Sunday, March 30, 2014

New ACC poster: many STEMI patients present with subtle ST elevation.

New ACC poster: many STEMI patients present with subtle ST elevation. Their prognosis is similar to those who meet STEMI "criteria". They need early reperfusion.

However, this study could have missed many occlusions because they only studied patients who did get immediate primary PCI.  They did not study the NonSTEMI patients who were later found to have limited coronary flow and might have benefited from immediate reperfusion.

The ECG told the whole story, but no one listened: ECG interpretation skills are critical to patient outcomes.


This was sent by a medical student somewhere in the world who will remain anonymous.  Details are scant so that it cannot be recognized.

The minute this medical student saw the first ECG, he knew the diagnosis without any further information.  Reading ECGs is hard, but can be done with commitment to learning, which comes from an awareness of its importance.  My most talented blog readers are paramedics because they have to put themselves on the line every time they activate the cath lab.  And they teach me a lot.  One of my most talented readers is a health care assistant (a nursing assistant) who has taken a keen interest in ECGs.  He can beat nearly anyone.  So you don't have to be highly trained.  You don't have to be a genius. You need to be interested and understand the value of the ECG.   It is not the ECG which is nonspecific, it is the interpreter.


A female in her 60s presented with 3 days of nausea, vomiting, and diarrhea, and not feeling well.  She complained of jaw pain and shortness of breath.  There was a 30 second episode of syncope, and another one the previous evening, without any tonic clonic movements, tongue-biting, or incontinence. She was ill appearing.  She had a remote history of lung cancer many years ago, cured.  She had no other medical  history.

She had this ECG recorded:
ECG 1: QTc is 484.  What do you think, especially compared to the previous, pasted below?

Previous ECG. completely normal

The diagnostic features of the first ECG were entirely missed by a whole team of emergency physicians, cardiologist, surgeons and others, even as the patient became increasingly hypotensive to a systolic BP of 60.  The lactate was elevated and pH low.  They were worried that the syncope was seizure and that she had brain mets.  Then they were worried about sepsis as an etiology of hypotension.  Then the notes mention "cardiogenic shock" but without any reference to a cardiac echo or to a chest x-ray.  Was there pulmonary edema?  Not mentioned in physicians'  notes.  Then she had some RUQ tenderness which led to a long process of evaluation for an abdominal source of sepsis, which turned up negative.  Initially fluids were given, then stopped in favor of pressors, as a CVP line showed CVP = elevated.

Another ECG was recorded:
ECG 2: Findings are still present and have evolved to a small degree

At time 6 hours, Troponin T returns at between 0.50 and 1.00 ng/mL (not giving exact number, but significantly high)

Now having frequent PVCs.

Now chest pain free.  Cardiologist note says: "Elevated troponin explained by type II MI due to her shock."  "Repeat ECG showing no STEMI, only non-specific ST-segment and T-wave abnormalities, unchanged from prior"

Transferred to surgery for exploration but diagnostic studies were too indeterminate to be certain of intra-abdominal pathology.  Besides, the surgeons say she is "too unstable for surgery."

Day 2:

A cardiac echo was done which showed normal LV function but moderate RV systolic dysfunction and diastolic septal flattening consistent with right ventricular volume overloadRight ventricle: moderately enlarged, hypocontractile free wall, moderate global decrease function.

Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI.

Still the pieces were not put together.

Another ECG is recorded:

ECG 3: More evolution, but not recognized.

I have only shown you 3 of the many ECGs recorded over the 3 days, all of which were diagnostic but not diagnosed.

After midnight (now day 3), she complains of shoulder pain and dyspnea.  Troponin was repeated and returned higher still.

She was taken to the cath lab.

What was the diagnosis?  See below.

Outcome and Analysis:

ECG 1 is diagnostic of inferior and right ventricular MI.  There is a junctional bradycardia.  There is less than 1 mm of STE in inferior leads with diagnostic reciprocal ST depression in aVL.  Additionally, there is ST elevation in V1 which, in the presence of inferior MI is diagnostic of Right ventricular MI.  This is the etiology of the syncope and hypotension and shock and elevated CVP. and right ventricular echo findings..  Furthermore, there are T-wave changes in V2 and V3 which are highly suggestive of ischemia, but difficult to localize: anterior? posterior? right ventricular?  In any case, these further support the diagnosis of coronary occlusion or near occlusion.  ECG 2 is similar, also with a junctional rhythm that is resulting in inverted P-waves in inferior leads (retrograde).  ECG 3 is yet more evolved.

When they finally did it, the cath showed a 100% RCA thrombotic occlusion at the ostium (proximal, before the RV marginal branch), confirming all clinical and ECG findings (except for diarrhea).  There was also disease of the LAD and Left circ.

She turned out to not have any abdominal pathology.
All cultures were negative.
There were multiple complications.

This was an inferior and right ventricular MI and once the first ECG was recorded, the diagnosis could have been made: everything about the presentation, after the ECG, screamed this diagnosis.


I cannot read the minds of the physicians involved, but I suspect there were two components to the delayed diagnosis:

1. Atypical presentation (nausea, vomting, and diarrhea)
2. Failure to regognize subtle but diagnostic features of the ECG.

Many say generally that the ECG is often a "non-diagnostic" test, or a nonspecific test.  Most often, it is the interpreter who is nondiagnostic and nonspecific.  The ECG here told the whole story, very specifically.  It was the failure of accurate interpretation which led to a 2 day delay in diagnosis and significicant myocardial loss and much unnecessary diagnostic and therapeutic intervention.

The ECG told the whole story, but no one listened.

Friday, March 28, 2014

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

A male in his 60s presented complaining of dysnpea and chest pain.  He was tachypneic and ill appearing.

I was texted this ECG.  The physician worried about PE mostly, but also MI:
My response was: "incomplete RBBB.  No evidence of acute MI.  Certainly could be PE.  What does the cardiac echo show?"

The bedside echocardiogram showed a serpiginous echogenic structure in the right atrium that was also flowing in and out of the right ventricle.  The RV was enlarged.

I am sorry that I had to take this video down because my colleague wants to submit it to an academic journal.  I have left the still frame in.

Still frame of the video: Blue circle show thrombus snaking throughout right atrium and right ventricle.

The patient was given IV tPA and rapidly improved.  A subsequent ultrasound showed no more thrombus.

Thursday, March 27, 2014

COPD exacerbation, what do the ECG and bedside echo show?

A woman in her 60s presented with a COPD exacerbation.  She also complained of some sharp chest pain with coughing. She was in moderate distress consistent with a moderate COPD exacerbation.  An ECG was recorded:

The computer reading was: "Anterior ST elevation due to early repolarization."

The treating physicians were alarmed by the first ECG due to the apparent hyperacute T-wave in V3.  They applied the LAD occlusion vs. early repol formula (see sidebar for excel applet and see previous posts), using computerized QTc of 416, STE60V3 of 3.0 (it may be 3.5) and R amplitude in V4 of 13, and found a value of 23.9 which is greater than 23.4 and indicates LAD occlusion.

So they sought out a previous ECG:

Here is one from 2 weeks prior:
What do you think?

Now they were even more worried, as the acute ECG is much different.  However, this patient did not have chest pain that was in any way typical.  They were appropriately reluctant to activate the cath lab, but did call the cardiologist, who was also appropriately worried.

A bedside ED cardiac echo was done during the evaluation:

The embed code has stopped working consistently.  You can see the video by clicking here:

First bedside ultrasound, subcostal view from Stephen Smith on Vimeo.

Here is an annotated still picture of one frame from above:
The blue arrow points toward the tricuspic valve and the base of the RV.  The red arrow points toward the mitral valve and the base of the LV

Second ultrasound, apical view from Stephen Smith on Vimeo.

What do these cardiac echo clips show?

First video clip: This clearly shows the bases of both the right and left ventricles are beating vigorously, but the apex is hardly moving at all.

Second clip: It is easy to see the base of the heart contracting, but although the image quality of the apex is poor, one does not see much motion there

At this point, the patient started having crushing chest pain and another ECG was recorded:
Now there is increased ST elevation in V3. See outcome below.

A formal ultrasound with Definity contrast was being done at approximately the same time as the onset of severe chest pain.  It showed:

--Regional wall motion abnormality-distal septum anterior and apex akinetic, large.
--Regional wall motion abnormality-distal inferior wall akinetic.
--Regional wall motion abnormality-lateral akinetic.
--There good contractility of the base of the heart.

--Normal left ventricular size.

--Decreased right ventricular systolic performance severe.
--Regional wall motion abnormality-right ventricle .


This ultrasound and the bedside ultrasounds show "apical ballooning", all highly suggestive of Takotsubo stress cardiomyopathy (which is likely to accompany a stressful event such as a COPD exacerbation), but it is also compatible with acute LAD occlusion.  The crushing chest pain, wall motion abnormalities, hyperacute T-waves and ST elevation were possibly due to takotsubo stress cardiomyopathy but also possibly due to LAD occlusion.  The patient was taken to the cath lab and had no obstructive LAD lesion and no culprit.  The troponin I peaked around 1.5 ng/ml.

Can one distinguish on the ECG between takotsubo stress cardiomyopathy (SCM) and acute STEMI???  Not reliably!  There are some ECGs that are clearly due to stress cardiomyopathy (widespread T-wave inversion).  But when the ECG is recorded during the ST elevation phase, I know of no reliable way to differentiate these.  I reviewed this topic in this post.  To sum it up very briefly, if it appears to be an infero-antero-lateral STEMI, it is more likely to be SCM than if the ST elevation is in one coronary distribution (e.g., anterior, as in this case); however, again, this is not more than 80% reliable.  The cellular pathophysiology of SCM is identical to STEMI (severe transmural ischemia), but it is due to catecholamine stress and small vessel constriction (NOT due to epicardial coronary flow obstruction); and that is why the ECG is nearly identical.

Here are several more cases of SCM.

Does cardiac ultrasound definitively differentiate the two entities?  In the acute phase, apical ballooning is highly suspicious for SCM, but large wall motion abnormalities may also be seen in patients with proximal LAD occlusion in a type III (wraparound) vessel, affecting anterior, lateral, and inferior walls.  These STEMI cases also have widespread ST elevation as in SCM.

Is the Right Ventricle involved in Takotsubo Stress Cardiomyopathy?

RV SCM has been described, appears to accompany LV takotsubo cardiomyopathy up to 25% of the time and be associated with worse LV function.   See this article: and also this article:


There is no more vexing ECG mimic of acute STEMI than SCM because the underlying cellular pathophysiology is the same.  It is unusual to make the diagnosis without an angiogram.

Monday, March 24, 2014

Elderly woman in Shock. EKG from #smaccGOLD pre-conference EKG workshop.

We had a great pre-smaccGOLD EKG conference, with Louise Cullen moderating and featuring Ed Burns, Hussam Tayib, John Larkin, Roger Harris, Trevor Jackson.

The smaccGOLD conference was incredible and the conference will be in Chicago next year!!  May 20-22, and I suspect there will be another EKG workshop the day before (May 19).  I will be proposing an Emergency Cardiology workshop as well, so stay tuned for more.

Here is a great description of the conference:

Participants brought there own ECGs, and this was one:

An elderly woman smoker with a couple days of intermittent chest pain presented in shock.  She had no past medical history and was on no medications.  She was delirious and agitated and required ketamine for sedation. 

Here is her ECG:
Is this VT?  Atrial Fib with RVR?  Sinus?  SVT?  And what about the QRS?  ST-T abnormalities?  See below.

Is this VT?  Atrial Fib with RVR?  Sinus?  SVT?  And what about the QRS?  ST-T abnormalities?

Answer: Sinus Tach with junctional premature beats (thanks to Jason Roediger and K. Wang for pointing that out!--these are not PABs or PVCs), RBBB, LAFB.  Subtle Antero-lateral ST elevation with inferior reciprocal ST depression.  Q-wave in V1 (QR where there should be rSR') suggests old or subacute MI.  This is a very dangerous combination and is almost always due to LAD or left main occlusion.


These very abnormal ECGs must be approached systematically unless you are very experienced and have instant morphology recognition.  Even then you are best off verifying your recognition with a systematic approach:

1. rate
2. rhythm
   2a. Fast?
      i. P-waves?
      ii. Regular or irregular?
      iii. If irregular, regularly irregular or irregularly irregular?
      iv. Wide or narrow?
      v.  Is it constantly fast? Sudden changes in rate?  Gradual changes in rate?
      vi.  Are there premature beats?
   2b. Slow?
      i.  Are there P-waves
      ii.  Do P-waves conduct?
      iii. Are P-waves at regular intervals?
      iv. Are QRS at regular intervals?
      v.  Are P's and QRS associated?  (no block)
      vi. Are P's and QRS dissociated? (block vs. dissociation only)
      vii.  Is QRS wide? (Escape or BBB)

3. QRS
   3a. Axis
   3b. Intervals (QRS, QT: look for LAFB, LPFB, RBBB, LBBB, IVCD)
   3c. Voltage
   3d. R-wave progression
   3e. Q-waves
   3f. S-waves
   4a. Voltage Proportional to QRS?
   4b. Appropriate/Inappropriate discordance/concordance to QRS?
   4c. T and QRS axis close to each other?
   4d. ST axis?

Here is an annotated ECG:
See full description below.  Black arrows point to P-waves that are hidden in preceding QRS but do conduct.  Red arrows point to easily seen P-waves.  These are easily seen because they follow a premature beat which does NOT reset the sinus node.  The blue arrow points to a P-wave that is hidden by BOTH the preceding T-wave and the onset of the following PVC.  The green arrows point to premature beats.  Are they PACs or PVCs?  This is very difficult to ascertain: if PVCs, they have a remarkably similar morphology to the conducted (LAFB, RBBB) QRS; if PACs, where is the premature atrial activity and why does it not reset the sinus node?  My conclusion is that they are PVCs that originate from near the posterior fascicle. 

Here is a more systematic analysis:

1. the rate is 120
2. one can see P-waves (black, red, and blue arrows)
3. P-waves are regular
4. QRS is irregular, but Regularly irregular, with beats 3, 5, 12, and 19 coming early (PAC vs. PVC vs. JPB.  These are Junctional premature beats, as the QRS is identical to the normal QRSs and there is no visible atrial activity).
5. There is some P to QRS dissociation (also beats 3, 5, 12, and 19)
6. QRS is wide


Axis is left
End of QRS is where black lines are
QRS duration in about 160 ms
Q-wave in V1
There are Deep S-waves in II, III, aVF and V2-V6.
There is a large R-wave in aVL and V1
Thus, the QRS morphology is LAFB and RBBB


The ST segment begins at the end of the QRS, at the black lines
There is ST elevation, see ST segment after black line in V2, V3, aVL


Taken to cath lab and had a proximal LAD occlusion, arrested and was unable to be resuscitated.

Here are two other similar ECGs:

First one (one of my most popular posts ever)
Second one (an incredible resuscitation with great outcome and also very frequently viewed)

Tuesday, March 18, 2014

Ventricular Fibrillation During Echocardiogram, Then Spontaneous Reversion Without Defibrillation

A 47 yo male presented to the Echo Lab one day after being seen in the ED for syncope.  During the echocardiogram, the tech noted that the heart stopped.  The monitor showed ventricular fibrillation.  Before the patient could be defibrillated, he spontaneously reverted to an organzied rhythm:

Ventricular Fibrillation, then a period of asystole, then a slightly wide escape rhythm.  One might question whether this is polymorphic VT, especially torsade.  I have a very long strip and it is definitely ventricular fibrillation, also as read by an electrophysiologist.

This happened several times before other personnel arrived with resuscitative equipment.

A 12-lead ECG was recorded:

There is no significant ST elevation, but there is ST depression in I, II, aVL and V4-V6.  The QTc is 465 ms, just barely longer than normal and not enough to cause torsade.

So the question comes up: what did he ECG look like at presentation to the ED the evening before?  Here it is:
Note how there is significicant ST elevation in V1 and V2 that is not there on the top (next day) ECG.  Note also that the T-waves are very prominent on the ED ECG, unlike the next day ECG.  The ST depression was present at that time as well.

I applied the LAD Occlusion vs. Early Repol Formula to this ECG: 

STE at 60 ms after the J point = 0.5 mm, computerized QTc = 460 ms, and R-wave amplitude in V4 = 7 mm; formula value = 25.45 which is greater than 23.4 and indicates that this is probably not normal variant ST elevation.

When the two are compared, it becomes clear that the ED ST elevation and T-wave are pathologic.

The patient was having anterior transient ST elevation ACS (technically not MI, as many have admonished me!!) at the time of the ED visit.  Serial troponins were normal.

An angiogram showed "100%" mid-LAD but with very faint antegrade flow.  He also had severe 3-vessel disease and underwent CABG 2 days later and did well.  The artery was occluded or nearly occluded at the time of the ED ECG.  This was the etiology of the ischemia and ventricular fibrillation. 

Spontaneous reversion of V Fib:

Spontaneous reversion is a rare but documented cause of syncope.  Here is one case report.  I have spoken with two electrophysiologists who report seeing this in the electrophysiology lab.   Frequently, what appears to be ventricular fibrillation is really polymorphic VT, as the two appear very similar morphologicially.  More often, I am shows a strip of Ventricular fibrillation that along with an erroneous interpretation that it is "Torsade," even though the patient was pulseless and required defibrillation.  Torsade should only be diagnosed in the context of a significantly long QT on the baseline ECG.  465 ms is not long enough.  Also, this morphology does not look like polymorphic VT (either Torsade or non-torsade PMVT).


1. ACS with 100% LAD occlusion
2. Syncope
3. Ventricular Fibrillation with Spontaneous

Friday, March 14, 2014

Pseudonormalization of Wellens' Waves

A male in his 60's complained of intermittent chest pain all day.  He was vague as to whether there was active chest pain, but it was definitely better at the time I talked to him.

Here is his initial ECG:
There is minimal ST elevaton and there are subtle T-wave inversions in V2-V5, highly suggestive of Wellens' syndrome
In Wellens' syndrome, the artery is open.  T-wave inversion, as I've pointed out countless times (and hope I'm not belaboring) is indicative of reperfusion of the infarct-related vessel.

BP was elevated, pulse lowered to 45.  He received ASA, Plavix 600mg, Heparin, and a Nitro drip.

As a matter of course, I ordered another ECG 15 minutes later:

The increasing T Wave inversion is Diagnostic of LAD ACS.

Once the diagnosis is made, the patient must go to the cath lab if pain cannot be controlled or the ECG shows any evidence of re-occlusion.  Re-occlusion is diagnosed by pseudonormalization of the T-wave (becoming upright).

The patient stated his pain was perhaps 4/10.

I ordered another ECG:
The T-waves are now upright and there is slightly more ST elevation (though this by no means meets "STEMI" criteria - these critieria are very insensitive for LAD occlusion).  If you apply the early repol/LAD occlusion formula (see sidebar Excel applet), using a computerized QTc of 413, the value is 26.6, which is significantly greateer than 23.4 and confirms the diagnosis of LAD occlusion.

I immediately activated the cath lab.  Because this was a highly unstable lesion, in discussion with the interventionalist, we gave a load and drip of eptifibated (Integrilin).

A bedside Echo of course showed an anterior wall motion abnormality.

His pain again subsided.

A 4th ECG was recorded, pain free:
Reperfusion T-waves are again present.

The artery is open again.

The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow.

Initial troponin I returned at 1.5 ng/ml.  Peak was 8.1 ng/ml.


1. Pay attention to T-wave inversions
2. Obtain serial ECGs
3. Patients with objective evidence of ACS whose pain and ECG abnormalities cannot be controlled must go for emergent PCI
4. LAD occlusion may be very subtle, with minimal ST elevation
5. T-wave inversion is a sign of reperfusion and open artery.
6. Normalization of T-waves in this context is "Pseudonormalization" and is diagnostic of re-occlusion

Tuesday, March 11, 2014

Incessant Regular Wide Complex Tachycardia

A male in his 50's presented after a witnessed syncopal episode. He reported multiple syncopal events over the last 1-2 months with increasing frequency, as well as recent fatigue.  He had a remote history of in-hospital cardiac arrest during surgery.  He had no anginal symptoms, no CP or SOB.  Prehospital tracings were concerning for monomorphic sustained regular wide complex tachycardia with repeated runs of bigeminy, and no clear evidence of a current of injury.

In the ED, he had VT on the monitor, and the following 12-lead ECG:
There is a regular monomorphic wide complex tachycardia with no P-waves. The computer measured the QRS at 126 ms, but it may be longer, depending on where the QRS ends, and that is not easy to ascertain.  There is left axis deviation and a large R-wave in V1: this is the RBBB-LAFB pattern and suggests either SVT with aberrancy of RBBB/LAFB, or VT with a focus of re-entry in the posterior LV, perhaps posterior fascicle.  A posterior fasciclar VT would usually have a relatively narrow QRS; if this is indeed 126 ms, that would be appropriate for posterior fascicular VT. 

It is most likely to be VT:  There is a large upright R-wave in aVR.  However, if the computer is correct, the QRS is not as wide as it should be for VT.  However, it could be fascicular.  Strongly supporting VT are the beats that follow the sinus beats; these are not preceded by P-waves (no sinus beat and no premature atrial beat either).  Therefore, the ectopic beats are ventricular.  And since the ectopic beat has the same morphology as the tachycardia, the tachycardia is almost certain to be VT.

Arguing against VT is the fact that RS wave in V3 has a duration of only about 80 ms from the start of the R-wave to the nadir of the S-wave (greater than 100 is expected in most VT) and that the QRS duration is short.  However, these would be expected in a posterior fascicular VT.  Fascicular VT, because it starts in the conducting system, looks more like SVT with aberrancy than it looks like VT.  It is also usually much more stable than standard VT (and this patient tolerated his dysrhythmia fairly well, was stable during this ECG, although it did result in syncope).

He was started on an amiodarone bolus and drip, with no response.  Then he was given several boluses of lidocaine and a lidocaine drip.  At a dose of 4mg/min, the VT stopped and the following 12-lead was recorded:
Ventricular bigeminy with couplets, all with the same morphology as the VT.  This proves that the first ECG is indeed VT, because the wide complexes here are definitely PVCs, (not PACs with aberrancy as there are no P-waves) and thus these are not supraventricular beats with aberrancy but definitely ventricular beats.

The patient was given Magnesium with a goal level of 2.5 mEq/L and K was targeted at 4.0 mEq/L. Aspirin, heparin and clopidogrel were given for suspicion of ischemic etiology.  Accordingly, the cath lab was activated.  Coronaries were normal.  Left Ventriculography showed a diffusely hypokinetic ventricle with dyssynergic contraction pattern. There were frequent PVCs during the injection. Visual estimated ejection fraction was approximately 30-40%.

The patient was transferred to the ICU post cath. He was continued on Amiodarone drip in addition to Lidocaine drip.  He had this ECG recorded:
Sinus rhythm with a slightly prolonged QRS

He continued to have high frequency ventricular ectopy with 30 beat runs of VT which were well tolerated. In the morning, he had a 30 beat run of monomorphic VT and then had an episode of severe bradycardia down to the 20's, with loss of pulses and need for brief CPR.  The patient was given 2 mg of atropine and was then transcutaneously paced for 5 minutes during which time he woke up and was alert.  He was sedated and intubated.  Etiology was not entirely clear, but amiodarone was suspected as partly to blame and it was stopped.  A transvenous pacer was placed.  He remained stable on a lidocaine drip.

Later, the patient went for EP study, and because it would be prolonged, he underwent general anesthesia.  No dysrhythmia could be induced under general anesthesia.  He was brought back awake the next day and dysrhythmias were inducible and able to be mapped.  It was found to be a posterior fascicular idiopathic VT.  It was successfully ablated.  The electrophysiologist did not think the bradycardia would be a persistent problem, so did not implant a permanent pacer, but did place a loop recorder to further study this problem.

A cardiac MR was done which showed normal LV function, RV enlargement concerning for possible arrhythmogenic right ventricular dysplasia (this is unlikely, as the VT was of LV origin).  There was no evidence of myocardial scar or edema.

Verapamil may have been useful to terminate this VT and keep the patient in sinus rhythm, and is certainly worth a try.  It was suggested by the electrophysicologist, but not given.  Posterior fascicular VT is usually verapamil sensitive.


1. Posterior fascicular idiopathic VT, ablated.  Temporarily best controlled with lidocaine.
2. Syncope due to #1
3. Temporary LV dysfunction due to dysrhythmia.

Here is another case of idiopathic posterior fascicular VT.

See this excellent full text article (Thakur RK et al.  Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:497-501.)

Friday, March 7, 2014

Inferior STEMI? Read the ECG systematically.

Leads V1 and V2 appear to be reversed.  Otherwise, what is it?

This diagnosis may be obvious to some, but it is easy to let your eyes be drawn to the ST elevation in II, III, and aVF, with reciprocal ST depression in aVL.  Then one forgets to read the ECG systematically: rate, rhythm, intervals, axis, voltage, QRS abnormalities, ST segment, T-wave, U-wave.

If one is systematic, then before seeing the ST-T abnormalities, you will see the short PR interval and the long QRS, which is long because of a delta wave.

ST- and T-wave abnormalities must always be read in the context of the QRS.  An abnormal QRS (LVH, LBBB, RBBB, WPW, Brugada, Hyperkalemia, IVCD, etc.), or abnormal depolarization, leads to abnormal repolarization (abnormal ST-T).

In this case, all the ST-T abnormalities are due to the abnormal depolarization through an accessory pathway, producing a delta wave and abnormal depolarization.  Even without a delta wave and short PR interval, the voltage of this magnitude (LVH) could also produce such a pseudoSTEMI pattern.

The patient presented with chest pain and palpitations.  The ST-T abnormalities did indeed distract the treating physician, who felt embarassed at initially missing what to him/her in retrospect was obvious.

The mind plays tricks on us and so we have to read these systematically.

This is very important for radiographs as well.  In my experience, most misreads of radiographs are not from lack of knowledge, but from distraction, from missing the obvious because you are looking for something else or see something distracting.  This is frequently true of ECGs.

Here are some other examples of pseudoSTEMI due to WPW.

Monday, March 3, 2014

Pseudo High Lateral STEMI -- How not to be deceived by ST elevation in aVL

This ECG was shown to me with no other information:

My response was: this is normal variant ST elevation in I and aVL. 

"Why?" I was asked.  First, I will say that many of my interpretations are subjective, based on pattern recognition that is not always translatable into a rule.

But I believe I can at least partly transform my interpretation into a rule here:   Even though there is some minimal reciprocal ST depression in lead III, the ST elevation is in the setting of a well-formed R-wave in aVL.  Moreover, there is a proportionally (proportional to the R-wave) small T-wave.  T-wave size and morphology is at least as important as ST elevation in diagnosing MI.  Also, there are well-formed J-waves in I and aVL.

High lateral MI is the MI location that is most difficult to diagnose largely because the R-wave voltage in Lead aVL is often very small, and thus any ST elevation or T-wave amplitude may also be small, though when scrutinized it is often proportionally excessive.  This does not apply here.  There is plenty of R-wave amplitude with which to judge the ST segment and T-wave.

There are no other findings on the ECG to support MI:

1. Lateral MI is frequently associated with posterior MI, but here there is no precordial ST depression

2. High lateral MI from first diagonal occlusion (D1) is frequently associated with ST elevation in V2.  Well there is indeed ST elevation in V2, but this is normal variant ST elevation:  if you use the Smith formula, STE60 V3 = 1.5, computerized QTc = 392, and R-wave amplitude is 10.5 mm; formula = 21.50 (significantly less than 23.4, so very unlikely to be MI).

3.  There is no ST elevation in V5 and V6.

Pretest Probability

If this were a person at risk for STEMI: risk factors, older age, crushing chest pain, I would highly recommend serial ECGs, immediate formal echo, etc.  But not cath lab activation.

In this case, as it turned out, the patient was less than 40, had no risk factors, and had primarily abdominal pain and vomiting. 

Certainly I would not obect to serial ECGs, but no more aggressive investigation is warranted.

Also, do not hesitate to consult someone with more expertise.  This is usually, but not always, a cardiologist


It turns out that the cath lab was activated, coronaries were normal, and the patient ruled out.

Unfortunately, this happened on a late in the evening, so that the cath team had to be called into the hospital and it was an unfortunate use of resources.

All serial ECGs were identical.  The patient ruled out by serial troponins.


1. Use cath lab resources wisely, especially depending on your institution's own resources
2. Remember the importance of proportionality
3. Remember the importance of the T-wave in STEMI
4. Soft ECG findings should be more deeply scrutinized when the pretest probability is low
5. f you are worried, use other resources, especially immediate high quality echo, to look for wall motion abnormality.

Recommended Resources