ECG Blog #428 — How Much to Do at Age 92?

I was sent the tracing in Figure-1 — with the following information:

• 92-year old patient with a history of "known arrhythmia" and hypertension.
• The patient was asymptomatic at the time ECG #1 was obtained — with the ECG presumably being recorded because an irregular rhythm was heard on auscultation. 

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• How much should we do for this 92-year old patient?
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• Extra Credit: Which arm or leg is most responsible for the artifact seen in today's initial ECG?

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

Answer to EXTRA Credit Question:

To begin with the answer to the Extra Credit Question — I suspect the cause of the abnormal baseline deflections seen in Figure-1 is muscle tremor artifact (See Bouthillet T — ACLS Med Training, Dec, 2015). A quick LOOK at the patient would confirm this — but I unfortunately do not have any information about the patient's appearance.

• NOTE: The abnormal baseline deflections in Figure-1 are maximal in leads I,III and aVL — modest in lead aVF — and minimal in lead II, as well as being minimal in the 6 chest leads. Therefore — the "culprit" extremity most responsible for the artifact in today's tracing is the LA (Left Arm).
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• As discussed in detail in ECG Blog #255 — We can identify the "culprit" extremity because the relative size of the artifact deflections in Figure-1 manifest the relative dimensions expected when a single extremity is primarily responsible for a certain type of artifact.
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• PEARL #1: That one extremity is primarily responsible for a certain type of artifact — can be quickly recognized by the finding of approximately equal artifact amplitude in 2 of the 3 standard limb leads (ie, in leads I and III for Figure-1) — and, minimally or not seen at all in the 3rd standard limb lead (ie, artifact is minimal in lead II). 
• By Einthoven’s Triangle (See ECG Blog #255) — the finding of equal artifact amplitude in Lead I and Lead III, localizes the “culprit” extremity to the LA ( = Left Arm) electrode.
• The greatly reduced artifact amplitude in lead II is consistent with this — because, derivation of the standard bipolar limb lead II is determined by the electrical difference between the RA ( = Right Arm) and LL ( = Left Leg) electrodes, which are not affected if the source of the artifact is the left arm.
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• SHORTCUT (To find the "culprit" extremity in seconds!): When 2 of the standard limb leads show approximately equal maximal artifact amplitude — and the 3rd standard limb lead shows minimal or no artifact — then whichever augmented lead shows maximal amplitude indicates the "culprit" extremity (which in Figure-1 is Lead aVL = which means that the LA is the "culprit" extremity).

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Back to Today's CASE:

• How would YOU interpret the rhythm in Figure-1?
• How much should we do for this 92-year old patient?

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

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MY Initial Thoughts:

From an arrhythmia standpoint — I found the rhythm in today's case to be fascinating. 

• That said — this patient is elderly and asymptomatic, which raises the questions as to, How much evaluation? — and — What clinical management would be optimal?

We are told in the brief information given — that today's patient has a history of a "known arrhythmia". Thus, the 1st issue that comes to mind in today's case is — What is the arrhythmia that this patient is "known" to have?

• By far — the most common cause of an irregularly rhythm in an asymptomatic elderly patient is AFib (Atrial Fibrillation).
• IF this patient had AFib — then determination of the need for rate control and/or informed consent by the patient (and/or by the family, if the patient is no longer mentally competent) regarding the pros and cons of anticoagulation — would be indicated.
• The above said — I was not made aware of additional specifics of this patient's medical history — and, the rhythm in today's case is not AFib.

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HOW to Interpret Today's Rhythm:

The "good news" — is that the elderly patient in today's case is asymptomatic. This means that we have at least a moment of time to try to figure out the rhythm in Figure-1. My initial observations include the following:

• The rhythm is obviously irregular. 
• There are 2 different QRS morphologies. These are: i) Beats #1-thru-4; beat #11; and beats #15,16 — all of which are at most, boderline prolonged, with an rS configuration in the long lead II rhythm strip; and, ii) The remaining 10 beats — all of which are of normal QRS duration, and manifest an RS configuration in the long lead rhythm strip.
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• The first 4 beats are regular at a rate of ~95-100/minute — and, they are not preceded by P waves. These first 4 beats manifest marked LAD (Left Axis Deviation) — being positive in lead I — but virtually all negative in simultaneously-recorded leads II and III.
• Beats #11 and #15,16 manifest an incomplete RBBB morphology (ie, with a nearly equiphasic R=S for beat #11 in lead V1 — and, with wide, terminal S wave for beats #15,16 in lead V6). This combination of incomplete RBBB + LAHB morphology for beats #1-thru-4; beat #11; and beats #15,16 — suggests that these 7 QRS complexes are all fascicular beats that arise from the LPH (Left Posterior Hemifascicle).
• NOTE: Since fascicular beats are ventricular beats — this means that the first 4 beats in Figure-1 constitute a short run of NSVT (Non-Sustained Ventricular Tachycardia), albeit an NSVT at the modest rate of ~95-100/minute.
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• The remaining 10 beats in Figure-1 manifest a narrow QRS complex in all 12 leads — and, are therefore supraventricular.

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QUESTION: 

• In Figure-1 — Is the underlying rhythm sinus?
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•     HINT: Is there a predominant P wave morphology?

ANSWER: The easiest way to tell if an underlying sinus rhythm is present — is to LOOK for: i) A predominant P wave morphology (ie, in which the P wave in lead II is upright with a constant PR interval); and, ii) A consistent R-R interval before the predominant P wave morphology. 

• As can be seen in Figure-2 — it appears that both of these features are present in today’s rhythm.

Figure-2: I've labeled sinus P waves with RED arrows.

NOTE in Figure-2 — The underlying rhythm is sinus!

• RED arrows in Figure-2 highlight what appear to be similar-looking upright P waves in the long lead II rhythm strip. At least before beats #6, 7 and 9 — the preceding R-R interval is very similar, suggesting these 3 P waves represent normal sinus-conducted beats.

Now that we have identified that, with the exception of fascicular beats #1-4; 11; 15,16 — the underlying rhythm in today's tracing is sinus — We can focus our attention on the remaining beats in today’s tracing:

• Beats #5; 8; 12; 13; and 17 — all occur earlier-than-expected — are all preceded by a P wave with a P wave morphology that is different from that of the RED arrow P waves — yet all manifest the same supraventricular QRS morphology as the 3 sinus-conducted beats ( = beats #6,7,9). 
• These 5 beats ( = beats #5,8,12,13,17) — are therefore PACs (Premature Atrial Contractions).

Putting It All Together:

I summarize in Figure-3 — what we have thus far determined for today’s arrhythmia:

• There are 2 distinct QRS morphologies in today’s rhythm.
• Beats #1,2,3,4 — beat #11 — and beats #15,16 — represent the first QRS morphology, in which there is slight QRS widening with a pattern consistent with incomplete RBBB/LAHB conduction. Based on the regularity of beats #1-thru-4, and the absence of sinus P waves in front of these 4 beats — these must be fascicular beats from the LPH.
• Since QRS morphology of beats #11,15,16 is so very similar to that of beats #1,2,3,4 in the long lead II rhythm strip — all of the beats marked by a RED circle in Figure-3 are fascicular beats.
• The finding of 4 consecutive beats of ventricular etiology at an accelerated rate — means that beats #1-thru-4 represents a 4-beat run of NSVT.
• YELLOW arrows highlight a negative deflection occurring just after the QRS of these first 4 beats. Because no such negative deflection follows the QRS of the other 3 fascicular beats (each of which is preceded by a RED arrow sinus P wave) — we know that the 4 YELLOW arrows in Figure-3 must represent 1:1 VA conduction (ie, retrograde P waves) that follow these first 4 fascicular beats.

Figure-3: Further labeling of today's tracing.

Additional Findings in Today's Rhythm:

As noted earlier — the underlying rhythm in today's tracing is sinus, since there is a predominant P wave morphology in the form of similar-looking upright P waves with constant PR interval in front of beats #6,7; 9,10; 14 (RED arrow P waves in front of these beats in the long lead II rhythm strip).

• PEARL #2: Seemingly on-time RED arrow P waves also appear in front of fascicular beats #11,15,16 — but with a shorter PR interval. This observation provides further support that beats #11,15,16 are of ventricular etiology (ie, The shorter PR interval of these on-time RED arrow P waves represents transient AV dissociation).
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• PEARL #3: Did YOU notice the slightly smaller S wave amplitude of fascicular beat #11? The reason for this — is that beat #11 is a fusion beat (ie, the RED arrow P wave in front of beat #11 partially conducts — resulting in "fusion" between fascicular beat morphology and the RS morphology of supraventricular beats). As per ECG Blog #128 — identification of fusion beats in this setting proves a ventricular etiology.
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• Finally in Figure-3 — I've selected different colors to represent the different P wave morphologies of the 5 PACs (colored P wave arrows before beats #5,8,12,13,17).

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LADDERGRAM Illustration:

For clarity — I offer my proposed laddergram in Figure-4.

• RED arrows represent sinus P waves. Slight variation in the P-P interval is the result of sinus arrhythmia.
• The first 4 beats represent a 4-beat run of fascicular NSVT. Dotted lines extending from these first 4 fascicular beats represent conduction back to the atria (resulting in the YELLOW arrow retrograde P waves).
• The different colored circles within the Atrial Tier — represent PACs arising from different sites within the atria.
• I've drawn the laddergram to reflect that I suspect each of the later 3 fascicular beats ( = beats #11,15,16) are fusion beats — though it is admittedly difficult to detect significant difference in QRS morphology between fascicular beats #15,16 vs QRS morphology of the pure fascicular beats #1-thru-4.

Figure-4: Laddergram illustration of today's rhythm.

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CASE Conclusion: Clinical Implications ...

There is no specific "classification" that fits all aspects of today's rhythm. The occurrence of so many PACs of different P wave morphologies brings to mind features of MAT (Multifocal Atrial Tachycardia) — but there are too many consecutive P waves of similar origin to be consistent with the concept of "true" MAT, in which P wave morphology and the PR interval varies from one-beat-to-the-next (ie, We see too many consecutive on-time RED arrow sinus P waves).

• PEARL #4: As discussed in ECG Blog #366 — Rather than strict definition of "MAT" — many patients manifest variations along the spectrum of MAT, in which there may be multiple P wave morphologies sandwiched between periods of fairly normal on-time sinus P wave activity. Such is the case in today's rhythm.
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• Clinically: Even when "pure" MAT is not present — rhythms with multiple PACs of multiple morphologies often "behave" in similar fashion to MAT in that: i) Severe pulmonary disease and/or "sick" patient with multisystem comorbidities (ie, acid-base and/or electrolyte abnormalities; shock; multi-system failure) are often the cause; and, ii) The BEST treatment is to "find and fix" the underlying cause (as per ECG Blog #366).
• As to the rest of the 12-lead ECG in today's case — supraventricular complexes (ie, beats #10,12,13 in leads V1,2 + beats #14 and 17 in leads V5,V6) — show increased voltage consistent with LVH — and ST-T wave changes consistent with LV "strain" — but this does not appear to be acute.
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• Finally: Today's rhythm further defies classification — because it includes frequent ventricular beats with a 4-beat run of fascicular NSVT.

MY Suggestion for Management:

Since today's patient is 92 and asymptomatic — We do not want to "do too much to him". Simply stated — "It is hard to make an asymptomatic patient feel better!"

• The above said — it is good to appreciate that even though today's arrhythmia does not fit the full definition of "MAT" — this rhythm does behave clinically in similar fashion as does MAT. Therefore — We should look for simple potentially "fixable" exacerbating factors, such as electrolyte imbalance (ie, Check serum K+ and Mg++ levels, as well as other electrolytes) — hypoxemia (Check O2 saturation levels) — heart failure, sleep apnea, dehydration, etc.
• If nothing "easily fixable" turns up abnormal — it may be that this 92-year old man has been in this rhythm for years! In that case — we may want to leave him alone.

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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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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 #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #128 and ECG Blog #129 — on Fusion beats.
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• ECG Blog #366 — MAT explained.
• ECG Blog #199 — More on 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 — on Wandering Atrial Pacemaker.

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 ...

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ADDENDUM (5/3/2024):

• Some additional information on MAT … 

ECG recognition of MAT (3:20 minutes Video).

 

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

ECG Blog #427 — To Cath this Elderly Patient?

The ECG in Figure-1 — was obtained on the scene by EMS (Emergency Medical Services). The patient was a man in his 90s, who ~1 hour earlier, noted the onset of severe CP (Chest Pain). He was hemodynamically stable — but clearly distressed with a sense of “impending doom” at the time ECG #1 was recorded.

• Despite the patient’s age — he was independent, lived alone, had good mental function — and had family support.

QUESTIONS:

• How would YOU interpret the initial ECG in Figure-1?
• Given the patient’s advanced age — Should the cath lab be activated?
• — OR — Are the QS waves in the chest leads indication of a completed infarction?
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• Extra Credit: How many beats are seen on this ECG? 

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

MY Thoughts on Today's CASE:

The format for recording today's ECG is different than that used in most medical systems that I've encountered.

• As illustrated in Figure-2 — only 7 beats are seen. For clarity — I've numbered these 7 beats in each of the 4 groups of 3 leads.
• The advantage of this type of recording system is that for these 7 beats — we get to see QRS morphology for each of these 7 beats in each of the 12 leads.
• The disadvantage of this type of recording system — is that 7 beats is a very small sample for assessing events occurring on this ECG. For example — if the 1 PVC ( = beat #5) would not have occurred until 3 beats later, then we would not have seen any PVCs on this tracing.
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• PEARL #1: My exposure over the past decade to numerous international ECG internet forums has taught me how numerous the different ECG recording formats are. It's worth routinely spending a few initial moments for verifying what recording format is used for the ECG you are about to interpret. With minimal practice — it becomes EASY to recognize the identical timing for each of the 7 beats in today's tracing — with the 5th beat always being the PVC (which confirms that this particular format only views 7 beats — but shows us QRS morphology for these 7 beats in each of the 12 leads).

Now that we have identified the recording format used for today's tracing — We can begin our systematic interpretation.

• Six of the 7 beats in today's tracing manifest a narrow QRS complex — that when measured, is irregularly irregular (ie, Although difficult to appreciate visually — caliper measurement reveals a variable R-R interval for the first 4 beats — with an obviously shorter R-R interval between beats #6 and 7).
• P waves are absent. This defines the rhythm as AFib (Atrial Fibrillation), here with a controlled ventricular response (ie, overall heart rate between ~70-to-100/minute).
• Beat #5 is a PVC (Premature Ventricular Contraction) — because it is early, not preceded by a P wave, and manifests a markedly wider and very different-looking QRS morphology in almost every lead compared to the other 6 beats.
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• The QTc looks normal.  
• There is no chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• Q waves are present in leads III, aVF — with QS complexes in leads V1-thru-V5, with no more than a tiny initial r wave in lead V6.
• R Wave Progression — never occurs because of the persistence of these chest lead QS complexes.
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• Regarding ST-T Wave Changes: There is marked ST elevation, with straightening of the ST segment takeoff in leads V2-thru-V6. This J-point ST elevation attains 2-3 mm for leads V2,V3,V4 — being slightly less than this in leads V5,V6. Given that ST elevation is usually not seen in lead V1 — the 1 mm of ST elevation seen in this lead in today's tracing is abnormal.
• ST-T waves in the limb leads are also abnormal. The much broader-than-expected and "fatter"-at-their-peak T waves in leads I, II and aVL are hyperacute. There is subtle ST elevation in lead aVF — and ST-T wave flattening in lead III.
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• IMPRESSION: In this patient who presents with severe, new-onset CP — today's ECG is diagnostic of an extensive, ongoing antero-lateral STEMI.

CASE Follow-Up:

The decision was made not to activate the cath lab. Repeat ECG showed further progression of ST-T wave changes. The patient was at that point transferred for cardiac cath and PCI. Unfortunately the patient arrested before catheterization could be completed — and could not be resuscitated.

Figure-2: I've labeled today's ECG to illustrate that only 7 beats are seen. Did YOU notice the abnormal ST-T wave in the PVC? (within the BLUE rectangle in lead V3).

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COMMENT: 

• Advanced age is not a contraindication to cardiac catheterization. More important than chronologic age is functional status (This patient was living alone, fully independent, with good mental function and with family support).
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• PEARL #2: The presence of Q waves (including deep QS waves — as are seen in leads V1-thru-V5 in Figure-2) — is not necessarily an indication of completed infarction or of permanent damage. Surprisingly — even large Q waves may develop in as short a time period as 1-to-2 hours. Such Q waves may sometimes regress — and even completely resolve. Comparison with a prior ECG would be needed in order to determine the presence and extent of any previous infarction — and clinical follow-up would be needed to determine whether any new Q waves will be permanent.
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• PEARL #3: It may sometimes be difficult to distinguish between active, ongoing infarction — vs LV aneurysm that developed following a prior infarction — vs superimposed new infarction, that occurs on top of prior infarction. That said — the shape and relative disproportionality of the elevated chest lead ST-T waves in Figure-2 — compared to S wave depth in the leads being looked at, are diagnostic of an acute ongoing event until proven otherwise. The amount of J-point ST elevation with LV aneurysm is at most modest (clearly less than what we see in leads V2-thru-V5 of today's tracing) — and longstanding elevated ST segments typically do not manifest such straightening of the ST segment takeoff, as is evident in leads V2-thru-V6.

PEARL #4: Assessment of ST-T wave morphology of one or more PVCs may sometimes prove insightful for determining whether or not an acute OMI is ongoing. While clearly not needed in today's case (because assessment of the diffuse and marked chest lead ST elevation is already definitive for an acute STEMI) — on occasion, ST-T wave morphology will be diagnostic for an acute OMI only in PVCs.

• The PVC within the BLUE rectangle in lead V3 of Figure-2 — illustrates a shape of ST elevation that simply should not be there for a PVC in the absence of an acute OMI.
• An example of a case in which the diagnosis of acute OMI was made purely by assessment of ST-T wave morphology in a PVC can be found HERE (See My Comment at the bottom of this page in the October 8, 2018 post in Dr. Smith's ECG Blog). 

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Acknowledgment: My appreciation for this case that is anonymously contributed.

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Related ECG Blog Posts to Today’s Case:

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

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

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs. 
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

ECG Blog #426 — Are STEMI Criteria Met?

The ECG in Figure-1 — was obtained from a 70-ish year old man with episodic CP (Chest Pain) over the previous 2-3 days, being awakened from sleep now for a more severe CP episode.

QUESTIONS:

• In view of this history — How would YOU interpret this ECG?
• Should you activate the cath lab?

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

MY Initial Thoughts on Today's CASE:

Although it is difficult from the brief history we are given, to determine the true onset of whatever might be happening — the patient's age, persistence and severity of CP are clearly cause for concern.

• Which lead(s) immediately "caught YOUR eye"?

ANSWER:

The ST-T waves in 5 leads immediately captured my attention. I have labeled these leads in Figure-2 with RED and BLUE rectangles.

• WHY did these leads capture my attention?

Figure-2: I've labeled with RED and BLUE rectangles the 5 leads that immediately "caught" my eye.

The Most Abnormal Leads in Figure-1:

When assessing a patient for a possible acute OMI — I like to begin with leads that I know are definitey abnormal.

• PEARL #1: If when assessing a patient with new CP — you see 1 or 2 leads in which you know the ST-T waves are definitely abnormal — it then becomes much easier to identify more subtle changes in neighboring leads that support your impression of an acute ongoing event.

Applying PEARL #1 to Today’s CASE:

The initial ECG in today’s case shows sinus rhythm at ~80/minute— normal intervals (PR-QRS-QTc) — normal axis — and no chamber enlargement. Although there are QS complexes in leads V1,V2 — this is not necessarily abnormal, and R wave progression is appropriate (with transition where the R wave becomes taller than the S wave is deep — occurring normally, here between leads V2-to-V3). 

• Lead III and Lead V3 (within the RED rectangles in Figure-2) — are the 2 leads in ECG #1 that I absolutely knew were abnormal.
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• The QRS complex in lead III is tiny (ie, the R wave in lead III is at most 2 mm tall). And, although the T wave in this lead is not “tall” in terms of its absolute height — this T wave in lead III is clearly disproportionate in size, with respect to its QRS complex (ie, The T wave in lead III is almost twice as tall as the R in this lead — with this T wave being “fatter”-at-its-peak and much wider-at-its-base than-it-should-be, given the dimensions of the QRS in lead III). 
• Once we recognize in this patient with new CP, that the ST-T wave in lead III is clearly hyperacute — it becomes much EASIER to recognize that the T wave in neighboring lead aVF is also disproportionately taller and “fatter”-at-its-peak than it should be, given modest height of the R wave in this lead aVF.
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• PEARL #2: It’s important to appreciate by the above principles — that even though by itself, I would not necessarily interpret the ST-T wave in neighboring lead II as “abnormal” — in the context of new CP, in which we have just identified hyperacute T waves in the other 2 inferior leads ( = leads III and aVF) — Doesn’t the T wave in this 3rd inferior lead ( = lead II) also look “fatter”-at-its-peak and wider-at-its-base than it should, especially given modest amplitude of the R wave in this lead?  
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• PEARL #3: In my experience, the EASIEST way to convince myself that ST-T wave changes in leads III and/or aVF are acute — is to LOOK FOR the “magical” mirror-image opposite relationship that almost always exists between the ST-T waves in leads III and aVL when there is acute inferior OMI (See ECG Blog #167 and Blog #184, among many other posts). 
• KEY Point: It is rare with acute inferior OMI not to see reciprocal ST-T wave changes in lead aVL. This is an important distinguishing point between inferior lead ST elevation that is normally seen with a benign repolarization variant (in which you will not see reciprocal ST-T wave changes in lead aVL) — vs with acute inferior OMI, in which you will!
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• Clearly, in Figure-1 — the ST-T wave flattening, with shallow T wave inversion that we see in lead aVL is a subtle finding (within the BLUE rectangle in aVL) — BUT — in the context of a patient with new CP and hyperacute T waves in the inferior leads — I interpreted the ST segment flattening with shallow T wave inversion in lead aVL as being consistent with a reciprocal change.

PEARL #4: Because of the common blood supply of the RCA (Right Coronary Artery) — and the LCx (Left Circumflex) artery (ie, both of these coronary arteries usually supply both the inferior and posterior walls of the left ventricle) — it is very common when you see ECG evidence of acute OMI in one of these anatomic areas, to also see it in the other anatomic area (See ECG Blog #193 — and Blog #351, among many others).

• Applying this PEARL #4 to the initial ECG in today’s case — I was hoping to find further support that the subtle ST-T wave changes in 4 of the limb leads were real — by also finding ST-T wave changes in the chest leads suggestive of acute or recent posterior OMI.
• In a patient with new CP — there should be no doubt that the ST-T wave in lead V3 in Figure-2 (within the RED rectangle in lead V3) is abnormal! Given the tiny amplitude of the QRS complex in this lead — the T wave in lead V3 is at least equally tall as the R in lead V3, with this T wave being “fatter”-at-its-peak and wider-at-its-base than it should be, given small size of this R wave.
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• PEARL #5: Normally — there should be slight ST elevation with a gently upsloping ST segment in leads V2,V3. Thus, the ST-T wave in neighboring lead V2 is also abnormal — in that the ST segment in this lead is flat without any ST elevation (ie, within the BLUE rectangle in V2).

Putting It All Together:

In view of the history of new CP — today’s initial ECG is diagnostic of an acute OMI ( = an MI with acute coronary Occlusion).

• While additional assessment can certainly be undertaken — the point to emphasize is that the ECG in Figure-1, in association with the history of new, severe CP that awakened this patient from sleep — is all that is needed to know that prompt cath with PCI should be done as soon as this is possible.
• There is no need to wait for Troponin results to come back before the patient is taken to cath. This is because even if the initial Troponin came back normal — this rules out nothing! (ie, An initial hs-Troponin may occasionally be normal with acute OMI). Therefore — there is no need to wait for Troponin results, because these results will not alter the need for prompt cath.
• Serial ECGs should of course be obtained — but, there is no need to wait for a 2nd ECG before the patient is taken to cath — since given the history of new, severe CP and hyperacute ST-T waves in multiple leads — regardless of whether a 2nd ECG looks better or worse — prompt cath is needed.
• Assuming arrangements are made for prompt cath — there will almost always be "a moment" before cath is done that a repeat ECG can be obtained, which will be helpful in assessment. But the point to emphasize, is that the decision to perform prompt cath need not wait until that 2nd ECG is done.
• As is also emphasized often in this ECG Blog — spontaneous reperfusion of the "culprit" artery is common — and, IF this occurs before a 2nd ECG is done, ST-T wave changes may "look better" (See References to related Blog posts below). But — What spontaneously opens — may just as easily spontaneously reclose — which is why even if a 2nd ECG "looks better" — prompt cath with PCI is still needed to prevent spontaneous reocclusion of the "culprit" artery at a later point.
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• Finally — this is not be called a NSTEMI (because this term would falsely imply that there has not been acute coronary occlusion — and that PCI will not be of benefit). The term "NSTEMI" has been overused, and is often applied by "default" (ie, because millimeter-based criteria for a STEMI are not seen on any of the ECGs that have been done). Instead, we know from discussion above and the pathophysiology involved, that acute coronary occlusion (ie, an OMI) is by far the most likely explanation for events in today's case.

KEY Point: All extra testing in today's case would serve to do is delay — with resultant risk of losing more myocardium that might be saved by PCI from prompt intervention. Therefore — as soon as you know there has been acute OMI — cardiac cath with PCI is indicated (without further need to "confirm" what you have already confirmed).

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Acknowledgment: My appreciation to Si Cocksey (from Manchester, UK) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

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

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

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).