may be present, but subtle (and sometimes only recognized when compared to a prior baseline ECG on the patient — or when compared with serial ECG changes over time). 
• PEARL #1: Even with an ongoing, extensive acute MI — the initial high-sensitivity troponin may sometimes be normal.
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• PEARL #2: It is important to note and correlate the presence and relative severity of symptoms with each serial ECG that is done. This is because the course of an acute OMI ( = an acute MI that results from acute coronary Occlusion) — is not always predictable. Instead, even before treatment — there may be spontaneous reopening of the "culprit" vessel — which often can be recognized by reduced CP that occurs in association with improved ECG changes.
• Spontaneous reopening of the "culprit" vessel may result in "pseudo-normalization" of ECG changes (IF the ECG is recorded "between" the stage of acute ST elevation — and the later stage of coronary reperfusion as ST elevation evolves into ST depression and T wave inversion). 
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• KEY Clinical Point: This "pseudo-normalization" stage still mandates prompt cath with PCI, because what spontaneously reopens — may just as easily reocclude at any point in time if not prevented by PCI.

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CHALLENGE:

With the above caveats in mind — Take Another LOOK at today's initial ECG in Figure-1:

• Which single lead in ECG #1 tells the tale? 

ANSWER (shown below):

I highlight the answer to the above "Challenge Question" in Figure-2:

Figure-2: I highlight the KEY lead in today's initial ECG.

 

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Regarding ST-T Wave Changes in Figure-2:

As per the title of today's ECG Blog — one KEY lead "tells the tale".

• ST-T wave changes in the limb leads show nonspecific ST-T wave flattening — but nothing that looks acute.
• I've highlighted within the RED rectangle in Figure-2 the single lead ( = lead V3) that in a patient with new severe CP is clearly abnormal. While a slightly elevated, gently upsloping ST segment is common and normal in leads V2,V3 — there is definite straightening of the ST segment in this lead on the initial ECG — and the amount of ST elevation (seen with respect to the dotted RED line in this V3 lead) is excessive. This represents a hyperacute ST-T wave in lead V3 until proven otherwise! 

PEARL #3: To emphasize that lead V3 is the KEY lead in today’s initial ECG — without which I would not have diagnosed acute OMI. But since we know (for the reasons stated above) that in a patient with new CP, that the ST-T wave in lead V3 is hyperacute — I also interpreted the 2 neighboring leads in Figure-2 ( = leads V2 and V4) as abnormal and consistent with acute LAD OMI until proven otherwise:

• Lead V2 — The amount of ST elevation in lead V2 is not necessarily excessive, given how common slight ST elevation is normally seen in anterior leads V2,V3. But in the context of lead V3 definitely showing a hyperacute ST-T wave — I thought there was a bit more “straightening” of the initial part of the ST segment in lead V2 that I would normally expect (at least in the 1st complex in this lead).
• Lead V4 — While not necessarily abnormal if looked at as an isolated finding — I thought the amount of ST elevation in neighboring lead V4 to be a bit more than is usually expected in this lead. And, at least for the middle complex in this lead — there seemed to be a bit more-than-expected ST segment straightening.
• 
  
• To EMPHASIZE: If not for lead V3 — I would not have interpreted leads V2 and V4 as necessarily abnormal. This is especially true in view of: i) The surprisingly good R wave progression that we see in ECG #1 — with an R wave of already 7-8 mm by lead V2 (whereas there is commonly “loss of R wave” in anterior leads with acute LAD OMI); and, ii) The complete lack of abnormality in the remaining chest leads ( = leads V1,V5,V6). It is lead V3 that "tells the tale"!

PEARL #4: As stated earlier — an initial ECG will not always be diagnostic. The KEY is to appreciate that in most patients — the process of an acutely evolving coronary occlusion is dynamic — sometimes showing dramatic changes in as short a period as between 5-10 minutes (See ECG Blog 115 for a case in which such dramatic ST-T wave changes occurred in just 8 minutes!).

• The “Take-Home” Message from today's case is clear — IF you are at all uncertain about whether your patient with CP is or is not acutely evolving an OMI — Repeat the ECG soon and often — until you can confidently answer this question!

Today's CASE Continues: 

Given any uncertainty you might have as to whether today's patient was evolving an acute OMI — the initial ECG should have been repeated within 15-20 minutes.

• The ECG was only repeated 80 minutes later. To facilitate comparison in Figure-3 — I have put these first 2 ECGs together. What do YOU see?

Figure-3: To facilitate comparison — I've put the first 2 tracings in today's case together. What has changed? (To improve visualization — I've digitized the original ECG using PMcardio).

Comparison between ECG #1 and ECG #2:

The BEST way to compare serial ECGs — is to put them side-by-side, as I have done in Figure-3.

• Given our concern regarding lead V3 in ECG #1 — I began assessment of ECG #2 by looking at this lead, and at its neighboring leads.
• Compared to ECG #1 — there is now unmistakeable straightening of the ST segment takeoff in lead V3 of ECG #2, with reduced T wave amplitude.
• Lead V4 in ECG #2 — is now unmistakeably elevated (with straightened ST segment takeoff).
• Each of the remaining chest leads also show differences. There is subtle-but-real ST elevation now in leads V1, V2 and V5 — and some ST depression in lead V6 than was not previously present. 
• 
  
• Limb lead changes in ECG #2 are subtle — but in the context of the above noted chest lead changes, I believe the slightly increased inferior lead T wave amplitude and ST-T wave flattening in lead aVL is real.
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• PEARL #5: Did YOU Notice the loss of R wave amplitude in ECG #2? There is now a QS pattern in lead V2, with noticeably reduced R wave amplitude in leads V2-thru-V5 compared to ECG #1. 

BOTTOM Line: If there was doubt about the diagnosis from ECG #1 — the repeat ECG in Figure-3 is now clearly diagnostic of acute LAD OMI because: i) Dynamic ST-T wave changes are seen in virtually all leads compared to the initial tracing — including progressive ST elevation in leads V2-thru-V5; and, ii) Loss of R wave amplitude in these chest leads.

• The Important LESSON: Given the history of new-onset severe CP — acute LAD OMI can be diagnosed (or at least strongly suspected) from the initial ECG in today's case. But even if there was uncertainty about ECG #1 — definitive diagnosis could have been made much sooner by repeating this initial tracing within 10-15 minutes (instead of waiting 80 minutes).

CASE Conclusion: 

The diagnosis of acute LAD OMI was made once the repeat ECG in Figure-3 was obtained. Given unavailability of cardiac catheterization — Streptokinase was administered.

• ECG #3 was recorded after completion of Streptokinase infusion — in association with clinical improvement. What do YOU see?

Figure-4: Comparison of ECG #2 — with ECG #3, recorded after completion of Streptokinase. (To improve visualization — I've digitized the original ECG using PMcardio).

 

Regarding the Post-Streptokinase ECG in Figure-3:

Streptokinase infusion was effective!

• Other than slight residual ST elevation in leads V1,V2 — ST elevation in other chest leads has essentially resolved!
• Although there has been loss of R wave amplitude compared to the initial ECG — there has been no further loss of R wave amplitude since ECG #2.
• There is now terminal T wave inversion — that begins in lead V2, and extends through to lead V6. In association with clinical improvement of this patient — ECG #3 now shows reperfusion T waves consistent with effective thrombolytic infusion.

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Acknowledgment: My appreciation to Kianseng Ng (from Malaysia) 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 #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).
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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.
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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 #417 — AFib with Aberrancy?

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) for shortness of breath. 

QUESTIONS:

• How would YOU interpret the ECG shown in Figure-1?
• Given the irregular irregularity of beats #4-through 17 — Is this a run of AFib (Atrial Fibrillation) with aberrant conduction?

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

Initial Thoughts on the ECG in Figure-1:

Today's ECG is challenging because despite the marked change in QRS morphology beginning with beat #4 — monomorphic VT (Ventricular Tachycardia) is usually a regular (if not, at least fairly regular) rhythm. This raises the question if beats #4-thru-17 might represent a run of AFib with aberrant conduction?

• HINT: The KEY to interpreting today's rhythm lies with assessment of atrial activity. What do YOU see?

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Does this Earlier Tracing Help?

Another ECG had been recorded on today's patient shortly before the ECG shown in Figure-1. 

• Does this earlier tracing (shown in Figure-2) help to determine the etiology of the run of irregular wide beats in Figure-1?

Figure-2: A 2nd ECG in today's case. This tracing was recorded shortly before ECG #1. Does this earlier tracing help to determine the etiology of the wide beats?

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My Approach to Today's Rhythm:

Atrial activity is present in association with each of the beats in both of today’s tracings. This atrial activity provides the KEY clue for determining the etiology of the wide beats. 

• Using calipers facilitates the process.
• 
  
• HINT: We need to look for P waves not only in front of the wide beats — but also during and just after the wide QRS complexes in order to complete our search for atrial activity. 

QUESTION:

I’ve put both tracings together in Figure-3.

• How do the colored arrows provide the answer?

Figure-3: I’ve put both tracings in today’s case together — and have labeled atrial activity with colored arrows.

The ANSWER to Today’s Rhythm:

The first 3 beats in ECG #1 are sinus conducted — with RED arrows highlighting on-time sinus P waves.

• Note that a 4th on-time sinus P wave occurs just before the 1st wide beat in the long lead II rhythm strip seen in Figure-3 ( = the 4th RED arrow in ECG #1 that appears just before beat #4).
• Note also that a subtle negative deflection occurs at the very end of the 2nd wide QRS complex ( = the 1st YELLOW arrow in the long lead II rhythm strip of ECG #1). This YELLOW arrow represents a retrograde P wave.
• KEY Point: The above events prove that beat #4 and beat #5 are PVCs (Premature Ventricular Contractions).

Several points should be emphasized regarding ECG #1:

• The reason we know that the subtle negative deflection ( = that 1st YELLOW arrow in ECG #1) that appears at the end of beat #5 is definitely a retrograde P wave — is that we see no such negative deflection at the end of beat #4. This is as expected — because an on-time sinus P wave appears just before beat #4, and this renders the atria refractory to retrograde conduction.
• Of interest — retrograde P waves (highlighted by YELLOW arrows) are seen at the very same point (ie, just after the QRS complex) of beats #6-thru-17.
• Further support that the subtle negative deflections at the end of the wide beats are indeed retrograde P waves — is forthcoming from our ability to see these retrograde P waves in other leads in the 12-lead tracing (= YELLOW arrows in multiple other leads in ECG #1).
• Returning to the long lead II rhythm strip in ECG #1 — Beat #17 is followed by a brief pause, after which the 5th RED arrow in this tracing highlights resumption of sinus rhythm with beat #18.
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• PEARL #1: The polarity of a P wave that appears shortly after a QRS complex helps to distinguish between sinus P waves, PACs (Premature Atrial Contractions) and retrograde P waves. Sinus P waves should be positive in lead II. They are often (albeit not always) negative in lead V1. PACs may either be positive or negative. But retrograde P waves should be negative in inferior leads (II,III,aVF) — and positive in leads aVR and V1 (as seen by the YELLOW arrows in ECG #1).
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• PEARL #2: The fact the 4th sinus P wave in ECG #1, as shown in Figure-3 ( = the 4th RED arrow in the long lead rhythm strip) is completely on-time, and is followed by a wide beat that is preceded by a PR interval too short to conduct — proves that beat #4 is a PVC. (Since the PR interval before beat #4 is too short to conduct normally — this means that beat #4 must be coming at least in part, from below the AV Node).
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• PEARL #3: QRS morphology of wide beats #5-thru-17 is very similar to QRS morphology of beat #4. This strongly suggests that despite the irregularity of beats #4-thru-17 — this represents a run of irregular VT.
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• PEARL #4: Beat #4 is a fusion beat. As noted in PEARL #3 — QRS morphology of beat #4 looks very similar (but is not identical) to QRS morphology of beats #5-17 (ie, The R wave of beat #4 is slightly shorter than the R wave of each of the 13 wide beats that follow it). To prove “fusion” — there should be a logical reason for a beat to manifest an intermediate morphology between sinus-conducted beats and pure ventricular beats — and this logical reason is present in ECG #1 — because the on-time 4th RED arrow sinus P wave (that is seen just before beat #4) has no more than a very brief moment of time to conduct to the ventricles before ventricular beat #4 arises. (For more on fusion beats — See ECG Blog #128 and Blog #129).  
• KEY Clinical Point: The finding of a fusion beat — provides further support that not only is beat #4 in ECG #1 at least in part of ventricular etiology — but also, that each of the wide beats that look like beat #4 ( = beats #5-17) are also of ventricular etiology, such that we have proven that beats #4-thru-17 represent a run of irregular VT! (See ECG Blog #133).

PEARL #5: One of the main reasons I chose today’s case is to emphasize that although monomorphic VT is usually a regular rhythm — it is not always a regular rhythm (See the ECG Media Pearl in today’s ADDENDUM below). 

• Most of the time when monomorphic VT is not regular — the amount of “irregularity” is minimal. That said — Today’s case represents an example in which we know the rhythm is VT despite the marked irregularity that we see in ECG #1.
• 
  
• The reason most monomorphic VT manifests a regular (or at least almost regular) R-R interval — is that this rhythm is most often the result of a stable reentrant circuit. There may be a brief "warm-up" or "cool-down" period until a regular R-R interval is established (in which case there is gradual acceleration or deceleration of the rate — either at the beginning or the end of an otherwise regular run of VT).
• The above said — On occasion, there may be focal triggered activity that results in the marked irregularity of the monomorphic VT seen in ECG #1 (Zhang et al — Circulation 139:1750-1752, 2019). 
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• P.S.: The reason for specifying the “monomorphic” form of VT as the VT rhythm that is usually regular — is that by definition, PMVT (PolyMorphic Ventricular Tachycardia) is a very irregular VT rhythm that quickly leads to hemodynamic instability (See ECG Blog #231).

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Regarding ECG #2 in Figure-3:

• As noted earlier — the bottom tracing in Figure-3 was recorded shortly before ECG #1. What additional information is provided by ECG #2 — that was not evident in ECG #1?

ANSWER:

In addition to further confirmation that the wide beats in today’s 2 tracings are ventricular in etiology — ECG #2 provides insight to the potential cause of the today’s VT rhythm.

• In Figure-3 — Beats #1,2; 8, 10 and 15 in ECG #2 are PVCs, with beats #1 and 2 forming a ventricular couplet ( = 2 PVCs in a row). We know these 5 wide beats are all of ventricular etiology — because the underlying atrial rhythm continues throughout this tracing despite these wide beats (ie, the 2 PINK arrow P waves slightly deform the initial upslope of the R wave of beats #8 and 10 — therefore with a PR interval too short to conduct. The 3 WHITE arrow P waves are contained within the QRS of wide beats #1,2,15 — thereby making it impossible for these P waves to conduct).

PEARL #6: 12 leads are better than one! 

• Although we see no evidence that WHITE arrow P waves are hidden within the wide QRS beats #1,2 and 15 in the long lead rhythm strip of ECG #2 — We do see a precisely on-time positive notch in lead V6 (2nd RED arrow in this lead). This confirms that regular P waves do continue throughout today's rhythm. 
• The above observation illustrates the concept of how use of simultaneous leads can provide insight not forthcoming from a single lead (in this case — looking for evidence of atrial activity not only in the long lead rhythm strip — but also in simultaneously-recorded leads V4,V5,V6).

PEARL #7: Most of the time, assessment of ST-T wave morphology of ventricular beats will not be a reliable indicator of a recent or acute event. As a result — We are only able to reliably assess ST-T wave morphology for acute changes in leads I,II,III of ECG #1, because these are the only 3 leads in which we see ST-T waves for sinus-conducted beats. These 3 leads suggest left axis deviation consistent with LAHB (Left Anterior HemiBlock) for sinus-conducted beats #1,2,3 — with nonspecific ST-T wave flattening, but no acute changes.

• In contrast to our inability to optimally assess ECG #1 for ischemic changes — the chest leads in ECG #2 clearly show suspicious changes for a recent acute event in sinus-conducted beats #11,12,13 (that manifest abnormal straightening of the ST segment takeoff in anterior leads V2,V3) — and — in sinus-conducted beats #14 and 16 (that show ST segment coving with symmetric T wave inversion in leads V4,V5,V6 — as well as a small amount of residual ST elevation in lead V4).
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• Clinical IMPRESSION: Given the minimal amount of ST elevation in the chest leads of ECG #2 — in association with symmetric T wave inversion in leads V4,V5,V6 — I suspect reperfusion T waves following recent LAD (Left Anterior Descending) coronary artery occlusion as the cause of the irregular VT and PVCs that we see in today’s 2 ECGs.

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LADDERGRAM Illustration:

To facilitate appreciation of the mechanism of today’s arrhythmia — I’ve added laddergrams for ECG #1 and ECG #2 in Figure-4.

• Following 3 sinus-conducted beats — beat #4 in ECG #1 (TOP laddergram) is a fusion beat ("F"), after which a run of irregular VT is seen ( = beats #5-thru-17). After a brief (post-ectopic) pause — sinus rhythm resumes with beat #18.
• YELLOW arrows in ECG #1 represent retrograde P waves that are conducted back to the atria.
• Note that I show the point of fusion for beat #4 at a relatively high point in the ventricles. Because QRS morphology of beat #4 closely resembles QRS morphology during the run of VT (with the main difference in morphology being slightly less R wave amplitude for the fusion beat) — the ventricular impulse contributing to beat #4 passes through most of the ventricles before encountering the sinus-conducted contribution to beat #4.
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• In ECG #2 (BOTTOM laddergram) — beats #1,2; 8, 10 and 15 represent PVCs. These 5 ventricular impulses conduct only a short distance backward (ie, into the AV Nodal Tier) before encountering the downward directed sinus-conducted impulses that prevent retrograde conduction of these PVCs from reaching the atria.

 

Figure-4: Laddergram illustration for the 2 ECGs in today’s case.

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Acknowledgment: My appreciation to Seung-Lyul Shin (from Incheon, South Korea) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
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• ECG Blog #198 — Can VT be Irregular?
• ECG Blog #403 (ECG Video) — Case of a regular WCT rhythm.
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• ECG Blog #128 and ECG Blog #129 — Reviews the concept of Fusion beats.
• ECG Blog #393 — Case of multiple Fusion beats.
• ECG Blog #133 — AV Dissociation, Fusion prove VT ...
• ECG Blog #382 — Another case in which Fusion confirms PVCs.
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
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• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.

 

ADDENDUM (2/17/2024): 

—  —

ECG Media PEARL #15 (5 minutes Audio) — Is Monomorphic VT a regular rhythm? — with attention to the 2 Caveats that emhasize how: i) Fast AFib may look regular; and, ii) Monomorphic VT is not always perfectly regular.

 

ECG Blog #416 — Is the Rhythm and ECG related?

Imagine the only information provided for the ECG in Figure-1 — is that it was obtained from a 60-year old man with new CP (Chest Pain).

QUESTIONS:

• In view of this brief history — How would YOU interpret this ECG in Figure-1?
• Is the cardiac rhythm related to the 12-lead ECG?

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

MY Thoughts on the ECG in Figure-1:

The goal of practicing clinicians is to interpret both parts of the tracing in Figure-1 ( = the cardiac rhythm and the 12-lead ECG) — in an optimal time-efficient manner. 

• To accomplish the above goal — our interpretation of these 2 Parts of today’s tracing need not necessarily be complete on our initial assessment. 
• Instead — in an acute case such as today’s (ie, in which the patient presents for new CP) — I favor spending no more than 5-to-10 seconds looking at the rhythm (to ensure that no immediate treatment is needed for this rhythm). 
• I then turn my attention to the 12-lead ECG to assess whether an acute OMI is likely to be present (in order to quickly determine IF prompt cardiac cath and potential PCI might be needed).
• 
  
• PEARL #1: Although I favor limiting the amount of time spent assessing today’s complex rhythm to no more than 5-to-10 seconds — I still favor using the systematic Ps, Qs, 3R Approach (See ECG Blog #185) because: i) With minimal practice — you’ll find this systematic approach actually speeds up your assessment, rather than slowing it down; and, ii) Your accuracy in interpretation will improve (such that even if you do not arrive at a definitive diagnosis — you will limit diagnostic possibilities).

 

My Quick Assessment of Today’s Rhythm:

By the Ps, Qs, 3R Approach:

• The rhythm in Figure-1 is clearly not Regular. That said — it is supraventricular (because the QRS complex is not wide). The overall Rate is slow, dropping in places to less than 50/minute. P waves are present — but the PR interval appears to be continually changing (ie, which raises the question as to whether any of the P waves are Related to neighboring QRS complexes?).
• 
  
• To EMPHASIZE: The above targeted assessment by the Ps,Qs,3R Approach should not take more than 10-20 seconds. This is all the information that you need for an initial Quick Assessment of the cardiac rhythm. 
• NOTE: Although the rate of the rhythm is quite slow in places — IF the patient is hemodynamically stable, then there is no emergent treatment needed (ie, There is no immediate need for a more precise interpretation of the rhythm). This means that you can now turn your attention to the 12-lead ECG to determine IF prompt cath is (or is not) immediately needed in this patient with new CP.

PEARL #2: Looking first at the cardiac rhythm — I was not initially sure IF some form of 2nd-degree AV block might be present. That said — I instantly knew that today’s rhythm was unlikely to be complete AV block because the ventricular response is so irregular! 

• Most of the time when there is complete (3rd-degree) AV block — the ventricular response will be regular (or at least almost regular). This is beause IF none of the P waves are able to conduct to the ventricles (as would be the case if complete AV block was present) — a regular escape focus (either from the AV Node or from the ventricles) will usually take over the rhythm. The marked irregularity seen in Figure-1 is simply too variable to arise from a normally functioning escape focus.

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Turning Attention to the 12-Lead ECG:

At this point in our interpretation — We need to focus on the 12-lead ECG. I've highlighted in Figure-2 the KEY leads that should capture your attention. In sequence, over the next 20-to-30 seconds — your eye should focus on the complexes within the RED — then light BLUE — then dark BLUE rectangles.

• In this patient with new CP — What do YOU now know?
• What intervention is needed?
• What does this tell us about the likely etiology of the rhythm?

Figure-2: I've highlighted the KEY complexes in the 12-lead ECG.

Interpretation of Today’s 12-Lead ECG:

In view of the history of new CP — YOUR assessment of the 12-lead ECG in Figure-2 should acknowledge the following:

• Within the RED rectangle: — The "shelf-like" flat ST segment with abrupt angulation into a prominent upright T wave in lead V2 is immediately diagnostic of acute posterior OMI (where the “O” in “OMI” indicates an acute MI that is due to acute coronary Occlusion). 
• KEY Clinical Point: Normally, there should be gentle upsloping of a slightly elevated ST segment in leads V2 and V3 — such that our "eye" should immediately recognize the abnormal shape of the complex within the RED rectangle (that tells us “posterior OMI” until proven otherwise). 
• 
  
• Within the 3 light BLUE rectangles: — Because of their common blood supply, posterior OMI is regularly associated with inferior OMI. Consequently — confirmation that the abnormal shape of the ST-T wave in lead V2 is truly the result of acute posterior OMI will be forthcoming IF limb leads are diagnostic of acute inferior MI. Note within each of the light BLUE rectangles — that there are small-but-real Q waves with subtle-but-real ST elevation. Especially in view of the modest QRS amplitudes — the ST-T wave in lead III clearly looks hyperacute (ie, disproportionately "fatter"-at-its-peak and wider-at-its-base than it should be — with subtle terminal negativity of the T wave).
• 
  
• Within the dark BLUE rectangle: — The "magical" mirror-image opposite ST-T wave picture in lead aVL to that seen in lead III removes all doubt. Given tiny amplitude of the QRS in lead aVL — the disproportionate area within the depressed ST segment in this lead is a reciprocal change that confirms acute inferior OMI (Note terminal T wave positivity in lead aVL — that also reflects the mirror-image of the subtle terminal T wave negativity in lead III).
• 
  
• BOTTOM Line: In less than a minute — We can confirm that in today’s patient, who presents for evaluation with new CP — the ECG in Figure-2 is diagnostic until proven otherwise, of acute infero-postero OMI (most likely from acute RCA occlusion). Prompt cath for PCI is clearly indicated!
• 
  
• PEARL #3: An advanced clinical concept — is that acute inferior MI is commonly associated with 2nd-degree AV blocks of the Wenckebach (Mobitz I) type. Awareness of this common association made me instantly suspect that some type of Wenckebach conduction is probably operative in today's rhythm — even though I admittedly do not see any pattern of consistent group beating, or any repetitive PR intervals that typically clue me in to Mobitz I conduction defects.

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A Closer Look at Today's Rhythm:

To Emphasize: The important "Take Home" Message from today's case — is that in this patient with new CP — the ECG in Figure-2 is diagnostic of acute infero-postero OMI (most likely from acute RCA occlusion) — and that prompt cath for PCI is needed.

• Whatever the specific etiology of today's arrhythmia is, the “good news” is — that this rhythm will most probably improve with reperfusion of the "culprit" artery.
• 
  
• That said — I found today's arrhythmia fascinating, and worthy of more in-depth analysis. (NOTE: The laddergram solution I propose below for today’s rhythm is complex and clearly Beyond-the-Core. That said — I believe my description and step-by-step construction of the laddergram below should prove insightful to any level provider.). 
• 
  
• As a reminder — learning to draw laddergrams does take some time and is not needed to become experienced and skilled in clinical arrhythmia interpretation. But — learning how to read laddergrams that are already drawn is EASY — and all clinicians (regardless of their level of experience) can quickly begin to benefit from the insight provided by laddergram illustration.
• For readers with an interest in learning either how to read and/or draw laddergrams — I have added LINKS to more than 100 laddergrams (many with step-by-step illustration) at this site = https://tinyurl.com/KG-Laddergrams —

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How to Proceed for “Solving” Today’s Arrhythmia:

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PEARL #4: At this point — Label the P waves!

• The simple step of labeling P waves is tremendously helpful in visualizing potential relationships between atrial activity and neighboring QRS complexes.
• Using calipers facilitates the process. I simply set my calipers at a P-P interval determined by selecting the distance between 2 P waves that I can identify with certainty. Because "ventriculophasic" sinus arrhythmia is so commonly seen with 2nd- and 3rd-degree AV blocks — We need to factor in the reality that the P-P interval between sinus P waves will often vary slightly.

Take a LOOK at Figure-3 — in which I've labeled sinus P waves with RED arrows throughout the rhythm strip.

• Are any PR intervals the same?
• Do you think any of the QRS complexes in Figure-3 are being conducted? If so — How can you tell that P waves are conducting these QRS complexes?

Figure-3: I've labeled P waves with RED arrows.

MY Thoughts on Figure-3:

• RED arrows highlight a fairly regular atrial rhythm (with slight variation in the P-P interval due to ventriculophasic sinus arrhythmia).
• As noted earlier in PEARL #2 — today’s rhythm is unlikely to represent complete AV block. This is because of the marked irregularity of the ventricular rhythm (whereas complete AV block most often manifests a regular, or at least fairly regular ventricular rhythm).
• Most R-R intervals in the long lead II rhythm strip contain 2 P waves between QRS complexes — which means that at least 1 of these P waves is not conducted. This strongly suggests that the irregular rhythm in Figure-3 represents some form of 2nd-degree AV block (ie, either Mobitz I [ = AV Wenckebach] or Mobitz II).
• IF this is true — then the fact that the QRS complex is narrow everywhere — that the PR interval is not constant — and, that the 12-lead ECG is diagnostic of an acute infero-postero OMI — suggests some form of 2nd-degree AV Wenckebach is operative (because with Mobitz II — the PR interval is constant for consecutively conducted beats — the QRS is almost always wide, and anterior rather than inferior infarction has occurred).
• BUT — If the rhythm in Figure-3 indeed represents some form of AV Wenckebach — it is not a "typical" form of AV Wenckebach, because there is no consistent pattern of group beating — and, similar PR intervals are lacking, whereas they are commonly seen with this Mobitz I form of 2nd-degree AV block. Instead — the PR interval in front of each of the 9 beats in today's tracing is constantly changing — which raises the question as to whether any of the P waves are being conducted to the ventricles?

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The LADDERGRAM: 

At this point I needed a laddergram to help me work out what might be a plausible mechanism for today's complex arrhythmia.

• NOTE: As I've commented on in a number of previous 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 for more on Dual-Level AV Wenckebach — which is what I suspected in today's complex rhythm in which the PR interval constantly changes — and, in which 2 P waves are contained within most R-R intervals).

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Figure-4: 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.

NOTE: Because I suspected dual-level AV block within the AV Node — I divided the AV Nodal Tier into 2 parts by drawing in a horizontal BLACK dotted line).

Figure-5: 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 9 supraventricular beats in this tracing. Once again, since conduction of narrow-QRS beats through the ventricles is generally rapid — I drew in near-vertical lines for each of the 9 narrow QRS beats in the Ventricular Tier.

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NOTE: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figure-4 and Figure-5). 

• Now the challenge begins! — with the task of trying to figure out which of the P waves in the Atrial Tier are being conducted to the ventricles.
• 
  
• PEARL #5: The BEST clue that a P wave is conducting a QRS complex to the ventricles — is when, in association with an underlying sinus rhythm (ie, in which there are no PACs or PJCs) — you see a QRS complex that clearly occurs earlier-than-expected. This concept is best illustrated in Figure-6.

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Figure-6: Of the 9 beats in Figure-6 — The QRS complex that most clearly occurs earlier-than-expected is beat #8. By PEARL #5 — this suggests that beat #8 is a QRS complex that is being conducted to the ventricles. Since beat #8 is neither a PAC nor PJC (because the underlying sinus rhythm remains quite regular — and a PAC or PJC would have reset the underlying sinus rhythm) — it must be that P wave "n" is conducting beat #8, albeit with a markedly prolonged PR interval (represented by the dark BLUE lines that pass through the 2 levels within the AV Nodal Tier).  

P wave "o", which falls right at the beginning of beat #8 — has too short of a PR interval to conduct (as I have represented by the light BLUE butt end that shows non-conduction of this impulse).

Figure-7: I fully acknowledge that because of the complexity of today's arrhythmia — some "Trial and Error" was needed along my way toward drafting the most logical solution to the laddergram for today's rhythm.

The position of P wave "l" (occurring so soon after the previous QRS complex) — seemed extremely unlikely to be conducting beat #7. This is especially true because P wave "m" appears in a much better position to conduct beat #7. I therefore drew in a light BLUE butt end to indicate non-conduction of P wave "l" — and dark BLUE lines that pass through the 2 levels within the AV Nodal Tier to indicate conduction of P wave "m". Note that the incline of the RED line within the lower AV Nodal Tier is greater than the incline of the dark BLUE line — consistent with a PR interval that is increasing until P wave "o" is non-conducted. (This makes for 3:2 AV Wenckebach conduction cycle within the AV Nodal Tier).

Figure-8: I next looked at P waves "p" and "q". One of these 2 P waves will most probably be conducting beat #9 to the ventricles. Because P wave "q" seems much better positioned to be conducting (ie, with a slightly, but not excessively prolonged PR interval) — I felt reasonably sure that P wave "p" was not conducting. This meant that 2 P waves in a row (P waves "o" and "p") were not conducting. This finding supported my suspicion of dual-level AV block within the AV Node, as the most logical explanation for there to be consecutive non-conducted P waves in a 2nd-degree AV block that is not Mobitz II. (I show this non-conduction of P waves "o" and "p" by successive butt end RED lines at each of the 2 levels within the AV Nodal Tier).

Figure-9: I next turned my attention to P waves "j" and "k". Once again, it seems logical that 1 of these 2 P waves will probably be conducting beat #6 to the ventricles. And once again, because P wave "k" seems much better positioned to be conducting (ie, with a slightly, but not excessively prolonged PR interval) — I felt reasonably sure that P wave "j" was not conducting. (This makes for a 2:1 AV conduction cycle — presumably by association being a 2:1 AV Wenckebach cycle).

Figure-10: At this point — a pattern for conduction of atrial impulses seemed to be established. By assessing atrial activity within each R-R interval — it became easier to intuit which P waves seemed least likely to be conducting — therefore suggesting that the remaining P wave(s) were indeed conducting neighboring QRS complexes to the ventricles.

P wave "i" seems perfectly positioned to conduct beat #5 to the ventricles (in a similar way that P waves "k" and "m" seemed well positioned to be conducting beat #6 and beat #7, respectively). IF this assumption is correct — then P waves "g" and "h" are not conducting any QRS complex to the ventricles. As was the case for P waves "o" and "p" — this makes for 2 non-conducted P waves in a row (which is why I drew successive butt end BLUE lines for P waves "g" and "h" at each of the 2 levels within the AV Nodal Tier).

Working my way backward — I next noticed how much earlier-than-expected beat #3 occurs, which as per PEARL #5 — strongly suggests that beat #3 is being conducted to the ventricles. But the PR interval of P wave "e" until neighboring beat #3 is clearly too short to conduct! Therefore, it must be that P wave "d" is conducting beat #3, albeit with a very long PR interval (in the same way we deduced that P wave "n" is conducting beat #8 with a long PR interval).

This left me with P waves "b" and "c" — which given the "pattern" of conduction observed up to this point, rendered it EASY for me to postulate that P wave "c" was much better positioned for conducting its neighboring QRS complex ( = beat #2) than P wave "b".

Finally — There is P wave "a" and beat #1. Although impossible to know for certain (because we do not see what happens before beat #1) — I drew in what seems to be the most logical conduction for this first part of today's rhythm (The PR interval between P wave "a" and beat #1 clearly seems too short to conduct).

Figure-11: My "finished" laddergram. Note that despite the lack of similar groups of beats that repeat (and the lack of repetitive PR intervals) — STEPPING BACK from Figure-11 does illustrate the concept of dual-level AV Wenckebach, in which there is progressive lengthening of PR intervals (represented by progressive increase in angulation within each of the 2 AV Nodal levels) — until 1 or 2 P waves in a row are dropped — with typical Wenckebach periodicity beginning again after the brief pause.

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Final COMMENT: 

Today's rhythm is difficult to interpret! That said — there are important lessons to be learned from review of today’s case.

• Precise determination of the etiology of today's arrhythmia is not needed for optimal initial management of today's patient! Instead — my Quick Assessment of the rhythm (which should not take more than 10-20 seconds to complete) is all that is needed for optimal initial management of today's patient.
• The KEY finding in today's ECG — is recognition in this patient with new CP that the tracing in Figure-2 is diagnostic of acute infero-postero OMI — and that prompt cath is needed for PCI.
• Whatever today's rhythm turns out to be — the "good news" is that the bradycardia and degree of AV block is likely to improve as soon as there is reperfusion of the "culprit" artery (Therefore need for prompt cath with PCI).
• 
  
• Being able to draw a laddergram of today's complex arrhythmia is not essential for optimal initial management of today's patient. That said — it is good to be aware of the entity known as dual-level AV Wenckebach as a less common, but nevertheless important form of 2nd-degree AV block. My hope is that review of my step-by-step approach to solving today's arrhythmia proves insightful for suggesting when dual-level AV Wenckebach should be suspected.
• Learning to read laddergrams that are drawn is EASY. Hopefully my step-by-step laddergram approach increases appreciation of the Wenckebach conduction pattern occurring in today's rhythm that is not otherwise obvious.
• 
  
• Finally — I will emphasize that my finished laddergram in Figure-11 is not the only possible solution to today's arrhythmia. More than a single solution is possible for many complex arrhythmias. What counts — is that my laddergram is a possible solution — and that some form of 2nd-degree AV block with periods of Wenckebach conduction is present.

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Acknowledgment: My appreciation to Adem Med Ahmed (from Mauritania) and Ahmed Elbakery (from Yemen) 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 Laddegrams (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.
• 
  
• 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). 
• 
  
• 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.
• 
  
• 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 #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• 
  
• 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 "culprit" artery.
• 
  
• ECG Blog #351 — reviews the diagnosis of acute posterior OMI. To see this illustrative case presented as an ECG Video — Please check out ECG Blog #406 (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).
• 
  
• 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 (2/10/2024):

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.

—  —

ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

• 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 the AV 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).

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Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

• PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
• PDF File: Posterior MI and the “Mirror Test” —

 

Figure-12: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

—  —

ECG Media PEARL #10 (10 minutes Audio) — 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 "culprit" artery.