ECG Blog #496 — When III and V1 Show the Same?

The ECG in Figure-1 was obtained from a middle-aged man — who presented with syncope and dyspnea.

QUESTIONS:

• Should you activate the cath lab?
• If so — Why?
• If not — Why not?
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• What are the wide beats?
• Are these wide beats a result of today's diagnosis?

Figure-1: The initial ECG in today's case — from a middle-aged man with syncope and dyspnea. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts on Today's CASE:

The underlying rhythm in Figure-1 is sinus — because there are upright P waves in the long lead II rhythm strip with for the most part, a constant and normal PR interval (RED arrows in Figure-2).

• The PR interval is shorter in front of each of the wide beats (ie, in front of beats #2,4,8,12,and 16).
• The wide beats are PVCs (Premature Ventricular Contractions).

PEARL #1: We know that each of the above-noted wide beats is a PVC — because there is transient AV dissociation.

• Note that each of the RED arrow sinus P waves that we see in the long lead II rhythm strip in Figure-2 is on time! This means that wide beats #2,8,12 and 16 are completely unrelated to the on-time sinus P waves that precede these beats (This is because the PR interval in front of beats #2,8,12 and 16 is simply too short for these RED arrow P waves to be able to conduct to the ventricles!).
• Note also that the RED arrow P waves that occur after each of these wide beats is also on time! The only way this can happen — is if these wide beats "arise from below" (ie, arise from the ventricles).

There is more proof that wide beats #2,8,12 and 16 are PVCs:

• There is no reason for these wide beats to conduct with aberrancy — because these are late-cycle PVCs (that occur at the end of diastole, at a point in the cycle that is virtually certain to be after the refractory period is over). Instead — aberrantly conducted supraventricular beats almost always occur earlier in the cycle, at a point when part of the conduction system is still refractory.

Figure-2: I've added RED arrows to Figure-1 — to highlight that there is an underlying regular sinus rhythm.

PEARL #2: Final proof that the wide beats in Figure-2 are PVCs — is forthcoming from beat #4, which is a fusion beat (See the Laddergram in Figure-3).

• The laddergram explains why wide beats #2,8,12 and 16 do not alter the occurrence of on-time sinus P waves (ie, These PVCs do not conduct far enough backward to affect SA Node impulses that continue to regularly depolarize the atria).
• The situation is different for beat #4 — which is preceded by a PR interval that is longer than the PR interval before each of the other wide beats. As a result, this 3rd RED arrow is able to conduct a short distance through the ventricles until it meets (ie, "fuses" with) ventricular beat #4. The result is a fusion beat, in which QRS morphology of beat #4 is intermediate between that of the wider ventricular beats — and the normally conducted sinus beats (See ECG Blog #217 — for illustrated discussion on how AV dissociation facilitates distinction between PVCs vs aberrantly conducted beats).

Figure-3: Laddergram of the long lead II rhythm strip.

QUESTIONS: 

• What kind of PVCs are the wide beats in Figure-3? (ie, Can you localize from where in the ventricles these PVCs arise?).
• Is the site of origin of these PVCs relevant to today's case?

To answer the above questions — Take a LOOK at Figure-4 — in which I've enclosed within dotted RED rectangles the appearance of these PVCs in each of the 12-leads.

Figure-4: I've enclosed within the dotted RED rectangles the appearance of the PVCs within each of the 12 leads.

PEARL #3: The PVCs in today's ECG appear to arise from the RVOT (Right Ventricular Outflow Track).

• The PVCs that we see for beats #12 and 16 — manifest a pattern similar to LBBB conduction in the chest leads (ie, predominantly negative in anterior leads V1,V2,V3 — and all upright in lateral chest leads V5,V6). PVCs with a LBBB-like morphology arise from the RV (Right Ventricle).
• In the limb leads — beats #2 and 8 manifest a vertical (if not somewhat rightward) frontal plane axis. Given the predominantly positive QRS morphology in the inferior leads — this suggests that the electrical impulse is traveling toward the inferior leads, because these PVCs arise from high in the ventricles (in this case — from the RVOT).
• NOTE: Clinical relevance of the site of origin for today's PVCs will become evident momentarily.

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Return to today's initial ECG — and the presenting history:

• Today's History: The patient is a middle-aged man who presents for syncope and dyspnea. 

For clarity in Figure-5 — I've reproduced and labeled this initial ECG.

• As discussed above, the rhythm in today's ECG is sinus (upright P waves in the long lead II rhythm strip) — with late-cycle PVCs that originate from the RV Outflow Track.
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• Note the Q waves in leads III and aVF (BLUE arrows in these leads) — and — T wave inversion in multiple leads (RED arrows in Figure 5).

QUESTIONS:

In view of the above history: 

• How do you interpret the 12-lead ECG in Figure-5?
•    — Should you activate the cath lab?

Figure-5: I've reproduced and labeled the initial ECG in today's case.

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MY Interpretation of Today's 12-Lead ECG: 

For clarity in Figure-6 — I've approached interpretation of today's initial ECG from a different perspective than that shown in Figure-5. I've labeled KEY findings from this new perspective in Figure-6:

• The rate of the regularly-occurring sinus P waves in Figure-6 is fast (about 115/minute) — so the underlying rhythm is sinus tachycardia.
• An S1Q3T3 pattern is present (ie, S wave in lead I — with both Q wave and T wave inversion in lead III).
• The rSr' in lead V1, in association with terminal narrow S waves in lateral leads I and V6 — is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• S waves persist across the chest leads — and are still present in leads V5,V6 of Figure-6 (whereas normally there are predominant R waves without S waves in the lateral chest leads).
• Symmetric T wave inversion is present in multiple leads in sinus-conducted beats (RED arrows in Figure-6 — with a lesser degree of T wave inversion also seen in lead aVF).

Figure-6: I've labeled KEY findings in today's ECG (See text).

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Putting It All Together: 

Rather than ischemia from an acute cardiac event — the sum total of ECG findings described above in Figure-6, in this patient who presented with syncope and dyspnea (but not chest pain) — strongly suggests an acute PE (Pulmonary Embolus).

• PEARL #4: When there is T wave inversion in the chest leads — IF there is T wave inversion in both lead V1 and lead III — Think acute PE (and not of an acute cardiac event). This is precisely what we see for the ECG in Figure-6.
• Acute RV "strain" manifests on ECG as T wave inversion (and/or ST depression) that is present in anterior leads and/or in inferior leads (especially in lead III). When seen in both anterior and inferior leads, in association with sinus tachycardia and other ECG findings consistent with acute PE (as shown in Figure-6) — suspect submassive PE. These ECG findings were recognized in today's case — and confirmed by pulmonary CT scan.
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• PEARL #5: The fact that the frequent PVCs in today's initial ECG arise from the RVOT — is consistent with the diagnosis of acute PE!

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By way of review — I add in Figure-7 below a list of ECG findings to look for when considering the diagnosis of acute PE. The presence of several of these findings, in association with a suggestive clinical history — should merit further evaluation with pulmonary CT scan.

• Today's patient certainly presented with a suggestive clinical history (syncope and dyspnea — but no chest pain).
• The ECG in Figure-6 is notable for sinus tachycardia — RV "strain" (with diffuse chest lead T wave inversion + T wave inversion in lead III) — S1Q3T3 — incomplete RBBB — persistence of S waves (still present in lead V6) — as well as frequent PVCs originating from the RVOT.

Figure-7: ECG findings associated with acute PE (from ECG Blog #443 — in which Echo and Pulmonary CT Scan findings are reviewed in detailed discussion of another case).

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for this case and this tracing.

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For More on the Diagnosis of Acute PE: 

• Please check out my ECG Blog #443 — as this post thoroughly reviews the ECG, Echo & Pulmonary CT Scan evaluation for suspected acute PE, and provides LINKS to other cases.
• Also check our the July 28, 2025 post in Dr. Smith's ECG Blog for another illustrative clinical case (Case write-up by Dr. Magnus Nossen — with review in My Comment at the bottom of that page).