You are told that the ECG in Figure-1 has generated 2 different interpretations among emergency care providers. These 2 interpretations are: i) That the wider beats in the long lead II rhythm strip are PVCs (Premature Ventricular Contractions); vs, ii) That the wider beats (ie, beats #2; 5,6; and #8,9) are PACs (Premature Atrial Contractions) — with the QRS widening being the result of aberrant conduction.
QUESTIONS:
- Which of these 2 interpretations do you favor?
- How would YOU interpret this tracing?
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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
MY Thoughts on the ECG in Figure-1:
This is a complicated tracing.
- PEARL #1: In most cases — I prefer to begin my assessment of an ECG by a brief look at the rhythm before I focus on the 12-lead tracing (that typically appears just above the long lead rhythm strip). This sequence is especially relevant in today’s tracing — because determining the etiology of the 5 wider beats in the long lead II rhythm strip is essential for knowing how to interpret the 12-lead tracing above it (See below for the reason why).
- PEARL #2: The wider beats in Figure-1 are neither PVCs (in the way we generally apply this term) nor aberrantly conducted PACs — because none of these beats occur more than the tiniest amount earlier-than-expected (ie, these beats are not “premature” in the usual sense of occurring noticeably early in the cycle).
- QUESTION: Does the PR interval remain constant in front of each of the 9 beats in Figure-2? If not — Why not?
ANSWER:
The PR interval appears to shorten slightly in front of each of the wider beats (ie, in front of beats #2, 5,6; 8,9).
- Focusing for a moment on just the long lead II rhythm strip — the fact that the PR interval remains constant and, is slightly longer in front of beats #1; 3,4; and #7 — suggests that these beats are sinus conducted (which I have labeled "S" in Figure-3).
- The widest beats in Figure-3 — are beats #2,6 and #9. These are ventricular beats (labeled "V" in Figure-3) that occur very late in the cycle. The P waves that precede these beats with a shorter PR interval compared to sinus-conducted beats — simply do not have enough time to conduct to the ventricles.
- This leaves us with beats #5 and #8 — which manifest a QRS morphology that is intermediate between sinus-conducted beats #1; 3,4; 7 — and ventricular beats #2,6,9. Note that both QRS morphology and T wave morphology of beats #5 and #8 are intermediate between sinus-conducted beats and ventricular beats. Thus, beats #5 and #8 are fusion beats (labeled "F" in Figure-3 — See ECG Blog #128 and Blog #129 for more on fusion beats).
- NOTE: One of the things that makes today's tracing so challenging — is that the P-P interval (highlighted by the RED arrows) is not constant throughout the tracing. Instead, there is an underlying sinus arrhythmia in Figure-3 — which makes it more difficult to distinguish between sinus-conducted beats vs ventricular beats and fusion beats (ie, Because of the sinus arrhythmia — it is more difficult to determine if ventricular beats occur "early" with respect to the underlying sinus rate).
Now that we have identified which beats in today's tracing are sinus conducted — we can focus on ST-T wave morphology of these sinus beats in each of the 12 leads to assess for potential ischemic change (See Figure-4).
- Remember: No clinical history was provided with today's tracing — so we do not yet have indication as to why there might be ventricular beats.
QUESTION:
Focusing in Figure-4 on the 3 sinus-conducted beats in the limb leads (ie, beats #1,3,4) — What do YOU suspect as the reason for the ventricular beats in the long lead II rhythm strip?
To facilitate assessment of the ST-T waves of sinus-conducted beats in the limb leads — I've enclosed beat #1 (in leads II,III) — and beats #3,4 (in lead aVF) within RED rectangles.
- QRS complexes in each of these inferior leads show QS waves (which are fragmented in leads II and aVF) and hyperacute ST-T waves (with straightening of the ST segment takeoff, widening of the T wave base — and some ST elevation).
- Confirmation that these inferior lead ST-T wave changes are real and indicative of an acute inferior OMI — is the reciprocal ST depression that is seen in oppositely-directed lead aVL (and in lead I to a lesser extent).
QUESTION:
Focusing in Figure-4 on the 1 sinus-conducted beat in the chest leads ( = beat #7) — Is there also evidence of posterior OMI? (within the BLUE rectagle in leads V2 and V3)?
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ANSWER:
While fully acknowledging how subtle the answer to this question is (ie, because the lead change only allows us to see a small portion of the ST-T wave for beat #7) — there probably is associated posterior OMI because: i) The ST segment of beat #7 in lead V2 appears flat, if not slightly depressed (whereas normally there is slight, upward sloping ST elevation in leads V2,V3); and, ii) Given how frequently posterior OMI accompanies inferior OMI — this subtle ST flattening and depression to me is enough to strongly suggest associated posterior OMI.
- PEARL #4 (Advanced Point): While fully acknowledging that it is much more difficult to assess ST-T wave morphology of ventricular beats for ischemia — I thought the T waves of the ventricular beats and of the fusion beats (ie, beats #5,6; 8,9) were disproportionately taller-than-expected! This suggests that these disproportionately tall chest lead T waves of these ventricular beats represent posterior reperfusion T waves.
- The deep QS waves in the inferior leads are therefore consistent with what appears to be an established infero-postero infarction.
- PEARL #5 — As discussed in ECG Blog #108 — AIVR (Accelerated IdioVentricular Rhythm) is a common reperfusion arrhythmia. The occurrence of late-cycle (ie, end-diastolic) PVCs is a similar phenomenon that is commonly seen with either spontaneous reperfusion, or reperfusion of the "culprit" artery as a result of treatment with either PCI or thrombolytics.
Conclusion:
Today's ECG suggests recent (and/or ongoing) infero-postero OMI — with ECG signs of reperfusion, in the form of taller-than-expected chest lead T waves and late-cycle ventricular beats.
- There are no PACs — because there are no early P waves.
- Because of slightly variable P-P and R-R intervals — it is impossible to know if some of the ventricular beats might be "premature". But PVCs in the usual sense are not present.
- To Emphasize: This is a very challenging tracing. BUT — If we look at all of the "parts" of this tracing, we are able to put together a "story" that indeed makes sense.
- PEARL #6: Whenever I see AIVR and/or late-cycle ventricular beats — I consider the possibility of recent infarction, now with reperfusion (which is precisely what we see in today's case).
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The Laddergram:
My proposed laddergram for today's ECG is shown in Figure-5.
- Beats #1, 3,4; 7 are sinus-conducted.
- I've drawn the laddergram assuming that beats #2, 6 and 9 are pure ventricular beats.
- I've drawn beats #5 and 8 as fusion beats, with the P wave in front of beat #8 penetrating slightly further into the ventricles than the P wave in front of beat #5. As a result — beat #8 looks more like the sinus-conducted beats.
- Note: I cannot rule out the possibility of a slight amount of fusion for the other 3 ventricular beats, since we do not know what ventricular beats occurring prior to a neighboring P wave would look like.
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Acknowledgment: My appreciation to Drs. 黄建成 and 许惠洋 and Kianseng Ng (from Malaysia) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
- 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 #218 — Reviews HOW to define a T wave as being Hyperacute?
- ECG Blog #108 and ECG Blog #321 — for more on AIVR.
- ECG Blog #128 and ECG Blog #129 — for more on fusion beats.