Wednesday, July 20, 2016

A 12 year old with Wide Complex Tachycardia

A previously healthy 12 year old presented to the ED with a "fast heart rate" that had started about 1.5 hours prior to presentation.  She was reportedly a healthy child and active in several sports. She had a fairly active day and had been swimming off of a boat when her symptoms started. Her mother thought that she was just anxious, so took her home and had her try some deep breathing exercises. 

When this didn't help she presented to the ED and had this ECG recorded: 


Here is a higher resolution image, but missing V4-V6:
There is regular monomorphic tachycardia with RR interval of about 0.285 sec (285 ms), for a rate of 210 bpm 
QRS duration is about 120 ms.
What do you think?











Comment: This is a wide complex tachycardia (but only minimally wide!).  

Differential Diagnosis

NOT atrial fibrillation because it is regular.  

NOT polymorphic VT (Torsades de Points, caused by Long QT or Catecholaminergic VT) because all the QRS are identical.

1. SVT with aberrancy
2. AV nodal reciprocating tachycardia (AVRT, antidromic SVT, using an accessory pathway, as in WPW).
3  Ventricular tachycardia (VT)
      a.  "idiopathic" fascicular VT, which has a structurally normal heart
      b.  "Standard" VT, which occurs in a structurally normal hearts such as cardiomyopathy

So let's think it through: 

1. SVT with aberrancy:

A. Sinus tachycardia (a form of SVT) with aberrancy:  Sinus tach can beat this fast in a child.  But there are no P-waves.  

B. Paroxysmal SVT (PSVT) with aberrancy.  

The morphology is similar to RBBB (large R-wave in V1, large S-wave in V6) plus left anterior fascicular block (LAFB) (rS in II, III, aVF, and qR in aVL, which gives it a left axis deviation, away from inferior leads).   

Is it PSVT with RBBB + LAFB?   Unlikely.
       i.    There is absence of rsR' in V1,  typical of RBBB.   
      ii.    QRS duration of 120 ms is atypical for RBBB.  
      iii.   RBBB Aberrancy implies a refractory right bundle.  Although the right bundle is the bundle most likely to be refractory, a child of 12 years should be able to fully conduct at a rate of 210.   

Thus, SVT with aberrancy is unlikely.

2. Antidromic AVRT

Antidromic AVRT travels down through the accessory pathway and up through the AV node.  After traversing the accessory pathway, it must transmit through myocardium (not through specialized conducting Purkinje fibers), which is slow.  Thus, there should be an initial wide depolarization, akin to a delta wave. 

If you thought it was AVRT, it would be easy to test with adenosine.  AVRT depends on the AV node for its circuit and will be terminated by an adequate dose of adenosine.

3.  Standard VT (structurally abnormal heart)

Unlikely in a healthy child who has been playing sports all day.  But it is possible to have myocarditis or other unknown cardiomyopathy.  Standard VT is rarely this narrow, at only 120 ms, though the age of the patient could narrow it.  A bedside ultrasound assessment of would be helpful: normal heart and good contractility would be strong evidence against this diagnosis.

4. "Idiopathic" Fascicular VT (structurally normal heart).  ["Idiopathic" VT is not really idiopathic any more, but rather is known to be due to reentry.  Most are posterior fascicular VT or right ventricular outflow tract VT (RVOT).]

Posterior fascicular VT is a wide complex tachycardia with RBBB and LAFB morphology. It initiates in the posterior fascicle.  A re-entrant rhythm that starts in the posterior fascicle will initiate a rapid depolarization down that fascicle (resulting in a short duration r-wave in inferior leads), then an upward directed depolarization through myocardium (wide) to the anterior-superior LV (resulting in S-waves in inferior leads and an R-wave in aVL).  It will also transmit to the right ventricle and result in an RBBB-like morphology.  

One must also consider RVOT, right ventricular outflow tract tachycardia.  However, the morphology is wrong for RVOT (see below).

A normal bedside ultrasound would be helpful.


Case Progression, as described by the treating physician:

"My initial thought was this was either SVT with aberrancy or V-tach. She was stable with an SBP of 146. Her only complaint was shortness of breath but she was not in any visible distress though she appeared anxious. I asked about family history and she did not have any family history of cardiac problems or arrhythmias. She denied any stimulant use or ingestions." 

"The rate was regular so I decided to try adenosine. I did this first with 6 mg then with 12 mg. Nothing happened, not even a decrease in HR, and I thought that this could be V-tach so I called the pediatric cardiologist at Children's who told me I was pushing the medication wrong and that I needed to do it with a three way stop cock. He said to keep upping the dose until the rhythm broke." 

"I didn't think this sounded right but I did it anyway (in retrospect I should have insisted he look at the EKG first). When this didn't work he finally looked at the strip and agreed that this could be fascicular V-tach. We discussed transfer and he suggested Verapamil. I did give her a 5mg dose and she rapidly converted (2nd EKG). She remained stable and was transferred to Children's. She will have an ablation next month."

"Can you comment and let me know if I should have been immediately onto V-tach?   I don't think Adenosine was the wrong thing to try first. If a patient like this were unstable I would have tried electrical cardioversion. " 

"Any thoughts other than this?" 

"How did you know when I showed it to you that it was from the posterior fascicle?"

Here is the post cardioversion ECG:
Sinus Tach, otherwise normal


Comment:

I knew when I looked at the ECG that it was fascicular VT because of all the features discussed above.  Adenosine certainly will not hurt this, but it will not help either.  Had it been AVRT, adenosine would probably have converted it.

Verapamil in VT: One might be squeamish about giving such a strong negative inotrope as verapamil to someone with VT.  This is due to the fact that most VT occurs in structurally abnormal hearts, especially in ischemic cardiomyopathy, with a low ejection fraction.  Giving verapamil to a patient with VT due to cardiomyopathy could indeed be disastrous.

Thus, our minds associate disaster with verapamil and VT.  In fascicular VT, we should not carry this association.  Of course, if you are hesitant about giving verapamil, just confirm good LV function (good contractility) with bedside ultrasound.

Just for contrast, here is another "idiopathic" VT.  This is a case of right ventricular outflow tract VT (RVOT VT).  RVOT is adenosine responsive.  I presented the case here.
Notice that this tachycardia, in contrast to the above, mostly depolarizes toward the inferior leads.  Late depolarization is also towards the left (wide R-waves in V5, V6), more akin to left bundle branch block. 

Both RVOT and posterior fascicular VT occur in structurally normal hearts and are usually very well tolerated.

Fascicular VT from the posterior fascicle is responsive to verapamil.   RVOT, by contrast, is indeed responsive to adenosine.  Therefore, I would not be surprised it if often gets misdiagnosed as SVT with aberrancy after it converts with adenosine.

Learning Points:

1. Wide complex tachycardia in a child with an otherwise normal heart is likely to be one of the "idiopathic" VTs such as fascicular VT.

2. Fascicular VT (not RVOT) originates in the posterior fascicle, and therefore has RBBB/LAFB morphology.

3. Fascicular VT usually has a relatively narrow QRS (up to 140 ms), whereas VT in a structurally normal heart usually has a wider QRS (not always!).

4. Fascicular VT is verapamil responsive.

5. If you can, ascertain good contractility before giving verapamil.

6. Adenosine will often work for RVOT, which has an LBBB morphology with an inferior axis.




Thursday, July 14, 2016

Dyspnea and Convex ST elevation, Marked LVH, with Bedside Echos

Case 1.

Chief complaint: A 60-something African American male with 5 days of increasing SOB with dyspnea on exertion.

This male in his 60's has a PMH of CAD with MI and CABG, HTN with LVH, hyperlipidemia, and mild HF with only moderately reduced ejection fraction (and some diastolic dysfunction as well).

He presents with 5 days of worsening shortness of breath with orthopnea as well as chest pain.  His BP is 191/90.  He also has a history of venous thromboembolism and has not been taking his anticoagulants.  He was also off of his BP meds (lisinopril, amlodipine and carvedilol).

Here is his ED ECG (ECG #1):
There is 2-3 mm of ST Elevation in V2.  
There is an upwardly convex ST segment in V2 and V3.
The computer read ****STEMI****Of note, the S-wave in V2 is almost 50 mm. This is severe LVH.
Thus, the ST/S ratio is no more than 0.06 (6%)
Note there is also a very prominent negative P-wave in V1, diagnostic of left atrial enlargement and supportive of severe LVH.









Here is his previous ECG (ECG #2):
Here all ST segments are concave upward.  There is slightly less ST elevation.  There is no convexity.
Thus, the convexity is new.
I cannot explain the marked difference in voltage from ECG #1.
They both used 1 millivolt per 10 mm in both limb leads and precordial leads
Bedside ultrasound:

The lung ultrasound (not shown) had B-lines, all but diagnostic of pulmonary edema.

Bedside ultrasound parasternal long axis view is shown below.  


There is severe LVH.  There appears to my eye to be less than optimal systolic function and also less than optimal LV diastolic function.


Here is the short axis view:

Same interpretation as above.


Here is the chest X-ray:


There is obvious pulmonary edema.


Clinical Course:

--The D dimer was barely elevated at 327 ng/mL (upper limit of normal: 230 ng/mL).
--The initial troponin I was 0.083 ng/mL (99% = 0.030); this patient does not have baseline elevated troponin (does not have chronic myocardial injury, which is not uncommon in patients with heart failure), so this was a new troponin elevation.  

That is to say, there appears to be acute myocardial injury. 

--The Creatinine was 1.5 mg/dL, with a GFR of 69 ml/min (low).
--The NTproBNP was 1564 pg/mL (slightly elevated -- normal for patients with GFR less than 60 is 1800 pg/mL).

The emergency physicians correctly interpreted the ECG repolarization abnormalities as being entirely due to LVH combined with some injury due to acute heart failure exacerbation and hypertension, and understood that the newly elevated troponin (with rise and fall) was due to demand ischemia (type 2 MI) due to hypertension and acute heart failure.

They administered furosemide.  

Learning point: 
1. ST Elevation with Convexity in the presence of LVH does not necessarily mean STEMI
2. The ST/S ratio in STEMI would be significantly higher.  

See discussion at this post: 

LVH with anterior ST Elevation. When is it anterior STEMI?


Clinical course continued:

They gave furosemide and obtained a CT pulmonary angiogram which ruled out pulmonary embolism.  He was not given any BP management.

Comment on management:

1. With B-lines and this chest x-ray and only a minimally elevated D Dimer, CTPA is unnecessary.  The diagnosis is clearly acute decompensated heart failure.

2. This patient should get some immediate treatment to lower blood pressure (afterload reduction).  IV nitroglycerine is best, but requires ICU monitoring. For a patient who is only moderately ill and does not require an intensive monitoring, a good choice, especially for African Americans with renal dysfunction, is afterload reduction with IV hydralazine (see references below).   Often, in a patient who has not been taking his/her antihypertensive, I simply give those medications immediately in the ED. As this usually includes either an ACE inhibitor or an angiotensin receptor blocker, this is often sufficient.

Vasodilator Therapy of ADHF
http://circ.ahajournals.org/content/123/21/2414
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808524/


Clinical Course continued:

Subsequent troponins were 0.078, 0.076, 0.064

A formal echo showed:

Decreased left ventricular systolic performance - mild.
The estimated left ventricular ejection fraction is 45-50%.
Regional wall motion abnormality-anterior and septum.
Regional wall motion abnormality-inferior.
Left atrial enlargement, moderate.
Diastolic septum measurement = 1.25 cm (LVH)
 Based on Doppler indices, the LV filling pressure is markedly elevated.

The patient improved simply by re-starting his hypertension medications, lowering his BP, and with one dose of furosemide.

2.5 weeks later, after recovering from acute decompensated heart failure, his ECG continued to show high voltage and convexity, although he was recovered from the acute heart failure.



Case 2:

A middle-aged patient with a history of severe persistent asthma, heart failure with preserved ejection fraction (HFpEF), and pulmonary hypertension presented presented very short of breath.  Here was her first ECG (ECG #3):
The computer read this as ****STEMI****
Note the marked ST elevation and the convex ST segments.

This is her previous ECG from earlier in the year (ECG #4):
Much less ST elevation and less convexity


A previous formal echo showed:

Hyperdynamic systolic performance.
The estimated left ventricular ejection fraction is 80 %.
There is no left ventricular wall motion abnormality identified.
Left ventricular hypertrophy concentric severe

She improved with therapy for asthma in the ED and had this ECG recorded 5 hours later (ECG #5):
Improved ST Segments and convexity has resolved.


There was no myocardial infarction.  All troponins were negative.  She improved with therapy for asthma and was discharged from the ED.



Learning Points:

1. Patients with LVH who are in acute respiratory distress, especially with elevated BP and/or acute decompensated heart failure, frequently have convex ST elevation.  This does not imply STEMI.

2. The ST/S ratio in STEMI with LVH is not established.  The article by Armstrong et al. which is discussed in the referenced blog post above did not have appropriate methodology and their ratio of 0.25 is far too high.  There certainly should be a ratio higher than 0.10 and probably higher than 0.15.  (Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy. Am J Cardiol. 2012;110(7):977-983. doi:10.1016/j.amjcard.2012.05.032










Friday, July 8, 2016

A 65 Year Old Man with Chest pain and Precordial ST Elevation

This case was sent by Sam Ghali (@EM_RESUS)


A 65-year-old gentleman presented to the ED complaining of chest pain.  He asked my thoughts on his presenting ECG:
Computerized QTc is 409 ms
What do you think?














Here is my response:

Strongly suspect normal variant or chest leads placed too high.
Possibly STEMI, but I strongly doubt.
In my life, I have seen one saddleback (such as this) that was a STEMI.
Outcome?


Here is Sam's analysis and outcome:

The obvious question at hand here: Is this acute LAD occlusion? 

There is an rSR' in V1 and S-waves in the lateral leads, but QRS less than 120 ms, thus an incomplete RBBB. There is significant ST-elevation in V1-V3, which meets ACC/AHA STEMI Criteria in these leads (greater than or equal to 2.0 mm in an male greater than or equal 40 yo). Also concerning for coronary occlusion, the T-waves are upright, large, and broad in appearance (especially in proportion to the QRS). There is inferior ST-depression in II, III, and AVF which in LAD occlusion is reciprocal to anterior ST-elevation. What speaks against LAD occlusion is the very well-developed R-waves in V3-V4. (As the ECG evolves in LAD occlusion, there is a loss of R-wave height as R-waves transition to Q-waves; however you wouldn't necessarily see this early on). There is concave-up ST-elevation which makes occlusion less likely, but by no means rules it out. What is also unusual in this case is the “saddleback” morphology of the ST-segment elevation.

A prior ECG would be helpful here, but there was none. A bedside echo looking at LAD distribution wall motion might also be helpful but due to logistical reasons this too was not an option. The decision was made to activate the cath lab. 

Outcome

The cath revealed chronic total occlusion of the RCA, with good collateral flow. There were multiple 40-50% lesions throughout the LAD and it’s Diagonals, as well as in the Circ. There was no acute occlusion.   Serial troponins were negative.  Echo did not show LVH.

I shared the case with Steve Smith to gain his expert insight, but here are my comments:

1. STEMI Criteria are imperfect - not nearly sensitive nor specific enough for strict use

2. Even with other ECG features taken into account, diagnosing acute LAD occlusion can be very difficult. The Subtle Anterior STEMI formula which may provide diagnostic guidance here, technically should not be used in the presence of inferior ST-depression.

3. While “saddleback” ST-elevation is less likely to be coronary occlusion, it is still possible for STEMI to have this morphology.

4.  Ultimately, if after all measures there is still concern for acute LAD occlusion, the diagnosis may be best excluded in the cath lab.

Smith comments:

This is saddleback ST elevation, such as one commonly sees in LVH or in type 2 Brugada.  It can also happen if chest leads are placed too high.  It is rarely due to STEMI.  (I was a bit surprised to hear that the echocardiogram did not show any LVH).

The inferior ST depression is probably a false positive.  If you look at the PR segment, it is downsloping.  This is a frequently encountered atrial repolarization wave, and this wave is persistent after the end of the QRS, causing a mimic of ST depression.

Atrial Repolarization wave mimicking ST depression:
You can read about it at this post.
You can watch a K. Wang video about this at this post.

Thus, the formula can be used.  The R-wave amplitude in V4 is the single most powerful predictor of early repol vs. LAD occlusion: a high amplitude, which here is very high at 25 mm, goes strongly against LAD occlusion.  The formula value here, using STE60V3 of 2.5 mm, is very low at 18.97.

Even if the QTc were very long, at 460 ms, the formula value would still be very low at 21.98 (less than 22.0), which would all but rule out LAD occlusion.

That said, one cannot entirely rule out STEMI with the formula and such a case should always of course be approached carefully.

If available, I would do a stat formal echo rather than activate the cath lab.



Friday, July 1, 2016

Middle-aged Diabetic with Syncope, Diaphoresis, Nausea, and Dizziness

This middle-aged male with history of 3 previous stents, 2 in the RCA, had Syncope, Diaphoresis, Nausea, and Dizziness.

He called 911 and the medics recorded an ECG that looks just like his first ED ECG:
There is inferior ST elevation and reciprocal ST depression in I and aVL, with reciprocal T-wave inversion in I and aVL.













This ECG was texted to me (while out on a beautiful point on an island!) with the question: "Would you activate the cath lab?"

I responded: "Yes or at least get stat echo.  It is 90% certain to be occlusion."

Outcome: The coronaries were clean.  The troponins were negative.  The subsequent ECGs did not evolve (this latter is the best evidence that there was no MI, as transient ACS can have all of the following negative: Cath, troponins, and Echo).

It turns out that the patient had a similar false positive activation 1/2 year ago because this is his baseline ECG.  

He must carry a copy with him wherever he goes!!

Sometimes you just have to have a false positive.  You must activate anyway.  You cannot let an ECG like this go without action unless you know it is the baseline.

If there is any doubt, it would be reasonable to find an old EKG and/or to get an emergent echo.

Pretest probability: This also points out (again) that when patients do not have chest pain, especially if they do not at least have dyspnea, the probability that their ECG represents a STEMI decreases considerably.


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.\