OMI? Subendocardial ischemia? Does it matter in this clinical context?

 Written by Pendell Meyers

A woman in her 70s with known prior coronary artery disease experienced acute chest pain and shortness of breath. The chest pain was described as severe pressure radiating to both shoulders. Vital signs were within normal limits.

She presented to the Emergency Department at around 3.5 hours since onset. She had taken aspirin at home.

Here is her triage ECG:

What do you think?

The ECG shows sinus rhythm with normal QRS complex morphology and significant subendocardial ischemia (SEI) pattern (ST depression in many leads, worst in lateral areas including leads II, V5-6, with reciprocal STE in aVR). One could argue or wonder if there is both subendocardial ischemia AND posterior OMI pattern, since the STD in V4 may be equal or possibly slightly worse proportionally than V6. 

But thankfully, when the clinical context is clearly and highly concerning for ongoing ischemia from ACS, this distinction doesn't matter much. Whether an ECG shows a pattern of OMI, SEI, both, or neither, the patient with ongoing ischemia needs to be considered for emergent reperfusion therapy. 

The Queen of Hearts is totally blinded to clinical context, and an upcoming model (that can independently report OMI vs SEI) identified SEI with high confidence.

While it is not necessary to have a prior baseline ECG in this case, there was one available:

Within normal limits.

Her history and ECG were interpreted as very concerning for acute coronary syndrome which might benefit from acute reperfusion therapy.

No posterior leads were performed.

She was emergently transferred to a PCI center. 

In the cath lab she was found to have severe multivessel disease, and the ostial circumflex was described as the culprit lesion. The note documents that the first view of the LCX showed 99%, TIMI 2 flow, but then (before intervention) was seen to fully occlude in real time (100%, TIMI 0).  Soon after the witnessed occlusion, the patient suffered ventricular fibrillation arrest, from which he was immediately resuscitated with 1 defibrillation. The procedure was described as very complex due to severe multivessel CAD, but ultimately PCI was successfully performed to the ostial LCX. It was noted that the other vessels may require later staged PCI and intravascular lithotripsy.

Pre-intervention.

Post-intervention.

Here is her ECG within 30 minutes of PCI:

Improved, but still with ischemia.

Here is her ECG 8 hours later:

Almost back to normal.

High sensitivity Troponin I:

(prior baseline within normal limit)

185 ng/L

638 ng/L

13,916 ng/L

(none further measured)

Echo:

EF 45%, hypokinesis of the inferior wall and basal to mid posterolateral segments.

Final Diagnosis: "STEMI"  (of course, as you can see in the ECGs above, this is not true, by definition this was NSTEMI. But the "final diagnosis" commonly just reflects whether the patient was given emergent therapy or not, regardless of the definition of STEMI/NSTEMI).

In other words, millimeters really don't matter!

Smith: This SEI pattern is one of global subendocardial ischemia, not of transmural ischemia.  The ST depression vector is towards lead II, so the STE vector is towards aVR. This STE in aVR is NOT analogous to STE of STEMI/OMI because there is no ventricular wall that corresponds to aVR--there are only atria on the top (or "base") of the heart.  This STE is RECIPROCAL STE, reciprocal to the ST depression.  

This SEI pattern is often attributed to "Left Main Occlusion".  This idea is erroneous.  Patients with complete left main occlusion usually die before arrival in the ED.  When they do not die, there are a variety of ECG patterns, shown in the post below.   This pattern is indeed consistent with left main ischemia (artery open but with insufficient flow), but it is also consistent with subtotal LAD ischemia and even with a culprit in any of the 3 epicardial vessels in addition to stenosis in the others ("3 vessel ACS"). 

Additionally, if we had an ECG recorded during complete occlusion of the circumflex with TIMI-0 flow, it would likely show Aslanger's pattern, which is inferior OMI plus SEI simultaneously.  With SEI alone, the ST depression vector would be towards lead II (so the STE vector is towards aVR), but with circ occlusion, there would also be an STE vector towards lead III.  The combined vector is exactly to the right, such that the only leads with STE are III and aVR.  These are not "consecutive" leads, so there is only a single lead with STE and it often does not meet 1 mm.

The pattern is defined as: 

(1) any STE in lead III but not in other inferior leads, 

(2) STD in any of leads V4 to V6 (but not in V2) with a positive or terminally positive T-wave, 

(3) ST in lead V1 higher than ST in V2

This figure shows the ST vector in Aslanger's:

See this post for 8 cases of total Left Main Occlusion: How does Acute Total Left Main Coronary occlusion present on the ECG?

See what happens when a left main thrombus evolves from subtotal occlusion to total occlusion.

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MY Comment, by KEN GRAUER, MD (12/31/2024):

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Assessment of today's case should be quick and to the point.

• The patient is an older woman with known coronary disease — who presents with severe CP (Chest Pain) of 3.5 hours duration.
• As per Dr. Meyers — the patient's initial ECG (TOP tracing in Figure-1) — shows sinus rhythm — diffuse ST depression (seen here in 8/12 leads) with ST elevation in lead aVR > V1 (RED arrows in aVR, V1).

As emphasized often in Dr. Smith's ECG Blog (See My Comment in the July 25, 2024 post and the March 1, 2023 post) — the ECG "picture" that we see in Figure-1 of today's case shows a supraventricular rhythm with diffuse ST depression — except for ST elevation that is seen in lead aVR (and to a lesser extent in lead V1). This picture defines the clinical entity known as DSI (Diffuse Subendocardial Ischemia). Recognition of DSI means we need to consider the 2 Categories of diagnostic entities that typically produce this picture:

• Category #1: Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• 
  
• Category #2: Subendocardial Ischemia from some other Cause (ie, sustained tachycardia — be this sinus tachycardia or some other arrhythmia; shock or profound hypotension; respiratory failure; GI bleeding; anemia, "sick patient", etc.). 

KEY Points:

• DSI does not indicate acute coronary occlusion! While true that many patients with DSI do have severe coronary disease — they generally do not have acute coronary occlusion at the time they are seen (although today's case illustrates a patient who developed acute coronary occlusion after ECG #1 was recorded, during the time that cardiac catheterization was being performed).
• That said, depending on the clinical setting — a significant number of patients who present with the ECG picture of DSI will turn out not to have coronary disease as the cause.

The 2 ECGs in Figure-1 illustrate these KEY concepts:

• In today's case, given that the patient was an older woman with known coronary disease — who presented with new CP — severe coronary disease (ie, Category #1) was almost certain to be the cause of the DSI pattern that we see in ECG #1.
• In contrast, despite the pattern of DSI seen in the BOTTOM tracing in Figure-1 (ie, with diffuse ST depression and ST elevation in aVR>V1) — entities other than coronary disease that are listed under Category #2 should be strongly considered because of the tachycardia! This ECG is taken from the July 25, 2024 post in Dr. Smith's ECG Blog. The patient was a younger adult with drug overdose and respiratory arrest, leading to the sinus tachycardia that we see in this bottom tracing (PINK arrows highlighting sinus P waves in other leads — because the fast rate rendered lead II P waves difficult to identify).

Today's "Take-Home" Message:

• The ECG pattern of DSI is usually easy to recognize — because in a supraventricular rhythm, there is diffuse ST depression (generally in at least 6 leads — often most prominent in lateral chest leads) — in association with ST elevation in lead aVR>V1.
• This pattern of DSI does not mean there is acute coronary occlusion.
• Many (but not all) patients with DSI have severe coronary disease.
• The presence of tachycardia in association with the ECG pattern of DSI serves as a clue that rather than severe coronary disease — one or more of the entities listed above in Category #2 may be the cause.
• And, as per Dr. Smith above — ST elevation in lead III (but not in other inferior leads) — in association with a pattern that is otherwise consistent with DSI — suggests Aslanger's pattern, in which there is inferior OMI plus severe disease in other coronary vessels.

Figure-1: Comparison between the initial ECG in today's case — with the ECG shown in the July 25, 2024 post (See text).

 

Dizziness in a 40-something with recent stent for inferior OMI

Dizziness is so unlikely to be OMI without an obvious ECG, that I am going to pretend that this patient presented with chest pain.

The PMCardio Queen of Hearts app asks you, before giving an interpretation of OMI ("STEMI-Equivalent"), whether the patient's clinical presentation is high risk for OMI.  If no, then she will tell you that the case is outside of the intended use group.

So let's pretend this is acute chest pain.  (Anyone can get acid reflux and present with chest pain, no matter the appearance of their ECG, right?)

This was interpreted as hyperacute T-waves in the inferior leads.

What do you think?  

There was a previous ECG for comparison, from an admission for inferior-posterior-lateral OMI (see in particular the pre-discharge ECG, below):

Previous active OMI

Predischarge ECG of previous active OMI

Notice that the T-waves in III and aVF are inverted.  

This further alarmed the providers, and led them to believe that these inferior T-wave are pseudonormalized and hyperacute.

What do you think?  Compare to inferior leads in the presentation ECG:

These T-waves do appear to be large and newly upright.  

However, they are NOT hyperacute

I can see instantly that they are not hyperacute, and so can Pendell.  But I cannot give an objective reason why not.  

Pendell and I have been attempting to numerically define hyperacute T-waves, and although we are making some great progress, our system so far cannot match our subjective accuracy (accuracy determined by angiographic/troponin/echo outcomes).  In fact, our system falsely called many of the T-waves in this ECG as hyperacute.

The Queen of Hearts also knows which large T-waves are hyperacute and which are not:

She knows that it is not OMI

(Unfortunately, most providers no longer have access to the Queen of Hearts because 1) it is not yet FDA approved and 2) thus a provider can only use it in the context of research.)

Why are the inferior T-waves upright when they were inverted on the last ECG?  Why is this not pseudonormalization (which implies re-occlusion)?

The last ECG was 6 months prior.  Over weeks to months, T-waves normalize after acute OMI.   If T-waves become upright in the hours or days after reperfusion (either spontaneous or due to intervention), then that is a sign of re-occlusion!  But you expect normalization if the time period is weeks to months.

Here are 9 cases that involve re-occlusion.

20 cases with pseudonormalization

Case continued

The patient was moved to the critical care area, and cardiology was consulted.  Cardiology correctly interpreted the ECG and did not want to activate the cath lab.  Of course, all other evaluation for possible acute MI is indicated and was undertaken, especially serial troponins.

Further ECGs were recorded:

25 minutes

Are those T-waves slightly smaller?  Maybe, but still the first ECG is NOT hyperacute.

47 minutes

Maybe smaller still?

Next day 

Now they are clearly smaller.

The patient ruled out for MI by serial troponins < 3 ng/L.

Why did they get smaller?  Was it unstable angina?  (Well, really, in this case, there was no angina, only "dizziness")

I don't think so.  I think that T-waves can have some evolution even without infarction.

But beware, because unstable angina does still exist in the era of high sensitivity troponin.

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MY Comment, by KEN GRAUER, MD (12/29/2024):

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I found today's case of interest because it addresses the theme of distinguishing "hyperacute" T waves (ie, indicative of ongoing acute OMI ) — vs T wave evolution not associated with an acute cardiac event.

In  the November 27, 2024 post — Drs. Smith and Meyers describe their ongoing work in association with clinician-researchers at Powerful Medical on developing an objective, mathematically derived and clinically-correlated definition of "hyperacute" T waves. KEY variables being integrated into their logistic regression formula include:

• AUC (Area Under the Curve) of the T waves being looked at.
• Increased Symmetry (as defined by time from T-wave onset-to-peak — compared to time from T-wave peak until T-wave end).
• ST Segment Upward Concavity (objectively measured — with reduced concavity correlating to increased likelihood of hyperacuity).

And so, I found it insightful that both Drs. Smith and Meyers immediately knew that despite the ST-T wave changes seen between today's initial ECG compared to the pre-Discharge ECG of this patient that was recorded following extensive acute infero-postero-lateral STEMI — the T waves in ECG #1 (that I've reproduced in Figure-1) are not hyperacute!

• As shown by Dr. Smith in his above discussion — serial ECGs on today's patient over the course of a day did show changes in ST-T wave appearance. Yet clinical follow-up confirming the absence of acute OMI also confirmed that the T waves in today's initial ECG were not hyperacute.

The above said — I thought it worthwhile to take another LOOK at the 2 key ECGs in today's case.

• When I first saw ECG #1 in today's case, being told to consider a clinical presentation of acute CP — I was clearly concerned.
• The T waves in the inferior leads of today's initial ECG are clearly disproportionately taller-than-expected considering modest amplitude of the QRS in these respective leads (RED arrows in Figure-1). That said — the ST segments in these inferior leads are not elevated, and these inferior lead ST segments manifest a peculiar concave-up slope.
• That said — the tiny, artifact-laden QRS complex in lead aVL manifests a very small amplitude mirror-image opposite picture compared to the ST-T wave picture in the inferior leads.
• Lead V1 in ECG #1 is also abnormal — with a tiny amplitude incomplete RBBB pattern manifesting disproportionately increased ST segment coving and T wave inversion that resolves by lead V2.
• 
  
• IMPRESSION: While I can appreciate how the peculiar inferior lead ST segment upsloping may detract from calling these T waves "hyperacute" — told to consider a history of new CP in association with ECG #1 — serial troponins with repeat ECGs are clearly indicated! (notwithstanding the appropriate decision by cardiology not to activate the cath lab at this time).

Comparison between ECG #1 and ECG #3:

Availability of a previous ECG on today's patient (as seen in Figure-1) — further clarifies that there is a difference in ST-T wave appearance in virtually all 12 leads when one compares ECG #1 with ECG #3.

• I found Dr. Smith's interpretation insightful, that despite the obvious ST-T wave differences between the 2 tracings shown in Figure-1 — the T waves in today's initial ECG are still not "hyperacute" (especially since their appearance is not the result of an ongoing or recent cardiac event).
• It turns out that ECG #3 was recorded ~6 months prior to ECG #1. I wish we could see the evolution of ST-T wave changes in ECG #3 at various points during those interim 6 months.
• Regardless — the serial ECGs shown above by Dr. Smith still show some evolution of ST-T wave appearance over the day that this patient was in the hospital.
• BOTTOM Line: As per Dr. Smith, "T waves can have some evolution even without infarction." That said — prudence dictates that even in those cases in which T waves may not fit the definition of being "hyperacute" — a history of new CP and clear differences in ST-T wave appearance (compared to the last previous ECG on record) — mandates ruling out an acute event (even though this does not necessarily mandate activation of the cath lab).

Figure-1: I've labeled the initial ECG and the pre-Discharge ECG in today's case.

 

Tachycardia in cardiology clinic, what is the rhythm?

Submitted anonymously, written by Willy Frick

A man in his 70s with a history of remote MI (details unavailable) and prior stent placement presented to cardiology clinic for routine follow up. He complained of days to weeks of palpitations and dyspnea. His clinic ECG is shown.

What do you think?

In an elderly patient complaining of palpitations, we have an ECG with heart rate 140 bpm. This is an arrhythmia until proven otherwise. The first step is in defining the atrial activity. The best leads for atrial activity are typically leads V1 and II, although individuals may vary. Inspecting V1 for atrial activity, there is nothing convincing for sinus activity. The second beat is preceded by a possible sinus beat, but it does not seem consistent.

Looking at lead II, there is a small deflection before the QRS. You might wonder if this is a P wave.

However, if you draw a vertical line to compare to neighboring lead I, you see that this is actually part of the QRS!

The slurred onset in lead I is suspicious for pre-excitation. But even in a pre-excited SVT, there will be some atrial activity. Can we find it?

Have another look at the V1 rhythm strip below and see if you can find any evidence for atrial activity before reading further.  (As always, click on the image to enlarge it!!)

With close inspection, you may notice a few unusual waveforms. I've pointed out some of the most believable candidates for atrial activity.

This raises the possibility of AV dissociation. A good way to test this is to use calipers to march out the P waves in both directions. Remember that sinus activity is not always perfectly regular. It can vary slightly from one beat to the next.

Allowing for a little bit of this fudge factor, we can pick two of the closely spaced arrows above and march them in either direction to get the following figure:

Some of the caliper tips fall in the middle of QRS complexes where it would be impossible to appreciate a buried P wave, but otherwise they march perfectly with irregular deflections in the waveform! This is a critical finding. This proves AV dissociation, and by extension ventricular tachycardia.

The cardiologist evaluating the patient in clinic did not recognize this. The note lists a diagnosis of "tachycardia," which is described as "narrow complex." (The QRS duration is approximately 144 ms, certainly not narrow.) The note says vagal maneuvers were unsuccessful, and recommends evaluation in the ER. The note says the patient's wife will drive him to the ER.

Repeat ECG obtained in ER:

Fortunately for the patient, his ventricular tachycardia spontaneously resolved. The current ECG shows sinus tachycardia with old inferior infarct. (Strictly speaking, the clinic ECG also had sinus tachycardia underneath the ventricular tachycardia.) He was admitted to cardiology. Serial troponin was undetectable. Documentation lists a diagnosis of "sinus tachycardia."

As an aside, sinus tachycardia at a rate of 140 in an elderly man is seriously concerning and demands an explanation. This would be approximately 95% of the patient's maximum predicted sinus rate. This demands an explanation -- sepsis, hemorrhage, withdrawal, etc. Calling sinus tachycardia raises more questions than answers.

After ruling out for ACS, the patient underwent angiography where he was found to have severe stable disease, which was already known. He was discharged with a plan for outpatient PCI to his chronically occluded RCA. There was no mention of ventricular tachycardia.

Fortunately for the patient, the person who submitted this case discovered it while reading ECGs. The submitter started the patient on amiodarone and arranged implantation of a defibrillator.

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MY Comment, by KEN GRAUER, MD (12/27/2024):

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Superb discussion by Dr. Frick in today's case, that highlights a series of important points regarding the ECG recognition of stable VT (Ventricular Tachycardia). I'll add the points that I note below.

• For clarity and ease of comparison in Figure-1 — I've labeled and have put the two 12-lead ECGs from today's case together.

For How Long can a Patient remain in Stable VT?

Today's case is remarkable in that this man in his 70s with a known history of prior MI and prior stent placement was misdiagnosed as having an SVT (SupraVentricular Tachycardia) by a cardiologist. Vagal maneuvers were tried — but were unsuccessful.  The patient was then sent to the ED for evaluation not by ambulance — but driven to the ED by his wife. And all the while — this patient was in stable VT!

• By history (since this patient had complained for days-to-weeks of palpitations and dyspnea) — it is possible that this patient could have been in stable VT for days-to-weeks!
• 2 major factors most probably led to the misdiagnosis of today's arrhythmia: i) This patient's history was over an extended period of time (ie, palpitations over a period of days-to-weeks); — and ii) This patient was hemodynamically stable throughout initial evaluation by his cardiologist (including during the performance of vagal maneuvers).
• As I've noted on a number of occasions in Dr. Smith's ECG Blog (See My Comments in the posts from September 20, 2023 — January 10, 2024 — and April 2, 2022 to name just a few) — I am aware of many cases of sustained VT in which the patient remained awake and alert for hours. I'm also aware a number of cases (including one at my former hospital) — where the patient was awake and alert in sustained VT for several days. 
• The LESSON is clear: Just because a patient remains awake and alert with an adequate blood pressure for an extended period of time — does not rule out the possibility of sustained VT. If the ventricular rate is not excessively fast (such as ~140/minute for today's initial ECG) — and the patient has reasonable LV function — then it is possible possible to remain in sustained VT for hours, and even days.
• The literature supports the premise that it is possible to remain in sustained VT for days at a time (Symanski & Marriott — Heart-Lung 24:121,123, 1995). In this case report — the 69-year old woman (who incidently had a history of both coronary disease and cardiomyopathy) — remained in sustained VT for 5 days without hemodynamic deterioration. During this time, she was treated in the hospital with multiple antiarrhythmic medications including Adenosine, Verapamil and Digoxin. On her 5th hospital day — she was given Amiodarone, which successfully converted the rhythm. Luckily — she "survived" the above treatment course (as each of the first 3 drugs that were given could have been fatal, given their tendency to precipitate VT deterioration in the setting of severe underlying coronary disease). NOTE: Although this case study is from 1995 — the misdiagnosis of wide tachycardias "because the patient is stable" remains all-too-common in 2025.

The Importance of Statistics and QRS Morphology:

The fact that the older man in today's case has known coronary disease — means that even before looking at his initial ECG — statistical odds that his regular WCT (Wide-Complex Tachycardia) rhythm will be VT are at least 90%.

• These statistical odds that the rhythm is VT can be further increased by noting the following in ECG #1: i) QRS morphology is not typical for any known conduction defect (ie, Instead of predominant negativity in the chest leads with LBBB until at least lead V4 — the QRS shows definite positivity already by lead V2); — and, ii) Instead of a rapid initial depolarization vector (as is so often seen with SVT rhythms) — the initial QRS depolarization vector is delayed (as well as fragmented) in multiple leads (such as leads III and V2-thru-V6).
• NOTE: The only exception that might account for the unusual QRS morphology seen in today's initial ECG — might be if a prior baseline ECG in sinus rhythm could be found showing the same unusual QRS morphology. Given that this patient was initially seen and treated (undergoing vagal maneuvers) in cardiology clinic — there may have been time to quickly find a patient record with a previous ECG in sinus rhythm.

What to Know about AV Dissociation:

Dr. Frick skillfully reviews in sequential detail the steps he followed to identify AV dissociation in ECG #1. As he emphasizes — defining the existence of an underlying independent atrial rhythm proves that the other rhythm in this tracing that manifests regular but wide QRS complexes must be ventricular in etiology.

• KEY Point: In my experience of meticulously searching for AV dissociation in every WCT rhythm I have encountered over a period of decades — it is rare to find it! Unfortunately, the desire of wanting (hoping) to "see" AV dissociation often leads emergency providers astray.
• The reality is that definitive diagnosis of VT is not nearly as difficult when the rate of the WCT rhythm is not overly fast. This is because diagnostic fusion beats and AV dissociation are much more likely to be seen in these relatively slower ventricular rhythms. The problem arises with relatively faster WCT rhythms — because underlying regular atrial activity so often gets hidden within wide QRS complexes and wider accompanying ST-T waves.
• My Experience: Most cases of supposed "AV dissociation" that I have seen others identify — turn out to be artifactual "blips" rather than true AV dissociation. This is important — because IF you are able to truly identify AV dissociation (as Dr. Frick does in today's case) — then you have definitively diagnosed VT. But if you only think that you may be seeing AV dissociation in a regular WCT rhythm — then it is best not to include this information in your assessment because it is much more likely than not to misguide you.
• PEARL: It is best not to diagnose AV dissociation unless you are 100% certain of this finding. And, the only way you can be 100% certain there is AV dissociation — is if you are able to walk out underlying independent regular atrial activity through at least a substantial portion of the rhythm strip. Finding 2, 3 or 4 "blips" that do not walk out further is not "proof" of AV dissociation.

Before I read Dr. Frick's description in today's case — I also suspected AV dissociation. This is because despite all of the fragmentation of QRS complexes that we see in ECG #1 — the overall tracing is surprisingly "clean" without significant artifact. This is why I suspected those small negative deflections that we intermittently see throughout the long lead V1 rhythm were "real".

• I highlight the 2 deflections I chose for setting my calipers to the P-P interval that I suspected (using RED arrows in ECG #1).
• In similar fashion as Dr. Frick — I then highlighted (using PINK arrows in Figure-1) periodic signs of additional atrial activity.
• Final "proof" of true AV dissociation was forthcoming when I was able to add (using YELLOW arrows placed at a similar P-P interval) markers in places where it was obvious that underlying regular atrial activity could easily be hidden.

Figure-1: I've labeled the initial ECG and the repeat 12-lead ECG in today's case.

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The Post-Conversion Tracing:

I found several features of the repeat ECG (after spontaneous conversion of the VT rhythm) to be especially interesting.

• We now see regular narrow QRS complexes in ECG #2 — that are conducted with a constant and normal PR interval at the same atrial rate, and with the same P wave morphology as was present in ECG #1 (RED arrows in the long lead V1 rhythm strip in ECG #2). This adds further confirmation that we truly were seeing AV dissociation in ECG #1.
• I suspect that this underlying atrial rhythm is not sinus — because no clearly upright P wave is seen in simultaneously-recorded lead II in the post-conversion tracing (dotted BLUE line showing this P wave's appearance in lead II of the post-conversion tracing). Instead — it looks like underlying atrial activity in both tracings of Figure-1 is from a low atrial rhythm. The low amplitude of these ectopic atrial P waves is another reason why AV dissociation is so subtle in today's case.
• Finally — Dr. Frick details how today's patient was found to have severe, stable coronary disease without evidence of an acute event. However, when I first saw ECG #2 — I had a different impression. Instead, in the setting of large inferior lead Q waves — my "eye" was attracted by: i) A small-but-real amount of inferior lead ST elevation (at least in leads II and III) — with suggestion of reperfusion T wave inversion in lead aVF; — ii) Potentially recent reciprocal change (subtle abnormal ST segment flattening in lead aVL); — and, iii) Potential posterior lead reperfusion T waves in the form of increased T wave positivity in leads V1,V2,V3. I therefore suspected that the cause of this patient's VT may have been recent infero-postero OMI, now with evidence of reperfusion T waves.
• NOTE: Tachycardia is still present in this post-conversion tracing ( = ECG #2). It is important to appreciate that at times — tachycardia may accentuate ST-T wave changes (ST elevation and/or depression) that are no longer present when the heart rate slows. As a result — I recognized that additional follow-up would be needed to determine the significance (if any) of these ST-T wave findings I describe in ECG #2 (and as per Dr. Frick — subsequent evaluation did confirm that none of these changes were acute). 

How comfortable are you with transcutaneous pacing?

Written by Willy Frick

A woman in her 70s is hospitalized with undifferentiated shock after being found down at home. Her family had not heard from her and called EMS. Paramedics found her bradycardic, hypotensive, and tachypneic. She was resuscitated and admitted to ICU for presumed sepsis.

Several days into hospitalization, she continued to have occasional episodes of sinus rhythm and sinus bradycardia with periods of Mobitz I AV block and 2:1 block. Her clinical team initiated transcutaneous pacing. Here is her cardiac telemetry. (Note: these are three consecutive strips of lead V1 from top to bottom.)

Do you notice any problems?

Here is the exact same strip, with the arterial pressure waveform included:

See if you can figure out what the problem is.

Hint: What does the arterial waveform correspond to on the ECG?

The problem here is complete failure to capture. The amount of current delivered is not above the minimum threshold required to cause myocardial contraction. The patient is getting some electrical stimulation, but nothing useful is happening.

The transcutaneous pads are delivering shocks at a rate of 70 per minute. You can see the purple lines (correctly) interpreted by the telemetry software as pacing spikes. And you can see a sharp deflection in the ECG from pacing artifact. The mistake here is thinking that the sharp pacer artifact deflection is a QRS complex. In fact, the only QRS complexes here are the patient's own native rhythm!

Here is the same image with orange arrows pointing out the patient's native P waves and blue arrows pointing out the patient's native QRS complexes. (Dotted lines indicated buried waveforms).

Now it becomes apparent that the arterial tracing corresponds exactly to the native QRS complex, and has no relationship at all to the pacing spikes. This patient is getting painful electrical shocks at a rate of 70 per minute which is providing no benefit whatsoever. Meanwhile, the patient's native rhythm is sinus bradycardia with adequate perfusion.

There may be some blocked P waves in there, it is hard to be sure with all the pacer artifact. The patient did have Mobitz I AV block both before and after this.

Here is where the pacing pads were turned on. Notice that the native QRS continues on unaffected by the pacing spikes.

Fortunately, this patient did not actually need any pacing. In fact, later on the patient's native rhythm was actually faster than the pacing efforts.

Cardiology turned the transcutaneous pacer pads off and recommended observation only. It is extremely lucky for this patient that she did not actually need any pacing. If she had needed pacing, she would have died.

So, how do you confirm that there is true capture of myocardium if you need to perform transcutaneous pacing?

• If you have an arterial line already, you should see the heart beat with every pacing impulse.

• If you do not have an arterial line, use bedside ultrasound to verify myocardial contractility corresponds to pacing.
• If you don't have ultrasound (but you should), then palpate a pulse! This can be harder than it sounds. Transcutaneous pacing will also capture skeletal muscle causing twitching. Your best bet is a femoral artery. And to be clear: It is completely safe to touch a patient who is being transcutaneously paced. I have done it many times.

• Pacing can be painful even if not capturing.  

• When in doubt crank the output all the way up. The dial will usually be labeled "OUTPUT," and the units will be mA.

Learning points:

• Do not confuse pacing artifact with myocardial capture

• Confirm capture by inspection of arterial line or palpation of a pulse

• When in doubt, crank the output

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MY Comment, by KEN GRAUER, MD (12/24/2024):

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Clinical implications of the content in today's post by Dr. Frick cannot be overstated — TCP (TransCutaneous Pacing) can either be lifesaving or producing of the opposite effect if basic troubleshooting measures are not attended to.

• In an effort to reinforce these measures presented by Dr. Frick in his above discussion — I've reproduced the following Section from my ACLS-2013-ePub.

Pacing CAVEATS: Is there Capture?

Effective TCP capture can be obtained in many (not all) patients. That said — there are pitfalls inherent in the process of determining IF effective electrical and mechanical capture are occurring. Consider the 4 rhythm strips shown in Figure-1:

QUESTIONS:

• Is there effective capture for rhythm strips A,B,C and D in Figure-1?
•   — How can you tell?  Clinically — What should you do? 

Figure-1: Pacing caveats. Is there effective capture for rhythm strips A,B,C,D? (adapted from Grauer K: ACLS-2013-ePub — Section 15, KG/EKG Press).

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ANSWER to Panel A:

The underlying cardiac rhythm in Panel A is asystole. Pacer spikes are seen at a rate of 75/minute (occurring every 4th large box) — but there is no sign of capture. 

• Suggested Approach: Increase current (gradually from ~50ma up to a max of 200 ma); correct other factors (ie, acidosis, hypoxemia). Treat asystole.

 

ANSWER to Panel B:

The pacer rate is ~100/minute. There is now electrical capture of every-other-beat in Panel B (as evidenced by a wide QRS complex with broad T wave occurring after every-other pacing spike).

• Suggested Approach: Since there now is sign of ventricular capture (at least for every-other pacing spike) — increasing current further will hopefully result in capture of every spike. Increase current (up to a max of 200 ma); correct other factors (ie, acidosis, hypoxemia).

ANSWER to Panel C:

Each pacer spike in Panel C now captures the ventricles by the end of this rhythm strip (evidenced by a wide QRS complex after each spike, followed by a broad, oppositely directed T wave).

• Suggested Approach: Look for objective signs to confirm that pacing is working clinically (ie, Check for pulse and BP; pulse ox pleth wave; and ET CO2 readings that should improve if the pacemaker is truly effective).

ANSWER to Panel D:

The rhythm in Panel D shows a regularly-occurring negative deflection after each pacing spike. That said — We suspect this may be pacer artifact and not indicative of true ventricular capture because there is no broad T wave (as there should be if this was paced! ).

• Comment: Verifying that true ventricular capture has occurred with external pacing is at times easier said than done. Reasons for this include the indirect nature of external pacing and a tendency for electrical artifact to be produced by the electrical activity generated from the pacemaker.
• Electrical artifact is usually "blocked out" from the ECG monitor (by integrated pacemaker software that eliminates a 40-to-80 msec. period that occurs just after the pacer spike from the ECG recording). BUT on occasion — a portion of this electrical artifact may persist beyond the "blockout" period. When this happens – the electrical artifact that regularly appears on the ECG monitor at fixed interval immediately following each pacer spike may “masquerade” as ventricular capture. It is important not to be fooled into thinking these “phantom” QRS complexes represent true capture. 

Suggested Approach: In addition to awareness of this phenomenon — You can verify that ventricular capture has truly occurred by:

• Being SURE the QRS after each pacing spike is wide and has a tall broad T wave. (In contrast — the QRS of electrical artifact is narrow and does not have any T wave! ).
• Palpating a pulse with each paced complex (and being certain not to confuse wishful thinking from pacer-generated muscle twitching as a “pulse” ).
• Checking for other evidence of perfusion (Can you get a BP? Is there now a pulse ox pleth wave? — and — Does ET CO2 increase as it should if the pacer is truly effective?)