Monday, March 18, 2019

IVCD, Saddleback STE in III, with reciprocal STD in aVL: Is it pseudoOMI or OMI? Echo with Speckle Tracking gives the answer.

A 77 y.o. woman with a history of hypertension and congestive heart failure presented for acute onset chest pain and shortness of breath. She stated that she woke up in the morning with a central chest pressure with associated shortness of breath. She had been feeling well the day before.

She had no h/o CAD but had a history of "unspecified cardiomyopathy"

No old EKGs or angiogram were available.

This ECG was texted to me with no information:
What do you think?

There is ST elevation in inferior leads, with reciprocal ST depression in aVL, so one must strongly suspect acute inferior MI.

However, 3 features made me think that it could be a false positive (pseudoOMI):
1) There is LVH
2) There is an intraventricular conduction defect, with QRS duration of 125 ms
3) There is an RSR' (saddleback) in lead III

My response was that the diagnosis of inferior OMI is probable but not certain.

I was looking at it on my phone when I gave that opinion; looking at the full size version I am more convinced of OMI than I was at the time.

Case continued:

The emergency physicians were also not certain.

So they did a bedside point of care cardiac ultrasound,

Here is the parasternal short axis:
The area on the lower left of the image has poor contractility

Apical 4-chamber

This shows, to my interpretation, an apical wall motion abnormality, and of the distal septum

This one was done with Speckle Tracking Strain Echocardiography.

The lavender line is associated with the lavender sector where it says "inferior".
That sector is clearly not moving as well as the upper right.
But you don't have to depend on your Gestalt.
You can see the graph.
The deeper the graph (deepest is yellow, which is anterior), the better the contraction.
The lavender sector contracts less than 10 on the scale, so there is indeed an inferior wall motion abnormality.

You might wonder why the inferior wall looks so medial.
The location depends on the operator who tells the machine what wall is what by placing dot markers on the endocardium.  So if the inferior wall is not accurately marked, it will identify the wrong wall.

Here are more cases with Speckle Tracking

Here is an article we wrote on the topic:

Rowland-Fischer A. Smith SW.  Laudenbach A.  Reardon R.  Diagnosis of acute coronary occlusion in patients with Non–STEMI by point-of-care echocardiography with speckle tracking. American Journal of Emergency Medicine 34(9):1914e3-1914e6; Sept 2016.

Here is the case we describe in the report: Ultrasound Before ECG for Chest pain? Whoever gets there first. Use of Speckle Tracking.

Case Continued:

The initial troponin I was 0.012 ng/mL (URL = 0.030 ng/mL)

The Cath lab was activated.

A 2nd troponin returned at 0.047 ng/mL (elevated)

The resident wrote that the cath showed only an OM occlusion.  

She asked 2 very astute questions: 
"Could an OM occlusion cause an inferior MI?"
and related:
"Could the EKG abnormalities be baseline and he really had an occlusion that did not manifest on the EKG?"

My answer:

In a left dominant system, an OM could supply the inferior wall, but that would be unlikely.  In this case, due to the EKG abnormalities, it is likely.  But the proof would be in the subsequent ECGs: did they evolve?  If the EKG abnormalities are a result of the ischemia, the ECG will always evolve.  The ST segments will resolve, or there will be T-wave inversion, or both.

Did the EKG evolve?

First, the full angiogram:

LM normal
LAD normal
LCx large codominant, normal appearing until point of occlusion in mid-vessel
    --So this OM does indeed supply the inferior wall.
RCA supplies PDA only, normal.

PTCA of LCx OM2 branch performed. Distal vessel difficult to visualize.  Flow eventually restored after multiple passes with thrombectomy aspiration catheter.

Here is the post PCI ECG:
The ST elevation is resolved (and the reciprocal ST depression)
Therefore the ECG abnormalities were definitely a result of the ischemia.

The post PCI troponin was 22.4 ng/mL

Formal echo later:

Moderate to severe decrease in left ventricular systolic function with an estimated EF of 30%.
Regional wall motion abnormality--apical septal, mid anteroseptal, mid to apical anterior, and apical lateral hypokinesis.
Regional wall motion abnormality--basal to mid inferior and inferolateral hypokinesis.

Comment by KEN GRAUER, MD (3/18/2019):
There are a number of reasons why I really like this case: iAs per the title chosen by Dr. Smith — it’s a great example of how combined use of ECG + Echo with Speckle Tracking makes the diagnosis; iiIt illustrates some important points about ECG assessment when the initial ECG shows an unusual form of intraventricular conduction defect (IVCD);  andiiiIt shows how the follow-up (ie, 2nd) ECG confirms the diagnosis.
  • For clarity — I’ve put both tracings in this case together, and have labeled some key findings (Figure-1):
Figure-1: The 2 ECGs shown in this case (See text).
COMMENT: As per Dr. Smith, it’s important to emphasize that in this older patient with underlying heart disease and new-onset chest pain — acute OMI must be assumed until proven otherwise. That said — I was initially less certain of this diagnosis from inspection of ECG #1 alone, without the benefit of a prior tracing for comparison ( = My Opinion).
  • In favor of acute OMI until proven otherwise from ECG #1 — all 3 inferior leads show subtle-but-real ST elevation — and, there is mirror-image opposite reciprocal ST depression in lead aVL. I’ve added horizontal RED and BLUE lines to these leads to facilitate recognition.
  • My reservation about whether or not these changes were acute stemmed from how atypical the IVCD in ECG #1 was. The QRS complex is wide. Although the QRS does not look overly wide in a number of leads — one takes the widest QRS that you are clearly able to see for measurement of QRS duration, and I measure 0.12 second for QRS width in leads V2 and V3. Therefore, there is a conduction defect. However, the triphasic ( = rsR’) complex in lead I (quadriphasic in lead aVL) is distinctly atypical for LBBB — as is the narrow R wave in lead V6. Typical LBBB also does not produce a 6mm R wave as early as lead V2, as we see here in ECG #1. This defines the conduction defect in ECG #1 as a nonspecific IVCD — because it does not conform to either typical RBBB or LBBB. Assessment of ST-T wave changes, as well as chamber enlargement is often more difficult in the setting of IVCD. (NOTE: I did not say “impossible” — but I did say that it’s often more difficult to assess acute ST-T wave changes in the setting of an unusual IVCD, such as the one we see here).
  • As per Dr. Smith — there is also LVH in ECG #1, and the presence of LVH can be a confounder for recognizing acute MI on ECG. I will emphasize that ECG criteria for diagnosis of LVH are different, and often much more difficult to ascertain in the presence of any conduction defect (RBBB, LBBB or IVCD). This is because the sequence of both ventricular depolarization and repolarization is altered when there is a conduction defect. As a result — recognition of ST-T wave changes of LV “strain” is less reliable — and, the usual numerical criteria established for ECG diagnosis of LVH are different and not well established. That said — the finding of very deep anterior S waves (ie, ≥25-30mm in V1, V2 or V3) has been correlated with high statistical likelihood of LVH. This criterion is met by the 32mm S wave in lead V2 of ECG #1.
  • Finding a prior ECG on this patient would have been invaluable for proving that the limb lead changes in ECG #1 were acute. Unfortunately, a prior ECG on this patient was not available. This highlights the value of Echo in the ED — with demonstration of a localized wall motion abnormality confirming the need for immediate cath (Our THANKS to Dr. Smith for these beautiful Speckle Tracking Echo videos! ).
COMMENT on ECG #2: There are a number of important findings to highlight on ECG #2, performed after successful PCI:
  • As per Dr. Smith — the inferior lead ST elevation and reciprocal ST depression in lead aVL has resolved in ECG #2.
  • NOTE: QRS morphology in leads I and aVL in ECG #2 is even more unusual than it was in ECG #1 — in that both leads I and aVL now show quadriphasic (rsR’s’) complexes, with a near isoelectric deflection. Extra-notched QRS complexes (ie, fragmenting) — is also seen in leads III, aVF; and in the S waves of leads V5 and V6. Such fragmentation often indicates “scar” — either from underlying cardiomyopathy, prior infarction or both.
  • It should be appreciated that R wave progression is markedly different in ECG #2, compared to ECG #1. That is, transition (where the R wave becomes taller than the S wave is deepoccurred between leads V3-to-V5 in ECG #1 — but it never occurs in ECG #2 (ie, the S wave remains predominant through to lead V6 in ECG #2). I would generally not expect this marked change in R wave progression to be the result of reperfusion — which raises the question of whether chest lead electrodes were placed in the same position when recording both tracings? Awareness of this difference in R wave progression is essential when attempting to compare serial ST-T wave changes!
  • That said, despite this marked difference in R wave progression between these 2 tracings — there should be little doubt that there has been evolution of the ST-T wave. Note the much more modest T wave amplitude (within the dotted BLUE rectangles) in ECG #1. In contrast — the T waves in all chest leads of ECG #2 are clearly more peaked and manifest a narrower base (within the RED rectangles). I interpret these as evolutionary reperfusion ST-T wave changes — that add further support to the acuity of the findings we saw in ECG #1.
OurTHANKS to Dr. Smith for providing this superb teaching case!

Friday, March 15, 2019

A 50-something with chest pain presents to a Non-PCI capable facility

An avid reader sent me this case.  He learned to read subtle ECGs here.


A 50-something presented with chest pain.  A triage ECG was recorded and shown to the ED physician:
What do you think?
The QTc-B was 427 ms

This was texted to me with no information, and here is my reply:

"I think it looks like an LAD occlusion."  

Why did I say this?  
--There is minimal STE in V2, but in the presence of a tiny QRS.
--The ST segment in V2 is convex upward, or at best straight
--The QRS starts with a Q-wave 
--There is a fragmented QRS (down-up-down-up-down-up)
--There is ST elevation in V3 with a rather straight ST segment

If you ignore the convexity, and use the 4-variable formula, we get:

STE60V3 = 3.0
QTc = 427
RAV4 = 12.5
QRSV2 = 2

Value = 21.73.  This is a very high value and strongly supports LAD occlusion.  The best cutoff was 18.2 with approximately 85-90% sensitivity and specificity.

The reader then told me the details:

"The ECG was shown to my partner, who thought it was normal.  He signed it as "No STEMI" (which is technically true)."

"I then signed up for the patient on the board without having seen the ECG."

"Then I saw the ECG and thought to myself "Oh, my God!""

"I too thought it looked like an LAD occlusion."

"I then saw the patient clutching his chest."

"I gave aspirin and heparin bolus, and called for a helicopter to transfer to the PCI facility."

"I was afraid they would not even accept the patient."

"The helicopter arrived and we recorded another ECG 25 minutes after the first, just as he was being loaded onto the stretcher:
Now it is an obvious STEMI (see leads V3 and V4)

Then I gave 50 mg (full-dose) TNK-tPA (tenecteplase) 


The cardiologist at the receiving institution reported that the patient was pain free on arrival.  [No EKG data was provided. This is important because if the ECG does not show evidence of reperfusion, immediate angio +/- PCI is indicated regardless of pain status]

"He said the patient was nearly pain free on arrival to their ER because of the TNK-tPA and thus, since he got TNK, protocol is to wait 3-24 hours because of the risk of bleeding.  If he were still having significant chest pain, they would have taken him immediately."

Because he was pain free, they waited 14 hours (until the next AM) to take him to CATH:  


100% occlusion of the old stent in the LAD (with a 95% stenosis proximal to the stent), 90% stenosis of RCA, and 70% stenotic circumflex, so he stented all three.

Whether there was TIMI 3 flow was not stated.

His troponin I peaked at 76 ng/mL.

Great work by the reader!!!

Comment by KEN GRAUER, MD (3/15/2019):
This is an important example of shape recognition. The case was submitted by an avid follower of Dr. Smith’s ECG Blog. The patient was a man in his 50s, who presented to the ED with chest pain. His initial triage tracing is shown in ECG #1. Forty-five minutes later — a 2nd ECG (ECG #2) was obtained. For clarity — I have put both tracings together in Figure-1.
  • Dr. Smith has expertly detailed the reasons why the QRST appearance in leads V2 and V3 of ECG #1 is diagnostic (until proven otherwise) of acute LAD occlusion.
QUESTION: Aside from leads V2 and V3 — How many other leads in ECG #1 are abnormal?
  • ALSO  Do you think there may be a problem with lead placement in ECG #1?
Figure-1: The 2 ECGs shown in this case (See text).
COMMENT: As per Dr. Smith — considering that this ECG was obtained in an ED, leads V2 and V3 are all but diagnostic of acute LAD occlusion. That said, this tracing was interpreted as “normal” when first seen. As a result — it is worth dissecting the findings in ECG #1.
  • In addition to the findings noted by Dr. Smith — the SHAPE of the QRST complex in lead V2 should “jump out” at you! The frowny” shape (ie, coved) ST segment that is topped off by a fatter-than-it-should-be T wave peak is simply disproportionate to the tiny QRS complex in this lead. This is a “picture” that in a patient with new chest pain — should be saying to you, “I’m an acute OMI until you prove that I am not."
  • To support the presumption that lead V2 is acute — we need to find at least one neighboring lead with ST elevation. As noted by Dr. Smith — the 2mm of J-point ST elevation with “rather straight” takeoff in lead V3 is clearly abnormal. NO more than these 2 neighboring leads in this patient with new chest pain should be needed to justify prompt transfer to the closest PCI facility.
BUT — it is Important to Recognize the OTHER Findings:
  • With proximal (as opposed to mid- or distal) LAD occlusion, in addition to anterior chest lead ST elevation — there will often be associated limb lead changes in the form of ST elevation (which may be subtle) in lead aVL inferior lead ST-T wave depression. In ECG #1 — there is suggestion of slight ST elevation in lead aVL — and, there are subtle-but-real ST segment flattening changes in each of the 3 inferior leads. Of these, lead aVF is the most marked — in that it clearly shows a straightened (if not slightly depressed) ST segment, with abrupt angulation that leads into a taller-than-it-should-be T wave given the tiny amplitude of the QRS complex in this lead aVF. NOTE: These limb lead changes are subtle! Butin the context of clearly abnormal ST elevation in V2 and V3 in this patient with new chest pain — I believe they strongly support the likelihood of acute proximal LAD occlusion.
  • Next in the context of clearly abnormal ST elevation in leads V2 and V3 — I interpreted the slight-but-real ST elevation in neighboring leads V1 and V4 as abnormal. I felt this offered further support that acute proximal LAD occlusion was ongoing. Retrospectively — I felt a look at ECG #2 (in Figure-1confirmed that the subtle ST elevation that I just alluded to for leads V1 and V4 of ECG #1 was real — because abnormalities in both leads V1 and V4 have clearly become more evident in this 2nd ECG obtained 45 minutes later.
Finally — I suspect there is malposition of at least lead V2 in ECG #1. This is because R wave progression as we move from lead V1-to-V2-to-V3 in ECG #1 just doesn’t make physiologic sense (ie, practical disappearance of the S wave in lead V2, with this multiphasic, almost null QRS complex — that then shows return of a substantial S wave in lead V3). Realizing that much has changed in ECG #2 with evolution of the infarct and development of deep anterior Q waves (QS complexes) — Doesn’t progression of QRS complexes and ST-T waves across chest leads in ECG #2 appear to be more logical?
  • Given that ECG abnormalities were initially not recognized in ECG #1 — it is quite possible that suspecting malposition of one or more chest leads, and immediately repeating the ECG might have resulted in a repeat tracing with more leads showing abnormal findings that might have been picked up earlier.
BOTTOM LINE: The fact that ECG #1 was initially interpreted as “normal” in this patient with new chest pain — means there is still “work to be done” in the area of ECG interpretation education.Rather than strict adherence to numerical stemi guidelines:
  • Remember that the prevalence of acute cardiac disease is greatly increased in an adult of a certain age who presents to an ED with new-onset chest pain.
  • When the amount of ST segment deviation is modest — ST segment SHAPE takes on much greater importance.
  • Although changes may be subtle — it’s essential to scrutinize all 12 leads, to see if a consistent “story” is being told. Doing so reveals that no less than 8 of the 12 leads in ECG #1 show at least subtle abnormal findings — which, when interpreted together in association with the clearly abnormal appearance of leads V2 and V3, make a convincing case for acute LAD occlusion until proven otherwise.
Our THANKS to the avid reader who shared with us this insightful tracing!

Wednesday, March 13, 2019

What is this rhythm? And what else does it show?

This was sent to me by my friend Sam Ghali (@EM_RESUS),, with no information.

Sam frequently just sends ECG without saying anything else.  About anything! Which is always fun for me because when Sam sends one it is always a difficult ECG.

Here it is:
What do you think?

These were my thoughts:

Rate and Rhythm: 
The rate is 126.  I see no definite P-waves.
There are two different morphologies of QRS.  Both are extremely wide, the 1st at 200 ms and the 2nd at about 160 ms.
The 9th beat (if you don't count the half beat at the start as the first one) is an early beat (a PVC), followed by the 2nd rhythm.  The PVC terminates one VT and starts another!
This is two different VT rhythms on the same 12-lead!

Ischemia?: V4-V6 have clear ST Elevation.

I wrote back:

I think this is VT with 2 different foci.
Beat 9 is an early beat that triggered the change, a PVC.
It also shows acute STEMI.

I sent this to Ken Grauer and he agreed.

Sam replied:

"Yup.  What's the culprit?"

I replied:


He replied:

67 yo guy. Altered, in shock. Looking at the chart apparently no actual CP but abdominal pain, SOB, etc. 

Yup. 100% Prox LAD (ostial).

March 14:

Now I see it differently, thanks to Christopher Watford's comment:

Alternative rhythm interpretation: ST w/ RBBB (small P-waves possible in leads I/III, approx 140 ms PRi), interrupted by a premature beat (focus unknown, possible fusion given intermediate shape), returning to ST w/ RBBB this time with LAFB due to the timing change by the premature beat.

I'm considering this as a possibility due to the identical rates of the first and second rhythms (both have RR's of approximately 470 ms).

I agree with LAD occlusion based on concordant changes in V4-V6.

Really neat ECG.

Comment by KEN GRAUER, MD (3/13/2019):
Fascinating tracing provided by Dr. Sam Ghali — enticingly without the benefit of any history. Having now looked at this tracing a 2nd time (and a 3rd time — and then a few more times …) — I have to amend my initial interpretation. I fully acknowledge that I do not know the etiology of this rhythm.
  • For clarity — I have labeled the beats in the long lead rhythm strip (Figure-1).
QUESTION: How would YOU approach interpretation of this arrhythmia?
  • HINT: Appreciation of ECG findings noted below will be greatly facilitated by use of calipers.
Figure-1: The very challenging tracing submitted by Dr. Sam Ghali. We are not given any history … (See text).
MTHOUGHTS: Among the challenges posed in interpreting this tracing, is determining the width of QRS complexes. We know the QRS is wide. I wasn’t certain where QRS complexes ended — and where the ST segment in various parts of the tracing began ...
  • I have added vertical BLUE lines for each set of 3 leads in Figure-1 to show where I think the QRS complex ends.
There are 3 long lead rhythm strips in Figure-1— taken from leads V1, II and V5. It is probably easiest to appreciate events by focusing on the long Lead IRhythm Strip:
  • The rate of the rhythm is ~130/minute.
  • As per Dr. Smith — there are 2 different QRS morphologies. The first 8 beats in the long lead II manifest a small q wave with a predominantly upright, notched QRS complex ( = morphology Xas per the label above beat #8). Beats #10-thru-21 in the long lead II manifest a predominantly negatively notched QRS complex ( = morphology Zas per the label above beat #10).
  • The QRS complex for both of these 2 morphologies is wide. Assuming we are not dealing with hyperkalemia or some other toxicity — this suggests we are either dealing with a ventricular rhythm (or rhythms) — or, a supraventricular rhythm with one or more conduction defects.
  • I do not see clear sign of P waves. One can question whether there is a small, upright P wave preceding beat #10 — but if so, I did not appreciate this anywhere else. I therefore assumed no atrial activity.
  • Beat #9 occurs earlyWithout calipers — it is probably easiest to appreciate that beat #9 occurs early by looking from beat-to-beat in the long lead V5 rhythm strip. With calipers — you’ll instantly measure the shorter R-R interval preceding beat #9. It is right after this early beat — that beginning with beat #10, QRS morphology changes.
  • Morphology of both the QRS complex, as well as of the ST-T wave of beat #9 complex Y”) in the long lead II rhythm strip is intermediate between QRS and ST-T wave morphology of the beat that precedes it beat #8 = X”) — and the beat that follows it beat #10 = Y”). This initially suggested to me, that beat #9 with its intermediate morphology is a Fusion beat — which if true, would identify at least one of the tachycardias as ventricular in etiology.
MInitial Impression of the Rhythm:
  • As Dr. Smith noted above — my initial impression was that there were 2 wide tachycardias of different morphology — and that this represented 2 different foci of VT.
  • In support of this — there appears to be Selevation in leads V4V5 and V6 (seen to right of the vertical BLUE line in these leads, that marks the end of the QRS complex). A large acute STEMI, as this ST elevation seemed to suggest — would provide a reason to develop VT.
M2nd Impression:
  • I looked again at the QRS morphology we are provided with for beats #1-thru-5 in leads I, II, III; and V1 and V5 (seen to the left of the vertical LIGHT BLUE line in these leads). This QRS morphology is clearly consistent with a RBBB, in addition to the presence of multiple Q waves. The qR pattern in leads II and III, in association with the S wave in lead I is almost consistent with LPHB (usually the S in lead I is deeper with LPHB). Given the apparent absence of sinus P waves — perhaps this represented junctional tachycardia for beats #1-thru-8 (with bifascicular block as a consequence of the large ongoing STEMI) — with a Fusion beat ( = beat #9) — followed by a run of VT ( = beats #10-thru-21)?
M3rd (and FinalImpression:
  • I initially thought the rate of the 1st tachycardia (ie, beats #1-thru-8) was different and slightly slower than the rate of the 2nd tachycardia (ie, beats #10-thru-21). However, on careful measuring (and remeasuringwith calipers — other than beat #9, which occurs early — the R-R interval of all other beats on this tracing is identicalThe finding of identical rates for runs of beats with different QRS morphologies is rarely due to chance. I therefore think that despite the apparent fusion beat ( = beat #9) — that there is a single tachycardia occurring in Figure-1.
BOTTOM LINE: don’t know for certain what this rhythm is. Opinions from any electrophysiologists (or others who may be wiser than me) as to what may be going on are welcome!
  • Regardless of the rhythm — there appears to be lateral chest lead ST elevation consistent with a large ongoing STEMI. (This was borne out by cath results provided by Sam Ghali — which showed 100% proximal LAD occlusion).
  • Could the rhythm in Figure-1 be a single supraventricular tachycardia with underlying RBBB — that then manifests changing conduction defects (ie, switch to LAHB conduction following the early beat #9)?
  • Could there be atrial activity that we are just not seeing well due to lots of baseline artifact?
  • Could the rhythm in Figure-1 be some unusual form of VT (ie, Bundle Branch Reentrant VT — or some other form of reentry, perhaps through an occult accessory pathway)?
  • COMMENT — Sometimes, one has to proceed clinically despite uncertainty about the precise rhythm. Apparently, this patient was in shock on presentation. If so, given lack of sinus P waves — immediate cardioversion of this wide tachycardia would seem indicated regardless of the mechanism of the rhythm. Hopefully, this would result in conversion to sinus rhythm — at which point attention to the ongoing STEMI could be addressed.
  • Some of the best ECG learning cases are those in which we don’t have a definitive answer.
  • For more Fusion Beats, and what they mean — CLICK HERE.

ADDENDUM: GREAT comment by Christopher (below) — which I am reproducing here. For clarity — I’ve added arrows for potential atrial activity (Figure-2).

Figure-2: Christopher’s comment + addition of arrows to my Figure-1(See text).
  • I previously pointed out the possibility of a P wave following the early beat, occurring before beat #10 (BLUE arrow). The reason I was not convinced this was a sinus P wave — was that I didn’t (and still don’t) see any indication of sinus P waves preceding beats #1-thru-8 in this long lead II, despite the isoelectric baseline with more than enough space to fit a P wave in before these first 8 beats ...
  • That said — as per the PURPLE arrows ( = Christopher’s theory, which is perhaps the most plausible) — there is suggestion of a small deflection preceding beats #11-thru-21.
  • As per my “3rd Impression” — the identical rate for both QRS morphologies that we see in this tracing is unlikely to be due to chance — and strongly argues that there is one single tachycardia here, which most probably results from acute STEMI with sinus tachycardia RBBB (for beats #1-thru-8) — followed by the early beat (not a “fusion” beat, despite looking so much like it is fusion ... ) — which due to the shorter recovery time precipitates LAHB in addition to RBBB for the last 12 beats in the tracing. THANK YOU Christopher!

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