ECG Blog #498 — Should you try Adenosine?

The ECG in Figure-1 was obtained from a middle-aged man with uncontrolled diabetes and presumed septicemia. 

• The patient's blood pressure was borderline low in association with the ECG in Figure-1. Rapid IV infusion to restore fluid volume was begun.

 

QUESTIONS:

• How would you interpret the initial rhythm in Figure-1?
• Is today's patient hemodynamically stable?
• Should you try Adenosine? 

 

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

Is the Patient Hemodynamically Stable?

We are provided with limited clinical information on today's patient — namely, that he is a middle-aged man with uncontrolled diabetes, presumed septicemia, and a borderline low BP. Clearly, we need to find out more about what is going on ...

• The 1st Thing to do — is to LOOK at the patient! The KEY Question to address is whether or not the patient is hemodynamically stable!
• As per the 6-minute Audio PEARL in the ADDENDUM below — sometimes, "Ya just gotta be there!" in order to determine if the patient is "stable enough" to continue assessing the rhythm (ie, to distinguish between VT vs some type of SVT rhythm) — and/or — to continue with medical management without need for immediate electricity (ie, with synchronized cardioversion).
• This is because IF the patient is not hemodynamically stable because of the rhythm you are treating — then it no longer matters whether the rhythm is VT (Ventricular Tachycardia) — or some type of SVT (SupraVentricular Tachycardia) rhythm — since regardless, immediate cardioversion will be indicated!
• On the other hand — IF the patient is hemodynamically stable with the rhythm you are treating — then by definition, there is at least a moment-in-time for you to further assess the rhythm diagnosis.
• 
  
• PEARL #1: To determine hemodynamic stability — Sometimes, "Ya just gotta be there ... ".

Regarding today's initial ECG that is shown in Figure-1:

• It is hard to be certain from the verbal description we are given IF the borderline low BP of today's patient is a result of today's fast rhythm — or, if instead — this patient's precarious medical condition (with marked volume depletion from uncontrolled diabetes and septicemia) is the cause of his hypotension and tachycardia.
• That said — Let us presume since capable providers decided to treat this patient with rapid IV volume infusion — that synchronized cardioversion was not immediately needed in today's case.  

My Approach to the Rhythm in Figure-1:

Assuming that today's patient is hemodynamically stable — Let's work under the assumption that we have at least a moment-in-time to better assess the initial rhythm in Figure-1. As always — I favor the Ps, Qs,3Rs Approach (as described in ECG Blog #185).

• The rhythm in Figure-1 is fast and Regular.
• The QRS is narrow — so the rhythm is supraventricular.
• Sinus P waves are not seen (so there are no P waves to be Related to neighboring QRS complexes).
• Therefore — the rhythm in Figure-1 is a fast, regular SVT rhythm without clear sign of sinus P waves.

PEARL #2: As discussed in ECG Blog #287 — Recognition that the rhythm in today's initial tracing is a regular SVT without clear sign of sinus P waves (ie, without a definite upright P wave in lead II) — should prompt consideration of the following differential diagnosis LIST:

• i) Sinus Tachycardia (IF there is a possibility that sinus P waves might be hiding within the preceding T wave); 
• ii) A Reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an AP [Accessory Pathway] located outside the AV node is involved); 
• iii) Atrial Tachycardia (ATach);
• iv) Atrial Flutter (AFlutter) with 2:1 AV conduction. 

PEARL #3: Knowing the actual Rate of a regular SVT rhythm can be extremely helpful in working through the differential diagnosis of the tachycardia. This is because:

• Point #1: While not impossible — Sinus Tachycardia becomes much less likely in a non-exercising adult IF the rate of the unknown tachycardia exceeds ~170/minute.
• Point #2: Untreated AFlutter most commonly presents with a ventricular rate that is close to 150/minute (~130-170/minute range). This is because the untreated rate of flutter in the atria of adults is most commonly close to 300/minute — which with 2:1 AV conduction, results in a ventricular rate close to ~150/minute. Therefore — AFlutter also becomes unlikely when the rate of an unknown SVT rhythm exceeds ~170/minute (as this would require a ventricular rate of over 340/minute if 2:1 AV conduction was maintained).
• CAVEAT: In contrast, an SVT rhythm for which the ventricular rate is in the range of ~140-150/minute, provides NO Clue to etiology — because each of the most common diagnostic possibilities (ie, Sinus Tach — ATach — AFlutter — AVNRT/AVRT) may all present with a ventricular rate in the range of ~140-150/minute.

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Estimating Rate when the Rhythm is Fast:

LOOK again at the rhythm in Figure-1:

• QUESTION: How fast is today’s initial rhythm?

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PEARL #4: I favor the Every-Other-Beat Method for rapid estimation of a fast heart rate. I illustrate this Method with a short Video PEARL in the ADDENDUM below — but a picture is worth 1,000 words.

• NOTE: Sometimes it is easier instead of assessing the R-R interval for every-other-beat — to assess the R-R interval for every-third- or every-fourth beat.

Applying this Method to today’s initial rhythm:

• Looking every-third-beat is easiest in this example — because there is a 3-beat period in this rhythm in which a part of the QRS at the beginning and at the end of this 3-beat period falls either on (or almost on) a heavy grid line (as seen for the 2 vertical BLUE lines just under lead I of Figure-2).
• Using the Every-Third-Beat Method — the amount of time that it takes to record 3 beats (BLUE numbers in lead I) is just over 5 large boxes (RED numbers in this Figure). Therefore — ONE THIRD the rate is a little slower than 300 ÷ 5, or a little slower than 60/minute.
• Therefore — the actual rate for the rhythm in Figure-2 is a little less than 60X3, which comes to a rate of ~170-175/minute. 

Figure-2: Illustration of the every-other (in this case, every-third) beat approach for rapid estimation of a fast heart rate.

PEARL #5: By far (!) — the most commonly overlooked entity in the differential diagnosis LIST cited above in Pearl #2 — is AFlutter (Atrial Flutter). Therefore, even though the ventricular rate in today's SVT rhythm is slightly above the usual range for AFlutter — the BEST way to avoid missing AFlutter is to always at least consider this diagnosis whenever you have a regular SVT rhythm that is not excessively fast (ie, less than ~180/minute), and for which clear sign of sinus P waves is absent.

PEARL #6: Using calipers facilitates finding the diagnostic "sawtooth" pattern of AFlutter. When looking for AFlutter — I take advantage of the fact that new AFlutter most often presents with 2:1 AV conduction.

• To look for this — I simply set my calipers at precisely half the R-R interval — and then using this interval — I look for leads in which I can "walk out" 2:1 conduction.
• I have done this in Figure-3 — in which slanted RED lines that occur at precisely twice the ventricular rate can be walked out in at least 4 leads. Given the ventricular rate that we estimated in Pearl #4 to be ~170-175/minute — this corresponds to an atrial rate of ~340-350/minute.
• The "sawtooth" pattern of the baseline with AFlutter is best appreciated by stepping back a little bit from the tracing. My "Go-To" Leads when looking for subtle signs of atrial activity are leads II,III,aVF; — lead aVR — and lead V1 (with "sawtooth" flutter waves seen in 4 of these leads in Figure-3).

Figure-3: Using calipers facilitates finding "sawtooth" flutter waves that are highlighted by slanted RED lines in leads II,aVR,aVF and V1.

Should You Try Adenosine for Today's Rhythm?

To emphasize — It would not be "wrong" to give Adenosine for today's rhythm. This is because most of the time — there are no longterm adverse effects from using Adenosine, because its duration of action is so short.

• PEARL #7: Although Adenosine usually does not produce longlasting adverse effects — this drug is not entirely benign. Adverse effects are not always shortlived (See Figures-9 and -10 in the ADDENDUM below).
• Adenosine works great to convert reentry SVT rhythms such as AVNRT and AVRT — but it generally does not convert AFlutter. Instead, what the drug typically does with AFlutter is to transientlly slow AV conduction — which facilitates seeing underlying flutter waves that had previously been hidden within the QRS and/or ST-T waves.
• My Thought: The reason I would not choose Adenosine for today's rhythm — is that we are already quite certain that the rhythm is AFlutter (as shown in Figure-3) — so that there is little to learn by giving Adenosine. If on the other hand, we were less certain that today's rhythm was AFlutter — then it would be perfectly appropriate to give Adenosine as a diagnostic-therapeutic maneuver.

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Today's CASE Continues:

Adenosine was given. The result is shown in Figure-4.

• What do you see?

Figure-4: Repeat ECG after IV Adenosine.

ANSWER:

The first 9 beats in Figure-4 show a continuation of the regular SVT rhythm that we saw in Figure-3. Thereafter, the rate-slowing effect of Adenosine is seen:

• Beginning with beat #10 — there is marked rate-slowing which reveals underlying flutter waves that are best seen in leads II, aVR, aVF; and V1,V2.
• Although it is not easy to see the ECG grid in Figure-4 — flutter waves appear to be regular in the above-cited leads, at a rate slightly greater than 300/minute (ie, with flutter waves slightly less than 1 large box in duration).
• We see 2 ventricular beats near the end of the tracing (beats #15,16).
• BOTTOM Line: Use of Adenosine confirmed that the rhythm in the initial ECG of today's case was AFlutter with 2:1 AV conduction, in which flutter waves were hidden within the QRS complex and the T wave that follows.

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The CASE Continues:

Within 2 minutes — the rate-slowing effect of Adenosine wore off, and the rhythm returned to what we saw in Figure-3.

• With the goal of slowing the ventricular response — the patient was treated with several doses of IV Metoprolol. A dose of IV Digoxin was given.
• Clinically — the patient improved.

The repeat ECG is shown in Figure-5.

• Is the patient now in AFib?

Figure-5: The repeat ECG after IV Metoprolol and Digoxin.

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ANSWER:

The "good news" — is that the patient improved clinically. Presumably — treatment of the patients uncontrolled diabetes and septicemia contributed to this clinical improvement.

• At first glance in Figure-5, the long lead V1 rhythm strip at the bottom of the tracing "looks" like AFib. That said — there is a regular irregularity to this rhythm. This is perhaps best appreciated in the long lead II rhythm strip that appears below the long lead V1, in which 2 "families" of similar duration R-R intervals are seen (highlighted by double BLUE and double RED arrows in Figure-6).

Figure-6: Colored double arrows highlight the regular irregularity of the rhythm in the long lead II.

In Figure-7 — We look closer at the long lead II rhythm strip that appeared at the bottom of Figure-5:

• RED arrows in Figure-7 highlight that although the ventricular response is not completely regular — the underlying rhythm remains AFlutter.

Figure-7: Looking closer at the long lead II rhythm strip that we saw at the bottom of Figure-5 — We can see that the underlying rhythm of AFlutter persists, albeit with an irregular ventricular response.

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Putting It All Together:

As we have seen in a number of previous ECG Blog posts — it is common for AFlutter to manifest dual-leval Wenckebach conduction out of the AV node (See ECG Blog #243  — and ECG Blog #463, among others for laddergram illustration of this phenomenon).

• I believe the group beating that the 2 families of colored double-arrows in Figure-6 suggest reflect a complex form of dual-level Wenckebach conduction in response to the AV Nodal blocking treatment that today's patient received.
• My proposed laddergram of this conduction for a portion of Figure-7 is shown in Figure-8.
• Full discussion regarding Teatment of AFlutter extends beyond the scope of this ECG Blog. A nice review of this subject is by Stiell and Eagles: Clin Exp Emerg Med 11(2):213-217, 2024. Given uncertain duration of AFlutter in today's case, and the association of AFlutter with the acute problems of uncontrolled diabetes and septicemia — medical treatment with the goal of slowing the ventricular response while addressing the patient's medical problems was perfectly appropriate.
• If this patient had been hemodynamically unstable as a result of the rapid ventricular response from AFlutter — then immediate synchronized cardioversion would have been indicated. But the patient was improving with IV Metoprolol and Digoxin, which was therefore continued. Along the way —  the initial 2:1 AV conduction in response to AFlutter slowed, with Wenckebach conduction out of the AV node. And the patient improved.

Figure-8: My proposed laddergram suggesting dual-level Wenckebach conduction for the rhythm in Figure-7.

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Acknowledgment: My appreciation for today's case that was shared anonymously with me.

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ADDENDUM (9/27/2025):

ECG Media PEARL #27 (3:00 minutes Video) — Reviews the Rule of 300 for estimating heart rate — and — @ 1:25 minutes in the video, the Every-Other-Beat Method for Estimating Rate with fast rhythms (from ECG Blog #210).

 

—  — 

ECG Media PEARL #37 (6:00 minutes Audio) — Reviews how to determine IF Your Patient with an Arrhythmia is Hemodynamically Stable! (from ECG Blog #220).

Regarding Adenosine:

Adenosine is a wonderful drug for emergency treatment of reentry SVTs. Even in cases in which Adenosine does not convert the rhythm — it will often facilitate rhythm diagnosis by its transient rate-slowing effect. 

• Although Adenosine is usually safe (because of its ultra-short half-life) — side effects can occur, and these are not uniformly short-lived. Therefore — Adenosine is probably best avoided for treatment of rhythms for which the drug has little to no chance of being effective (ie, If you know that the SVT you are treating is AFib or AFlutter — then its better to use some other rate-slowing or antiarrhythmic agent — rather than risking side effects from a drug that is unlikely to work).

Figure-9: Pages 1 and 2 on Pros & Cons of using Adenosine (excerpted from my ACLS-2013-ePub).

 

Figure-10: Pages 3 and 4 on Pros & Cons of using Adenosine (excerpted from my ACLS-2013-ePub).

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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 #210 — reviews the Every-Other-Beat Method for estimation of heart rate when the rhythm is very fast.
• 
  
• ECG Blog #287 — for a regular SVT that was AFlutter.
• ECG Blog #409 — another regular SVT that was AFlutter.
• ECG Blog #229 — reviews distinction between AFlultter vs ATach (and WHY AFlutter is so commonly overlooked).
• 
  
• ECG Blog #240 — reviews the approach to a regular SVT rhythm.

ECG Blog #497 — Nonspecific ST-T Wave Changes

I was sent the ECG shown in Figure-1 — and told that it was from a previously healthy older man who had a witnessed collapse.

• This ECG was interpreted as showing, “nonspecific" ST-T wave changes. 

QUESTIONS:

• Do you agree with this interpretation?
• Any other concerns?

Figure-1: The initial ECG in today's case — from an older man with witnessed collapse. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on the ECG in Figure-1:

Given the concerning circumstances of a "witnessed collapse" — the ECG in Figure-1 is not normal.

• The rhythm in ECG #1 is sinus at ~85/minute. Intervals (PR-QRS-QTc) are normal. The frontal plane axis is horizontal (about zero degrees — given the isoelectric QRS in lead aVF). There is no chamber enlargement.

Regarding Q-R-S-T wave changes:

• My "eye" was immediately drawn to leads V2 and V3 (within the RED rectangle in Figure-2). Normally there is slight, upward-sloping ST elevation in these 2 leads. Instead — the ST segments are flat without any ST elevation at all (RED arrows in these leads). This abnormal finding, when seen in a patient with new symptoms — should suggest the possibility of recent or acute posterior OMI (Occlusion-based MI ) — as explained by the "Mirror Test" in ECG Blog #351.

Given the common blood supply of the inferior and posterior walls of the left ventricle — I next focused on the inferior leads.

• There is subtle-but-real ST segment coving in lead III, and to a lesser extent in lead aVF — in association with shallow-but-real terminal T wave inversion (BLUE arrows in these leads).
• Reciprocal changes are seen in lead aVL (ST segment straightening — with terminal T wave positivity).
• ST segment straightening, albeit without ST depression — is also seen in leads I, II; and in leads V5,V6.

KEY Point: The ECG in Figure-2 is not normal. While true that the above ECG findings are subtle, and might be described as "nonspecific" — given the clinical setting of a patient who had a "witnessed collapse" — there are ECG abnormalities in no less than 9/12 leads. 

• My concern was that ECG #1 could indicate a recent infero-postero OMI in a patient with significant underlying coronary disease. Additional evaluation was essential.

Figure-2: I've labeled today's ECG.

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Follow-Up of Today's CASE:

It turns out that this patient’s collapse was associated with no pulse and no respiration ==> cardiac arrest! The arrest was witnessed — and CPR was promptly initiated. EMS was quickly on the scene — and found the patient to be in VFib (Ventricular Fibrillation).

• EMS immediately defibrillated the patient — with prompt ROSC (Restoration Of Spontaneous Circulation).
• The patient arrived in the ED a short while later — sitting up, alert and oriented (albeit with no memory of what had just happened).
• At no time did the patient have any chest pain. He did not feel ill prior to collapsing, and had no specific symptoms that he could recall.
• The ECG in Figure-2 was recorded within minutes after achieving ROSC.

In the ED — the initial Troponin was normal.  

• Cardiology was consulted. Plavix, heparin and IV infusion of Amiodarone were all started — and the patient was transferred in timely fashion to a center with 24/7 access to cardiology services.
• Cardiac cath revealed multi-vessel coronary disease (I don't know further details of this patient's cath report).
• The patient's condition stabilized — and arrangements were made for CABG (Coronary Artery Bypass Grafting). The patient did extremely well — and was subsequently discharged from the hospital without neurologic deficit.

Additional Thoughts:

Today's case is a success story. Cardiac arrest was witnessed — CPR was promptly started — and, EMS was quickly on the scene to defibrillate the patient, with restoration of sinus rhythm.

• This patient never had chest pain.
• While I don't have access to all data on the case — the initial Troponin was negative. This is not uncommon. As per references in the ADDENDUM below — there will often be spontaneous reopening (reperfusion) of the "culprit" artery, even before any medical treatment is given. If the period of time that the "culprit" artery was occluded is brief — then even high-sensitivity Troponin may not be elevated (or only minimally elevated).
• If the moment in time that the initial ECG was recorded occurred in between the period of ST elevation — and the period of ST depression with the T wave inversion that is commonly seen with reperfusion of the occluded vessel — then the ECG may show pseudo-normalization, with no more than minimal ST-T wave abnormalities (consistent with the ECG picture seen in Figure-2 of today's case).
• Subtle signs in Figure-2 of reperfusion in today's case include: i) Terminal T wave inversion in leads III, aVF; — ii) Terminal T wave positivity in lead aVL; — and, iii) The flat, non-elevated ST segments in leads V2,V3 — with somewhat peaked and upright T waves in these leads.
• Today's patient had no symptoms prior to his sudden arrest. This older man was unaware that he had longstanding underlying coronary disease. The hint on his ECG to underlying multivessel disease is the presence of ST-T wave flattening in so many leads (ie, in leads I,II; V5,V6 — in addition to the abnormal findings in the infero-postero lead distribution). Presumably — this patient's arrest was the result of acute infero-postero OMI, that then promptly reperfused.

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Acknowledgment: My appreciation to Michael Moore (from Kansas, USA) for this case and this tracing.

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ADDENDUM (9/20/2025):

• For More Material — regarding the ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion). NOTE: The timed-contents of this Podcast #2 facilitate quickly finding whatever key concepts you wish to review.
• Check out near the top of the "My ECG Videos" page, those videos from my MedAll ECG Talks that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• 
  
• KEY Clinical Reality: Many of the acute coronary occlusions that we see never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

                                                                                                                        

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?
• 
  
• 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.
• 
  
• 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.
• 
  
• 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).