ECG Blog #388 — Why Does Lead V1 Look Funny?

The ECG in Figure-1 was obtained from an 18-year old woman — who moments before been resuscitated from out-of-hospital cardiac arrest.

QUESTIONS:

In light of the above clinical history ...

• How would YOU interpret her post-resuscitation ECG?
• Does this ECG in Figure-1 provide clue(s) to the etiology of this patient's cardiac arrest?

Figure-1: The initial ECG in today's case — obtained following resuscitation from cardiac arrest of an 18-year old woman.
(NOTE: The filter setting used a 150 Hz high-frequency cutoff.)

MY Initial Thoughts on Today's Case:

Today's tracing was sent to me. When I first saw this ECG — I had more questions than answers ...

• The "good news" — is that we clearly see sinus P waves in ECG #1, that document conversion to sinus rhythm (ie, upright P waves in lead II that precede each QRS complex with a constant and normal PR interval).
• The challenging part of the 12-lead tracing seen in Figure-1 — is WHY does an 18-year old woman have such a wide and bizarre QRS morphology? I suspected the answer resides in the reason why an 18-year woman might have a cardiac arrest.

Looking Closer at QRS Morphology in ECG #1:

At first glance — I thought we were simply looking at a very wide and bizarre QRS complex, especially in lead V1 (where the QRS looked to measure at least 0.15 second).

• The all-upright QRS in lead V1 — together with wide terminal S waves in lateral leads I and V6 — is consistent with complete RBBB (Right Bundle Branch Block).
• The rS configuration with predominant negativity in all 3 inferior leads — is consistent with associated LAHB (Left Anterior HemiBlock) — therefore RBBB/LAHB = Bifascicular Block.
• In addition — there seemed to be significant fragmentation (excessive notching of the QRS) — which usually is indication of underlying "scar" from infarction, cardiomyopathy, or other form of underlying structural disease.

CASE Follow-Up:

At this point — I learned answers to some of the questions I raise above:

• The 18-year old woman whose post-resuscitation tracing is shown above in Figure-1 — was found to have ARVC/ARVD (Arrhythmogenic Right Ventricular Cardiomyopathy or Dysplasia).
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• Genetic testing confirmed ARVC (The patient had a homozygous DSG2 gene — associated with both autosomal dominant and autosomal recessive forms of ARVC). 
• The patient's younger brother was also diagnosed with "a cardiomyopathy".
• Echo showed a markedly dilated cardiomyopathy (EF ~22% with global hypokinesis, including severely dilated RV with impaired RV function).
• MRI confirmed ARVC.
• An ICD (Implantable Cardiac Defibrillator) was inserted — and the patient was discharged from the hospital. This young woman did well for a year — but unfortunately suffered another cardiac arrest, from which she could not be resuscitated.

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About ARVC/ARVD ...

ARVD is a genetic disorder of the myocardium. As a result of a familial gene mutation — there is fatty infiltration of the RV free wall (Shah et al — Stat Pearls-NCBI-2022). First described by Guy Fontaine in 1977 — the disorder has a prevalence of ~1/5,000 in the general population.

• Clinically — the concern is the high risk of developing VT with a LBBB pattern (indicative of the RV origin of VT).
• Overall, by way of perspective — ARVD is an uncommon disorder. That said — ARVD appears to be an underestimated cause of SCD (Sudden Cardiac Death), especially among younger adults, in whom it accounts for ~20% of SCDs in those under 35 (Mu et al — Medicine 96(47):e8808, 2017). 
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• KEY Point: All-too-often the diagnosis of ARVD is only made postmortem. This is particularly unfortunate — because life-prolonging treatment (in the form of ICD implantation) is available.
• The ECG may provide revealing clues to the diagnosis of ARVD — but as discussed below, there are important caveats to be aware of when interpreting an ECG in which you are considering the possibility of ARVD.
• Echo may provide helpful clues (ie, by showing a dilated right ventricle, with a very thin RV free wall — and — impaired RV function).
• Definitive diagnosis may be made by endomyocardial biopsy — or more commonly in recent years, by MRI — in association with genetic testing.
• Genetic testing of relatives is essential to prevent undetected disease in family members.

Can You Diagnose ARVD from QRS Morphology During the VT?

As suggested above — ARVD is surprisingly common among the potential causes of sudden death in a “previously healthy” younger adult population. Many of these patients have no symptoms prior to their presentation with a 1st (and unfortunately – sometimes also their last) episode of VT. Among those patients who are successfully resuscitated — the question arises as to IF it is possible to diagnose ARVD as the cause from QRS morphology on the ECG obtained during the episode of sustained VT? Insight into this question is provided by 2 Hoffmayer et al manuscripts (JACC 58(8):831-838, 2011 — and — Front Physiol 3:23, 2012).

• VT in patients with ARVD usually arises from the RV. As a result — an “lbbb-like” QRS morphology is typically seen during VT in the chest leads. That said — the frontal plane axis may be variable, depending on where in the RV the greatest pathology is found, and whether RV fatty infiltration is diffuse or more localized.
• Another cause of variable (sometimes unpredictable) QRS morphology during ARVD-associated VT — is that some patients also have LV involvement, which can be the source of resultant VT (Ghannudi et al — Clin Med Insights Cardiol 8(Suppl 4):27-36, 2014).
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• Clinically — The differential diagnosis for an episode of sustained VT in a previously healthy young adult features some form of idiopathic VT (most commonly RVOT VT = Right Ventricular Outflow Track VT) vs AVRD. Overall, between these 2 principal considerations — RVOT VT is by far, the more common entity. That said, given the more lethal prognosis of ARVD — it is essential not to overlook this diagnosis (especially since ARVD is not as rare as is thought by many).
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• NOTE: The presence of QRS fragmentation and/or recognition of multiple QRS morphologies during repeat episodes of sustained VT are 2 ECG findings that favor AVRD (ie, RVOT VT typically lacks fragmentation [because by definition there is no underlying structural heart disease] — and RVOT tends to only manifest a single QRS morphology [whereas ARVD is more likely to manifest multiple VT morphologies, especially if fatty infiltration involves multiple areas within the RV]).
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• BOTTOM Line: QRS fragmentation and multiple VT morphologies are not reliably seen in all patients with ARVD. As a result — sensitivity and specificity of ECG characteristics during a VT episode are far from perfect for predicting which patients are likely to have ARVD. That said, clinically — this does not matter in an emergency situation because initial management (ie, with drugs or synchronized cardioversion) is essentially the same! And, in 2023 — virtually any young adult with an episode of VT should have follow-up evaluation including cardiac MRI to rule out mimics of severe underlying cardiac pathology, such as ARVD or sarcoidosis with cardiac involvement. Cardiac MRI will then tell you if ARVD is or is not present (Macias et al — JAFIB 7(4):106-111,2015).

When to Suspect ARVD from the 12-Lead ECG:

Awareness of the ECG signs of AVRD may facilitate diagnosis:

• T wave inversion in right-sided leads V1,V2,V3 is almost always seen — so much so, that the diagnosis of ARVD becomes unlikely if right-sided T wave inversion is missing.
• There may be localized QRS widening (to ≥110 msec.) in these right-sided leads.
• The most specific diagnostic ECG sign of ARVD is the Epsilon wave (Pérez-Riera et al — Ind Pacing Electrophys J 19:63-67, 2019). These elusive ECG deflections are thought to represent delayed potentials from slow intraventricular conduction (due to fatty infiltration, mixed with fibrous tissue within remnants of normal myocardium). 
• That said — Epsilon waves are often of limited diagnostic value, because: i) Technical oversights reduce detection, even in patients with these deflections; and, ii) Epsilon waves are generally a manifestation of more advanced disease.

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Why is it hard to pick up Epsilon Waves on ECG?

• There are several reasons ...  

Reason #1: The Wrong Filter Setting is Used ...

All too often — filter settings are ignored. Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. Greater filtering is generally used in monitor mode, with a common setting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) — is recommended for diagnostic mode, where more accurate ST segment analysis is essential.

• I've taken Figure-2 from the illustration by García-Niebla et al (Rev Esp Cardiol 69(4):438, 2016) — to show how selection of a 40 Hz cutoff frequency (that is commonly chosen in clinical practice in an attempt to "improve" tracing appearance) may result in reduction (if not disappearance) of fine ECG features such as the Epsilon wave, that is only optimally seen in Figure-2 at a cutoff high-pass filter setting of 150 Hz (BLUE arrows). 

 

Figure 2: Illustration of the effect of filter settings on the likelihood of seeing epsilon waves on a standard 12-lead ECG.

Reason #2: The Wrong Lead System is Used ...

I strongly recommend the section by Drs. Buttner and Cadogan in Life-In-The-Fast-Lane on the Fontaine Lead — https://litfl.com/fontaine-lead/ — as this concise review outlines what to know for optimizing your chance of identifying an Epsilon wave on ECG. I highlight below a few KEY points from this LITFL Review:

• Identification of an Epsilon wave is the most specific ECG sign of ARVD. These small deflections may be seen as a "blip" or "wiggle", most often occurring either at the end, or just after the QRS complex — but definitely before the T wave. Epsilon waves are best seen in leads V1,V2 — and a bit less well seen in V3,V4. On occasion — they may also be seen in other leads.
• LITFL cites a figure of 23% for the frequency of visualizing epsilon waves on a standard ECG in patients with ARVD. The filter settings used in association with citation of this figure are not mentioned — so given the tendency of all-too-often selecting a 40 Hz high-pass setting (instead of the optimal 150 Hz setting) — an even lower likelihood of finding epsilon waves might be expected on the ECGs sent our way in search of detecting Epsilon waves.
• In contrast — use of special placement of standard ECG machine electrodes called Fontaine Lead Placement — allows detection of Epsilon waves in up to 75% of patients! Rather than reproducing the user-friendly instructions on the LITFL site — I'll refer interested readers directly to their site — https://litfl.com/fontaine-lead/ —
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• Finally — Be aware of the variety of potential Epsilon wave shapes! These include: i) "Wiggle" waves; ii) Small upward spikes; iii) Small downward spikes; and/or, iv) Smooth amplitude deflections at the end of the QRS (which may result in prolongation of the QRS in right-sided leads by up to 25 msec.).

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Take Another LOOK at Today's Tracing:

"Armed" with the above insight regarding ECG detection of Epsilon waves — Let's take another LOOK at today's initial ECG (Figure-3).

• How would you now interpret the initial ECG in today's case?
• Do you see Epsilon waves in Figure-3? If so — in which lead(s)?

Figure-3: The initial ECG in today's case — that I've reproduced from Figure-1. This ECG was obtained following resuscitation from cardiac arrest of an 18-year old woman. (NOTE: The filter setting used a 150 Hz high-frequency cutoff.)

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ANSWER: Interpretation of Figure-3 . . .

I fully acknowledge that prior to 2010, when I started my ECG Blog and began my heavy involvement in ECG internet consultation — I had no direct experience with Epsilon waves. While I still find exposure to this intriguing ECG phenomenon uncommon — I've become much more comfortable with its detection.

• The ECG in today's case provides the BEST illustration of Epsilon waves that I too-date have seen.

Figure-4: I've labeled the ECG in Figure-3 — to highlight how to identify the numerous Epsilon waves present in today's tracing.

My Observations regarding Figure-4:

The rhythm in Figure-4 is sinus — as evidenced by regular upright in lead II P waves, with a constant and normal PR interval.

• As we noted in the beginning of today's post — the QRS complex is wide, with QRS morphology consistent with RBBB/LAHB.
• Note that there is T wave inversion in the anterior leads, as would be expected with ARVD (albeit the presence of RBBB itself could account for some of this anterior T wave inversion).
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• KEY Point: The reason for the bizarre shape of the QRS complex in lead V1 — is that the QRS in this lead is being prolonged by a huge Epsilon wave (dark BLUE arrow).
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• To assist in looking for Epsilon waves in other leads — I dropped a vertical dark BLUE time-line through the peak of the huge Epsilon wave in lead V1 — extending downward through the long lead II rhythm strip at the bottom of the tracing. Doing so defines the point in the 2 simultaneously-recorded long lead rhythm strips that marks the occurrence of the Epsilon wave.
• Using this reference point we defined for the Epsilon wave in the long lead II and lead V1 rhythm strips — I then extended upward a vertical light BLUE time-line to highlight the expected location of any Epsilon waves that might be seen in simultaneously-recorded leads I,II,III — aVR,aVL,aVF — and V4,V5,V6.
• The light BLUE arrow in lead II highlights a surprisingly large negative Epsilon wave that is present in this lead.
• Following these upward extended light BLUE time-lines — we can see that smaller, but definitely-present negative Epsilon waves are also seen in leads I, aVL, aVF, and V3-thru-V6.
• Another positive Epsilon wave is seen in lead aVR.

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing. 

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ADDENDUM (7/29/2023):

I summarize KEY features regarding Idiopathic VT in Figure-4.

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT.

 

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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 the Ps, Qs, 3R Approach to Rhythm Interpretation.
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• Please see My Comment at the bottom of the page in the June 3, 2023 post in Dr. Smith's ECG Blog — in which a case of ARVC is reviewed.
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• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
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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.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #197 — Review of Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #38 and Blog #85 and Blog #323 — 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 — Criteria for distinguishing VT vs Aberration.

ECG Blog #387 — 2 Minutes Later ...

The ECG in Figure-1 was obtained from an elderly man with a history of coronary disease — who contacted EMS for "burning" chest discomfort that woke him at 3am. Unlike his "usual" anginal episodes — this chest discomfort was not relieved by NTG. Some amount of time passed at home — during which his chest discomfort persisted

• The patient was hemodynamically stable at the time he was seen by EMS, when ECG #1 was recorded.

QUESTIONS:

• How would YOU interpret the initial ECG in today's case?
• In view of the above history — Does ECG #1 suggest an acute event? Should the cath lab be activated?

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

MY Thoughts on ECG #1: 

In view of the history — the initial ECG in today's case is clearly of concern! I see the following:

• Although there is no long lead rhythm strip — we can see that the rhythm is AFib with a controlled ventricular response (ie, irregularly irregular rhythm without P waves — and with a heart rate between ~70-110/minute).
• Regarding Intervals: There is no PR interval (since the rhythm is AFib). The QRS complex is narrow. The QTc is at most slightly prolonged. 
• Axis: Slightly leftward — but not leftward enough to qualify as LAHB (ie, predominantly negative QRS in lead aVF — but not predominantly negative in lead II).
• No chamber enlargement.
• Large, wide Q waves are present in leads III and aVF — consistent with this elderly patient's known history of coronary disease (ie, prior inferior infarction).

The most remarkable changes in ECG #1 relate to ST-T waves:

• In the Limb Leads — ST-T wave changes do not look acute. There is no more than minimal upsloping ST elevation in leads III and aVF — with volume of the upright T wave in these leads not disproportionate to the very wide and deep Q waves that are present. 
• The ST segment in the other inferior lead ( = lead II) is flat, but not elevated at all.
• There is some downsloping ST depression in high-lateral leads I and aVL — which is consistent with a mirror-image opposite ST-T wave picture compared to what we see in leads III and aVF.
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• BUT — in the Chest Leads — There definitely are ST-T wave changes of concern! This is especially true given the History in today's case.

PEARL #1: Normally, there will be slight, upward sloping ST elevation in anterior leads V2 and V3. Not only is this slight ST elevation missing from leads V2,V3 in ECG #1 — but the ST segment in these leads (as well as in neighboring leads V1; and V4,V5) is distinctly flat! 

• This picture of ST segment flattening (with loss of the normal slight ST elevation in V2,V3) — should be instantly recognized as abnormal, especially in a high-risk patient (such as in the elderly man with known coronary disease in today's case — whose episode of new chest discomfort was not relieved by NTG).

PEARL #2: When T waves in anterior chest leads are upright (as they are in Figure-1) — 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).
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• NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly much taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized. 

PEARL #3: 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 importance of correlating 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 (Chest Pain), 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, the ST elevation and reciprocal ST depression significantly improve.
• Reperfusion of the "culprit" artery is even more likely IF — in association with CP resolution, one sees "reperfusion" T waves (ie, T wave inversion) in areas where there had been ST elevation.
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• KEY Point: Somewhere in between the phase of acute ST elevation and return of ST segments to baseline — may be a "transition" phase of pseudo-normalization, during which time the ECG may look relatively normal (or show no more than nonspecific ST-T wave flattening). IF attention is not paid to the presence and relative severity of CP in association with each serial ECG — it could be extremely EASY to overlook recent OMI if the initial ECG is being viewed during this phase of pseudo-normalization.

PEARL #4: Perhaps the most difficult infarction location to recognize — is acute posterior MI. This is because none of the leads in a standard 12-lead tracing directly view the posterior wall.

• As emphasized in many of these ECG Blogs (See ECG Blog #285 and Blog #193 — among many others) — use of the "Mirror Test" facilitates recognition of acute posterior MI (ie, Instead of ST elevation — there is mirror-image opposite ST depression in anterior leads that provide a "mirror-image opposite" view of the posterior left ventricular wall). The message is clear — If, in a patient with new chest pain — ST-T wave depression is maximal in leads V2, V3 and/or V4 — consider acute posterior MI until proven otherwise.
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• KEY Point: In areas of the heart where an acute STEMI produces ST elevation — reperfusion T waves (that develop after the "culprit" artery reopens) will appear as T wave inversion. The opposite occurs with posterior MI — in which instead of T wave inversion, development of tall, upright T waves in leads V2, V3 and/or V4 signal the presence "reperfusion" T waves.

PEARL #5: As emphasized in ECG Blog #317 — Although posterior leads (ie, V7,V8,V9) are often advocated to facilitate recognition of acute posterior MI — use of posterior leads is not essential for this purpose.

• QRST amplitudes with posterior leads are reduced compared to mirror-image anterior lead amplitudes — because electrical activity from posteriorly placed V7,V8,V9 electrodes has to traverse the thick back musculature before it can pick up the heart's electrical activity. 
• MY Observation: In my experience over the past 40+ years of diligently looking for posterior MI — I have virtually never seen posterior leads diagnose a posterior infarction that wasn't already evident to me from application of the Mirror Test to the standard 12-lead ECG. NOTE: With just a little bit of practice — it becomes EASY to apply the Mirror Test to facilitate recognition of posterior MI.

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Putting It All Together:

Given the History in today's case (ie, of an elderly man with known coronary disease — who a number of hours before ECG #1 was obtained, was awakened by new CP that was not relieved by NTG) — I would interpret ECG #1 as suggestive of acute posterior OMI ( = Occlusion-based MI) — until proven otherwise.

• The modest amount of ST depression (which is maximal in lead V4) — in association with the T wave imbalance (T in V1>T in V6), with flat ST segments and disproportionately tall, peaked T waves in leads V1-thru-V4 — suggest there has been spontaneous reperfusion.
• The very deep and wide Q waves in leads III and aVF indicate that there has been inferior infarction at some point in time. Whether this inferior infarction is part of the recent posterior OMI is uncertain from the single ECG shown in Figure-1. After all — the onset of symptoms occurred some hours earlier — and there is still some ST elevation in lead III with reciprocal changes in leads I and aVL — so there could be an associated acute (or recent) inferior infarction. 
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• PEARL #6: Availability of a prior ECG on today's patient could have answered the question as to whether limb lead changes are "new" or "old". Finding a prior tracing on today's patient would also confirm my impression of recent (and/or ongoing) posterior OMI.
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• PEARL #7: Even without availability of a prior ECG — the history and ECG findings described above in the initial tracing justify cath lab activation. This is because even though the "culprit" artery may have spontaneously reperfused — What has spontaneously reopened might just as easily spontaneously close again — which is why prompt cath with PCI of the "culprit" artery is indicated to prevent reclosure.

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The CASE Continues:

En route to the hospital — another tracing was done 2 minutes after ECG #1. For clarity and ease of comparison — I've put this repeat ECG together with today's initial tracing in Figure-2.

QUESTIONS:

• How would YOU interpret the repeat ECG — which was recorded 2 minutes after ECG #1?
• Does this repeat ECG support my impression of recent (and/or ongoing) posterior OMI? 
• What important piece of clinical information are we missing in association with ECG #2?

Figure-2: Comparison between the initial ECG — and the repeat ECG done ~2 minutes later. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Repeat ECG: 

The frontal plane axis and QRS morphology is virtually the same in all 12 leads for both of the tracings in Figure-2. This tells us that lead-by-lead comparison for any change in ST-T wave morphology is valid!

• The AFib with controlled ventricular response is unchanged.
• I see no difference in limb lead ST-T wave appearance between the 2 tracings. 
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• BUT — there has been a definite change in ST-T waves in the chest leads! Specifically — there has been a significant increase in the amount of ST depression in leads V2-thru-V6 in ECG #2. This ST depression is now clearly downsloping — with reduced T wave amplitude.
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• PEARL #8: The fact that there has been unmistakable change in ST-T wave appearance between the serial tracings in Figure-2 — defines this development as a "dynamic" ST-T wave change. In a patient with new symptoms — the finding of ischemic-looking "dynamic" ST-T wave change by itself — is indication for prompt cath, with probable need for PCI (See ECG Blog #222 for more on this topic).
• As previously noted — acute posterior OMI produces ST depression in anterior leads (ie, a positive "Mirror" Test). The disproportionately tall (and abnormal-looking) T waves in several chest leads of ECG #1 are consistent with "reperfusion" T waves in this posterior infarction — which suggest that the "culprit" vessel had spontaneously reopened at some point before ECG #1 was recorded. The fact that ECG #2 now shows ischemic-looking increased ST depression in multiple chest leads, in association with reduced T wave amplitude — strongly suggests that the "culprit" vessel has now reoccluded!

PEARL #9: There unfortunately is no information in this case as to whether this patient's "burning" chest discomfort was increasing — was stable — or, was decreasing at the time that ECG #2 was recorded. 

• It's important to appreciate, that IF chest pain was increasing at the time ECG #2 was recorded — that this would strongly support our theory that the reason for the increased ST depression and decreased T wave amplitude in multiple chest leads, is that the "culprit" vessel has now reoccluded!
• The clinical importance of this association — is that indication for immediate cath becomes absolute (!) — IF chest pain increased at the time the "dynamic" ST-T wave changes that we see in ECG #2 were recorded.

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CASE Conclusion:

On their way to the hospital, the EMS crew requested cath lab activation — because they recognized the above "dynamic" ST-T wave changes.

• Unfortunately, the clinical significance of the serial ECG changes in Figures-1 and -2 were not recognized by providers in the ED. Cath lab activation was cancelled when the initial troponin was not elevation.
• Additional troponins were not ordered.
• Additional follow-up on this case is lacking ...

COMMENT: It is always difficult to attempt reconstruction of a case when information is lacking. That said — there are important lessons to be learned from events in this case. To the above 9 Pearls — I add the following.

• PEARL #10: There are several reasons why the initial troponin with acute OMI may fall within the "normal" range (ie, spontaneous reopening of the "culprit" artery may have occurred soon enough after acute occlusion — such that there is no initial troponin elevation). Despite the initial normal troponin in today's case — additional troponins should have been ordered on this high-risk patient with a worrisome history of new chest pain.
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• PEARL #11: There is no mention in today's case of a prior ECG ever becoming available. While understandable that previous ECGs for comparison will usually not be available to the EMS team dispatched to attend to the patient — it should have been EASY to find a prior tracing for comparison purposes in the ED on this patient with known coronary disease and prior anginal episodes. The chances are excellent that comparison of a prior tracing with ECG #1 — could have confirmed that the ST-T wave changes in today's initial tracing were acute. In 2023 — it should be EASY to locate and transmit previous ECGs for comparison from established patients.
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• Final PEARL: Appreciation of the pathophysiology described above in Pearl #3 is essential for optimal assessment of patients suspected of having an acute coronary event. Cath lab activation should not have been cancelled in today's case.

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Beyond-the-Core: Are there N-Waves in ECG #1?

I reviewed the concept of "N-Waves" in ECG Blog #354. 

• While writing up this case — it dawned on me that the best explanation for the extra positive "notch" that we see in leads III and aVF of ECG #1, but which disappears in ECG #2 (despite essentially no other change in inferior lead QRS morphology) — is that these small deflections in ECG #1 reflect N-waves.
• IF so — this subtle ECG finding would be consistent with recent OMI, most likely with the LCx as the "culprit" artery.
• Oppositely-directed small negative deflections are seen in high-lateral leads I and aVL in both ECG #1 and ECG #2.

What is an "N-Wave"?

In 2011 — Niu et al described the presence of an "N-Wave" — or delayed activation wave of the left ventricular basal region. Because this area of the heart is typically supplied by the LCx — this is likely to be the "culprit" artery when N waves are seen as part of the pattern of acute ischemia (Int J Cardiol 162(2): 107-111, 2013).

• As highlighted in the March 26, 2022 post in Dr. Smith's ECG Blog — N waves are recognized by the transient appearance of notching (usually ≥2 mm in size, with respect to the PR segment) — with resultant slight widening of the QRS complex. Because N-waves typically last <24 hours after acute occlusion — they may be smaller than 2 mm, depending on when during the process they are seen.
• As opposed to J-wave notching (that is more likely seen in the chest leads) — N-waves are usually seen in one or more of the inferior leads, and/or in leads I, aVL.
• 
  
• MY Thoughts: When I first read about N-waves — I was hesitant to use this ECG finding in my assessment, for fear of "overcalling" occasional QRS fragmentation as being something else. But I thought both the case I presented in ECG Blog #354, as well as today's case — are consistent with being probable N-waves in these 2 patients with chest pain and ECG signs consistent with posterior OMI from a LCx culprit. I wish we had cath confirmation on these 2 cases.

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Acknowledgment: My appreciation to David Baumrind (from Eastern Long Island, NY, USA) 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 the Ps, Qs, 3R Approach to Rhythm Interpretation.
• 
  
• 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. 
• 
  
• 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.
• 
  
• ECG Blog #260 — ECG Blog #222 — 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.
• 
  
• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
• 
  
• 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).
• ECG Blog #317 — reviews why posterior leads are not essential for diagnosis of acute posterior MI.
• 
  
• 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.
• 
  
• ECG Blog #350 and ECG Blog #377 — regarding T Wave Imbalance in the Chest Leads.
• 
  
• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
• 
  
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• 
  
• 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 (7/22/2023):

• 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.