An Elderly Male with "Indigestion"

This case was contributed by Brooks Walsh, an ECG enthusiast who has contributed frequently, and edited by Smith

Case

An elderly male called EMS after he developed “indigestion.” The paramedic recorded  a series of ECGs; the initial ECG is representative here:

Computer read: “Normal ECG”

What do you think?

Algorithm is either Glasgow or Marquette 12 SL

This ECG is diagnostic of LAD occlusion because of terminal QRS distortion in lead V3.  See explanation below.

Smith sent this to the Queen of Hearts years later.  Here is the result:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

Two doses of nitroglycerin reduced the patient’s symptoms during transport. He was almost asymptomatic when he arrived in the ED. The paramedic interpreted this as a STEMI.

An ECG was obtained in the ED:

There is ST elevation in V2-V4.  Is it normal ST elevation (early repol?) or LAD occlusion?

The computer read this as “Early repolarization, otherwise normal ECG.”

What to you think?

Comment: the T waves in V2 and V3 are massive compared with the R waves, nearly diagnostic of hyperacute T waves.

Can you employ the Subtle Anterior STEMI calculator?

The Subtle STEMI calculation is used to differentiate a subtle anterior acute coronary occlusion from early repolarization (ER).  ER is unlikely, given the age, but there is STE in both the anterior and lateral leads, and the J-points are either notched or slurred in many of those leads. Also, the STE is concave-upwards, further supporting ER as a “STEMI-mimic” in this case, though in approximately 40% of acute LAD occlusion, upward concavity is present in all of leads V2-V6.

Use of calculator (formula) on the EMS 12-lead: The EMS 12-lead had QTc 401 ms, with STE60V3 of 2.0 mm, and RA in V4 of 18 mm, resulting in a value of 20.2.   (Even making STE60V3 = 3.0 mm, and RA in V4 15 mm only moves the result to 22.4.)

Thus, using the Subtle Anterior STEMI calculator, the EMS ECG is strongly predicted to be ER, while that in the ED is borderline, and changed markedly depending on the baseline used in V3.

How about using the calculator on the ED 12-lead?

The ED ECG is more equivocal.
The QTc 439 ms, with STE60V3 of 2.0 mm, and RA in V4 of 16 mm, resulting in a value of 23.1   However, even small changes in RV4, and especially in V3STE60, tilt the result on ether side of 23.4!

However: one should not use the calculator in this patient!

The patient has overt evidence of anterior acute coronary occlusion, and so the formula might provide false-negative results.

In this case, there is "terminal QRS distortion," which in our study was a sign of "obvious" MI and thus an exclusion.  We have studied this (will be published) and found that it does not occur in early repol.

Terminal QRS distortion was defined as the absence of both a J-wave and an S-wave in either of V2 or V3.   In this case (see image below), there is virtually no S-wave in lead V3, nor is there a J-wave. The EMS 12-lead shows that the S wave (blue arrow) does not descend below baseline. The ED 12-lead, obtained in the context of improving symptoms, shows an S wave (red arrow) that just barely dips below the baseline.

This is terminal QRS distortion, and it has been discussed before here and here. 

An ECG was found from 2 months prior: 

There is no ST Elevation, normal R- and T-waves, normal S-waves in V2 and V3.  

The old ECG served as confirmation, but was not necessary to activate the cath lab. 

Pretest Probability
In a recent case with marked ST elevation, I argued that the pretest probability was low and one should therefore investigate more before activating the cath lab.  In that case, the patient did not have chest pain but was 36 years old.  This patient does not have chest pain but is elderly and that increases the pretest probability by a huge amount.  Furthermore, because of terminal QRS distortin, this ECG cannot be early repolarization, whereas that previous ECG with approximately 5 mm of ST elevation was indeed due to early repol. 

Additionally, a bedside echo was performed while waiting for the cath lab team to arrive, and it showed characteristic hypokinesis of the LAD distribution (apex and distal septum) on the apical 4-chamber view:




Outcome:

The cath lab was activated and a 99% LAD obstruction was found and opened and stented

It is easy to be led astray by the computer....

I saw this ECG lying around:

The computer called this "normal" with no other comment.
what do you think?

It is amazing that the computer called this normal, as there are clearly abnormal QRST's in beats 3, 4, and 5.

What are they?

I looked the case up on the McKesson system because one can highlight the run of abnormal beats in lead II across the bottom (see red box) and then one is able to see these abnormal beats in all 12 leads:

Now what do you think?

One could easily be fooled into thinking these are hyperacute T waves.

But the queen was not fooled by this into thinking it is OMI.  

The PM Cardio app does diagnose WPW.  The app called it Left anterior fascicular block.   It clearly recognized it as not normal.  

 





This is clearly WPW.  Among these beats there is clearly a short PR interval and delta waves.  The QRS is very abnormal due to the pre-excitation.

I looked at the patient presentation and it was unrelated (no tachycardia, no palpitations, etc.).  The ECG findings were not recognized by the emergency physicians.   The patient had been admitted to the hospital and no one had noticed.  No final ECG interpretation had been placed in the record before the patient was discharged, and he was discharged without recognition of the diagnosis of WPW.

On record review, the patient had been seen in the ED in previous years for palpitations and the ECGs were actually normal, with no evidence of WPW.  He had been diagnosed with anxiety (which he may indeed have, but it is common for patients with later-diagnosed SVT to be diagnosed with anxiety or panic attack).  No doubt he had been having runs of tachycardia due to WPW.

I am certain that when the final read was placed by the interpreting physician that it would have been correct.  In this instance, I put that final interpretation into the system, added the diagnosis, and notified the primary care physician.

Learning Point:

You cannot trust the computer interpretation!  You must carefully look at every tracing yourself.  Use the computer's interpretation, but do not rely on it.

I suggest:

1. Read it yourself while hiding the computer interpretation
2. Then read the computer interpretation (it may see things that you did not)
3. Then look again

Dr. Ken Grauer has an excellent post on computer interpretations:
http://ecg-interpretation.blogspot.com/2016/05/ecg-blog-126-computerized-ecg.html

Also, see Ken's insightful comments on this case below:

GREAT case Steve! Thanks for citing my ECG Blog #126, in which I review a practical approach for optimizing benefits of computerized interpretations. I am equally amazed as you in this case that the computer did not pick up on at least some abnormality … but the key for anyone who is less than a true ECG expert lies in your 1st suggestion = HIDE the computerized interpretation BEFORE you look at what the computer said. Had that been done, the WPW that is obvious on this tracing would not have been missed.

Often overlooked is the concept that patients who have an accessory pathway may conduct normally at some times and abnormally at other times. And sometimes, they may split the relative amount of conduction passing over normal and accessory pathways even from beat-to-beat (known as a “Concertina effect). The “good news”, is that finding a Concertina effect suggests a relatively longer refractory period for the accessory pathway — and therefore a relatively lower risk of sudden death (http://casereports.bmj.com/content/2013/bcr-2013-009328.full ).

The interesting thing to me is how the 2nd beat in the long rhythm strip in your example would look relatively “normal” by itself. However, when compared to the 1st beat in the rhythm strip, we clearly see the difference. So there is FUSION between normal conduction (PQRST morphology of the 1st beat) — and purely conducted WPW beats ( = beats #3,4,5). Note how there once again is a different degree of fusion for the 6th beat in the long lead II rhythm strip. So we are alternating between normal and accessory-pathway conduction in this rhythm strip … Note also how differently delta waves appear in different leads. Delta waves are EASY to recognize in leads I and aVL (because they are positive). Delta waves are negative in leads III and aVF — and in lead II to we see a multiphasic almost isoelectric initial component to the delta wave. It is because of some fusion with normal conduction and this near isoelectric delta wave appearance that by themself, it would be difficult to identify WPW from beats that look like beat #2 and beat #6 in the long lead rhythm strip.

Anterior STEMI? Or Benign Early Repolarization?

This was posted a few years ago.  I'm highlighting it again, with comments from Ken Grauer below.

This was sent to me by Jason Winter, of Facebook Clinical Electrocardiology Page https://www.facebook.com/EKG.ECG/

This is a 36 yo m with h/o TBI and epilepsy.  He had a seizure this morning and rolled out of bed unable to get up.   There were no injuries and no chest pain and he appeared well.  He complained of 3 days of diarrhea and abdominal pain.  The medics recorded a prehospital ECG: 

The computerized QTc is 397 ms
Jason writes: "What's your thoughts Steve?"
Jason was very skeptical of STEMI.
What do you think?

Jason,

I agree.

V4 especially looks like early repolarization.  There is high R-wave voltage.

The formula for differentiating LAD occlusion from early repolarization requires ST elevation at 60 ms after the J-point (here 5 mm), computerized QTc, and R-wave amplitude.  Unfortunately, the R-wave is cut off on this ECG but it appears as if it would be at least 20 mm.  This results in a value of 22.883.  While one should be suspicious of any value greater than 22.0, this does not indicate LAD occlusion.

Note: In our study, we excluded from analysis cases with 5 mm of ST elevation because they would be "obvious," not subtle, anterior MI.  But this measurement was at the J-point, which on this ECG is 4 mm.  STE at 60 ms after the J-point is substantially higher than at the J-point. 

Pretest probability: Especially when there is no Chest pain, or there are very atypical symptoms, one should be very suspicious of the diagnosis of coronary occlusion unless the ECG is crystal clear.

More analysis: V4 has a high J-point, after which the ST segment is comparatively flat, without a correspondingly massive T-wave.  The T-wave is, in fact, small compared to the large R-wave.  This also argues against STEMI.

What was the outcome?

Outcome

"I later found out that this is a patient who regularly calls paramedics to c/o chest pains and he had fooled many of them. And the cath lab is alerted most of the time."

So this was the patient's baseline ECG.

Learning point

This is not to suggest that such an ECG should summarily be dismissed, but that in a patient with a low pretest probability and such an ECG may indeed have early repolarization, and further investigation might be undertaken before any cath lab activation.

Look for old ECGs
Do serial ECGs
Do echocardiography

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

MY Comment by KEN GRAUER, MD (10/1/2020):

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

From time to time — it's helpful to "resurface" prior cases that convey timeless important lessons. The diagnostic problem posed in today's repost from June 17, 2016 is a perfect example of this. 

• The ECG in this case was not indicative of acute LAD occlusion. Instead — it represented this patient's "baseline" tracing.

KEY POINTS from this CASE:

• The presenting history often provides invaluable clues to the likelihood of an acute cardiac event. (The patient is a 36yo man who was seen for a seizure. There was no chest pain. This is a "low prevalence" history for an acute cardiac event.).
• Always look for prior ECGs for comparison. (Previous ECGs in this case were very similar to the one we were asked to interpret).
• Check for old records. (Turns out that the patient regularly called EMS for complaints of chest pain that frequently led to cath lab activation.)

ACKNOWLEDGMENT:

When I first looked at the ECG in this case — I was concerned about potential LAD OMI. After all — there is ST elevation in virtually all chest leads, with ST segment straightening in leads V3 and V4 (with no less than 5 mm of J-point ST elevation in lead V3!). In addition — slight ST elevation in lead aVL and T wave inversion in each of the inferior leads looked consistent with reciprocal changes.

• BUT — This is a prehospital ECG!

For clarity — I have reproduced the ECG in this case in Figure-1, in which I've labeled with RED arrows an important finding seen in 4 KEY leads.

Figure-1: I've labeled today's ECG to show where QRS complexes are cut off.

My THOUGHTS on ECG #1: 

It’s important to recognize WHY I added the 4 RED arrows to Figure-1:

• There is a limit to the amount of voltage that prehospital ECGs in most EMS systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit. Careful scrutiny between the 4 RED arrows and the horizontal RED lines reveals the abrupt cutoff from this truncation. Therefore — We have NO idea as to how deep the S waves in leads V2,V3 are — nor how tall the R waves in leads V4,V5 are.
• 
  
• Among other examples of this phenomenon (in which prehospital ECGs give a false impression of the relative amount of anterior chest lead ST elevation) — is the case from the February 6, 2020 post in Dr. Smith's ECG Blog (Please see My Comment at the bottom of the page in that post).
• 
  
• In Figure-1 — I suspect that much of the reason for the seemingly marked ST elevation in lead V3 arises from LVH, with exceedingly deep S waves in leads V2 and V3.
• A cardiomyopathy with dilated chambers might also explain the RAA (tall, peaked P waves in the inferior leads) — and the ST-T wave depression in the inferior leads (ie, ST-T wave changes of LV "strain" may sometimes be seen in inferior leads in patients with marked LVH).
• 
  
• NOTE: The “easy solution” for resolving the problem of excessive QRS amplitude, with resultant truncation of complexes — is to record the ECG at HALF standardization. Unfortunately, this option might not be available for pre-hospital tracings (but it can be done once the patient arrives in the ED for their initial hospital tracing).

FINAL Thoughts on this Case:

Although LVH with extremely deep anterior S waves (in leads V2,V3) may explain the marked ST elevation in lead V3 of Figure-1 — the S wave is not deep in lead V4. In addition — there is ST segment straightening in both leads V3 and V4 — and, at least for the middle complex in lead V5, I thought the ST segment coving looked potentially worrisome.

• To Emphasize — If I was seeing this patient for the 1st time in the ED without any medical records or prior ECGs available for comparison — and — IF the history was of new-onset cardiac-sounding chest pain — I would not be able to rule out the possibility of an acute cardiac event on the basis of this single ECG alone. But knowing this information (as described above) — allows us to rapidly identify the ECG in Figure-1 as one more manifestation of this patient's baseline ECG. It's worth remembering that this ECG does not represent acute LAD occlusion!

  

Just as hyperacute T-waves can be reciprocal to T-wave inversion (last case),.....

Just as hyperacute T-waves can be reciprocal to T-wave inversion (last case),..... 
....T-wave inversion can be reciprocal to STEMI of opposite wall!

This case was sent by Arthur Lee.

Case:

A 50 yr old woman presented after a syncopal episode, with sweating and left arm numbness. There was no chest pain or SOB, at least none reported by Dr. Lee. Here is her presenting ECG:

Arthur asked: "How do we interpret the anterior T-wave inversion? Are they reperfusion T-waves of the anterior wall?"

What do you think?

Answer:

There is very abnormal T-wave inversion in aVL which is typical of subtle transmural/subepicardial (due to occlusion) ischemia to the inferior wall.  This is reciprocal T-wave inversion.  The high lateral wall is reciprocal to the inferior wall.

Similarly, the precordial T-wave inversions in V2-V4 are reciprocal to posterior wall transmural/subepicardial (due to occlusion) ischemia.

This ECG is typical of a very subtle and/or early inferoposterior MI.  It is incorrect dogma that posterior MI has upright T-waves.  That is wrong because the T-wave orientation depends on many factors, including the lead strength of the well perfused (normal) anterior wall (contributing an upright vector) and the state of the artery supplying the posterior wall.   If open, it will contribute an upright vector -- (posterior reperfusion T-waves); if closed, it will contribute a negative, inverted vector because it is 180 degrees opposite to an upright (hyperacute) vector towards the posterior wall.
This negative vector can overpower the upright vector produced by the anterior wall and result in inverted T-waves.

Thus, this is a subtle inferoposterior MI, and the T-wave in III should then be scrutinized for any hyperacute features.

Indeed, when you look at the T-wave in lead III, it has just as much amplitude (voltage) as the QRS in lead III.  This is not normal.  This supports inferoposterior MI as the diagnosis.

Given that this patient has no chest pain, one must be skeptical of such a diagnosis.  She does however have diaphoresis and arm numbness.



Fortunately, the symptoms resolved and the following ECG was recorded:

All inverted T-waves are now upright and the hyperacute T-wave in lead III has normalized.
This confirms the previous interpretation and is diagnostic of reperfusion.

Outcome:

She ruled in for MI by troponins and went for angiogram.  An 80% thrombotic RCA was stented.

How do you explain these inferior hyperacute T-waves?

Alberto Pinsino, a cardiology fellow from Milan, Italy, sent this case:

Dr. Smith,

I would be interested in knowing your opinion about this case..

The Case

A 59-year-old Asian woman with hypertension and hypercholesterolemia and no past history of CAD came to the ED of a major teaching hospital with waxing and waning chest pain worsened by minimal efforts which had been ongoing for 5 days.  

She had visited the same ED two days before for the same reason.  The EKG is not available but described by the on-call cardiologist as “non specific repolarization abnormalities.”  The troponin was negative and she was discharged on ibuprofen with a diagnosis of pericarditis.

My comment: you diagnose pericarditis at your (and your patient's) peril!  It is relatively rare and usually when the ECG diagnosis of pericarditis is made, it turns out, in retrospect, to have been MI and a misread ECG.  Remember that unstable angina still exists.

At presentation, this EKG was recorded: 

Alberto's interpretation: "Inverted biphasic T waves in V1-V4, inverted T waves in D1-aVL."
Smith comment: I agree, consistent with Wellens' syndrome of the anterolateral wall, due to proximal LAD ACS.

Bedside echo was normal. First troponin was 16 ng/L (0.016 ng/mL), second 22 ng/L, third 28 ng/L (so, just barely positive: cut-off at our institution is 13 ng/L).

In the telemetry ward, 18 hours later, the patient had chest pain and another EKG was taken as shown in image 2 

Alberto's interpretation:  "There are deeply inverted T waves with minimal ST depression in V2-V3 and D1-aVL, hyperacute T waves in the inferior leads, especially III and aVF, long QT. Looks like Wellens' Syndrome." 

The crux of Alberto's inquiry:  "Why are there "hyperacute T-waves" in inferior leads??"

Smith answer: The Wellens' syndrome has evolved as it normally does, with increasingly inverted T-waves in the affected anterolateral territory.   These large upright and fat T-waves in inferior leads, especially lead III, are NOT hyperacute inferior T-waves.  These T-waves are reciprocal to the large inverted T-waves in aVL (high lateral).  III and aVL are 150 degrees opposite each other.  When there is a large Wellens' inverted wave in aVL, added to the already upright inferior T-wave, there MUST be a large upright T-wave in lead III.

So this large upright T-wave in lead III is analogous to what I call posterior reperfusion T-waves: tall, wide, upright T-waves in lead V2 after reperfusion of the posterior wall.  They are reciprocal to what would be recorded from the posterior part of the heart (inverted Wellens' waves), and added to the upright anterior T-waves.

Question: How can you tell if a large upright wave is hyperacute or if it is reciprocal to an inverted wave?  

Answer: You can tell mostly based on the state of the patient.  If the patient is symptomatic (should usually be chest pain), then the large fat T-wave is hyperacute.  Serial ECGs should show evolution to STEMI in that lead.   If, on the other hand, the patients is now pain free, then the ischemia is in the territory of the inverted T-wave and that is a reperfusion T-wave.  The hyperacute T-wave is only a reciprocal view.

The remainder is the Case Continued.

During the night, she experienced other episodes of chest pain – image 3 is an EKG while on chest pain at time 22 hours – and was put on iv nitrates.

In the morning, another EKG was collected while pain free as shown in image 4, time 33 hours. 

Troponin at this time was 7 (negative) In the cath lab, patient had a tight LAD stenosis which was stented and noncritical stenosis on the ostium of PDA (right dominance) and LM.

Here is the angiogram:

EKGs 5 and 6 below show, respectively, EKG after cath lab (time 37 hours) and EKG collected the day after the procedure (inverted T waves still present but less deep, shorter T waves in the inferior leads). Patient was pain free after stenting.

She was discharged three days later, still pain free.

I would be interested in knowing your opinion about this case. I think it is clearly a Wellens syndrome, but I am really having a hard time to explain the hyperacute T waves – if they really are hyperacute - in the inferior leads.  

Kind regards,

Alberto Pinsino

Here is a comment from Ken Grauer:

Our thanks to Alberto Pinsino for submitting this case. GREAT explanation by Dr. Smith as to why the  ST-T wave changes seen in leads III and aVF are reciprocal to the deep T wave inversion elsewhere rather than primary hyperacute changes. I’d simply add that 2 additional clues why these ST-T wave changes in leads III and aVF are much more likely to reflect reciprocal changes rather than primary hyperacute T waves are: i) that lead II shows no more than minimal ST-T wave changes. With acute evolving inferior STEMI, we’d expect a similar ST-T wave appearance in lead II as in the other 2 inferior leads; and ii) With acute inferior STEMI, we often see accompanying anterior ST depression consistent with posterior involvement. But instead of the usual “shelf-like” ST depression that is most commonly seen with acute posterior MI in these anterior leads — there is deep, symmetric T wave inversion that is different than the typical morphology of a posterior stemi-equivalent pattern. On the other hand, this anterior deep T wave inversion is consistent with a Wellens pattern from a tight LAD lesion. Molto grazie to Drs. Pinion and Smith for posting this case!

Dyspnea, Right Bundle Branch block, and ST elevation

An elderly male called 911 for acute onset of shortness of breath and vomiting.  EMS found him with a heart rate as high as 180 and hypoxic with O2 saturations in the 80's.

A prehospital 12-lead was obtained:

There is atrial fibrillation (irregularly irregular, no P-waves) with a rapid ventricular response.
There is right bundle branch block (RBBB).
There is ST elevation in V2-V5.
Is this acute STEMI??

On arrival in the ED, the patient had this ECG recorded:

Atrial fibrillation with RVR.
ST Elevation in V2-V5.
Is this acute STEMI?

Note the well-formed Q-waves in the leads with ST elevation!  This suggests old MI.

Comment: Old MI with persistent ST elevation, otherwise known as "LV aneurysm" morphology, usually has QS-waves (deep S-wave without a subsequent R-wave).  But RBBB alters the sequence of ventricular activation such that the wave of depolarization ends by going to the right.  Thus, an R-wave which would otherwise be absent is present in right precordial leads.

Normally, RBBB has rSR'.  But with old infarction, the initial r-wave is obliterated and one is left with a QR.  This can occur in acute STEMI with RBBB, but should raise the suspicion for LV aneurysm.



Let's look at a second instructive case in which the patient alternated between RBBB and normal conduction:

Note classic anterior LV aneurysm morphology (QS-waves in V1-V3 with ST elevation).  There is ST elevation, but the T/QRS ratio is less than 0.36 in all of leads V1-V4, indicating that it is not acute STEMI.
I derived and validated this rule.

The patient with the above ECG presented twice with chest pain and RBBB, with this ECG:

There is ST elevation in V1-V4 without the deep QS-waves.
But there is RBBB.  The patient has an intermittent, possibly rate-related, RBBB.
This fools you into thinking that there is no ECG aneurysm morphology.
However, the typical aneurysm morphology is transformed by the RBBB!!
This patient received inadvertant thrombolytic therapy twice because this morphology was not understood. Neither time was it an acute MI.  

Back to the first case:

The patient's record was available.  It revealed that the patient had a known LV aneurysm with this ECG 4 months prior:

Same, except there is a slower ventricular response.

The Previous Echo
--Left ventricular ejection fraction is 29%
--Decreased left ventricular systolic performance, severe.
--Regional wall motion abnormality-distal septum anterior and apex diastolic
distortion with dyskinesis (aneurysm) large.
--Regional wall motion abnormality-distal inferior wall akinetic (part of LV
aneurysm)
--No evidence for left ventricular thrombus


Further history revealed that he had nausea and vomiting earlier in the day and that he might be dehydrated. His inferior vena cava was "collapsing" on ultrasound (this is not always reliable).  On the other hand, there were B-lines and reported pulmonary edema on CXR.  The ejection fraction on bedside ultrasound was consistent with the previous echo.

On history, he claimed to have been taking his chronic AV nodal blockers for atrial fib.

Exam revealed lower extremity cellulitis, but there was no fever.

Thus, the clinical picture was confusing.  A Diltiazem drip was started, with some improvement but a fall in blood pressure.

The ultimate interpretation of the data was that some dehydration and sepsis had led to high adrenergic state and rapid ventricular response, which led to decreased ventricular filling and, paradoxically, pulmonary edema.

He improved greatly with both fluids and diltiazem.

There was no acute coronary syndrome.

Troponin I peaked at 0.829 ng/mL (consistent with demand ischemia and type 2 MI).

Learning Points:

1. LV Aneurysm can mimic acute STEMI
2. RBBB distorts the ECG of LV aneurysm morphology, further mimicking acute STEMI.
3. Most Atrial Fib with RVR is due to acute disease superimposed upon chronic atrial fib
4. Management of fluid status and rate control in chronic atrial fib can be very complex.\

Wide Complex Tachycardia with Fusion and Capture Beats. Not what you think.

This late middle-aged patient presented with acute hypoxic respiratory failure, with chest discomfort and apparent pulmonary edema, with a decrease in systolic function.

Here is her 12-lead ECG:

There is LBBB with sinus rhythm at a rate of about 100. This was new LBBB.
There is no concordant ST elevation or excessively discordant STE.
Notice the morphology of the P-waves and QRS in lead II

She was appropriately taken to the cath lab because of ischemic symptoms and pulmonary edema with new decrease in LV function.  At angiogram, no evidence of ACS was found.

While in the ICU, she remained tachycardic and had this rhythm strip recorded:

Wide complex tachycardia.
What is the rhythm?  Is it still sinus?

Perhaps it will help if I circle a couple complexes:

It is a wide complex.
Note two different narrower complex beats (circled). 

1. The third QRS complex (second of the two circled) is "narrow," preceded by a P-wave.  

If this were an unknown WCT, it could easily be interpreted a as "capture beat"  and be "diagnostic" of VT. 

2. The second QRS complex (first of the two circled) is wider than the third beat, but narrower than the other wide-complex beats. 

If this were an unknown WCT, it could easily be interpreted a as "fusion beat" and be "diagnostic" of VT. 

Such beats, which are fusion or capture beats, are said to always indicate that the wide complex tachycardia is VT.

But this is clearly sinus tachycardia. How can there be capture and fusion beats?

These are "pseudo" fusion and capture beats. 

Here is the explanation and learning points:

First, a couple definitions (of fusion beat and capture beat): Both typically occur in cases of VT with AV dissociation.  In fact, it is generally said that in wide complex tachycardia, the presence of a fusion beat or a capture beat implies VT with nearly 100% specificity.  

Capture beat: A sinus impulse reaches the atrioventricular node and the ventricle in a nonrefractory phase between the wide QRS complexes, and produces a beat with a normal QRS duration. 

Fusion beat:  A sinus impulse reaches the atrioventricular node and the ventricle during a ventricular beat (ectopic beat or VT beat) and they coincide to produce a hybrid complex. 

The below was written by our electrophysiologist, Dr. Rehan Karim:

Explanation of Mechanism:

-  If you measure the sinus rate (and march-out P-P interval), it stays fairly constant before and after those "fusion" and "capture" beats.

-  However, if you measure the ventricular rate (R-R interval), the "fusion beat" comes in early. This essentially would occur if there is a PVC originating from the ventricle that is ipsilateral to the bundle-branch block (e.g., LV PVC in the setting of LBBB).  In standard LBBB, the LV activation is delayed, and if a PVC originates from LV at the right time, it can activate the LV at the same time that the RV is being activated by the right bundle.  In other words, the right and left ventricles get activated simultaneously which, compared to the LBBB, shortens the QRS!  This thus results in a relatively narrow beat (AKA "fusion" beat).

- If you closely look at the PR interval on the third beat ("capture beat"), it is slightly longer than the other PR intervals during the wide-complex beats.

- The PVC from the second beat (1st of the two beats in question) has some degree of "retrograde concealment" into the Right bundle, therefore, slightly prolonging refractoriness of the Right bundle. Important concept here is, when we call bundle branch "block" - it is not always a "true block", but rather a "delay". If Right-bundle has faster conduction than Left-bundle, then it will give rise to LBBB type pattern on EKG. In this situation, both the RBB and LBB get delayed so now the QRS complex looks narrow ("capture") beat, but with a slightly prolonged PR interval.

I remained a bit confused by this, so Rehan wrote this:

-  The second of those two narrower beats ("capture" beat) does NOT have a PVC in it.

-  Here is how delaying in both RB and LB can shorten the QRS:  If two people are racing and one of them is slow (delayed), then the faster one will win (BBB). However, if for some reason, you slow down the fast person (trip him over to make him fall so he becomes slow too) - then both will reach at the same time, but the finish line will be reached later (hence longer PR).

-  The PVC from the blocked (slow) side goes trans-septal and collides with the opposite bundle. This prolongs the refractory period of the bundle so the faster bundle also becomes slow for the next beat. So now, both the bundles conduct slow and you have narrow (capture)beat after a slightly prolonged PR interval.

Similar situation can occur with any WCT. Therefore, the statement "Presence of fusion and capture beats are diagnostic of VT" is not always true.

Learning points:

1. Bundle-branch "block" is not always a "block" but rather a "delay"

2. PVC from the side where bundle branch conduction is delayed or "blocked" would result in fusion complex that would be narrower than the wide-complex tachycardia.

3. Similar delay in both bundle branches would result in a narrow QRS complex, but with a relatively longer PR interval.

4. Presence of "fusion" and "capture" beats would favor VT, but are not "diagnostic" of VT, as they could occur in SVT with aberrancy.
5. Supraventricular tachycardia with aberrancy (sinus tachycardia is a type of SVT) can have capture and fusion beats!

I guess your readers may need a cup of coffee before they read this :)

Rehan.