Why is this patient in shock?

This ECG was handed to one of my partners who was working in triage.  

The conventional algorithm stated "Nonspecific ST-T wave abnormalities."

What do you think?

My partner immediately diagnosed inferior OMI.  (Do you see: the subtle STE in III and aVF?  The terminal QRS distortion in aVF?  The ST depression in aVL?  The ST depression in V2-V4 of posterior OMI?  There is terminal T-wave inversion in III with terminal upright T-wave in aVL -- This strongly suggests reperfusion IF the patient's symptoms have subsided.  But they had not.)

He went to find the patient: Middle-aged man was working this afternoon when he developed sudden onset lightheadedness with diaphoresis, nausea, and had multiple episodes of emesis. The symptoms persisted for several hours, so his wife convinced him to come to the hospital.   He has no history of similar symptoms. 

This ECG is diagnostic regardless of whether the patient has chest pain or not.

He specifically denies chest pain or trouble breathing.  This was confirmed over and over with the patient.

All of my partners are good at recognizing OMI on the ECG.

He sent it to the Queen of Hearts:

 

And here is the Explainability:

Register for access to Queen of Hearts here

The patient was taken to the critical care area.  His systolic blood pressure was 80 mmHg and his lactate was 6 mEq/L.   The patient is in shock.

Why was he in shock?   ---The answer is on the ECG.

If you are not sure, maybe you will understand after seeing this ECG recorded 17 minutes later:

What do you think?

There is much more obvious STE in V1 that, especially in the context of inferior OMI, is diagnostic of right ventricular (RV) OMI (RV MI).   This implies a proximal RCA occlusion, proximal to the RV marginal branch which supplies the RV.  Not all proximal RCA OMI cause RV MI physiology (decreased RV cardiac output) and RV ECG ischemia: often the RV gets collateral circulation from the LAD which protects it from events like this.

He was taken to the cath lab and a total occlusion of the proximal RCA was found.

Angiographic findings:

1. Left main: no stenosis.

2. LAD: 40-50% ostial stenosis, otherwise luminal irregularities.

3. LCX: Large, nondominant. Supplies a large OM. Luminal irregularities,

but no stenosis.

4. RCA: proximal thrombotic or embolic occlusion with TIMI 0 flow. It

supplies an RPDA (inferior OMI) and RPLA (posterior OMI) without stenoses.

A post PCI ECG was recorded:

What do you think?

This was diagnosed as "uncertain rhythm with LBBB," but there are no P-waves, so I think it is post reperfusion accelerated idioventricular rhythm (AIVR), which because it initiates in the ventricle, has LBBB morphology.  

The OMI is still evident.  

In AIVR like this, you  can still use the Smith Modified Sgarbossa Criteria, and since there is proportionally excessively discordant STE in lead III (STE at the J-point divided by S-wave = 2.5/5.5 = 0.45; a value ＞25% in just one lead is diagnostic and＞20% all but diagnostic.)

Another similar ECG was recorded an hour later:

Also AIVR with persistent ischemia

--Normal left ventricular cavity size, wall thickness and systolic function; estimated ejection fraction is 55-60%.

--Regional wall motion abnormality in the mid to basal inferior segments.

--Moderately dilated right ventricle with moderately reduced right ventricular systolic function.

The estimated pulmonary artery systolic pressure is 17 mmHg + RA pressure.

Based on the appearance of the IVC, the RA pressure is significantly elevated. (Smith: this is because of decreased RV output, so it backs up into the RA)

So this too supports RV infarction.

Right Ventricular infarction (RV OMI)

RV infarction has very high mortality if not immediately reperfused, but the RV recovers very well if reperfused.  

Treatment of RV infarction prior to reperfusion: possibly some gentle hydration (see below) and norepinephrine to keep systolic BP high.  Unlike the LV which is perfused during diastole (because of very high chamber pressure during systole), the low pressure RV is perfused best in systole.  Keeping the systolic BP normal is very important for mitigating RV ischemia.  Even with an occluded RV marginal branch, collateral circulation can save the RV if the systolic pressure is high enough.

Gentle hydration: Caution to avoid excessive volume administration; overdistension of the ischemically dilated RV can lead to pressure on the septum and decreased LV output, similar to PE.  It can also result in the descending limb of the Starling curve, resulting in further depression of RV pump performance.  

The best single lead for RV infarction on the normal 12-lead is V1.  If there is not STD in V2, V1 has moderate sensitivity for proximal RCA occlusion.  But if there is any STD in V2, there is posterior OMI which "pulls down" the ST in V1 also, hiding the RV infarction.

We proved this: In inferior myocardial infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction

Such attenuation of the sensitivity in the presence of posterior OMI is also true for V4R (right sided leads) (Kosuge et al.)

More articles on danger of RV OMI:

Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction.  New Engl Journal.  You can support the diagnosis of RV MI using Right Ventricular Leads, particularly V4R, but Kosuge (above) showed that even V4R ST segment can be pulled down by the ST depression of posterior MI, leading to a false negative.

Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction.  JACC

Right ventricular dysfunction and risk of heart failure and mortality after myocardial infarction.  JACC

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MY Comment, by KEN GRAUER, MD (5/10/2024):

===================================

The "beauty" of today's case — is that the ECGs all tell a story, even before the history of this patient is known.

• I focus my comments on this story — in which I'll add some thoughts to Dr. Smith's excellent discussion. For clarity — I've labeled the 4 serial tracings in today's case.

==================================

Looking at the Initial ECG:

Even before delving into the KEY points that enabled Dr. Smith's partner to immediately diagnose the acute OMI ...

• Did YOU Notice the rhythm in ECG #1?
• 
  
•      HINT: The rhythm in ECG #1 is not sinus!

ANSWER:

• For the rhythm to be sinus — the P wave should be upright in lead II. The only 2 exceptions to this statement are dextrocardia and lead misplacement.
• The YELLOW arrows in lead II of ECG #1 show that no P wave is present in this lead. Instead — a small, upright P wave is seen in leads I and aVL (BLUE arrows in these leads). There is no lead reversal. This pattern, in which no definite P wave is seen in lead II — but an upright P wave is seen in leads I and aVL — is consistent with a low atrial rhythm.
• 
  
• KEY Point: A low atrial rhythm is most often a common normal variant — although in today's case, it may convey similar implications as would a junctional escape rhythm. That said, while clinical management of today's patient is not altered by not having a sinus rhythm — You can simplify life (and never overlook sinus rhythm again) by routinely spending the first 2-3 seconds of your inspection of every ECG you encounter by scanning the long lead II rhythm strip with your educated "eye" to make sure that each QRS is preceded by an upright P wave.
• NOTE: ECG #2 was obtained 17 minutes later. RED arrows in ECG #2 show the return of sinus rhythm (RED arrows in the long lead II of ECG #2). Beats #9 and 10 in ECG #2 occur early, and are probably PACs (with beat #10 probably being conducted with aberration).

Figure-1: I've labeled the first 2 ECGs in today's case.

Recognizing Today's OMI within Seconds!

With experience — Recognition of today's OMI should be accomplished in less than 20 seconds (even without knowing the history).

• Once we've established that the rhythm in ECG #1 is supraventricular (ie, a low atrial rhythm, as noted above) — my "eye" was immediately drawn to lead III (within the RED rectangle), which shows a large Q wave, ST segment coving with subtle-but-definite ST elevation, and terminal T wave inversion.
• Confirmation that the subtle ST segment elevation in lead III is real and acute — is forthcoming within seconds from the 2 frontal plane leads enclosed within the BLUE rectangles: i) In lead aVF — the Q wave and ST segment straightening with slight ST elevation conveys support from this neighboring lead to lead III; and, ii) In high-lateral lead aVL — we see the precise mirror-image opposite ST-T wave picture as we see in lead III. This reciprocal change is also seen in the other high-lateral limb lead ( = lead I) — and verifies the diagnosis of acute inferior OMI until proven otherwise.
• 
  
• We've emphasized on multiple occasions that the ST-T wave in leads V2 and V3 should normally show slight, gentle-upsloping ST segment elevation. Instead, lead V2 in ECG #1 (within the RED rectangle) jumps out as manifesting a flat (straight) ST segment without any ST elevation. Given that we've already established the diagnosis of acute inferior OMI — the ST-T wave appearance within this RED rectangle establishes the diagnosis of associated posterior OMI (which is further supported by abrupt transition to a predominant R wave already by lead V2).
• Within the BLUE rectangle in neighboring lead V3 — we see ST segment flattening and slight-but-real ST depression — thus providing further evidence of acute infero-postero OMI.
• NOTE: The time it should take for an "educated eye" to appreciate the above ECG findings within the 2 RED and 3 BLUE rectangles should be less than 20 seconds.

What about Lead V1 in the Initial ECG?

Acute posterior OMI produces maximal ST depression in leads V2, V3 and/or V4. Although less marked — posterior OMI typically also produces ST straightening with some depression in lead V1. Posterior OMI should not produce ST elevation or a hyperacute T wave in lead V1 — unless there is associated RV MI.

• KEY Point: As soon as the acute infero-postero OMI was recognized in ECG #1 — our "eye" should be drawn to the disproportionately tall and "fat" T wave in lead V1 of this tracing (within the PURPLE rectangle). As per Dr. Smith — the clinical importance of appreciating that the tiny QRS complex in lead V1 should not display a disproportionate hypervoluminous T wave — is that this finding is diagnostic of acute RV MI (thereby explaining this patient's hypotension). In addition, this finding localizes the "culprit" artery to the proximal RCA.

Comparison of ECG #1 and ECG #2:

With acute posterior OMI + RV involvement — there is interplay between right-sided ST elevation (from the RV MI) — and anterior ST depression (from the posterior OMI).

• In ECG #1 — ST segment flattening with slight depression from posterior OMI was most marked in leads V2 and V3.
• 17 minutes later with the recording of ECG #2 — we see marked increase in the ST elevation from the RV MI in leads V1,V2 — such that lead V2 no longer shows ST-T wave changes of posterior OMI (within the PURPLE rectangles in ECG #2). In contrast — the limb leads in ECG #2 show no significant serial change.

==================================

What about the Rhythm after PCI?

I found the post-PCI rhythms in ECG #3 and ECG #4 to be interesting, challenging — and clinically informative.

• I completely agree with Dr. Smith — that the "theme" of these post-PCI rhythms is the development of variations of AIVR (Accelerated IdioVentricular Rhythm) — which given the timing of this rhythm, suggests this is a reperfusion arrhythmia (that is often associated with successful reperfusion from PCI).
• AIVR is most often a transient occurrence in the post-PCI setting. Although the "atrial kick" is lost — most patientts will be hemodynamically stable (from the successful PCI), in which case no intervention is needed!

Figure-2: I've labeled the 3rd and 4th ECGs in today's case.

ECG #3 is Challenging!

The difficulties I had interpreting the first post-PCI rhythm ( = ECG #3) included: i) Finding P waves; and, ii) Determining why there were so many different QRS morphologies.

• I did not think any P waves were present in ECG #3 for the first 10 beats in the long lead II rhythm strip. I dropped a vertical RED line from the onset of the very wide QRS in lead I. This told me that the initial slurring and notching in lead II did not represent atrial activity — but instead formed the inital part of the QRS complex in this lead.
• Despite the resemblance to LBBB morphology in the first 10 beats (ie, with an all-upright R wave in lateral leads I and aVL — and a predominantly negative QRS in anterior leads V1,V2,V3) — the lack of atrial activity overwhelmingly favored a ventricular rhythm (rather than a junctional rhythm with LBBB) as the cause for QRS widening.
• 
  
• KEY Point: AIVR with LBBB-like morphology suggests that this ventricular rhythm is arising from the right ventricle — which is consistent with the acute RV MI producing shock in today's case.
• 
  
• Beats #12 and 13 — are sinus conducted (RED arrows highlighting definite sinus P waves in front of beats #12 and 13).
• Working backward — I thought the RED arrow in front of beat #11 was also a sinus P wave, albeit with a shorter PR interval than that seen before beats #12 and 13.
• The QRS complex of beat #11 is clearly wider than the QRS of sinus beats #12 and 13 — but not as wide as the 10 QRS complexes that preceed beat #11 (This is perhaps easier to appreciate by looking at the simultaneously-recorded beats in the 12-lead tracing above the long lead II rhythm strip). Therefore — beat #11 is a fusion beat! (a determination that further supports our deduction that beats #1-thru-10 are ventricular in etiology = AIVR).
• 
  
• The confusing part to me in ECG #3 — was the changing QRS morphology for beats #1-thru-10 in the long lead II rhythm strip. For clarity — I labeled the wide, equiphasic complexes with an "X" ( = beats #1-thru-7; #9) — and the wide predominantly negative complexes with a "Y" ( = beats #8 and 10).
• Whereas the R-R interval for complexes "X" were equal to each other — the 2 "Y" complexes were preceded by a slightly shorter R-R interval. 
• 
  
• MY THEORY: I suspect there are 2 ventricular sites, each producing their own version of AIVR. In support of my theory — Note that ~1 hour later, ECG #4 now shows all beats in the long lead II of this 2nd post-PCI tracing with the same QRS morphology — that is consistent with the predominantly negative morphology of complex "Y" (and with a slightly faster AIVR rate than was seen for AIVR by the "X" complexes in ECG #3). 
• The rate of AIVR with the "X" complexes is ~75/minute (an R-R interval = 4 large boxes).
• The rate of AIVR with the "Y" complexes is 85-90/minute (an R-R interval = 3.4 large boxes — and similar to the shorter coupling interval for the 2 "Y" complex beats in ECG #3).
• It is because the rate of AIVR with the "Y" complexes is slightly faster than the rate of the "X" complexes — that we see dominance of the "Y" AIVR in ECG #4.

Final Point: As per Dr. Smith — Despite the ventricular rhythm in these post-PCI tracings — We still see evidence of the OMI!

• While clearly more difficult to assess ST-T wave morphology when confronted with 2 different AIVR morphologies — the coved and markedly elevated ST segment in lead III of ECG #3 and ECG #4 simply should not be there!
• In the chest leads — Note the dramatic difference in the shape of the coved and markedly elevated ST segment in lead V1 of these 2 post-PCI tracings — compared to the upward concavity and much less elevated ST segments in lead V2 and V3. Isn't this similar to the "interplay" we saw in ECGs #1 and #2 between lead V1 ST elevation from RV MI — and lack of ST elevation in leads V2,V3 from the posterior OMI? 

A young man with palpitations.

A 30-something presented with chest pain, palpitations, and SOB.  He has had similar symptoms for 4 years, but has never been evaluated.

Here is his presenting ECG, which was sent to me real time, along with the 2nd ECG below:

Regular Narrow Fast without P-waves.  PSVT.  

It is very difficult to tell if this is:

 1) AVNRT or 

2) orthodromic AVRT 

(Orthodromic AVRT = WPW with orthograde conduction down the AV node and retrograde up an accessory pathway)

See Ken Grauer's discussion below in differentiating AVNRT from orthodromic AVRT.

Shortly after arrival, the patient spontaneously converted to this rhythm (also sent to me, along with the first):

What do you think?

The two ECGs above were texted to me with the text: "Young Guy came in in SVT but now in and out of irregular wide complex tachycardia. -- not sure if polymorphic VT vs. a fib with WPW."

My response: "Definitely not polymorphic VT.  Definitely atrial fibrillation.  Probably WPW but is very slow for atrial fib withWPW.  I would just cardiovert electrically."

Smith: the rhythm is irregularly irregular without P-waves.  There are delta waves and polymorphic QRS (but NOT polymorphic VT!).  So this looks like WPW with Atrial fibrillation.  What is unusual is that the rate is not REALLY fast, as you expect when there is atrial fib with an accessory pathway.  The shortest R-R inteval that I see is between the 6th and 7th beat and is 280 ms, which is not dangerously short.

Nevertheless, you NEVER want to give an AV nodal blocker to Atrial fib with WPW:

1. The reason to avoid AV blockers in WPW is that, in addition to blocking AVN, they actually enhance conduction via AP by shortening refractory period, which can produce VF.

2. Adenosine is considered safe for termination of AVRT in WPW, but the pro-arrhythmic effects of adenosine can rarely cause AF, so do not give AVN blocker to WPW unless you have defib pads placed.

The essential features of A Fib WPW are:

1. Irregularly irregular

2. Polymorphic

3. Wide

4. Some very short R-R intervals

Never give an AV nodal blocker to Atrial Fibrillation with WPW; it can result in ventricular fibrillation.  This means NO calcium channel blocker, beta blocker, adenosine, or digoxin.

Cardioversion can be done pharmacologically (usually procainamide), but why would you want to do that?  Only if you are unable to perform procedural sedation or if the patient refuses.

So electrical cardioversion was done (using etomidate sedation.  I prefer low dose propofol, just enough for amnesia, but not enough to result in serious hypotension).

Here is the post cardioversion ECG:

Definite pre-excitation (delta waves due to accessory pathway, "bypass tract").  Pre-excitation results in a short PR interval.

Electrophysiology note:  "In the context of pre-excited atrial fibrillation, we would recommend proceeding with mapping and ablation of accessory pathway (particularly given high risk features including his shortest pre-excited R-R interval is < 250 ms). It does appear likely that his pathway may anteroseptal, which does increase risk of damage to AV node."

More explanation from electrophysiology:

"ECG only records 10-seconds worth of data, therefore long rhythm strip is essential to make sure ample data is available. Fortunately in the stabilization room, they had recorded a long rhythm strip (Smith: not seen by me and not shown) during atrial fibrillation and some R-R intervals were very short approaching 250 msec."

He was taken for immediate ablation that day in the EP lab, but (explanation from electrophysiology) this ECG was recorded:

No pre-excitation, therefore, no ablation attempted

Electrophysiolgy explains: "These accessory pathways can be very superficial fibers and during the first procedure, it got mechanically “bumped” before turning on ablation and therefore NO ABLATION WAS PERFORMED in absence of preexcitation, given high risk location. Despite of waiting for an hour pathway conduction did not come back (but they do invariably come back after such mechanical bump). Therefore repeat procedure was performed with Cryo-ablation after the accessory pathway conduction had returned."

The next morning, this ECG was recorded:

What do you think?

The delta waves are back.  There is recurrent pre-excitation.

The Ablation was done.

He was taken for another ablation and this ECG was recorded:

Normalized.

He was discharged.

===================================

MY Comment, by KEN GRAUER, MD (5/8/2024):

===================================

I found today's case extremely interesting regarding a number of points about reentry SVT rhythms, with or without AP (Accessory Pathway) participation. I'll add the following points to Dr. Smith's excellent discussion.

• For clarity in Figure-1 — I've labeled the first 2 tracings in today's case.

Figure-1: I've labeled the first 2 tracings in today's case.

Can We Distinguish between AVNRT vs Orthodromic AVRT?

As per Dr. Smith — the principal differential diagnosis between the regular SVT reentry rhythms, is between AVNRT (AtrioVentricular Nodal Reentry Tachycardia — in which the reentry circuit is contained within the AV Node) — vs orthodromic AVRT (AtrioVentricular Reciprocating Tachycardia — in which the reentry circular first travels down the normal AV nodal pathway, and then conducts back to the atria over an Accessory Pathway).

• As I illustrated in My Comment at the bottom of the page in the March 6, 2020 post of Dr. Smith's ECG Blog — while not infallible, the finding of a very short RP' interval suggests the mechanism of the reentry SVT rhythm is AVNRT, in which the impulse travels back to the atria over the "fast" AV nodal pathway. This is because when the reentry circuit is entirely contained within the AV node — it takes minimal time to return to the atria.
• 
  
• In contrast — the finding of a moderately long RP' interval suggests that the mechanism of the reentry SVT rhythm is orthodromic AVRT, in which a "concealed" AP may be participating in the reentry pathway. Because the AP lies outside of the AV node — the time to circulate around the reentry pathway and conduct back to the atria (retrograde) is longer than when the entire reentry circuit is contained within the AV node.

As I illustrate in the March 6, 2020 post — retrograde conduction can often be seen during a reentry SVT rhythm! 

• IF you look for retrograde P wave conduction during a regular SVT rhythm — You'll begin to find it much more often than you might have imagined! On occasion — recognizing retrograde conduction may provide a KEY clue to the mechanism of a tachycardia.
• To LOOK for retrograde P waves: — i) Look in the inferior leads for a small negative notch that occurs at the very end of the QRS, or fairly soon thereafter; or, ii) Look for a small positive notch in lead aVR and/or lead aVL and/or lead V1; and, iii) Confirm that the notching you identified during the regular SVT rhythm truly reflects retrograde atrial activity (rather than being a part of the QRS or the result of artifact) — by noting that this notching is no longer present after conversion to sinus rhythm. (My Figure-2 in the March 6, 2020 post illustrates this confirmation).

Regarding Today's CASE: 

Unfortunately — I found the initial ECG in today's case equivocal with regard to my search for retrograde P waves:

• As shown in Figure-1 — the rhythm in today's initial ECG is a regular SVT (ie, Narrow-complex tachycardia) at ~190/minute, without sinus P waves.
• I initially thought the small negative notch at the very end of the QRS in lead II — and the small positive notch at the very end of the QRS in lead V1 — both represented retrograde P waves with a very short RP' interval (within the RED circles in these leads). If so — this would strongly suggest AVNRT of the "slow-fast" type (which is by far the most common form of AVNRT) as the mechanism of today's initial rhythm.
• That said — I thought the more-pointed-than-expected negative deflections in leads III and aVF — and the pointed tip of the upright T wave in lead aVL — might represent retrograde P waves, in which case the RP' interval would instead be moderately long (within the BLUE circles in these leads).
• 
  
• BOTTOM Line: Given conflicting findings regarding my search for potential retrograde atrial activity — I could not distinguish between AVNRT vs orthodromic AVRT on the basis of ECG #1 alone. Sometimes you can distinguish between AVNRT vs orthodromic AVRT — but not in today's initial tracing.

WHY CARE if the Mechanism is AVNRT vs Orthodromic AVRT?

While emphasizing that overall initial management of AVNRT and orthodromic AVRT are similar — there are some differences to be aware of that may have a role in treatment decision-making.

• WPW is recognized on ECG by the presence of 3 Findings: i) A short PR interval; ii) Delta waves in a number of leads; and, iii) QRS widening. 
• It's important to appreciate that patients with an AP may not always manifest these 3 findings that are characteristic of complete or predominant preexcitation. Instead — Patients with an AP may at times manifest partial or even no preexcitation (with the relative percentage of impulses traveling over the AP vs the normal AV nodal pathway being highly variable). IF the relative amount of preexcitation at any given time is minimal — then delta waves, PR interval shortening, and QRS widening may be barely (if at all) detectable.
• 
  
• APs may conduct forward (anterograde) and/or backward (retrograde). While APs are usually capable of conducting in both directions — forward or backward conduction may not be possible in some patients. This leads to the concept of a "concealed" AP — in which only retrograde conduction is possible over the AP. 
• Up to 15% of patients with a regular reentry SVT rhythm who are referred for catheter ablation may have a "concealed" AP, in which delta waves are never seen because forward (anterograde) conduction over their AP is not possible (Pappone and Santinelli — ESC: July, 2018). 
• 
  
• KEY Point: Synthesizing the concepts in the above bullets means that a significant percentage of the time when treating a new patient with a regular reentry SVT rhythm, but without clear sign of atrial activity — that despite never seeing delta waves, the patient may have a concealed AP (ie, that rather than AVNRT — the regular SVT may be orthodromic AVRT).
• The "good" news — is that initial treatment of such patients with a regular reentry SVT rhythm is the same (ie, Adenosine, Verapamil/Diltiazem, ß-Blocker) — because AV nodal blocking agents will successfully interrupt the reentry circuit in both AVNRT and orthodromic AVRT.
• The "less good" news — is that in up to 1/3 of patients with orthodromic AVRT — spontaneous AFib may develop at some point — presumably predisposed by "triggering" of AFib by AP-mediated reciprocating tachycardia (Ma et al — Exp Clin Cardiol 9(3): 196, 2004 — and Silverman et al. in J Investig Med: Jan, 2018). And, as per Dr. Smith — use of AV nodal blocking agents (ie, Adenosine, Verapamil/Diltiazem, ß-Blocker) are contraindicated in patients with AFib and WPW — because blockade of the normal AV nodal pathway may result in further acceleration of anterograde conduction over the AP, which may result in deterioration of the rhythm to VFib.
• The other "less good" news — is at least the theoretical risk that using an AV nodal blocking agent to treat a regular SVT might precipitate AFib if the patient had a "concealed" AP (ie, if instead of AVNRT — the rhythm was orthodromic AVRT). Fortunately — precipitation of AFib by giving an AV nodal blocking agent to a reentry SVT that turns out to be orthodromic AVRT is rare (and consensus remains to treat reentry SVT rhythms with AV nodal blocking agents).

What About the Rhythm in ECG #2?

I was intrigued by the spontaneous development of the rhythm in ECG #2 — just a short while after ECG #1 without administration of any medication!

• As per Dr. Smith — the rhythm in ECG #2 is irregularly irregular without P waves. While I hesitate in diagnosing delta waves in the absence of sinus P waves (because LBBB conduction may sometimes manifest initial QRS slurring) — the additional features of changing QRS morphology — and the finding of some very short R-R intervals alternating with some unexpectedly longer R-R intervals (ie, between beats #5-6) in this younger adult — suggested WPW with AFib (although definitive diagnosis of WPW was not made until the 3rd ECG was obtained, which showed return of sinus rhythm with short PR, delta waves and a similar-looking wide QRS).
• 
  
• PEARL #1: As we have highlighted in previous posts (See the March 11, 2020 post) — WPW can be immediately diagnosed when you see AFib with a wide QRS and an extremely rapid ventricular response (that at times attains a rate of between ~220-250/minute!).
• Unlike PMVT (PolyMorphic Ventricular Tachycardia) in which QRS morphology usually changes dramatically from one beat to the next — the changing QRS morphology typically seen in WPW with AFib tends to be more subtle (due to modest variation in the relative percentage of preexcitation).
• 
  
• PEARL #2: Not all patients with WPW are at high risk of developing potentially life-threatening tachyarrhythmias. The risk of developing VFib during AFib in a patient with WPW is greatly increased when the SPERRI (Shortest Pre-Excited R-R Interval) measures below 220-250 msec. This corresponds to a shortest R-R interval that is barely more than one large box in duration. We do not see this in ECG #2 — as the shortest R-R interval is 7 little boxes in duration ( = 280 msec. — as I've labeled between beats #6-7).
• How fast the ventricular response will be in association with AFib in a patient with WPW will depend on anterograde conduction properties of the AP. The overall rate of AFib in ECG #2 is ~150/minute (ie, There are 25 beats in the 10 second long lead II rhythm strip ==> 25 X6 = 150/minute). Since the ventricular response in ECG #2 is comparable to the rate range for any patient who develops new-onset AFib — definitive diagnosis of WPW was not made in today's case until the 3rd ECG was obtained.

FINAL Points in Today's CASE:  

• Even though the SPERRI value during AFib in today's case was not below 250 msec. — catheter ablation was indicated because this younger man was very symptomatic with not just one, but two WPW-related tachyarrhythmias (orthodromic AVRT and AFib).
• It is possible to have more than a single AP! (Goyal et al — StatPearls: July, 2023). While multiple APs in a given patient is not common — I initially wondered if that might be a possibility in today's patient, given the need for repeat ablation the next day. That said — the fact that morphology of the wide QRS was virtually identical in sinus rhythm after each ablation suggested this patient did not have more than a single AP (and in Dr. Smith’s discussion, under Electrophysiology Explains — we learn the reason the EP cardiology repeated the procedure the next day).
• Finally — Did you notice the very tall T waves in multiple leads after each ablation? This finding is typical for a post-ablation memory T wave pattern — which is often considered evidence of a successful ablation (Silverman et al — J Investig Med: Jan, 2018).