Friday, June 24, 2016

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?











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.
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













Monday, June 20, 2016

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?














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.



Friday, June 17, 2016

Anterior STEMI? Or Benign Early Repolarization?

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




  

Sunday, June 12, 2016

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:

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.










Friday, June 10, 2016

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!

Monday, June 6, 2016

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.\

Friday, June 3, 2016

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.

Friday, May 27, 2016

Acute Respiratory Distress, Hypoxia, and a Large Right Ventricle on Bedside Ultrasound

A 50-something presented in acute hypoxic respiratory failure, alert and in respiratory distress.  She required Bilevel positive pressure ventilation.

Pulse was 139 and BP 99/75.  She was diaphoretic.

A bedside ultrasound was done immediately:
video

Notice the very large RV and very small, but well functioning, left ventricle.

What do you think?
















There were also B-lines (not shown).

Here is here initial ECG:
What do you think?













There is sinus tach.  There is a large S-wave in lead I.  There is a Q-wave in III.  Do these indicate acute right heart strain, typical of pulmonary embolism?











No!

First, there is no full S1Q3T3 (no T-wave inversion in lead III; for significance of S1Q3T3, see notes at the bottom).

More importantly, there is also a large R-wave in lead V1.  This combined with the right axis deviation (S greater than R in lead I) is all but diagnostic of RV hypertrophy (in contrast to acute right heart strain) which is a chronic condition.  Notice there are also large upright P-waves in right precordial leads (though not in lead II).  These are also suggestive of right atrial hypertrophy, which often accompanies right ventricular hypertrophy.

Seeing this, the probability of PE was greatly diminished.  The B-lines on lung ultrasound was also very strong evidence against PE.

She turned out to have chronic pulmonary fibrosis and acute pulmonary edema.  The RV enlargement was chronic.

A previous formal echo was found:
Pulmonary hypertension. The estimated peak systolic PA pressure is 60 mmHg
plus RA pressure and diastolic pressure 13 mmHg plus RA pressure.   Right ventricular enlargement with distortion of the position of the interventricular septum consistent with right ventricular pressure
overload.  Decreased right ventricular systolic performance. The left ventricular is relatively small with decreased systolic performance. The estimated left ventricular ejection fraction is 39 %.
There are no convincing regional wall motion abnormalities.


After therapy for pulmonary edema, she improved.

Learning Points:

In the context of hypoxic respiratory failure and a large RV on echo, the ECG can help to differentiate acute right heart strain (which can be due to acute hypoxia, especially from pulmonary embolism) from chronic RV hypertrophy.

The presence of a large R-wave in lead V1 well differentiates acute right heart strain from chronic RV hypertrophy.



S1Q3T3


This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients who had clinical findings suspicous of PE, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), among patients with suspicion for PE, S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.


Monday, May 23, 2016

Syncope During Exercise in a 12-Year Old

This was sent by a paramedic who wishes to remain anonymous.

911 was called because a 12 year-old female had a "seizure" at the gym. 

On arrival, medics found the patient supine on gym mats, conscious but lethargic. Her skin was very pale, cold, and diaphoretic, and there was no radial pulse but only a palpable brachial.  Her lips were cyanotic and firefighters had already begun oxygen therapy. She complained of nausea and bilateral rib pain not worsened by palpation or inspiration. She did not have any obvious injuries on exam, but we noticed bladder incontinence. She was still cyanotic 15 minutes after the "seizure."

The patient's coaches stated that she was "warming up" for practice when she suddenly lost consciousness, fell, and had brief seizure-like activity. They denied seeing her sustain any other injuries aside from a ground-level fall onto a soft surface. She regained consciousness within a few minutes, but remained altered. 

Later on during transport, the patient was able to recall what happened: she was running when she became very dizzy and lost consciousness. The patient's family stated that she had no medical history, no previous seizures or similar episodes with exercise, and no family history of cardiac problems or sudden death. 

A monitor strip showed frequent PACs.


After a quick exam and history we took her out to the ambulance, where her first set of vitals were: BP 100/63, HR 72, SpO2 99%, RR 22. Her lungs were clear and she never complained of dyspnea.

A prehospital 12-lead was recorded:
Sinus rhythm.  There are clear ischemic (down-up) T-waves in II, III, aVF and V4-V6.
There is an rSr' in V1, but this is not abnormal.  It can especially be due to high lead placement.
The QRS duration is 98 msec (normal)
The computerized QTc is 461 ms (slightly long, but not dangerously so).

Case Continued:

After about 6 or 7 minutes on oxygen, the patient's cyanosis resolved and so did the premature beats. Her mental status and skin greatly improved. However, for the remainder of transport her systolic blood pressure remained in the 80s (86/56) despite improvement otherwise (I wondered later if the first BP was an incorrect reading). We started a fluid bolus and by the time we reached the ED, her only complaint was fatigue.


She was admitted to a children's hospital.

The followup was somewhat sketchy, as it did not come from medical records but from family via a third party:

She  was found to have an anomolous left main coronary artery which reportedly became "pinched" during exercise, causing severe ischemia with drop in cardiac output and syncope.  

She had surgery to move the artery and is reportedly doing well.  They are just having difficulty keeping her inactive. 

Learning Points:

1.  It may help to record an ECG in cases of "seizure"
2. Syncope in children can be due to ischemia, as well as due to pure rhythm disturbances such as long QT, WPW, Catecholaminergic polymorphic VT (CPVT), Brugada, AV block, etc.
3. Syncope during activity is particularly worrisome.

Check out this case:

A 16 year old girl has syncope while playing basketball.....



Here is my article on ED Syncope Workup:

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....





Friday, May 20, 2016

My Very Smart Colleagues are Getting Very Good at Diagnosing Subtle Occlusion

My very smart colleagues are getting very good at this!

A male in his 40's with a significant history of coronary disease and stents called 911 for sudden onset "terrible" left sided chest pain radiating to the jaw, with diaphoresis and vomiting.  He appeared very uncomfortable.

Here is his prehospital ECG, recorded approximately 15 minutes after onset of pain:

Normal


On arrival, another ECG was recorded 16 minutes after the prehospital ECG, approximately 30 minutes after the onset of pain:
There is a normal amount of ST elevation in V2-V4.
However, it is greater than in the prehospital ECG.
Upward concavity in all of V2-V6, no reciprocal ST depression, no Q-waves, no T-wave inversion.
The computerized QTc is 387 ms.
The LAD occlusion formula value, using:
ST Elevation at 60 ms after the J-point = 3 mm
Computerized QTc = 387 ms
R-wave amplitude in V4 =  9.5 mm
Formula = 23.32
This is just below the cutoff of 23.4, which would make LAD occlusion very likely.
I consider any value above 22.0 as suspicious, and needing serious evaluation.

_____________________________
Dr. Ken Grauer added the following nice points:

I would make the following points regarding serial ECGs in this case. ECG #1 is normal. One needs to compare serial tracings by going lead-to-lead. Even without use of the formula — there ARE changes that should be readily apparent from lead-to-lead comparison between ECGs #1 and 2. That is in V1 — the T wave is now positive in ECG #2; in V2 — the T wave is now disproportionately tall with respect to the QRS in this lead, and the J-point is now elevated; in V3 — both QRS complexes now show clear ST elevation with what looks like broadening of the T wave base, compared to relatively normal appearing ST-T waves in ECG #1. Given the history in this case — this lead-to-lead comparison should be more than enough to prompt immediate cath. That the formula has now become positive supports this clinical decision.
____________________________________



There was an old ECG for comparison from 8 months prior:
This has less than 0.5 mm STE in V2 and V3.  This is a significant change.


So there is a change in the ST elevation.

Kambara (see below) showed that early repolarization is dynamic; see this case and discussion: 

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.


However, in this case:
1. The formula is nearly diagnostic
2. There is definite increase in ST elevation
3. The patient has a classic clinical presentation for anterior MI

Possible Management Strategies:

1. It is very early in the patient presentation, and there has not yet been time for much ECG evolution.  Therefore, serial ECGs may be particularly useful
2. Do bedside cardiac ultrasound.  If there is clear wall motion abnormality, then activate cath lab.  If none, then do formal contrast echo or, if unavailable, then speckle tracking echo cardiography.
3. The ACC/AHA does recommend emergent angiogram for patients with ongoing, refractory chest pain and high suspicion of coronary syndrome, even in the absence of ECG or biomarker evidence of ischemia.  In this case, there is even very good ECG evidence.

As with 50% of STEMI, the initial troponin was negative (Initial cTnI = 0.028 ng/mL, 99% upper reference level = 0.030 ng/mL).

My very astute colleagues simply activated the cath lab after giving aspirin, heparin and ticagrelor.  The interventionalist was skeptical but gladly took the patient to the cath lab.

Here is the cath report:

--Culprit Lesion (s): 90% ruptured plaque in mid LAD proximal to the previously placed stent; initial flow in distal LAD TIMI III 
--The right coronary is occluded - in-stent - at the aortic ostium in the presence of L to R collaterals

The interventionalist remained skeptical even after the angiogram:

"Unstable angina/ACS with putative mid-LAD culprit (90% stenosis with TIMI III flow on initial angiography) - recommend continued troponin levels to define whether the current event represented an acute myocardial infarction.  Suspect chronic total occlusion of the ostial RCA (instent)"

Post PCI ECG:
All the previously noted increase in ST Elevation has resolved.QTc = 379 ms
This proves that the ST elevation was indeed due to ACS.
At the time of the ECG, there would have been TIMI 0 or 1 flow, but spontaneous reperfusion occurred, aided by adjunctive pharmacotherapy (ASA, heparin, ticagrelor)

What is the post-angiogram formula value?
STE = 1
QTc = 379
RAV4 = 11
Formula now = 19.971 (clearly normal)More evidence that the presenting ECG represents LAD occlusion.

Here is the subsequent formal echo:

The estimated left ventricular ejection fraction is 67 %.
Normal estimated left ventricular ejection fraction .
Left ventricular hypertrophy concentric .
Regional wall motion abnormality-anterior hypokinetic.


Here is the next day ECG:
There was such rapid and complete reperfusion that no reperfusion T-waves (Wellen's waves) did not evolve. This is somewhat unusual in patients who have a significantly elevated troponin.
Troponin I peaked at 4.44 ng/mL


Learning Points:

1. Pre-test probability is critical (here there is history of CAD and very typical presentation, with sudden onset, vomiting, and diaphoresis)
2. Use the Subtle LAD occlusion formula
3. Compare with previous ECG
4. Record serial ECGs
5. Compare with the prehospital ECG
6. Interventionalists' opinions are important, but not the gold standard (see reference below).


References

1. McCabe JM.  Physician Accuracy in Interpreting Potential ST-Segment Elevation Myocardial Infarction Electrocardiograms.  J Am Heart Assoc. 2013;2: e000268 doi: 10.1161/JAHA.113.000268
http://jaha.ahajournals.org/content/2/5/e000268.full.pdf+html

Although interventionalists performed the best among physician groups, there sensitivity for coronary occlusion in this study was 70% (specificity 89%).

All EKGs are at the end of this article and you can test yourself.  I had 93% sensitivity and 100% specificity. 

2. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.  

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.