Friday, September 22, 2023

This ECG was texted to me: normal variant early repolarization, or LAD Occlusion MI (OMI)?

This ECG was texted to me with no other information.  I assumed the presentation was consistent with acute MI.

What did I say?

"OMI.  Activate the cath lab."  

The T-waves in V2-V6 are diagnostic.  It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5.  

There is also some non-diagnostic STE in inferior leads.  There is zero reciprocal ST depression.  50% of LAD OMI have zero reciprocal ST depression!

But it looks a lot like normal variant STE (also known as "early repolarization".

Then I sent it to the Queen of Hearts PMCardio AI Bot and she gave this response:

The Queen is very good.

I also later used the 4 variable formula:

19.6 is all but diagnostic of LAD occlusion.

In spite of a relatively short QTc of 376 ms, the very low R-wave amplitude in V4 and the ST Elevation at 60 ms after the J-point in lead V3 contribute to a high final value.

Here is the clinical story:

A 40 year old male with no cardiac history presented with acute substernal chest pain that started 40 minutes prior to arrival.  He had been having similar episodes for the past week, lasting no more than 5 minutes.   He reported associated diaphoresis, radiation to the bilateral upper extremities and mild shortness of breath. 

The first ECG was recorded at 53 minutes after pain onset.

He was given NTG sublingual.

The pain began to improve and this ECG was recorded:

T-waves are not quite as tall, though still have a large AUC.
They continue to show OMI.

Then the pain completely resolved and another ECG was recorded:

There are now very subtle Wellens waves (Pattern A).  
[Subtle terminal T-wave inversion in V3-V6.  This is diagnostic of full reperfusion.]

An old ECG was found:
As you can see, this patient has zero baseline STE, and normal T-waves.  You never know if a patient's baseline has normal large STE or complete absence of STE, or somewhere in between.  
90% of normals have some STE in V2 and V3.

The first troponin was 21 ng/L (detectable but below the 99% URL of 35 ng/L).  A healthy young man would be expected to have a troponin that is undetectable (less than 3 ng/L)

The patient went to the cath lab: 

--Ruptured plaque in the distal LAD

--Diffuse coronary artery disease is noted in LAD branch vessels and a small LPL branch

--LAD is a large-caliber vessel that wraps around the apex (this explains the STE in inferior leads)

--First diagonal branch is a medium caliber with diffuse severe stenosis in the medial branch

--There is diffuse 40% stenosis in the proximal and mid LAD

--D2 is a small to medium caliber with tandem 70% stenoses in the ostial/proximal segment

--There is a hazy 95% stenosis in the distal LAD with angiographic characteristics of plaque rupture

--Apical LAD flow is TIMI-3 on initial angiography

It is important to remember that 20% of definite STEMI (OMI that everyone agrees are STEMI) have TIMI-3 (perfect) flow at angiography.  And you can see why: the artery may sponstaneously reperfuse, as it did here well before angiography, and documented with resolution of pain and evolution of the ECG to typical full reperfusion pattern

Peak troponin I was 8544 ng/L.  This is typical for a brief LAD OMI.

In some of our studies, this ECG would be classified as a false positive because the TIMI flow was perfect and the peak troponin was not over 10,000 ng/L!

Formal echo: 

--Normal left ventricular size, mildly increased wall thickness, and normal function. 

--Estimated left ventricular ejection fraction 55-60%.

--Regional wall motion abnormality--mid to apical anterior, mid anteroseptal, and apical septal akinesis.


MY Comment, by KEN GRAUER, MD (9/22/2023): 


Today's case is challenging — because our 1st look at the ECG in Figure-1 was without the benefit of any clinical information. I focus my comment on this initial ECG in today's case.

Take another LOOK at the ECG in Figure-1 ...
  • How can we know that this ECG should not be mistaken for a repolarization variant? 
  • Which 1 or 2 leads are KEY?

Figure-1: I've labeled the initial ECG in today's case.

MY Thoughts
 on the ECG in Figure-1:
Unlike Dr. Smith — I admittedly was not immediately certain that today's initial ECG represented an acute OMI. 
  • What lowered my confidence in calling ECG #1 a definite OMI — was the finding of somewhat similar-appearing, upright T waves with slight-but-real J-point ST elevation in so many leads (ie, leads I,II,aVF; V2-thru-V6)
  • My confidence was also lowered by the complete lack of any ST elevation or depression in lead aVL (which is usually my "Go To" lead when looking for confirmation of acute inferior OMI, or for acute LAD occlusion).

And then I looked closer ...
  • Unless the ECG in Figure-1 was obtained as "routine" in an absolutely asymptomatic patient (or unless a prior tracing on this patient could be found showing identical ST-T wave morphology) — the 2 leads enclosed within the dotted BLUE rectangles ( = leads V4 and V5— simply can not be interpreted as "normal".
  • Instead — leads V4 and V5 have to be interpreted as having hyperacute T waves that are clearly disproportionate to their respective QRS (ie, These T waves are taller in size — "fatter"-at-their-peak — and wider-at-their-base than expected, given the small R wave amplitude in these leads).

  • Once I identified leads V4 and V5 as definitely abnormal — I looked closer at neighboring leads. Looking more laterally, while the R wave in lead V6 was clearly taller than the T wave in this lead — in the context of knowing that leads V4,V5 were hyperacute — the T wave in lead V6 looked "fatter"-than-expected — and the base of this T wave was clearly widened.
  • Looking more proximally (in the context of knowing leads V4 and V5 were hyperacute) — lead V3 (and by extension, probably also lead V2) manifest a taller-than-expected and wider base than is generally seen with repolarization variants.

  • MY Impression Thus Far: Learning what the history in today's patient is — was clearly critical to optimal interpretation. That said — IF there was any history of recent symptoms, my interpretation would be multiple hyperacute chest lead T waves until proven otherwise.

Looking at the Limb Leads:
  • As noted above — I was surprised by lack of any ST segment deviation in lead aVL. That said —

  • The Qr pattern in lead III (BLUE arrow) — was clearly abnormal! Although the finding of an isolated Q wave in lead III is by itself not necessarily abnormal — this Q wave was much larger and wider, as well as followed by a small-but-definite terminal positive deflection (r') — which generally is not seen as a normal finding in lead III.
  • In support of this Q wave in lead III being abnormal — is the small-but-definite q wave in lead II (within the dotted BLUE circle).

  • Finally — I though lead aVF looked extremely suspicious! (ie, with a straightened ST segment takeoff — and considering tiny size of the R wave in this lead, a hyperacute-looking T wave).
  • P.S.: While by itself, the ST-T wave in lead I would not necessarily look abnormal — there is J-point ST elevation in this lead, that in the context of all of the other findings may well be part of the acute picture.

BOTTOM LINE: I have found it extremely helpful when assessing ECGs for possible OMI — to look for those 1 or 2 leads that I know do not look normal. Once I find 1 or 2 of those leads — closer scrutiny of the remaining 10 leads usually reveals enough abnormalities to support my suspicion.
  • As discussed above in Dr. Smith's excellent discussion — serial ECGs, correlated to severity of patient symptoms soon confirmed the acute event in today's patient. 

Wednesday, September 20, 2023

A 50-something with Regular Wide Complex Tachycardia: What to do if electrical cardioversion does not work?

Case submitted by anonymous. Written by Smith.  Ken's piece at the bottom is excellent.

A 50-something presented with sudden onset palpitations 8 hrs prior while sitting at desk at work. He had concurrent sharp substernal chest pain that resolved, but palpitations continued. Over past 3 months, he has had similar intermittent episodes of sharp chest pain while running, but none at rest. Past medical history includes coronary stenting 17 years prior. A brief chart review revealed his most recent echo in 2018, with LV EF 67%, “very small” inferior wall motion abnormality.

Initial ED ECG:

What do you think?

This was shown to me with no clinical information and I said "It is VT until proven otherwise."  Why did I say that?

1. It does not look like RBBB or LBBB; therefore, if there is aberrancy, it is atypical aberrancy

2. The rapidity of onset of the QRS is slow (in SVT with aberrancy, the first part of the QRS is through fast conducting Purkinje fibers and is therefore narrow).  Look at the R-wave in V4: it takes 60 ms to reach its peak.  It should be less than 30 ms.

3. It has a "Northwest Axis" (towards aVR).  Correspondingly, as Ken notes below, the inferior leads are 100% negative, which virtually never happens in SVT.

4. There is a 40 ms q wave in aVR.  

5. The 2 R-waves in V1 fulfill Brugada criterion of having the first R larger than the 2nd R (in true RBBB, the first r-wave is small and the 2nd R'-wave is large)

6. There is a deep S-wave in V5 and V6.

7. The 15th beat (2nd beat of V1-V3) appears to be a fusion beat, which is all but diagnostic of VT.

8. Ken notes AV dissociation.  I find AV dissociation in VT to be very difficult to differentiate from artifact, as there are always random blips on tachycardia tracings.

So there are MANY features of VT and virtually zero features of SVT with aberrancy.

Then we must consider clinical data other than the ECG, for a pretest probability:

Of all wide complex tachydysrhythmias, the majority are VT.

If you take old people with a history of MI (he had a stent), that percentage goes far higher since there is scar tissue that acts as a nidus for the PVCs that initiate VT.  The history of inferior wall motion abnormality confirms this.

Clinical course:

A bedside echo showed good contractility.

The interpretation was SVT with aberrancy (erroneous).

The choice was to use electrical cardioversion with sedation.

No adenosine was given (if you believe it is SVT, this is worth a try).  However, this is not SVT.  If it is VT, adenosine is safe but not effective.

Shocked x 2 without effect.  Pads were placed with ultrasound guidance, so they were in the correct position.

What to do now?

If you believe it is SVT, then try adenosine.

If you don't know what the dysrhythmia is, then try procainamide.  Procainamide is proven better and safer than amiodarone for VT (Procamio randomized trial) AND it also works for SVT.  So I would give procainamide.

Warning: if this is VT, a calcium channel blocker can result in shock and death.

K returned 3.6 mEq/L

2 g IV Mg was given. 10 mEq IV K (with plan for 40 mEq PO KCl) was given.

Heparin bolus (4000u), infusion  

Plan for rate control

25 mg IV diltiazem given

HR = 143

25 mg IV repeat dose diltiazem given

HR = 143

Diltiazem drip 10 mg/ hr for ~20 min

HR remained 140 - 155 

Then the patient developed Cardiogenic shock and echo had poor contractility

Amiodarone load given.   Patient intubated.

Repeat cardioversion was then successful.

Cardiology was consulted and the patient underwent coronary angiogram which showed diffuse severe three-vessel disease. 

Episodes of angina over past couple of months had been progressive. 

--High sensitivity troponin I rose to peak at 2900 ng/L.  

--Formal bubble contrast echo showed EF 35% with anterior, anterolateral and inferolateral akinesis.  

--Coronary angiogram shows diffuse severe three-vessel disease.  

--Patient will need CABG 

Learning points:

1. Calcium channel blockers must be avoided in VT (unless it is fascicular VT, which has a different morphology.  Read this post: 

Idiopathic Ventricular Tachycardias for the EM Physician

2. Pretest probability: Even before the ECG, a patient with a history of coronary stent has a 90% chance that his wide complex tachycardia is VT.

3. VT can be perfectly hemodynamically stable if the patient has good cardiac contractility.  The reason that VT is associated with instability is that so many cases of VT are in patients with very poor LV function.

2.  Learn to differentiate VT from SVT with aberrancy.  Here are many discussions of, and cases of, SVT with aberrancy.

3.  Electrical Cardioversion works for both, but when it does not, try procainamide (in addition to optimizing K and Mg).  Procamio randomized trial.


MY Comment, by KEN GRAUER, MD (9/20/2023): 


Assessment of the regular WCT ( = Wide-Complex Tachycardia) patient — is one of the most challenging problems in emergency medicine. Fortunately — initial management is similar in many cases, regardless of whether the rhythm is VT or some form of SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or aberrant conduction (ie, Synchronized cardioversion may be needed if the patient is at all unstable ...).
  • Today's case is insightful in many ways — especially since despite prompt electrical cardioversion, we are told that this patient "was shocked X 2 without effect".

My clinical impression of the initial rhythm in today's case was similar to that of Dr. Smith — namely that this initial rhythm has to be interpreted as "VT until proven otherwise". That said:
  • There is no need to "prove otherwise" in today's rhythm — because ECG #1 (that I've reproduced in Figure-1— already provides proof that this rhythm is VT.

  • Definitive diagnosis that ECG #1 is in fact VT is more than academic. This is because the treating clinicians failed to make an accurate rhythm diagnosis — and, as a result — the wrong treatment was continued, with nearly lethal consequence (ie, IV loading with Diltiazem — followed by IV Diltiazem infusion for ~20 minutes resulted in severe hypotension).

Take another LOOK at the initial ECG in today's case (Figure-1).

  • Why do I say there is proof in ECG #1 that the rhythm is VT?

  • IV Diltiazem (and/or IV Verapmil) can be a treatment of choice in selected hemodynamically stable patients with Fascicular VT. That said — How do we know that IV Diltiazem was contraindicated in today's case?

Figure-1: I've reproduced the initial ECG in today's case. Do you see proof that confirms VT?

Lessons from Today's CASE:
I've reviewed "My Take" on ECG interpretation of the regular WCT rhythm on many occasions in Dr. Smith's ECG Blog (See My Comment at the bottom of the page in the June 23, 2023 postamong many others).
  • The fact that the 50yo man in today's case has known coronary disease (including exercise-induced angina over the previous 3 months) — means that even before looking at his initial ECG — statistical odds that his regular WCT rhythm will be VT are at least 90%.

  • These statistical odds can be increased to over 95% likelihood of VT within a focused 5-to-10 second assessment that notes: i) There is extreme frontal plane axis deviation (ie, an all negative QRS in each of the inferior leads — which is virtually never seen in SVT rhythms)ii) QRS morphology in lead V1 is atypical for RBBB conduction because of the lack of an S wave, and the taller "left rabbit ear" (While this does not completely rule out the possibility of rbbb conduction — it does make SVT much less likely)andiii) The almost-all-negative QRS complex in lead V6 (which will almost always have more positive activity in supraventricular rhythms).

We are told that "the Patient was Shocked X2 Without Effect ..."
While possible that synchronized cardioversion had no effect — I suspect it more likely that something happened after these 2 shocks were delivered — but that the patient then quickly resumed his WCT rhythm.
  • This is clinically relevant — because obtaining hard copy of what happened immediately after synchronized shock was delivered (even if the WCT rhythm resumes quickly thereafter) will often provide ECG clues to a definitive rhythm diagnosis. And IF it these clues would have been recognized — the inappropriate use of IV Diltiazem might have been avoided.

We are told that this Patient had Palpitations that Lasted for Hours!
While difficult to quantify from the limited information available in today's case — it sounds like this patient may have remained in sustained VT for hours (ie, He presented 7.5 hours after the sudden onset of his palpitation symptoms).
  • Perhaps the reason clinicians in today's case thought the regular WCT rhythm that this patient presented in was SVT with aberrancy — was that the patient reported "hours" of palpitations?
  • As I discussed and documented in Lesson 1 of My Comment at the bottom of the page in the April 2, 2022 post of Dr. Smith's ECG Blog — certain patients may remain in sustained VT not only for hours — but even for days!

IV Diltiazem was Contraindicated!
As discussed often in Dr. Smith's ECG Blog — the entity of idiopathic VT is unique, in that ~10% of VT rhythms are seen in patients who do not have underlying structural heart disease (See My Comment at the bottom of the page in the February 14, 2022 post of Dr. Smith's ECG Blog).
  • The 2nd most common form of idiopathic VT is Fascicular VT — which interestingly does often respond to IV Verapamil or Diltiazem (See Figure-3 below in the APPENDIX for my Summary of Idiopathic VT).

  • That said — Today's patient does not have the simple form of Fascicular VT that responds to IV Verapamil or Diltiazem — because today's patient has underlying heart disease (as well as a history of exercise-induced angina in the 3 months prior to presentation). In addition — ECG features of the initial rhythm are atypical for the simple form of Fascicular VT likely to respond to calcium blockers (ie, marked QRS widening — extreme frontal plane axis deviation — almost-all negative QRS in lead V6).
  • Since today's patient does not have this simple form of Fascicular VT — he almost certainly has an ischemic (scar-based) form of VT. The reason IV Diltiazem and Verapamil are contraindicated in ischemic VT — is that these calcium channel blockers are negative inotropes and vasodilators (the consequences of which were seen in today's case when the patient developed hypotension and cardiogenic shock following IV Diltiazem).

How Can We Prove that ECG #1 is VT?
In addition to the clinical setting (Today's patient having known coronary diseaseand the above ECG features described by Dr. Smith and myself — there are 2 ECG findings that prove the initial tracing in today's case was VT. I've labeled these 2 ECG findings below in Figure-2:

Figure-2: I've labeled ECG findings that prove this rhythm is VT (See text).

There is a Capture Beat that manifests Fusion
As already noted — within seconds of seeing ECG #1, I was over 95% sure that the rhythm was VT.
  • It is not often that we see Fusion Beats in rapid regular WCT rhythms — because most of the time, the fast ventricular rate completely usurps any underlying supraventricular rhythm. However, when we do — this virtually proves that the WCT is VT — because unexpectedly narrow QRS complexes are unlikely to occur unless there is "capture" of a supraventricular impulse that somehow "gets through" and "fuses" with a ventricular beat.

  • I am always surveying regular WCT rhythms for a "break" in the rhythm — and/or for some unexpected change (ie, narrowing) in the QRS. My eye was therefore immediately drawn to the distinctly different-looking (and narrowerbeat #7 (that I have labeled F/C in Figure-2). And although beat #17 does not look much different from the other 23 beats in the long lead II rhythm strip — there is no doubt that this beat is different and narrower than all other simultaneously-recorded beats in leads V1,V2,V3. The only way for the ventricular beats in ECG #1 to become narrower (apart from rare "supernormal" conduction) — is if there is fusion with underlying supraventricular impulses (CLICK HERE — for more on Fusion Beats).

There is AV Dissociation in Today's Regular WCT!
Although the search for AV Dissociation is so often evoked among those criteria used to differentiate SVT from VT — the clinical reality is that it is uncommon (if not rare) for us to recognize AV dissociation in those cases of a regular WCT in which we otherwise do not know the etiology.
  • The diagnosis of VT is not nearly as difficult when the rate of the WCT rhythm is not overly fast. This is because diagnostic fusion beats and AV dissociation are much more likely to be seen in these relatively slower ventricular rhythm.

  • Today's regular WCT is ~140/minute — which is usually fast enough that identification of AV dissociation is typically challenging, if not impossible (ie, underlying sinus P waves will usually be hidden within QRS complexes and ST-T waves at this rapid a rate). That said — We can definitively diagnose AV dissociation in today's tracing!

  • Although it is often difficult to distinguish movement artifact from definite underlying P waves — the RED arrow P wave in the long lead II rhythm strip immediately caught my eye!

  • Once I knew that at least 1 definite underlying P wave was present — I diligently looked for more. This told me that the ORANGE arrow deflections were all clearly highlighting other underlying P waves. (There is no R wave in the QRS complex of ventricular beats in the long lead II rhythm strip — so the initial positive deflection seen at the beginning of the QRS of beats #2, 5, 8, 18, 21 and 24 is the superposition of regularly-occurring underlying sinus P waves on the QS complexes of the VT rhythm.)
  • Note that 2 consecutive ORANGE arrow P waves (in the T waves of beats #12 and 13) follow the RED arrow P wave — which told me the underlying sinus P-P interval. Even without calipers — the above process (which took me no more than seconds to recognize) indicated enough on-time regular P waves to confirm AV dissociation — which told me 100% that ECG #1 is VT.

  • In the "peace and quiet" of my office — Knowing the underlying P-P interval allowed me to map out (with PINK arrows) regular-occurring underlying sinus P waves throughout the rest of the rhythm strip (with many of these PINK arrow P waves producing extra "peaking" of T waves, as for the T waves of beats #3,6,9,16,19,22).

  • To EMPHASIZE: I knew there was AV dissociation from recognition of the RED and ORANGE arrow P waves — that with practice, can be recognized at the bedside without calipers in no more than a few seconds.

  • Final POINT: For there to be "capture" and "fusion" — an on-time sinus P wave should be seen to occur at a point in the cardiac cycle in which conduction of a supraventricular impulse would be likely. Note that the long vertical BLUE arrow extending upward from the PINK arrow P wave in the T wave of beat #16 does occur at a point in which conduction of the F/C complex would be likely.
  • CLICK HERE — for more on use of AV Dissociation in the diagnosis of VT.

The LESSON To Be Learned:
Recognition that the regular WCT rhythm at ~140/minute in today's case was an ischemic form of VT can be made in time-efficient fashion at the bedside.
  • Although detection of fusion, capture and/or AV dissociation will not often be found in those more-difficult-to-diagnose faster VT rhythms — these ECG findings were all present in todays case — allowing a definitive diagnosis if recognized.
  • But even if fusion, capture and AV dissociation were not identified — the diagnosis of presumed VT and treat accordingly until proven otherwise needs to quickly be made at the bedside.
  • It should be clear that today's patient did not have idiopathic VT — because the patient has known coronary disease. As a result — IV Diltiazem was contraindicated.
  • Hard Copy tracings need to be recorded during cardioversion — since even if the patient's regular WCT resumes soon after electricity is delivered — the etiology of the WCT will often be revealed. This may have provided key information confirming ischemic VT, that would have immediately favored either IV Amiodarone or IV Procainamide (instead of the diversion of using IV Diltiazem bolus and drip that led to shock). 


ADDENDUM (September 20, 2023):

Figure-3: Review of KEY features regarding Idiopathic VT (CLICK HERE — for the source of this Summary).

Sunday, September 17, 2023

Chest discomfort and a dilated right ventricle. What's going on?

Written by Magnus Nossen MD, peer reviewed and edits by Smith, Meyers, Grauer

A 60 something previously healthy female smoker sought medical attention after 2-3 days of intermittent chest discomfort. The chest discomfort was described as sharp. Episodes lasting 5-30 minutes. On the day of presentation she experienced another episode of chest discomfort accompanied by vomiting and throat pain. She was concerned about possible throat infection. She contacted her primary care physician. Due to the vague nature of her symptoms and the fact that she had chest discomfort and no clinical sign of throat infection she was referred for further work up. 

Upon admission she had ongoing slight chest discomfort. Vital signs unremarkable except borderline hypotension with a systolic BP about 102 mmHg. The following ECG was recorded. 

Here the image quality is enhanced using the PM Cardio app. What do you think?

The presenting ECG shows SR with narrow QRS complexes. There is normal R-wave progression in the precordial leads with no evidence of ischemia. In the limb leads there is T-wave inversion in lead aVL with a low amplitude QRS preceding the T-wave. There is some upwards concave ST segment elevation in the inferior leads with what seems to be well formed J-waves. 

First troponin I returned 3174 ng/l, at which point a repeat ECG was ordered. 

Not much difference from 1st ECG.

A bedside echo was performed. 

The bedside echocardiography showed a dilated and hypokinetic RV with an internal diameter (RVIDd) at the base about 4,0cm. The RV > LV. There is visible septal flattening with D-sign in the parasternal short axis. McConnells sign was present. (maybe not seen well on these echo-loops) The CW doppler at the tricuspid valve showed a maximum TR velocity of 2,55m/s with a TRP gradient of 26mmHg. 

Possible explanations for the echocardiographic findings could be grouped accordingly:
  • 1) Conditions causing volume overload of the RV. (E.g large ASD, partial anomalous pulmonary venous return, significant tricuspid regurgitation, carcinoid valvular disease, etc,)
  • 2) Conditions causing pressure overload of the RV. (Any cause of pulmonary hypertension. E.g COPD, Idiopathic PAH, acute or chronic PE, pulmonary valve stenosis, etc)
  • 3) Conditions affecting RV myocardial contractility, such as ARVD or RV infarction

The ECGs does not really show any signs of chronic RV dilation or hypertrophy. There is normal axis, normal R-wave progression in the precordial leads and no intraventricular conduction abnormalities. Furthermore there are no ST-T changes in the early precordial leads as could be expected if the dilation was caused by pulmonary embolus or ARVD. 

At this point an old ECG on file was found for comparison. 

Below, the limb leads of the baseline ECG (left) placed side-by-side with the limb leads of the presentation ECG (right). 

When placed side by side, the hyperacuity of the inferior T waves can be appreciated. It is also now easier to appreciate that the more bulky T wave inversion in aVL must represent reciprocal change from inferior wall hyperacute T waves. Also, looking through the retrospectoscope, the isoelectric ST segment in lead V2 on the presentation ECG becomes quite suspect for posterior wall involvement. 

                         Baseline limb leads                                      Presentation limb leads
Notice the T-waves in II, III, and aVF are substantially larger
On their own, this would not be diagnostic, but highly suspicious.
Just the fact of chest pain and highly elevated troponin is enough to activate the cath lab, but here you can see just how subtle hyperacute T-waves can be.

Based on the ECG changes, the echocardiographic findings, troponin level and rapid onset of symptoms the clinical picture seemed best explained by some acute process, making pulmonary embolus or acute MI most likely. An acute RCA OMI with inferior and right ventricular involvement fits way better than PE in this case, there really was no respiratory symptoms and O2 saturations and other vital signs were unremarkable, a right sided ECG was recorded and is shown below. 

The right sided ECG shows lack of any real R-wave in V3R-V6R. Also there is subtle but proportionally significant ST elevation in the same leads. The limb leads also seem to show some progression of inferior OMI findings. The cath lab was activated and the patient was found to have a 100% proximal RCA occlusion with TIMI 0 flow. Post PCI the patient became gravely hypotensive and "shocky". She stabilized on dobutamine and levosimendan infusions that could be discontinued after 24 hours. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). The tricuspid annular plane systolic excursion (TAPSE) improved from 15mm to 19mm within the first 24 hours. The LV EF was 57% at formal echo.

This case represents an RCA occlusion with inferior wall OMI findings on the ECG and echocardiographically predominant RV involvement. 

Purely isolated RV infarction is limited to patients with a dominant Cx or to patients who already have had an inferior wall MI who then later experience a proximal RCA occlusion. Isolated RV infarct will not show inferior wall OMI findings. RV infarction usually have ST-elevation or OMI findings in the right precordial leads overlying the right ventricle.

This is the ECG at discharge 3 days post PCI.

Here is an example of isolated RV infarction, from Dr. Smith's book:

Learning points: 

1) OMI can be very subtle and RV infarction may manifest poorly on the standard ECG.
2) Typical persistent chest pain with a sigificantly elevated troponin is OMI until proven otherwise, regardless of the ECG.
3) RV Failure leads to hypotension but NOT pulmonary edema (unlike LV failure)
4) Repeat ECGs, right sided ECG and bedside echo may be helpful in making a diagnosis of ACS.
5) McConnells sign can be seen in both RV infarction and acute RV pressure overload as with large PE

Here is a great case of Right Ventricular MI with both D sign and McConnell's sign:


MY Comment, by KEN GRAUER, MD (9/17/2023): 


I love cases when an unexpected outcome is so logically arrived at. Our THANKS to Dr. Magnus Nossen for sharing this case with us.
  • I focus my comment on the initial ECG in today's case — which I've reproduced in Figure-1, and to which I've added the previous tracing found on file.

Figure-1: Comparison between today's initial ECG — and the baseline ECG that was on file. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on the Initial ECG in Figure-1:
Key points in the history of today's patient — is that her symptoms of CP (Chest Pain) were intermittent over a 2-3 day period — without specific mention of when during this time period symptoms were greatest. As a result — the onset of any acute event that may have occurred is uncertain. In view of this history — I found ECG #1 of concern because of the following findings:
  • There is ST elevation in each of the inferior leads. Although the amount of ST elevation is not great in ECG #1, and there is J-point notching as commonly occurs with repolarization variants — the ST segment prior to the T waves in these inferior leads is straightened.

  • Lead aVL is definitely not normal. Although the tiny QRS amplitude in this lead makes assessment difficult — the J-point in lead aVL is depressed, the ST segment in this lead is abnormally coved — and the T wave relative to QRS amplitude is hypervoluminous and markedly disproportionate. The shape of this ST-T wave in lead aVL is a reduced-size mirror-image opposite picture of the ST-T wave in lead III — which in a patient with CP, could clearly reflect reciprocal changes of a recent or ongoing acute process.
  • In support of that these findings in lead aVL are not normal — the other high-lateral lead ( = lead I) is also not normal in appearance (ie, the ST segment in lead I is completely flat — in association with a smaller-than-expected T wave).

  • My IMPRESSION re the Limb Leads: I thought the above noted limb lead findings in ECG #1 were non-diagnostic — but clearly of concern. In this woman in her 60s, with a 2-3 day history of intermittent CP (potentially consistent with an event occurring at any point during that time period) — I thought the above ECG findings could reflect recent inferior OMI. Additional evaluation (and ideally finding a prior tracing for comparison) would be very helpful.

Regarding the Chest Leads in ECG #1:
  • The ST-T wave appearance in leads V2-thru-V6 is not normal. Instead — ST segments in each of these 5 leads is abnormally flat. This is especially noted in anterior leads V2 and V3 — which normally display a slight amount of upward-sloping ST elevation. In the presence of the above-noted limb lead findings — this lack of slight, upward-sloping ST elevation in leads V2,V3 — especially in association with an R wave in lead V3 that abruptly becomes tall (given the tiny r wave amplitude in neighboring lead V2) — could be consistent with recent posterior infarction, especially given concern from the limb leads about recent inferior OMI.

The Case Continued: 
  • The initial troponin value came back markedly elevated!
  • Repeat ECG (shown by Dr. Nossen above) — failed to show significant change.
  • Bedside Echo was performed.

 As dramatically shown in the bedside Echo by Dr. Nossen — the RV was greatly dilated and hypokinetic, narrowing the differential diagnosis to the entities he lists above in his discussion — with the lack of any ECG findings consistent with pulmonary disease and the markedly elevated troponin pointing to acute RV MI as the most likely diagnosis. Interesting additional aspects of today's case include:
  • Comparison with the "baseline" tracing ( = ECG #3 in Figure-1) — confirms that the subtle-but-real ST-T wave limb lead changes noted above in ECG #1 were new, as there was no ST elevation in the inferior leads and no ST depression in lead aVL of baseline ECG #3.
  • That said — the earlier-than-expected transition and ST segment flattening in leads V3-thru-V6 was present in the baseline ECG (if anything, with slight ST depression in the earlier tracing) — so these chest lead changes that I suspected represented posterior OMI in ECG #1 were not new.

  • Finally (as per Dr. Nossen) — the right-sided ECG that was done did show ST elevation that confirmed RV MI, albeit the amount of right-sided ST elevation was modest. 

Last Points:
The "good news" — is that bedside Echo was instrumental in recognition of acute RV MI.
  • Seeing the markedly dilated and poorly contractile RV on Echo — facilitated clinical ECG interpretation. Comparison of the initial ECG with the prior "baseline" tracing — confirmed acute inferior OMI, which "fit" with the cardiac cath finding of acute proximal RCA occlusion.
  • I suspect the real-but-relatively-modest ECG changes seen on the ECGs in today's case may be because: i) The acute event in today's case may have begun 2 or 3 days earlier (as suggested by the history)andii) Right-sided ST elevation in association with acute RV MI tends to be a transient event that often resolves within 24 hours (Nagam et al — Perm J: Vol. 21, 2017).  

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