Today's patient is an older man with a permanent pacemaker that was placed ~1 year ago for complete AV Block. He presents to the ED (Emergency Department) at this time — for new CP (Chest Pain) that began earlier in the day, and which has still persisted. The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded.
QUESTIONS:
- How would you interpret the ECG in Figure-1?
- Should the cath lab be activated?
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| Figure-1: The initial ECG in today's case. |
My Thoughts on Today’s CASE:
We are told that today's patient has a pacemaker — and that he presents for new CP persisting over the course of a day. Questions that arise include the following:
- Do we see evidence of this patient's pacemaker in ECG #1? If so — Is the pacemaker working appropriately?
- Can we assess the ECG of a patient with a pacemaker for ST-T wave changes of acute OMI? If so — Are there any worrisome findings in ECG #1?
ANSWERS: Can We Detect Acute OMI in a Paced Tracing?
As seen in Figure-2 — Pacemaker spikes are present (within the small RED circles in leads V4,V5). Similar tiny spikes are intermittently seen in other leads.
- At least in leads V4,V5 — we see these pacemaker spikes just before wide QRS complexes with a LBBB-like morphology — so the pacmaker appears to be appropriately capturing the ventricles at ~85/minute.
- It is at least sometimes possible to assess a paced ECG for ST-T wave changes of acute ischemia. Such assessment is made more challenging by QRS widening of paced beats (and resultant altered ST-T wave morphology) — but there are times when we can see evidence of acute OMI on a completely paced tracing.
- In such instances — application of Smith-Modified Sgarbossa Criteria help to identify abnormal ST-T wave findings despite complete pacing (See Pearl #4 in ECG Blog #282 for review of Smith-Modified Sgarbossa Criteria).
- There is no way that the 4+ mm of downsloping ST depression in lead V6 with terminal T wave positivity can be a "normal" finding (within the RED rectangle in Figure-2). If anything — we would expect secondary ST-T wave changes of LBBB or in a paced tracing to be oppositely directly to the predominantly negative QRS deflection in lead V6.
- In the context of this clearly abnormal downsloping ST depression in lead V6 — the more subtle flattened ST depression in neighboring lead V5 (BLUE arrow in this lead) is also abnormal.
- The next lead in Figure-2 to catch my "eye" — is lead V1 (within the BLUE rectangle) — as the relative amount of J-point ST elevation in this lead is clearly disproportionate to the modest size of the S wave in this lead (The relative amount of ST elevation in lead V1 does appear to satisfy the 25% criteria of Modified-Smith Sgarbossa Criteria outlined in ECG Blog #282).
- Given the clearly abnormal ST elevation in lead V1 — I thought the J-point ST elevation in neighboring lead V2 was also abnormal. While not satisfying the 25% criterion of Smith-Modified Sgarbossa — the J-point in this V2 lead is angled sharply (BLUE arrow in V2) — rather than manifesting a smoother transition as is normally expected between J-point and ST segment (Note the much smoother transition between J-point and ST segment in neighboring leads V3,V4 that I interpreted as normal).
- PEARL #2: The presence of coved ST elevation in leads V1,V2 with clearly abnormal ST depression in leads V5,V6 is consistent with Precordial Swirl — which suggests a proximal LAD occlusion (See ECG Blog #380 for more on Precordial Swirl).
- To address the question posed at the beginning of today's case: YES, the cath lab should be immediately activated given the history of new CP and the ECG findings in Figure-2.
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| Figure-2: I've labeled today's initial ECG. |
The CASE Continues:
A prior tracing on today's patient was found. To facilitate comparison in Figure-3 — I've put this previous ECG from ~8 months earlier together with today's initial ECG.
- Does availability of this prior ECG support your decision to activate the cath lab?
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| Figure-3: Comparison between today's initial ECG — and a previous ECG done ~8 months earlier. |
Comparison with the Prior Tracing:
Availability of the prior ECG on today's patient removes all doubt about the need to activate the cath lab!
- PEARL #3: The BEST way to hone your ECG interpretation skills — is to train your "eye" in recognizing subtle findings by follow-up comparison with subsequent tracings to see how more subtle findings on the original tracing evolved over time.
- Lead-to-lead comparison between ECG #1 and ECG #2 in Figure-3 shows significant changes in virtually every lead!
- Looking first at the 2 leads that made the diagnosis for us — it is easy to see how abnormal the ST-T waves in leads V5 and V1 of Figure-1 truly were!
- Looking further at the more subtle changes in leads V2 and V5 that I highlighted above — we can confirm the validity of my observations on seeing that there was more ST elevation in lead V2 in ECG #1 than there was on the prior ECG — and the subtle, flattened ST depression in lead V5 of ECG #1 was not at all present on the prior ECG.
- ST-T wave changes in other leads are present on comparison between the 2 tracings in Figure-3 — but those changes are not nearly as easy to detect — which confirms my PEARL #4 from today's case = It is usually more difficult to assess paced tracings for acute ischemia — but it is definitely not impossible.
CASE Conclusion:
The cath lab was activated. Cardiac cath revealed the following:
- There was significant 3-vessel disease.
- 90% distal stenosis of the LMain.
- 50% mid-LAD stenosis.
- 90% patent ostial stenosis of the LCx.
- 50% mid-RCA stenosis.
The LMain narrowed area was successfully stented to the patent LAD. The patient did well in follow-up.
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PEARL #5: Had I not been told — I may not have realized that today's patient had a pacemaker from the initial ECG shown in Figure-1. Pacemaker spikes are often difficult to detect for a number of reasons:
- There could be pacemaker malfunction.
- There could be signal interference and artifact and/or "noise".
- Modern pacemakers increasingly use bipolar leads — and bipolar leads generate smaller spikes on ECG.
- Filter settings are suboptimal. This is especially true when the low-pass filter is set below the standard value of 150 Hz. That said — even at 150 Hz, the percentage of patients whose pacemaker spikes will be visible on a standard ECG has been found to be far less than the percentage for detecting pacemaker spikes on ECG with a higher low-pass filter of 300 Hz (Sun et al — Chin Med J 132(5):534-541, 2019).
Regarding Filter Settings:
I suspect suboptimal Filter settings is the most common reason that pacemaker spikes are not readily seen on many tracings. All too often — filter settings are ignored.
- Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms.
- Greater filtering is generally used in monitor mode, with a common setting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation.
- In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) — is recommended for diagnostic mode, where more accurate ST segment analysis is essential.
- Modern bipolar pacemakers generate smaller pacing spike amplitudes compared to older devices, making them harder to detect on the ECG. Awareness that the filter setting is important — especially if you find yourself hopelessly looking for spikes in a tracing of a patient thought to have a pacemaker.
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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.
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