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.
• 
  
• 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).
• 
  
• 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.
• 
  
• 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.
• 
  
• 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. 
• 
  
• 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.
• 
  
• 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. 
• 
  
• 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.
• 
  
• 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.
• 
  
• 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.
• 
  
• 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. 
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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 — ECG Blog #222 — and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
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• 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).
• 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.
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• ECG Blog #350 and ECG Blog #377 — 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 (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. 

ECG Blog #386 — OMI or Something Else?

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who while performing his regular exercise routine, developed "slight" chest discomfort and "palpitations". These symptoms persisted for over an hour, which led the patient to contact EMS. Surprisingly — he was hemodynamically stable with minimal discomfort at the time his initial ECG in Figure-1 was recorded.

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• How certain are you of your diagnosis?
• Could the patient have WPW?
• What would you do?

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

MY Thoughts:

Surprisingly — Today's patient was hemodynamically stable in association with the rhythm shown in Figure-1. By definition — this means that there was at least a moment in time to contemplate the etiology of the rhythm before having to begin treatment. 

By the Ps, Qs, 3R Approach (as reviewed in ECG Blog #185):

• The QRS complex is obviously wide.
• I do not see P waves.
• The rhythm is Regular — at a Rate of ~230/minute.
• 
  
• Impression: The rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia) at ~230/minute, without clear sign of atrial activity. As I've often emphasized on this ECG Blog (See ECG Blog #220 and ECG Blog #361 — among many others) — Statistical odds in a middle-aged man with new symptoms, that a regular WCT without P waves will turn out to be VT — are at least 80-90%, even before we look at QRS morphology. As a result — Assume VT until proven otherwise!

We can easily increase the certainty of our diagnosis for today's rhythm that is shown in Figure-1 — by attention to QRS morphology:

• There is extreme axis deviation (ie, an all negative QRS not only in lead I — but also in each of the inferior leads)!
• The QRS is all positive in lead aVR (which implies the impulse is coming from below — and is therefore not supraventricular).
• The QRS is all negative in lead V6 (similarly implies an impulse coming from below).
• There is no biphasic complex in any chest lead (ie, the QRS is all positive in V1,V2 — and all negative in V3,4,5,6 — so no chest lead has any kind of RS complex).
• QRS morphology for ECG #1 does not resemble any known form of conduction defect. Instead — the QRS is amorphous.
• 
  
• BOTTOM LINE: I would estimate the odds that the regular WCT in Figure-1 is VT as >98-99%!

PEARL #1: Any one of the 5 bullets shown above would increase the odds that today's regular WCT is VT to >95%. Assuming today's patient is not hyperkalemic — taken together, the above 5 bullets regarding QRS morphology for today's regular WCT make it hard to imagine this rhythm is anything other than VT.

PEARL #2: An important confounder to be aware of as a non-VT cause of a regular WCT rhythm — is WPW. That said — QRS morphology in Figure-1 essentially rules out WPW.

• Activation of the ventricles over an AP (Accessory Pathway) — should generally proceed from the base of the heart toward the apex. This should result in at least some positivity of QRS complexes as one moves toward the lateral chest leads. The finding of all negative QRS complexes in leads V3-thru-V6 therefore strongly suggests that the arrhythmia-associated impulse is not traveling over an AP (Steurer et al — Clin. Cardiol 17:306-308, 1994).
• Although the sensitivity of this criterion for ruling out WPW is poor (ie, most VTs do not have all negative QRS complexes in 3 or more of the most lateral chest leads) — when you do see an all negative QRS in leads V4,V5 and V6 — this essentially rules out a WPW-related tachyarrhythmia.

The CASE Continues:

The rhythm in ECG #1 was interpreted as VT and treated accordingly. In view of the patient being hemodynamically stable — a dose of IV Amiodarone was tried, but without success. 

• Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. This resulted in the tracing shown in Figure-2.

QUESTIONS:

• How would YOU interpret the ECG in Figure-2?
• Is prompt cath indicated for a presumed acute MI?

Figure-2: How would you interpret this 12-lead tracing obtained immediately after synchronized cardioversion?

MY Thoughts on ECG #2:

The "good news" — is that synchronized cardioversion successfully resulted in sinus rhythm! That said — there are significant ST-T wave abnormalities. I see the following in ECG #2:

• Upright P waves in lead II, with a constant and normal PR interval that therefore confirms conversion to sinus rhythm — here at a rate of ~85/minute.
• The QRS is fragmented (notched) in several leads (ie, leads III, aVL, V3) — but is not prolonged.
• Given the heart rate — the QTc is at least borderline prolonged.
• The frontal plane axis is normal (about +60 degrees).
• There is no chamber enlargement.
• There is deep, symmetric T wave inversion in leads V3-thru-V6 (most marked in V3,V4). Nonspecific ST-T wave flattening is seen in the limb leads.
• 
  
• IMPRESSION: The rhythm is now sinus. There are marked ST-T wave abnormalities. The question arises as to whether these changes in ECG #2 represent acute infarction as the cause of VT? (with need for prompt cath with PCI?).

PEARL #3: It's important to be aware of a "memory" effect. This phenomenon may sometimes be seen following an episode of a sustained tachycardia — in which marked ST-T wave abnormalities not due to infarction may be seen for a period of hours, or even days!

• Despite the marked ST-T wave abnormalities in ECG #2 — I would suspect that these are not the result of acute infarction because: i) There is no ST elevation in this post-cardioversion tracing; ii) There is no reciprocal ST depression; and, iii) The shape of the ST-T wave changes is fairly similar in leads V3-thru-V6 — with no more than nonspecific ST-T wave flattening in the other 8 leads (ie, This post-conversion ECG just doesn't "look" like an acute infarction). That said — I was not 100% certain about this interpretation.

The CASE Continues:

• An initial hs-Troponin-I assay was positive, with a value = 94 ng/L (normal is <34 ng/L for a man of this patient's age). That said, immediately after sinus rhythm was restored — the patient's symptoms resolved! He remained pain-free.
• On questioning after restoration of sinus rhythm — the patient denied any preceding angina symptoms before this hospitalization.
• 
  
• Bedside Echo was done (4-Chamber view shown in Figure-3).

Figure-3: Bedside Echo 4-Chamber View (See text).

QUESTION:

• Does the bedside Echo in Figure-3 help to explain the abnormal ST-T wave findings in ECG #2?

ANSWER: The bedside Echo view in Figure-3 shows dramatic apical hypertrophy — with no more than a slit-like apical internal ventricular lumen. Despite this finding, overall ventricular function is preserved (Estimated EF = 54% — with no wall motion abnormality).

• KEY Point: Rather than acute coronary occlusion — this bedside Echo suggests that the primary problem can most likely be attributed to severe apical cardiomyopathy!
• This is consistent with the patient's history — in that the patient had no prior history of anginal symptoms — and the slight chest discomfort he experienced in association with his VT promptly resolved as soon as sinus rhythm was restored.
• 
  
• PEARL #4: Taking another LOOK at QRS morphology during VT (ie, in Figure-1) — the monophasic positive QRS in right-sided lead V1 and the all negative QRS complex in chest leads V3-thru-V6 — suggest a left-ventricular apical origin for his VT, which is completely consistent with the severe apical hypertrophy seen on Echo.

The CASE Continues: Additional Testing ...

Additional testing was done. Along the way — the decision was made to cancel the initial call for cardiac catheterization, and instead to obtain a less invasive CT coronary angiogram. 

Selected results of additional testing are noted below.

• A follow-up ECG done the next day ( = ECG #3 in Figure-4).
• Troponins were repeated — reaching a peak elevation of >31,000 ng/L!
• 
  
• CT coronary angiogram — No obstructive coronary disease.
• Cardiac MRI —  consistent with severe apical hypertrophy (See Figure-5). No sign of ARVC. EF ~60%. 

Figure-4: Comparison between the post-conversion 12-lead ECG — and the ECG repeated the next day.

Figure-5: Selected CT scan slice (IVS = InterVentricular Septum; LV Wall; slit-like LV cavity).

Figure-6: Selected Cardiac MRI view.

DISCUSSION:

There are many important aspects of this case.

• The patient presented in a regular WCT rhythm without P waves, at the rapid rate of ~230/minute (Figure-1). QRS morphology suggested with virtual certainty that the rhythm was VT. Since the patient was hemodynamically stable — brief trial with Amiodarone is reasonable and was attempted, but when this did not convert the rhythm — synchronized cardioversion was applied.
• 
  
• Synchronized shock successfully converted the rhythm to sinus — but there was marked ST depression on the 12-lead (Figure-2). Although essential to rule out OMI (ie, an acute coronary occlusion) as the cause of VT — the astute clinician in charge of the case cancelled the initial call to activate the cath lab because: i) The post-conversion 12-lead in Figure-2 lacked ST elevation and other ECG indicators of acute infarction; ii) The patient's symptoms immediately resolved once he was converted to sinus rhythm; iii) This previously healthy middle-aged adult had no history of angina nor other reason to suspect underlying coronary disease; and, iv) Bedside Echo suggested marked apical hypertrophy and no wall motion abnormality (Figure-3).

Subsequent testing supported the presumption of apical cardiomyopathy as the cause of this patient's sustained VT.

• CT coronary angiogram showed no obstructive coronary disease. 
• As seen in Figure-5 — this CT scan slice supports the bedside Echo finding of marked apical hypertrophy, resulting in minimal chamber volume for ventricular filling
• The selected Cardiac MRI view shown in Figure-6 — shows similar findings of marked apical thickening with good contractility, but no more than a slit-like LV cavity opening for LV filling.

Additional Teaching Points:

• Type-2 MI (Myocardial Infarction) — is defined by an increase in troponin with evidence of ischemia that is not due acute coronary disease, but which instead results from a mismatch in oxygen supply and demand (Smilowitz et al — Coron Artery Dis 29(1):46-52, 2018). Today's case is illustrative because it shows how high troponin may rise despite the absence of acute coronary occlusion! (ie, Severe subendocardial ischemia from sustained VT in a patient severe apical cardiomyopathy resulted in a peak troponin >31,000 ng/L in today's case).
• 
  
• Bedside Echo proved invaluable for providing a rapid explanation for the patient's sustained VT that obviated the need for prompt cath.
• 
  
• Post-VT ST-T wave abnormalities do not necessarily indicate acute coronary occlusion, even when troponin is markedly elevated. Comparison in Figure-4 of the immediate post-cardioversion tracing ( = ECG #2) — with the repeat 12-lead ECG done the following day ( = ECG #3) shows persistence of ST-T wave abnormalities (if anything, with slight increased T wave inversion seen in the inferior leads of ECG #3). Whether these ST-T wave changes are the result of "memory" following an episode of sustained VT — or — whether they are longstanding in this patient with apical cardiomyopathy (and/or some combination of both conditions) — is uncertain. But immediate resolution of chest pain once VT was converted — and — the normal CT coronary angiogram — essentially ruled out acute coronary disease as the cause.
• 
  
• P.S.: Despite marked apical hypertrophy — QRS voltage was not in the least increased in either ECG #2 or ECG #3. The ECG is an imperfect tool for detection of LVH. Echo is far superior for this purpose. 

CASE Conclusion:

• Today's patient was deemed high-risk. As a result — an ICD (Implantable Cardioverter-Defibrillator) was placed, and he was discharged on a ß-blocker.

 

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) 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 — Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• 
  
• ECG Blog #361 and ECG Blog #220 — Review in detail the clinical approach to a regular WCT (Wide-Complex Tachycardia).
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• ECG Blog #337 — The importance of the new OMI (vs the old STEMI) Paradigm (and My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog). 

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ADDENDUM (7/15/2023):

The original 3 ECGs in today's case were recorded using the Cabrera lead format. This ECG recording format is favored in Norway, Sweden, Germany — and in a number of other countries. 

• Given the ever expanding use of the internet — virtually all clinicians everywhere are likely to encounter this format at the very least, from time to time. As a result — I show in Figure-7, the initial ECG in today's case as it was originally recorded using the Cabrera format (Please see my Editorial Note near the top of the page in ECG Blog #365 for review of the basics of the Cabrera recording system). 
• 
  
• For comparison — I've reproduced in Figure-8 the post-conversion tracing shown in today's case (which I initially showed in Figure-2) — in which I've simulated the standard recording format used in the U.S. and most other countries (ie, I inverted lead aVR — and moved the location of various limb leads).

Figure-7: The post-conversion tracing in today's case — as it was originally recorded using the Cabrera format. (Given ever expanding use of the internet — it's good to become familiar with this recording format, that in many ways is more logical than the standard format we are used to — as discussed in ECG Blog #365). 

Figure-8: For comparison purposes — I've reproduced the post-conversion tracing in today's case that was shown in Figure-2. 

ECG Blog #385 — This Patient Arrested Soon After

The ECG in Figure-1 was obtained from a 60-year old woman — who presented to the ED (Emergency Department) for “palpitations”. Her vital signs were normal at the time this triage ECG was recorded. Blood was drawn, and the patient was promptly placed in a room to be seen — but on entering, the ED physician found her unresponsive in cardiac arrest. ROSC (Return Of Spontaneous Circulation) was achieved — but the patient did not recover neurologically.

• How would YOU interpret the ECG in Figure-1?  
• Do you see any indication on this ECG of WHY this patient was about to arrest?

Figure-1: The initial ECG in today's case. Is there any indication on this ECG of WHY this patient shortly after had a cardiac arrest?

Philosophical Overview:

All emergency providers from time-to-time encounter a patient who unexpectedly develops cardiac arrest — despite no obvious indication from their appearance that this was about to happen. This unexpected occurrence always prompts retrospective soul-searching as to whether any clinical signs may have been missed.

• What do YOU see in ECG #1? 

MY Thoughts on ECG #1:

As per my usual approach — I favor beginning my analysis with a brief look at the long lead rhythm strip before I begin to focus on the 12-lead. By the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm in Figure-1 is clearly not Regular. The heart Rate becomes quite slow in places (ie, with a couple of R-R intervals exceeding 6 large boxes in duration).
• The QRS complex is narrow in all 12 leads — which identifies the rhythm as supraventricular.
• P waves are present — with RED arrows in Figure-2 highlighting sinus P waves that are seen in front of most beats (as identified by the similar shape of these P waves, that are upright in lead II with a constant and normal PR interval).

Figure-2: I've labeled sinus P waves in today's tracing with RED arrows. Is there additional atrial activity?

QUESTION:

Take another look at Figure-2.

• How many additional P waves do you see on this tracing?
• 
  
•    HINT: There are more P waves than QRS complexes ...

PART #1 of My ANSWER:

In addition to the 8 RED-arrow sinus P waves in Figure-2 — there are 3 conducted PACs (Premature Atrial Contractions) — as I highlight in Figure-3 by the BLUE arrows placed in front of beats #2, 7 and 11.

• Note that these 3 beats ( = beats #2,7,11) each occur earlier-than-expected (ie, They are "premature").
• Although a slight variation is seen in P wave morphology of the sinus-conducted P waves in Figure-3 (ie, the P waves under the RED arrows) — P wave morphology for each of these 3 PACs is clearly different compared to the P waves of sinus-conducted beats (ie, the P waves under the BLUE arrows are notched). This difference in P wave morphology indicates a different site of origin.
• 
  
• Subtle Point — Did YOU notice that the QRS complex for each of these PACs is narrow and looks similar but not identical to the QRS morphology of sinus-conducted beats? (ie, The narrow s wave of premature beats #2,7,11 is not as deep as the narrow S wave of sinus-conducted beats). The reason for this slight variation in QRS morphology — is that these PACs are conducted with some degree of aberration (This difference in morphology is perhaps best appreciated by looking at beat #11 in simultaneously-recorded lead V4 in Figure-2).

Figure-3: I've labeled (with BLUE arrows) — the 3 PACs that are conducted in today's tracing.

PART #2: There are still more P Waves!

Did YOU See the 2 pointed deflections contained within the ST-T waves of beats #3 and 4 in Figure-3?

• We know that the 2 pointed deflections that appear under the YELLOW arrows in Figure-4 are real — because none of the other ST-T waves in today's tracing manifest a similar appearance — and — both of these 2 pointed deflections are followed by a pause not seen elsewhere on this tracing. This timing strongly suggests that these pointed deflections under the YELLOW arrows in Figure-4 represent blocked PACs! (that reset the SA node — thereby producing the brief pause that follows these blocked PACs).
• 
  
• PEARL #1: Another reason the 2 pointed deflections in today's tracing are likely to represent blocked PACs — is what I call, "The Birds of a Feather Phenomenon". As discussed in ECG Blog #348 — Since we know that today's rhythm shows an underlying sinus rhythm with PACs under the BLUE arrows — it is likely that other early-occurring deflections consistent with the timing of blocked PACs do in fact represent PACs.
• 
  
• PEARL #2: As cited in ECG Blog #252 — my favorite truism in arrhythmia interpretation is, "The commonest cause of a pause is a blocked PAC". Application of this truism cautions against overdiagnosis of AV blocks — and encourages us to always carefully scrutinize any unanticipated short pause for the possibility of hidden non-conducted atrial activity.

Figure-4: I've labeled (with YELLOW arrows) — the 2 blocked PACs in today's tracing.

What About the 12-Lead ECG?

Take another LOOK at the 12-lead ECG in today's case — which I've reproduced again in Figure-5. This ECG shows:

• A slightly leftward axis (ie, predominantly negative QRS in lead aVF) — but not negative enough to qualify as LAHB (ie, The QRS is still predominantly positive in lead II).
• No chamber enlargement.
• No Q waves.
• Slightly delayed R wave progression (ie, The R wave does not become more positive than the S wave is deep until between V5-to-V6).
• Nonspecific ST-T wave flattening in multiple leads.
• Subtle-but-real U waves (under the GREEN arrows).
• 
  
• IMPRESSION: I see no acute ST-T wave changes in Figure-5. That said — the finding of sinus rhythm with lots of PACs (some non-conducted) + nonspecific ST-T wave flattening in multiple leads + U waves — strongly suggests that there may be an electrolyte imbalance (ie, low K+ and/or low Mg++).

Figure-5: Take another LOOK at today's 12-lead ECG. What do the GREEN arrows suggest?

BACK to Today's CASE:

To recap the clinical presentation of today's case — this 60-year old woman presented to the ED for "palpitations". Vital signs were initially "normal" — but the patient shortly thereafter was found in cardiac arrest. While no one would predict an impending cardiac arrest from the initial tracing seen in Figure-5 — My admittedly retrospective assessment of today's ECG should suggest:

• A probable electrolyte disorder (ie, low K+ and/or low Mg++).
• An underlying sinus rhythm with lots of PACs of at least 2 different shapes. While the rhythm disorder in Figure-5 does not manifest enough irregularity or P wave variability to qualify as MAT — the finding of multiple PACs with more than 1 morphology should suggest similar clinical implications as the MAT rhythm described in ECG Blog #366 — which are for the provider to anticipate either severe pulmonary disease and/or multisystem disorders in a "sick" patient.
• 
  
• CASE Follow-Up: Lab work that had been drawn before the cardiac arrest — came back after the arrest. It showed marked hypokalemia with severe acidosis, hypoxemia, and signs of early CO2 retention. The difficult clinical lesson — is that sometimes patients may be sicker than they appear. 

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Acknowledgment: My appreciation to Chun-Hung Chen - 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.  

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ADDENDUM (7/9/2023) — Additional material relevant to today's case:

 

Figure-3: Summary of KEY points related to MAT.

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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 #199 and ECG Blog #366 — for Review of MAT.
• ECG Blog #65 — for an example of MAT in a patient with chronic pulmonary disease (plus more on the differential diagnosis of MAT).
• ECG Blog #200 — for an example of Wandering Atrial Pacemaker.
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• ECG Blog #289 —  Review of U wave recognition (and low K+/Mg++).
• 
  
• ECG Blog #348 — Reviews the concept of "Birds of a Feather" (with regard to recognizing aberrantly conducted PACs).
• ECG Blog #252 — The "Commonest Cause of a Pause" is a blocked PAC.
• 
  
• ECG Blog #140 — Example of alternating Bifascicular Block Aberration.
• ECG Blog #14 — Example of Blocked PACs.
• ECG Blog #15 — Example of a WCT rhythm with aberrant conduction.
• ECG Blog #33 — Example of PACs with varying degrees of Aberrant Conduction.
• ECG Blog #263 — Differentiation of WCT rhythms (ie, deciding between VT vs Aberrancy?).
• ECG Blog #211 — WHY does Aberrancy occur? (And why the most common form of aberrant conduction manifests RBBB morphology).
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• ECG Blog #70 — Reviews the Ashman Phenomenon (re aberrant conduction).
• ECG Blog #71 — Regarding the Ashman Phenomenon with AFib.

I link to 2 additional illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for MAT:

• The January 5, 2020 post in Dr. Smith’s ECG Blog — for an example of MAT.
• The September 30, 2019 post in Dr. Smith’s ECG Blog — for an example of “MAT”, but without the tachycardia ...