ECG Blog #377 — Is the 1st ECG Normal?

The patient whose initial ECG is shown in Figure-1 — is a middle-aged man who presented to the ED (Emergency Department) for new-onset CP (Chest Pain). He was hemodynamically stable at the time this tracing was done.

• The patient was still having CP at the time ECG #1 was obtained — although the severity of his CP was unclear (ie, It is not known IF this patient’s CP was increasing — the same — or decreasing — at the time the ECG in Figure-1 was recorded).

QUESTIONS:

• In view of the above history — How would YOU interpret the initial ECG?
• WHY is it important to correlate severity of this patient’s CP with ECG #1?

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

MY Thoughts on the Initial ECG in Figure-1:

Sinus rhythm at ~60/minute is seen in ECG #1. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement (ie, Although R wave amplitude is a bit tall in lead V5 — QRS amplitude does not quite satisfy voltage criteria for LVH). 

Regarding Q-R-S-T Changes:

• Q Waves — are not seen on this tracing.
• R Wave Progression — is normal, with transition (where height of the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

Regarding S-T T Wave Changes — These are non-diagnostic …

• In the Limb Leads — QRS voltage is fairly low. There is non-specific ST-T wave flattening, but this does not look acute.
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• In the Chest Leads — The most abnormal-looking lead is lead V5, in which there is a sagging ST segment, but without J-point depression. The overall ST-T wave appearance in this lead looks more like LV “strain” than ischemia. There is non-specific ST-T wave flattening in neighboring leads V4 and V6.
• T waves are upright and peaked in anterior leads V1,V2,V3. The slight J-point ST elevation that is seen in these leads is not abnormal in leads V2 and V3 (that commonly manifest slight ST elevation as a normal phenomenon) — but lead V1 usually does not manifest any ST elevation (and the J-point is slightly elevated in lead V1 of ECG #1). Finally — it is difficult to determine if T wave amplitude in lead V2 is slightly disproportionate to S wave depth in this lead.

PEARL #1: When T waves in the chest leads are upright (as they are in Figure-1 — with the exception of the T wave in lead V5) — then, the T wave in lead V1 will usually not be taller than the T wave in lead V6. Although this "Imbalance" of precordial T waves is not seen very often — in the “right” clinical setting, it has been associated with recent OMI (Occlusion-based MI), most often from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350).

BOTTOM LINE Regarding ECG #1:

The initial ECG in today's case is not diagnostic of an acute event. That said — in this middle-aged man who presented to the ED with new-onset CP — there are a number of ECG findings of potential concern. These include.

• Subtle-but-real nonspecific ST-T wave flattening in 5 of the limb leads. 
• T wave "imbalance" in the chest leads — in which the upright T wave in lead V1 is not only taller than the T wave in lead V6 — but, there is slight ST elevation in lead V1 — and a potentially disproportionately tall T wave in lead V2.
• Support that these findings may be acute — is forthcoming from the uncharacteristically flat ST-T waves in lateral chest leads V4,V5,V6. Against the sagging ST-T wave in lead V5 being a reflection of LV "strain" — is the positive T wave and lack of any ST segment sagging in more-lateral lead V6.
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• To Emphasize: As isolated findings — None of the above ST-T wave abnormalities are diagnostic of an acute event. But taken together, in association with the history of new-onset CP — We can not rule out an acute (or recent) cardiac event on the basis of this single tracing. Therefore — ECG #1 is not a "normal" tracing (and close clinical follow-up is essential!).

PEARL #2: It's important to appreciate that the course of acute MI from acute coronary occlusion — is often staggered. By this, I mean — that even without PCI or thrombolytic therapy, the "culprit" vessel may spontaneously reopen. Sometimes the "culprit" vessel stays open — but at other times, it may at any point in time reocclude. And, sometimes this process of spontaneous reopening and reclosing may occur multiple times in short succession.

• The reason it is important to always correlate the presence (and relative severity) of CP with each serial ECG recorded on the patient — is that doing so may provide insight as to whether the "culprit" vessel at any time during the process is likely to be open or closed.
• The "culprit" coronary artery is more likely to be occluded IF the patient has ongoing severe CP — especially if this occurs in association with ST elevation over the area of infarction.
• Spontaneous reperfusion is likely IF in association with reduction (or resolution) of CP — ST elevation and reciprocal ST depression significantly improve.
• Somewhere in between the phase of acute ST elevation and return of ST segments to baseline, followed at some point by development of reperfusion (ie, inverted) T waves — may be a "transition" phase of pseudo-normalization, during which the ECG may look relatively normal (or show no more than nonspecific ST-T wave flattening).

How Does Pearl #2 Relate to Today's Case?

As stated above — ECG #1 in today's case is non-diagnostic. The patient was still having CP at the time this initial ECG was obtained — but how severe his CP was is unclear from the information we have available (ie, it was not known IF his CP was increasing — the same — or decreasing).

• IF this patient's CP was still severe at the time ECG #1 was recorded — then the peaked anterior T waves with subtle ST elevation and a potentially disproportionate T wave in lead V2 might reflect early proximal LAD (Left Anterior Descending) occlusion.
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• IF on the other hand, the patient's CP was significantly less than it was at the time symptoms began — then the peaked anterior T waves and diffuse ST-T wave flattening elsewhere might reflect reperfusion T waves in a patient with posterior OMI.
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• Alternatively — ECG #1 may simply reflect nonspecific ST-T wave abnormalities in a patient who was not having an acute event. 

What To Do Clinically?

The point to emphasize — is that we simply can not arrive at any conclusion on the basis of the single tracing shown in Figure-1. Instead — optimal management would include the following:

• Repeat the ECG soon! (ie, within 10-20 minutes of the initial tracing). IF the patient is evolving an acute event — it often takes no more than minutes for dynamic ST-T wave changes to become evident that confirm the diagnosis. Additional repeat ECGs are indicated (as might be needed) — until such time that a definitive ECG diagnosis (of either acute OMI or no OMI) is made!
• Look for a prior ECG on the patient (which may provide insight as to whether subtle ECG findings, as were described above for ECG #1 — are new or old).
• Follow-up closely with serial troponins — to see if there is any elevation.
• Ideally obtain a stat Echo at the bedside (which if this shows a regional wall motion abnormality during chest pain — would confirm an acute evolving event).

Today's CASE Continues:

The repeat ECG (that was done ~2 hours later) — is shown together with the initial tracing in Figure-2. The patient was apparently still having CP at the time ECG #2 was done (although  it was unclear if the patient's CP had persisted at the same intensity — or — had waxed and waned during the 2 hours that passed between obtaining these 2 tracings).

QUESTIONS:

• In light of the above historical information (and in light of the initial ECG in Figure-1) — How would you interpret ECG #2?
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• Has there been an acute OMI? IF so — What is the "culprit" vessel?  

Figure-2: Comparison of the repeat ECG with the initial tracing. (To improve visualization — I've digitized the original ECG using PMcardio).

How to Compare Serial Tracings?

The method I favor for comparing serial tracings — is to pick one of the ECGs — and to interpret that tracing in its entirety by whatever systematic approach you are using. I usually start with the earliest tracing that was recorded — because you then know that any changes seen on a subsequent tracing are "new".

• We are looking for changes in the shape and amount of ST elevation and depression between the tracings that we are comparing.
• The challenge with ECG comparison — is that we have to distinguish between differences from one ECG to the next that are likely to be due to a worsening or improvement in the patient's coronary disease — versus — ECG changes that are likely the result of technical factors (ie, a shift in frontal plane axis or QRS morphology changes due to a difference in lead placement or in the degree of elevation of the patient's bed [some acutely ill patients are unable to lie flat — and this may alter QRST appearance]).
• After full interpretation of the initial ECG you have looked at — I go lead-by-lead when I compare serial tracings, holding both tracings right next to each other. This is because IF, for example — the QRS complex is predominantly positive in lead III or in lead aVF on the 1st tracing — but then becomes more-negative-than-positive on the 2nd tracing — then the frontal plane axis has shifted! — and — you'll need to consider this axis shift when determining whether any differences in ST-T wave morphology are likely to be due to technical factors or "true" evolution of the patient's cardiac condition.
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• Finally (as per PEARL #2 above) — I do my best to correlate the presence and relative severity of CP to ECG findings in each of the serial tracings. 

In Today's CASE: Comparing ECG #1 and ECG #2:

As noted above — a good 2 hours passed before the repeat tracing was obtained. Unfortunately — how severe symptoms were during this 2-hour period is uncertain.

• To Emphasize: Our goal in repeating the ECG, is to see if there have been “dynamic” ST-T wave changes since the initial tracing was done, since IF there has been significant change — this would confirm that an acute event was ongoing.
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• How Valid is Our Comparison? — Comparison between ECG #1 and ECG #2 with regard to QRS amplitude and morphology in the 6 limb leads — reveals no significant change. In the chest leads — R wave progression is similar in the 2 tracings, with no more than slight reduction in lateral chest lead R wave amplitude. This suggests that any differences in ST-T wave morphology between the 2 tracings will be clinically significant!

What are the Changes?

Comparison of ECG #1 and ECG #2 reveals a number of significant changes:

• The most "eye-catching" change in ST-T wave appearance between the 2 ECGs in Figure-2 — is in lead V2. The slight upsloping J-point ST elevation with prominent upright T wave that had been present in ECG #1 — has been replaced by slight-but-real shelf-like J-point ST depression, with reduction in the size of the terminally positive T wave. In a patient with new chest pain — this ST-T wave appearance in lead V2 of ECG #2 is consistent with a positive "Mirror" Test (as described in ECG Blog #285 — as well as in other Related ECG Blog links provided below).
• Support that this change in ST-T wave appearance in lead V2 of the repeat ECG is real — is forthcoming from clear ST-T wave changes in each of the other 5 chest leads!
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• In lead V1 — the ST segment is no longer elevated, as it had been in ECG #1. Note that the "imbalance" of precordial lead T waves is no longer present! (ie, The T wave in lead V6 of ECG #2 is now clearly taller than the T wave in lead V1).
• In lead V3 of ECG #2 — instead of slight upsloping ST elevation, leading to a large positive T wave — there is now flat ST depression leading to a biphasic T wave with terminal negativity.
• In lead V4 of ECG #2 — ST depression becomes more marked than it was in lead V3, now with frank T wave inversion.
• In lead V5 — the sagging ST segment seen in the initial ECG — has been replaced by straightening of the ST segment takeoff, now with a clearly positive T wave. This effect continues in lead V6 of ECG #2 — in which there is now unmistakeable J-point ST elevation, with straightening of the ST segment takeoff that leads into a hyperacute T wave.

PEARL #3: The fact that there are such definite differences in multiple leads of the repeat ECG in today's case — defines these differences as "dynamic" ST-T wave changes. In a patient with new CP — this ECG finding indicates acute OMI until proven otherwise (and provides clear indication for prompt cath!).

PEARL #4: Did YOU appreciate the change in ST-T wave appearance between the 2 ECGs in Figure-2 in leads I and aVL? To emphasize — the change is subtle. That said — recognition of this change illustrates the important concept of comparing tracings in the context of the entire ECG. The fact that there is no doubt about the changes in each of the 6 chest leads compared to ECG #1, makes me look that much closer at the remaining leads in ECG #2, for additional findings that may be more subtle. The fact that there is no doubt about new hyperacute ST-T waves in lateral chest leads V5,V6 in ECG #2 — tells me that the increased volume of the positive T waves in high-lateral leads I and aVL of this repeat tracing is real!

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Putting It All Together:

Although it would have been helpful to know how this patient's symptoms correlated to the timing of ECGs #1 and #2 — Knowing there was ongoing CP of some degree in association with these 2 tracings done 2 hours apart strongly suggests the following:

• Dynamic ST-T wave changes are seen. ST depression that is maximal between leads V2-to-V4 is diagnostic of acute posterior OMI. Hyperacute ST-T waves in all lateral leads (ie, in leads I,aVL; V5,V6) with new ST elevation in lead V6 of ECG #2 — is diagnostic of acute lateral OMI.
• Acute postero-lateral OMI in the absence of inferior lead ST elevation strongly suggests acute LCx (Left Circumflex) Occlusion as the "culprit" artery. Prompt cath with PCI is clearly indicated.

Today's CASE Concludes:

The cath lab was activated after ECG #2. Cardiac catheterization revealed total occlusion of the LCx — which was successfully reperfused with PCI (Percutaneous Coronary Intervention). There was insignificant disease in the RCA (Right Coronary Artery) and the LAD (Left Anterior Descending) coronary artery. 

• In Figure-3 — I've added the final ECG in today's case, done the day after PCI, with the patient pain-free.

QUESTION:

• How would YOU interpret the likely status of the "culprit" LCx artery at the time that each of the ECGs in Figure-3 were done?

Figure-3: Comparison of all 3 tracings obtained in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

How to Interpret the 3 ECGs in Figure-3?

The results of cardiac catheterization proved that the "culprit" vessel was the LCx — with occlusion of this vessel causing postero-lateral infarction.

• The initial ECG in today's case ( = ECG #1) — did not show expected findings of acute LCx occlusion, in that there is no ST depression in leads V1-thru-V4 — and no lateral lead ST elevation. 
• Instead — there is precordial lead T wave "imbalance", with the T wave in lead V1 taller than the T wave in lead V6 — and, with a disproportionately tall T wave in lead V2 (compared to S wave amplitude in this lead). This suggests that the "culprit" LCx had spontaneously reopened at the time ECG #1 was recorded. The surprisingly tall T waves in leads V1,V2,V3 are consistent with reperfusion T waves in the posterior wall distribution. The nonspecific ST-T wave flattening seen in the other leads in ECG #1 are consistent with probable "pseudo-normalization" on the way to developing reperfusion T wave changes.
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• As discussed in detail above — ECG #2 was obtained ~2 hours after ECG #1, without clear indication as to the relative severity of CP compared to CP severity at the time of symptom onset. I suspect the patient's CP had increased in severity at the time ECG #2 was recorded — since maximal ST depression in leads V2-to-V4, in association with hyperacute ST-T waves in all lateral leads (with new ST elevation in lead V6) strongly suggests that the "culprit" vessel had spontaneously reoccluded at the time this repeat ECG was obtained.
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• The final ECG in today's case ( = ECG #3) was obtained the day after successful PCI, at a time when the patient was pain-free. The fact that ST-T waves in ECG #3 look so similar in appearance to ST-T waves in ECG #1 — supports my presumption that the "culprit" vessel had already spontaneously reopened by the time the initial ECG in today's case was done.

PEARL #5: One of the KEY "Take-Home" Points from today's case — is how correlation between the presence and relative severity of CP with ECG findings on each serial tracing can provide invaluable information regarding the status (open or closed) of the "culprit" vessel at the time each ECG is done.

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) 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 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
• ECG Blog #367 — for another example of acute LCx OMI. 
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• ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
• ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
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• ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
• ECG Blog #230 — How to compare serial ECGs.
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• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
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• ECG Blog #350 — regarding T Wave Imbalance in the Chest Leads.
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• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.

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ADDENDUM (4/30/2023):

• I've added several Audio Pearls below with material relevant to today's case.

—  — 

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?).

—  —

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.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria. 

ECG Blog #376 — A 15yo with Fever ...

The 12-lead ECG and long lead rhythm strip in Figure-1 — was obtained from a previously healthy 15-year old male, who presented with fever and diarrhea. He was hemodynamically stable. No chest pain.

• How would YOU interpret the ECG in Figure-1?
• What is the cardiac rhythm?
• What do you suspect as the clinical diagnosis?

Figure-1: The initial ECG in today’s case — obtained from a 15-year old male with fever and diarrhea. What is the rhythm? What is the clinical diagnosis?

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NOTE: In the interest of optimizing clinical relevancy and time efficiency for arriving at the diagnosis — I highlight in step-by-step fashion my approach to today’s case.

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MY Thoughts on the Initial ECG in Today’s Case:

For cases in which the patient is hemodynamically stable — I generally like to begin by assessing the rhythm in the long lead II rhythm strip at the bottom of the tracing. After assuring myself that no immediate action is needed to treat the rhythm — I’ll often take a quick glance at the 12-lead ECG. Doing so in Figure-1 — it should be obvious that in addition to the irregular rhythm — that many of the leads in the 12-lead tracing show ST elevation or depression.

• PEARL #1: Common things are common. In a previously healthy adolescent (who is 15 years old in today's case) — the presentation of an acute febrile illness that is without a complaint of chest pain, is highly unlikely to be due to an acute MI. As a result — as soon as I saw the irregular rhythm and both ST elevation and depression on the 12-lead ECG — I immediately suspected acute myocarditis as the most probable cause of this abnormal ECG.

Assessing the Rhythm:

I favor use of the Ps, Qs, 3R Approach for assessing the cardiac rhythm (See ECG Blog #185). To emphasize — Use of a systematic approach to rhythm interpretation should not slow you down. For example — in no more than 10 seconds of reviewing the long lead II rhythm strip in today’s case — I was able to deduce the following:

• A certain number of P waves are present (RED arrows in Figure-2).
• The QRS complex is narrow — so the rhythm is supraventricular.
• The ventricular rhythm in Figure-2 is not Regular. Instead — there is a regular irregularity (ie, “group” beating) — in the form of bigeminal rhythm with alternating shorter-then-longer R-R intervals.
• At least some of the P waves in today’s rhythm are Related to neighboring QRS complexes. We know this — because many of the PR intervals repeat. Thus, in Figure-2 — We see that the PR interval before each QRS that ends a shorter cycle is the same! (ie, The PR intervals before beats #2, 4, 6, 8, 10 and 12 are all = 0.24 second — such that this tells us that each of these P waves is being conducted, albeit with 1st-degree AV block).
• We also know that while some P waves in Figure-2 are conducting — other P waves are not conducting (which we know because the RED arrow P waves that appear just before the onset of beats #5, 7 and 9 have a PR interval that is too short to conduct). 
• Since the QRS complex nearest to these P waves that are not conducting (ie, the QRS complex of beats #5,7,9) — is narrow and looks very much like the QRS of sinus-conducted beats #2,4,6,8,10 and 12 — we can presume that beats #5,7,9 are junctional beats. And because the AV Nodal escape rate in children and adolescents may be faster than in adults (ie, 50-to-80/minute — instead of 40-to-60/minute) — beats #5,7 and 9 may represent junctional escape beats.
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• Finally — The underlying atrial rhythm in Figure-2 is probably regular. IF this is indeed the case — then there will be more P waves than QRS complexes, which means that some form of 2nd-degree AV block is likely to be present. And, the finding of group beating — in association with a regular atrial rhythm — with a number of PR intervals that repeat — should strongly suggest Wenckebach conduction.
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• To Emphasize: We have not yet proved the above assumptions. That said — keeping in mind how “Common things are common” — and — following the Ps, Qs, 3R systematic approach to rhythm interpretation — allows us within seconds to suspect the most likely clinical and rhythm diagnosis in today's case.

Figure-2: The long lead II rhythm strip that appeared below the 12-lead ECG that was shown in Figure-1. RED arrows highlight that a certain number of P waves are definitely present. Is the underlying atrial rhythm regular?

HOW to Prove Our Assumptions:

The KEY step in proving our assumptions — is to establish that the underlying atrial rhythm in Figure-2 is indeed regular. This is EASY to do with the use of calipers.

• Set your calipers to the P-P interval suggested by any 2 consecutive P waves in Figure-2 that we can definitely identify. This could be the P-P interval defined between the 3rd and 4th RED arrows in Figure-2 — between the 5th and 6th RED arrows — or between the 7th and 8th RED arrows.
• Realizing that slight variation in the P-P interval is common (known as sinus arrhythmia) — the PINK arrows in Figure-3 suggest the probable location of underlying sinus P waves. In support that sinus P waves are probably hiding under each of these PINK arrows — is the presence in Figure-3 of a small “hump” or notch in each of these locations (when compared to the appearance of normal ST-T waves or QRS complexes in this rhythm strip). 
• 
  
• PEARL #2: Using calipers to “walk out” the P-P interval we selected makes it fast and easy to find the probable location (under the PINK arrows) of these regularly-occurring sinus P waves.

Figure-3: Using calipers makes it EASY to “walk out” the probable location of sinus P waves hiding under each of the PINK arrows. Note that a small “hump” or notch lies under each PINK arrow (compared to the normal appearance of ST-T waves and QRS complexes without PINK arrows). 

PEARL #3: The reason it is so helpful to identify an underlying regular atrial rhythm (as we have done in Figure-3) — is that doing so rules out other causes of group beating, such as PACs (including blocked PACs) and sinus pauses (as is commonly seen with Sick Sinus Syndrome).

• KEY Point: One of the KEY criteria for recognizing AV blocks — is that the atrial rhythm should be regular (or at least almost regular — as the P-P interval may vary slightly if there is sinus arrhythmia). In contrast — P waves that clearly occur too early or too late to be consistent with a sinus rhythm, are much less likely to be due to an AV block.

Putting It All Together: We’ve established that today’s rhythm is supraventricular with “group beating” — and with an underlying regular sinus rhythm. Some P waves conduct — but others do not. There are more P waves (ie, colored arrows in Figure-3) than QRS complexes — so, some form of 2nd-degree AV block appears to be present, although we've not yet established the precise mechanism.

• As emphasized in ECG Blog #326 (and as I review in the ADDENDUM below) — Mobitz I, 2nd-Degree AV Block (ie, AV Wenckebach) — is by far (!) the most common form of 2nd-degree AV block, especially when there is consistent group beating as we see in Figure-3.
• There are many different forms of AV Wenckebach — some of which do not show obvious progressive PR interval prolongation until a beat is dropped. For example — It is common to see junctional escape beats with AV Wenckebach (See ECG Blog #63 — for illustration of this phenomenon).
• The QRS complex is narrow (The QRS is typically narrow with Mobitz I — whereas it is almost always wide when Mobitz II is present).
• The PR interval is increased for those P waves that do conduct (which is commonly seen with Mobitz I — much more so than with Mobitz II).
• We do not see consecutively conducted P waves with a constant PR interval anywhere on today's tracing (as is required for there to be the Mobitz II form of AV block). 
• 
  
• BOTTOM Line: With regard to the rhythm in today's case — I knew within seconds that some form of AV Wenckebach was almost certain to be present (especially in view of the clinical scenario, that strongly suggested acute myocarditis as the underlying etiology).
  

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Taking Another LOOK at Today's 12-Lead ECG:

As emphasized above in Pearl #1 — Common things are common. ECG abnormalities in a previously healthy adolescent, who presents with an acute febrile illness — is unlikely to be due to an acute MI (all the more so in today's case — in which this 15-year old did not even have chest pain). For clarity — I've reproduced the initial tracing from today's case in Figure-4. I see the following:

• Regarding the Rhythm: Group beating is present in a bigeminal pattern, with regular sinus P waves (as described in detail above). This is almost certain to represent some form of AV Wenckebach.
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• Regarding Intervals: Conducted beats manifest a prolonged PR interval — the QRS is narrow everywhere — the QTc may be slightly prolonged.
• There is a vertical frontal plane axis (ie, the QRS is nearly isoelectric in lead I — if not slightly negative).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves — are seen intermittently in leads I,aVL; and in V1,V2 (ie, a tiny initial r wave is seen for some beats in these leads). 
• R Wave Progression — is appropriate, with transition (where the R wave becomes taller than the S wave is deep) occurring at a normal location between leads V3-to-V4.
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• ST-T Wave Changes — There is coved ST elevation in high-lateral leads I and aVL — as well as in lead V2 (and to a much lesser extent in lead V1). There is marked ST depression in each of the inferior leads. There is also ST depression in leads V2-thru-V4 (downsloping in lead V3) — with terminal T wave positivity in these leads.

BOTTOM Line: The ECG in Figure-4 is markedly abnormal. In addition to probable Mobitz I, 2nd-degree AV block — multiple leads show either ST elevation or ST depression that is not characteristic of any specific anatomic area for acute coronary occlusion (especially given the presence of AV Wenckebach, but in the absence of acute inferior ST elevation).

• As emphasized above — the History in today's case is most consistent with acute myocarditis — because the patient is an adolescent with an acute febrile illness, but no chest pain. 
• 
  
• PEARL #4: The ECG findings of acute myocarditis are highly variable. Virtually anything can be seen, depending on the specific etiology of the myocarditis, and the severity of illness. That said — One often sees Q waves and ST-T wave abnormalities that may be marked (with or without any of a variety of cardiac arrhythmias) — but which occur in a distribution that typically does not suggest a specific anatomic location. This is precisely what we see in Figure-4.
• At other times — the ECG of a patient with acute myocarditis may look very similar to that of an acute evolving infarction. Both entities manifest troponin elevation (that may be marked) — and sometimes cardiac catheterization (or Cardiac MRI, if available) may be the only way to distinguish between these 2 entities.
• To Emphasize: When the patient is older and presents with a history of cardiac-sounding chest pain — then acute infarction will be much more common than acute pericarditis, myocarditis, or perimyocarditis.

Follow-Up in Today's CASE:

The patient in today's case was diagnosed as having acute myocarditis. The patient did well with conservative management — and both ECG and the rhythm abnormality resolved as his clinical condition improved.

Figure-4: I've reproduced from Figure-1 the initial tracing in today's case.

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Beyond-the-Core: Laddergram Illustration ...

Certain complex arrhythmias may have more than a single plausible rhythm interpretation. The fact that this occurs in today's case — is what makes interpretation of today's rhythm so challenging.

• To Emphasize: Precise determination of the mechanism of today's arrhythmia is not needed for appropriate management. Instead — simply recognizing that some form of AV Wenckebach is likely to be present (as we describe above) — in association with an acceptable ventricular rate — is clinically sufficient, since a normal rhythm will most probably return as the patient's acute myocarditis resolves. That said — It may be insightful to review step-by-step construction of a laddergram when the mechanism of the rhythm is not immediately apparent.

Constructing the Laddergram:

• NOTE: For more on the basics of HOW to Read (and/or Draw) Laddergrams — Please see my ECG Blog #188 —

Figure-5: I find it easiest when constructing a laddergram — to first complete the Atrial Tier (that shows atrial activity). The BLUE arrows illustrate how I drop a vertical line from the onset of each P wave.

Figure-6: It is also usually easy to fill in the Ventricular Tier — which I do by dropping vertical lines down from the onset of each QRS complex.

Figure-7: Once the Atrial and Ventricular Tiers are filled in — We can begin "solving" the laddergram. I do this by connecting those P waves that I am certain are conducting — with the QRS in the Ventricular Tier that is likely to be produced. In today's case — this will be for the P waves in front of beats #2,4,6,8,10 and 12 — because these P waves all have the same PR interval.

Figure-8: The reason today's rhythm is so challenging — is that I see 2 possible mechanisms that may explain this arrhythmia.
— — — — — — — — 
Possibility #1: We have previously established that the PR interval of the YELLOW P waves is too short to conduct. I therefore suspected that beats #1,3,5,7,9 and 11 are junctional escape beats — which I have drawn in as small RED circles within the AV Nodal Tier. This leaves me with having to explain the path within the AV Nodal Tier to be followed by the YELLOW and WHITE P waves.

Figure-9: I thought it logical to postulate that the WHITE P waves are not being conducted because of the 2nd-degree AV block. Although we know that the YELLOW P waves are also not conducted (because their PR interval is too short to conduct) — these YELLOW P waves never have a "chance" to conduct (because the junctional escape rhythm takes over before these P waves can make it to the ventricles). Whether these YELLOW P waves would conduct IF junctional beats #1,3,5,7,9 and 11 did not occur is unknown.

Figure-10: There is a 2nd Possibility for the mechanism of today's rhythm. Some patients have dual AV Nodal Pathways — each with their own conduction properties. In such cases — there may be a marked difference in the PR interval for those P waves on the rhythm strip that are conducting (depending on which AV Nodal Pathway is being used). IF dual AV nodal pathways were operative in today's case — then the BLUE arrow P waves in Figure-10 may be conducting with a very long PR interval — and — it may be that the WHITE arrow P waves are the ones that are not conducted because of this unusual pattern of Mobitz I.

BOTTOM LINE:

As noted earlier — Complex arrhythmias may sometimes have more than a single plausible rhythm interpretation. I am not certain whether Possibility #1 or #2 is the correct explanation in today's case. That said, as noted earlier — Clinically, it does not matter!

• Some form of AV Wenckebach is present. The overall ventricular rate is more than satisfactory (ie, the average rate is over 80/minute) — and given the diagnosis of acute myocarditis — we anticipated that the AV conduction disturbance would resolve as the patient's condition improved. It did — and the patient recovered uneventfully.

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Acknowledgment: My appreciation to Chaim Katalan (Laniado Hospital, Israel) 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 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• 
  
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
• 
  
• ECG Blog #236 — Reviews the 3 Types of 2nd-Degree AV Block.
• ECG Blog #63 — for a case of AV block with junctional escape beats. 
• ECG Blog #192 — Reviews the 3 Causes of AV Dissociation (and emphasizes why AV Dissociation is not the same thing as Complete AV Block).
• ECG Blog #186 — When to suspect Mobitz I?

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ADDENDUM (4/24/2023):

One of the most problematic areas in arrhythmia interpretation is assessment of the AV Blocks. This doesn't have to be so difficult ... I review the basics in ECG Blog #186 — which are briefly summarized in the Audio Pearl below.

• In ECG Blog #236 — my 15-minute ECG Video Pearl #52 reviews how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block).
• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
• 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! (This is a free download).

—  —

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

• What follows below is a 7-page excerpt from my ACLS-2013 Arrhythmias (Expanded Version) book — in which I review the distinction between AV dissociation vs complete AV block.