Friday, March 24, 2017

A young man with sudden chest pain

A 30-something with history of 2 pack per day smoking complained of sudden left arm and chest pain while working construction.  It was very distressing for him.  He presented by private transportation, stating that his pain was decreasing.

At triage, he had this ECG recorded:
The computer read that there is incomplete right bundle branch block.
QRS duration 102 ms.
What do you think?

No significant abnormalities were seen in triage, and the patient had to wait 2 hours.  By the time he was roomed, his pain was gone.

A second ECG was recorded, pain free:
If you didn't see anything wrong with the first one, maybe you can see it now by comparison with this one.

His first troponin I, drawn 4 hours after arrival, was 1.6 ng/mL.

--There is subtle ST Elevation in inferior leads II, III, aVF, with reciprocal ST depression in aVL.  This is diagnostic of inferior injury.  The fact that it resolved with resolution of chest pain simply verifies this.
--There is also a decrease in the size of the lateral precordial T-waves.
--Notice that the ST elevation on the first ECG does NOT meet STEMI criteria. There is not 1 mm of STE in any lead.
--But that ECG is diagnostic of injury.

The patient was started on heparin.

Shortly thereafter, he had a run of ventricular tachycardia.  Therefore he was taken urgently to the cath lab.  [Patients with ACS who have persistent refractory pain, hemodynamic or electrical instability, or pulmonary edema, should go emergently to the cath lab]

The angiogram was clean!!  

An MRI was diagnostic of myocarditis.  

--There were no wall motion abnormalities (although they are frequently seen in myocarditis)
--No evidence of microvascular obstruction
--Delayed enhancement sequences obtained at 10 mins after gadolinium administration reveal multiple (at least 3) foci of delayed enhancement, measuring about 2 centimeters in the 
inferior septum, and approximately the same size in the inferior wall.
--There is subendocardial sparing demonstrated (this pretty much establishes myocarditis, as ischemia would preferentially affect the subendocardium.

Troponin I profile:

Time after arrival         Troponin I
4                                     1.613
6.5                                  5.887
13.5                              10.969
15.5                              11.347
19                                   9.001
21.5                                7.521
25                                   6.175  

Learning Points:

1.  Learn to recognize subtle injury. This could have been an early STEMI.  The patient's reperfusion time would have been delayed.
2.  It is particularly easy to miss these when you are shown an ECG completely out of clinical context, as often happens with triage ECGs.
3.  Injury NOT due to ischemia also is high risk: in this case, the risk of ventricular dysrhythmias.
4.  Myocarditis and STEMI are often indistinguishable.  They may have injury on ECG, wall motion abnormalities, and elevated troponins.  ACS may also have a negative angiogram if there is autolysis of thrombus!  MRI makes the diagnosis.

Here is another interesting related case:

A Young Woman with Chest Pressure and Subtle, Focal ST Elevation/Depression

The effect of targeted temperature management on QT and corrected QT intervals in patients with cardiac arrest

Just published online:

Tuesday, March 21, 2017

2 different wide complex rhythms (rate about 60) in a patient with chest pain

A male in his 40s presented to the ED by ambulance with acute chest pain, possibly waxing and waning.  He had been working out and felt dizzy and weak in addition to the chest pain.

He had a pacemaker in place that he stated was due to a congenital problem, later found to be due to congenital absence of atrial activity.  He had no history of coronary disease.

Here is his first ED ECG (ECG 1):
What do you think? (It is NOT paced)
See analysis below.

ECG 2: 25 minutes later
What do you think? (Still not paced)
See analysis below.

ECG 3: His prehospital ECG was located; it had been recorded 25 minutes before the first ED ECG:
What do you think?

ECG 1: 

1. There are no P-waves.  The rate is slightly above 60.  There are no pacer spikes, so either the pacer is not working or its rate is set below 60.
2. There is an RBBB and LAFB morphology, which means that either the junction is escaping and there is RBBB + LAFB, or there is a posterior fascicular escape.  A rate of 60 suggests that it is junctional and not fascicular.
3. V2 lacks the normal ST depression that one sees in RBBB.  In RBBB, the ST segment is usually discordant (opposite to) the positive R'-wave, with up to 1 mm of ST depression, also usually with an inverted T-wave, as seen in the "normal RBBB" ECG below.
4. Concordant STE in lead I
5.  Notice the slight ST elevation in V3, with up-down T-wave. This is highly suggestive of ischemia.
6.  There is very poor R-wave progression from V3-V6.
7.  There are Proportionally large T-waves from V3-V6.

In this situation, all these features are all but diagnostic of LAD occlusion.

Normal RBBB
Normal RBBB, with normal ST depression, up to 1 mm, in V2 and V3, and inverted T-waves.
Note the absence of ST elevation and the size of the T-waves in lateral precordial leads.

ECG 2:

Same analysis, except that now there is new ST elevation in V4-V6 and dynamic T-waves in V2 and V3, with slightly increased ST elevation in aVL with reciprocal ST depression in lead III.

ECG 3: Prehospital ECG:

1. This one is paced!! (Also at a rate slightly above 60)
2. Look at lead V6.  There is proporionally excessively discordant ST elevation at 2.5 mm.  Divide that by the preceding S-wave (6 mm), and the proportion of 2.5/6 = 42%.  I believe this is diagnostic of coronary occlusion.
3. The T-waves in V3-V6 are very abnormally large, highly suggestive of acute occlusion.

ECG in Ventricular Paced Rhythm with Coronary Occlusion

The Modified Sgarbossa criteria for left bundle branch block (LBBB), which I apply to ventricular paced rhythm, uses a hard cutoff of 25% in just one lead to diagnose coronary occlusion.  This is the third criterion (1st criterion is concordant STE of 1 mm in 1 lead, and 2nd is concordant ST depression of 1 mm in one of leads V1-V3); any one of the 3 makes the diagnosis.  Our research would indicated that the normal discordant proportional ST elevation is about 11% and that anything above 15% is very likely to be occlusion.  A 25% ratio was 99% specific, but a 20% proportion was still 94% specific in the validation study!

We are in the midst of a multicenter, international study to assess the Modified Sgarbossa Criteria in Paced Rhythm.  It is called the PERFECT study!  (Paced ECG Requiring Fast Emergent Coronary Therapy).

Many physicians still do not believe that STEMI can be diagnosed in the presence of ventricular paced rhythm.

One of my mentors, K. Wang, put up an image on Medscape of a Paced ECG that clearly showed STEMI and quizzed the readers and received this answer:
50% gave the wrong answer: you cannot diagnose infarction in ventricularly paced rhythms.

Case Continued:

The cath lab was activated emergently and the patient was found to have 100% occlusion of the first Diagonal off the LAD.  It was opened and stented.

The peak trop I was 33.9 ng/mL.

A subsequent echo showed:

--Normal left ventricular size, thickness estimated left ventricular ejection fraction is 50-55 %.
--Regional wall motion abnormality-distal septum anterior and apex,dyskinetic.
--Regional wall motion abnormality-distal inferior wall, dyskinetic.
--Asynchronous interventricular septal motion nonspecific.

Learning Points:
1. RBBB can obscure LAD occlusion, but you should suspect it in the absence of normal discordant ST depression in V2 and V3, or with hyperacute T-waves.
2. Paced rhythm obscures MI far less than believed.  Coronary occlusion can definitely be diagnosed in the presence of ventricular paced rhythm.
3. Even in normal conduction, acute coronary occlusion is frequently not evident on the ECG. This is also true with RBBB, LBBB, and Paced Rhythm.  There is little evidence supporting the notion that it is far more difficult in the latter three.

Sunday, March 19, 2017

Tachycardia, Dehydration, and New ST Elevation in a 20-something, then a Surprise.

A male in his early 20s presented intoxicated, with no CP or SOB.  An ECG was obtained for tachycardia.

First ECG:
Sinus tachycardia at 150.
There is inferior ST Elevation and Q-waves that appear to be Inferior STEMI.
There is reciprocal ST depression in aVL.
Is this STEMI?

The patient was very dehydrated.

The physicians were worried about STEMI, and so did a Point of Care Cardiac Ultrasound which showed IVC collapse and hyperdynamic function.

The patient had a previous visit with dehydration
There had been some, but less, STE
Not very similar to this one.

There was another previous visit with dehydration
Also not similar

He was given 2 liters of IV fluids.  A 2nd ECG was recorded 1 hour later:
Sinus tach at a rate of 120
Heart rate and ST segments are almost normalized 

What do you see now?
See below.

Unexpectedly, there is every other beat pre-excitation.  So the patient has WPW. This was never diagnosed before.  But I don't think this explains his ST segments.

Clinical course

3 serial troponins were below the 99% level of 0.030 ng/mL, but not undetectable.

K was 4.5 mEq/L.

The patient was rehydrated and discharged.


Why the PseudoSTEMI pattern?

I don't know for certain, and this ECG sure looks like inferior STEMI.  However, patients with STEMI generally do not have tachycardia unless they are in cardiogenic shock.  If such is the case, the patient should have high filling pressures and high right sided pressures and NOT have a collapsed IVC.  They should also not be hyperdynamic.

It is possible to be dehydrated AND have a STEMI, but in that case the best initial treatment is supportive: rehydration.  Then re-evaluation.

So it was perfectly appropriate to do a bedside ultrasound and, finding a hyperdynamic heart, to defer diagnosis of ACS and give fluids.  Even if this STE is due to ischemia, it is most likely due to demand ischemia, NOT due to ACS, and the best initial therapy is to hydrate.  In our many studies of type 2 MI, we found that 2-5% had ST elevation on the ECG.

Final comment:

I sent this to Ken Grauer, who is a fantastic ECG resource and has much experience with stress ECGs, and asked if this is a pattern he has seen in stress tests.  He stated "no," (in a few more words than that).

Friday, March 17, 2017

A 20-something with DKA and a regular wide complex tachycardia

Medics were called to see a 20-something type 1 diabetic with h/o DKA who had altered mental status.

He was found to have "Kussmaul" respirations and respiratory distress.

He was not in shock, his blood pressure was adequate, and pulses were strong.

He was put on the cardiac monitor:
Regular wide complex tachycardia.

A 12-lead ECG was recorded:
Regular Wide complex tachycardia at a rate of 200.
What do you think?
If you're the medic, what would you do?

Whenever there is a wide complex, especially in a patient with DKA, one should think of hyperkalemia (sinus rhythm, often with "invisible P-waves").

However, this rate is too fast for sinus tach and the morphology is not right for hyperkalemia.  Still, calcium is harmless and it is harmless to give 3 grams of calcium gluconate.

He arrived in the ED in the same condition.  He was hemodynamically stable but with altered mental status and respiratory distress.  Cardiac echo showed hyperdynamic performance.   Blood gas showed severe acidosis, with pH 7.00, pCO2 25 and HCO3 of 6.   K retured at 4.5 mEq/L.

He was treated with calcium, bicarbonate, and magnesium.  He was intubated.

He had this ECG recorded:
What do you think?
What do you want to do?
Suppose the patient did not have altered mental status from DKA and was not intubated?

Analysis: VT vs. SVT with aberrancy vs. sinus tachycardia with hidden P-waves.  (With a rate this fast, and no inkling of P-waves, sinus is very unlikely but if you were not sure, you could record Lewis Leads.)

This ECG is almost certainly supraventricular tachycardia with aberrancy.  Why?

First: pretest probability
The patient is young and without heart disease
Good LV function makes VT less likely (except for fascicular VT)

Second: the ECG itself:
1. There is an inferior axis.  The impulse originates cranially and propagates caudally.  In contrast, VT, because it originates in the ventricle, which is lower left, generally propagates toward the upper right.
2. More importantly, there is a typical right bundle branch block (RBBB) morphology:
    a. There is RR' in V1 and the R' is larger than the R.
    b. There is a rapid, narrow R-wave in V5 and V6, with a wide S-wave.

This latter makes SVT with RBBB aberrancy almost certain.

Thus, it is very likely that it will convert with adenosine.  The medics could have given adenosine and converted.  Since the patient was hemodynamically stable, there was no rush to convert and therefore it is OK that they left it alone.

If you're wrong and give adenosine to a patient with VT, don't worry.  Adenosine has been shown to be safe in Ventricular Tachycardia and is even recommended now in ACLS.

Of course, electrical cardioversion will work very well but generally requires sedation unless the patient is already obtunded.  This patient was intubated and sedated, so electricity is easy to use.

However, if this patient were not so sick with DKA that he needed to be intubated, adenosine would be the treatment of choice.

The patient was diagnosed with VT and electrically cardioverted.

Here is the post-cardioversion ECG:
Sinus Tachycardia with normal QRS and axis and nonspecific ST-T abnormalities

There is no baseline RBBB.  The right bundle generally has a longer refractory period than the left bundle, so that when there is a fast rate, it can result in RBBB aberrancy.  

The patient did well and was later diagnosed with SVT with aberrancy.

Learning Points:

1.  Adenosine is safe in regular wide complex tachycardia.  (But NOT in irregular polymorphic wide complex tachycardia, as this could be WPW with atrial fib)

2. If there is typical RBBB morphology, it is almost certainly SVT with aberrancy.  There are also fairly rare fascicular ventricular tachycardias which can mimic SVT with aberrancy.  However, you won't hurt them with adenosine.

Tuesday, March 14, 2017

Why did this patient have ventricular fibrillation?

A previously healthy 50-something collapsed while exercising.  He underwent CPR and defibrillation and was brought to the ED.

Here is his initial ED ECG:
What do you think?

1. Sinus tachycardia due to post arrest state.
2. I see no evidence of STEMI or even of subtle coronary occlusion.  I see no evidence of ischemia.
3. In some leads, there appears to be a very long QT, but it lead II across the bottom is used, it becomes apparent that the P-wave is mimicking the T-wave in some leads.  QT is normal.
4. There is no evidence of structural heart disease or congenital ion channel disease.
5. There are non-diagnostic Q-waves in inferior leads.  These could represent old inferior MI, which provides the substrate (scar) for ventricular fibrillation.

The patient went for emergent angiography.  Here are the findings:

LAD with obstruction, TIMI-1 flow, opened and stented.  Other diffuse non-obstructive disease.

The peak troponin I was only 0.85 ng/mL.

The next day formal echocardiogram was totally normal (no old MI).

In November 2016, this study was published in Resuscitation:

Millin MG et al.  Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis.  Resuscitation 2016, Vol.108, p.54-60.

The authors looked at many studies of patients with out-of-hospital cardiac arrest (OHCA) in which angiogram findings were correlated with ECG findings.  They found that 1/3 of patients who did not have STEMI on the ECG had culprit lesions that "required intervention."  They caution that this does NOT mean that all patients with cardiac arrest without ST elevation need emergent cath lab activation.  They caution that it is not clear which of these patients do need the cath lab or how to identify which will have culprits that need intervention.  Further study is needed.

However, here is a subgroup of OHCA that definitely should go:

Previously healthy patients who have ventricular fibrillation without a clear cause.  This includes, but is not limited to, patients with ECG findings such as:
1) Old MI with scar (Q-waves diagnostic of old MI)
2) Brugada syndrome
3) Hypertrophic cardiomyopathy.
4) Evidence of arrhythmogenic RV dysplasia
5) Evidence of chronic cardiomyopathy (along with echo evidence of very poor LV function).  Most of these patients are not previously healthy.
6) Other?

If no definite etiology can be found, the ventricular fibrillation was likely due to coronary ischemia (from acute coronary syndrome, with plaque rupture and thrombus) that is not evident on the ECG.

Common coronary findings in patients with ACS that results in OHCA:

1. Fixed tight lesion(s) which, during exercise, resulted in ischemia (not ACS, intervention not always needed, at least not emergently)
2. Thrombosis which was occlusive or nearly occlusive, but is no longer so because of some spontaneous thrombus lysis (requires intervention).   
3. Culprit lesion which showered downstream platelet-fibrin aggregates, resulting in small vessel ischemia.  These culprits are dangerous because the thrombus can propagate again and occlude the artery (requires intervention).
4. Thrombus with persistently limited flow, as in this case, even thought the ECG that does not show evidence of ischemia (requires intervention).
5. Other?

Learning point:

ST Elevation, and especially ST elevation criteria, are not sensitive for ACS and not even very sensitive for coronary occlusion.  ST depression may also not be present.  A high pretest probability, such as unexplained ventricular fibrillation, is ample reason to activate the cath lab.

Friday, March 10, 2017

How unreliable are computer algorithms in the Diagnosis of STEMI?

A 61 year-old with chest pain arrived to the ED by ambulance with resolving chest pain.  Here is his ED ECG:
The computer interpretation was "normal"
What do you think?

This ECG is NOT normal.  The T-waves in V2-V4 are very large in proportion to the QRS.   They are suspicious for hyperacute T-waves. There is low QRS amplitude.  

Can you trust a computer interpretation of "normal?" 
---Most of the time, but obviously not all the time.

  1. Hughes KE et al. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med 2017; 24(1): 120 – 24. PMID: 27519772
This recent study, discussed on Salim Rezaie's fine site REBEL EM, implies you can trust the computer interpretation of "normal." (

What to do?

Recording serial ECGs would be useful.  The chest pain is resolving, so if these are resolving hyperacute T-waves, then followup ECGs should show their size diminishing.

However, when I saw this patient, I knew that he had come by ambulance, so I knew there must be a prehospital ECG recorded somewhere and went to look for it.

I found it.

Here it is:
Need I say more?
Yes, I'll say more: see the computer interpretation:
"Normal variant ST elevation, consider early (repolarization)"
Why the medics did not see it, I'm not sure. 

The cath lab was activated, as it should be with transient STEMI.

See this case of transient STEMI:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death.

Angiogram: There was 80% obstruction of the LAD with a large thrombus and TIMI-2 flow; the thrombus was suctioned out.

All serial troponins were undetectable!

Had we not seen those subtle hyperacute T-waves, and then sought out the prehospital ECG, the patient would have ruled out, with one of three outcomes:

1. Subsequent thrombus propagation with re-occlusion, recurrent chest pain and diagnosis made (although perhaps late and perhaps only after an adverse outcome)

2. Undergone stress test with uncertain results.

3. Been discharged to home with potential disastrous outcome.

Learning Points

1.  Computer algorithms that make the diagnosis of "normal" are usually correct, but is usually good enough?

2. Computer algorithms are completely unreliable at diagnosing STEMI, with both poor sensitivity and poor specificity.  Here are two recent articles confirming this:

    a. The Comparison of Physician to Computer Interpreted Electrocardiograms on ST-elevation Myocardial Infarction Door-to-balloon Times.
    b. Electrocardiographic diagnosis of ST segment elevation myocardial infarction: An evaluation of three automated interpretation algorithms

3.  Always look for the prehospital ECG

4.  Hyperacute T-waves occur not only shortly after onset of chest pain (as the ST segment is about to rise, or "on the way up"), but also shortly after reperfusion (as the ST segment is resolving after reperfusion or "on the way down").

5.  With very brief occlusions, troponins may all be negative.  What would high sensitivity troponins have shown?  We don't know.

Thursday, March 9, 2017

Subtle Dynamic T-waves, Followed by LAD Occlusion and Arrest

This case was written by Sam Ghali: (@EM_RESUS).  Thanks, Sam!


A 42-year-old lady presented to the ED with complaints of intermittent episodes of chest pain associated with shortness of breath for the last 2 days. This was her ECG (it is unclear if this was with or without pain):
Computerized ECG Read: “Normal sinus rhythm. Normal ECG.”
What do you think?


Sam's analysis
"There is sinus rhythm with a normal rate. QRS axis is shifted somewhat to the left. Intervals are normal. Overall this is a very quiet ECG. 

But if you look closely at the precordial T-waves you see a hint of terminal T-wave inversion in V2, and biphasic T-waves in Leads V3 and V4."

As above, it is unclear from the history whether the patient was experiencing chest pain at the time of this ECG, but these right precordial t-wave  findings were appreciated and the patient was treated with medical therapy and admitted to the hospital. 

Troponin T returned at less than 0.010 ng/L (normal)

A repeat ECG was performed 1.5 hours after the first (without pain):
 The precordial T-wave inversions appear to be resolving. A biphasic T-wave is only really well-appreciated in V3 now. 

2 hours later (3.5 hrs after the initial ECG) she develops severe, crushing chest pain. Another ECG is obtained:
 She suddenly occluded her LAD with a very large territory of viable myocardium at risk! 

Shortly after this ECG she suddenly went unresponsive and into V-Fib. CPR was initiated and she subsequently entered into V-Fib storm. After multiple shocks, 300 mg of Amiodarone, and 100 mg of Lidocaine she stabilized and was taken emergently to the cath lab. She was found to have a 100% occlusion of her Mid LAD just after the takeoff of D1 - which was reperfused and stented. Her 2nd troponin (drawn before her reocclusion/arrest) ended up coming back barely elevated at 0.015 ng/mL! (normal, less than 0.010 ng/mL)<0 .010="" font="" ml="" nbsp="" ng="">

She ended up doing fine and in the next few days was discharged home in good condition.

Smith comment:

T-wave inversion such as seen in the first ECG can be seen with active non-transmural ischemia.  We usually see this sort of T-wave inversion AFTER chest pain has resolved and, in that case, it is called "Wellens' syndrome," and implies that when the patient had pain the LAD was occluded, but that it spontaneously reperfused and resulted in "reperfusion" T-wave inversion. In such a case, the T-wave inversion would evolve into deeper and more symmetric (pattern B) T-wave inversion and troponins would be positive.  

But in this case, it is due to active ischemia, resolves with resolution of ischemia, and has little if any troponin elevation.

Here is another similar case:

Dynamic T-wave inversion (apparent Wellens' waves), all troponins negative: Unstable Angina

Sam's Learning Points:

1. Don’t trust the computerized ECG reading. The computer is not designed to pick up such subtle ECG findings as seen in this case . If this patient was discharged from the ED she very likely would have died. We must be the experts and pick up these life-saving ECG findings!

2. ACS can be a very dynamic process. For example, a coronary plaque ruptures: the vessel can undergo occlusion, spontaneous reperfusion, maybe reocclusion, again reperfusion, etc. At the time we are seeing the patient and reading their ECG remember that we are only seeing a snapshot of this process in time.

3. Unstable Angina still exists. There are some that overestimate the sensitivity of contemporary troponin assays and have come to believe that unstable angina no longer exists. This is very dangerous thinking. It is unclear whether high-sensitivity troponins will ultimately do away with unstable angina, but we are certainly not there yet. This lady nearly “ruled out with 2 sets” as her 3-hour troponin barely made the lab cut-off by 0.005 ng/mL and could have just as easily returned negative.

Smith comment

Had she not re-occluded and arrested, her troponin would not have gone above 0.010 ng/mL.  She would have been discharged.  Then re-occlusion and arrest might have happened at home.  Thus, unstable angina exists and can be deadly.

The ECG is still important, regardless of negative troponins.

Friday, March 3, 2017

Another 40-something with intermittent chest pain

I was sent this ECG by a resident from elsewhere, with the following information:

"Young previously healthy man with several 10-20 minute episodes of chest pain over the past few hours, asymptomatic on presentation and during this ECG."

"What do you think?"

There are Q-waves in V2 and aVL.  The T-wave in V2 is too large for this Q to be due to old MI.  There is minimal STE in aVL and a proportionally large T-wave, with a reciprocally large T-wave in lead III and a biphasic down-up T-wave in aVF.
There is some STE in V2 and V3, but this cannot be called normal variant because there is a Q-wave in V2 and poor R-wave progression.
All of these are very worrisome for LAD or D1 ischemia.

Here is my response:

"Old MI with superimposed LAD or First Diagonal acute ischemia.  Q-wave in V2, aVL suggest old MI, but T-wave is too large in both to be old.  Alternative is subacute MI of these vessels."

"Please send info."


This is a 40-something who complained of several 10-20 minute episodes of chest pain over the previous few hours.  He had no prior medical history, but is a smoker with a positive family history of CAD.  He arrived at 7:30 pain free and had this ECG recorded at 7:32.  I will repost it here:
See above description

The first troponin was undetectable (cTnT, < 0.01 ng/mL) and he was sent to the observation unit for serial troponins without recording any more ECGs.

Smith comment: this is not acceptable.  One should at least perform many serial ECGs to look for either resolution or evolution of these T-waves.  Since his pain had resolved and was still gone, one would expect resolution of the large T-waves and minimal ST elevation and this would be diagnostic.

Case continued:

At 8:30 he complained that his pain was returning and another ECG was recorded at 8:42:
This is slightly BETTER than the previous  There are smaller T-waves, and less STE in aVL, and the reciprocally inverted T-wave in III is not as deep.  The down-up T-wave in aVF is now all up.
This ECG represents dynamic ACS

--Proving that serial ECGs recorded in the ED would have shown resolution of the T-waves.  
--Now they are growing larger from what would have been seen on an intervening ECG 

The ECG was interpreted as No Change.

Case continued:

At 8:50 he had "seizure like activity" that resolved (probably an episode of pulseless VT) and was moved to the ICU, where he had this ECG:
Obvious proximal LAD occlusion (STEMI)

Here is his next 12-lead:
Ventricular Fibrillation is not supposed to be captured on a 12-lead ECG!

This is after defibrillation and the patient had a pulse and was awake:
Slow and sick!  Take me to the cath lab!!

This was recorded just before he was taken to the cath lab:

Here is the angiogram:
Proximal LAD occlusion

Here annotated with arrows:

Learning Points:

1. Real ECG findings of coronary occlusion can be extremely subtle!
2. Learn to recognize hyperacute T-waves.
3. Learn to recognize down-up T-waves
4. Learn to recognize the reciprocity between aVL and III
5. Troponins are not reliable for diagnosis of early ischemia/occlusion
6. There is still a role for observation!

Wednesday, March 1, 2017

A 40-something with chest pain in the middle of the night

This was sent by one of our former residents.


"A 40-something year old man awoke with chest pain in the middle of the night.  He had a h/o HTN and positive family history of CAD.   He had no other risk factors.  His pain was very typical sounding, with nausea, diaphoresis, and SOB."

"He was given 4 aspirin given by EMS, and was given 3 NTG and his pain went from 8/10 to 3/10.  He looked a bit sick.  His prehospital ECG was pretty identical to this initial ED ECG as #1.   There was no prior for comparison."  

Initial ED ECG, time zero:
What do you think?

Thoughts from the doc who sent it:

"I had a ton of concern about his T waves being too big in the lateral precordial leads."

Smith comment: Agree!  The T-waves are not large at all, but relative to the small QRS, they are indeed huge!  The T-waves in I and aVL are also far too large, and have a reciprocally inverted and large T-wave in lead III.  The T-wave in V2 is far too large for that small QRS.

Case continued:

"We did a repeat ECG at about 30 minutes:"
No significant evolution, but some small resolution of T-wave size.

"I thought it showed no significant evolution.  My own bedside echo looked to have some septal WMA (but our machines are suboptimal and he was a little technically difficult)."

"So we did another repeat ECG:"
About the same

"The ECG was still the same.  The chest pain waxed and waned.  I gave another 3 rounds of NTG with improvement, but the pain was still there."

"I called cardiology and told them the story.  I told them very clearly of my concern for hyperacute T-waves, and the cardiologist said that this was an "overcall" and that they were normal.  Honestly, this was what I expected to hear them say."

The initial troponin then returned at 0.080 (99% = 0.045.  This slightly elevated troponin should clinch the diagnosis.  However, it apparently did not change management.

It is important know that it would be very common for the initial troponin to be entirely negative, as it is in about 50% of full blown STEMI.

But the ED doc did the right thing!

"Still concerned I called in the Echo tech in the middle of the night."

"I sent him to the ICU on Heparin and NTG drips.  About 20-30 min after admission, I heard the cath lab announcement overhead.  I look and he did in fact have a wall motion abnormality."  

"He went to the cath lab and there was a 100% mid-LAD occlusion with thrombus and also thrombus in the posterior descending artery but this artery was open (dual culprits!).  He got two stents: one in the mid LAD, restoring TIMI-3 flow, and also one in the distal Left Posterior Descending Artery.  All in all, he went to the cath lab in about 3-4 hours from arrival."

Here is the post-cath ECG:
These are normal T-waves.
Note the difference!!
Note that they are proportional to the small QRS!!

Learning Points:

1. Acute LAD occlusion can be very subtle on the ECG.  In a study by Marti et al., who took all patient with any suspicion of coronary occlusion to the cath lab, 13% of acute LAD occlusion had less than 1 mm of ST elevation in V2 and V3.
2.  Beware hyperacute T-waves!!
3.  When you are concerned about acute coronary occlusion, but the ECG is not definitely diagnostic, there is a middle way between cath lab activation and no activation: pursue agressively with diagnostic adjuncts: compare with old ECG, do serial ECGs, do high quality echo.
4. You are not held to the same Door to Balloon Time standard in these occlusions that to not meet STEMI criteria.  They will be called NonSTEMIs!  But these NonSTEMI patients have better outcomes with early reperfusion, compared to next day angiogram and PCI.
5.  If you are concerned about subtle coronary occlusion, pursue it with formal echocardiogram
6.  It is not the size of the T-wave, or the height of the ST segment, that makes the diagnosis, it is there size in proportion to the QRS!

Thursday, February 23, 2017

An unstable wide complex tachycardia resistant to electrical cardioversion

Thanks to our electrophysiologist, Rehan Karim, for his help with this post.


A very elderly inpatient suddenly had a rapid pulse by oximetry.  The nurse put him on the monitor and noticed a wide complex tachycardia.  The patient was alert with a normal blood pressure.  He had a history of myocardial infarction, with a known lateral wall motion abnormality and a chronic total occlusion of the circumflex.

A 12-lead ECG was recorded.
Click on image to enlarge
Regular, Monomorphic, Wide complex Tachycardia (WCT) at a rate of 190.
What do you think?

Interpretation: This is clearly Sustained Monomorphic Ventricular Tachycardia.

You may say that interpretation does not matter because electrical cardioversion works for any regular WCT, but you'll see in this case that electricity did NOT work and that interpretation may indeed matter.

How do we know it is VT?
Pretest probability
    1) Most regular WCT is VT
    2) In elderly patients, an even higher percentage is VT
    3) Patients with a history of MI have scar tissue and have an even higher risk of VT
    4) When there is poor LV function, VT is more likely still

Post-Test probability (the ECG alone, regardless of clinical factors)
    1) The QRS duration is very long (wide).  In lead V3, it appears to be about 180 ms. (1)
    2) There is a monophasic R-wave in lead V1 (RBBB morphology but without the typical rSR' of true RBBB).(2)
    3) The initial part of the QRS is very wide.  aVR takes 80 ms to reach its peak.  Moreover, the impulse initiates towards aVR, turns around and goes away (toward lead II), then turns back to aVR [see (4) below].(3)  

(1)  In WCT, a QRS duration of greater than 140 ms favors VT with only moderate specificity.  Duration of 160-180 ms strongly favors VT.
(2)  A monophasic R-wave in V1 heavily favors VT.
(3)  In VT, the impulse is initiated in myocardium, not in conducting fibers, and thus travels slowly before it arrives at a conducting fiber.  Therefore, the initial part of the QRS is slow (wide).  In SVT with aberrancy, the impulse is conducting through Purkinje fibers and thus the initial impulse is relatively narrow.
----For cases in which there is an LBBB-type morphology in lead V1 (small r-wave followed by deep S-wave): if there is any precordial lead which has an onset of R-wave to nadir of S-wave of greater than 100 ms, then VT is very likely.  Even though in V2 this interval is 120 ms, the rule does not strictly apply here because there is RBBB (not LBBB) morphology in lead V1 (an upright R-wave).
(4) Axis (not as helpful here as one might expect): As a general rule, with exceptions: in VT, the impulse starts in the ventricle (inferior and leftward) and travels up and to the right, resulting in an upright R in aVR.  This results in a "Northwest" axis, at between -90 and -180 degrees.  
----In this case, although aVR appears all upright, the axis is more complex.  Note that leads II, III, and aVF are positive, indicating an inferior axis.  Why the discrepancy?  If you look very closely, you'll see that the impulse starts toward aVR, turns back toward the inferior leads, and then turns toward aVR again, all in very rapid succession.  Such a convoluted pathway is also a good sign of VT.

There was a suggestion that retrograde P-waves were present and that this might indicated SVT.  However, I don't see any here, AND the presence of retrograde P-waves does not help to differentiate VT from SVT.   Retrograde P-waves can be seen both in SVT and VT.
----AV dissociation (P-waves, not retrograde, out of sync with the ventricle) heavily favors VT

See this post for an more complete overview of the ECG diagnosis of wide complex tachycardia:

Clinical Course

--The blood pressure began to drop.
--Adenosine 6 mg, then 12 mg was given without any change.
--Amiodarone 150 mg was given without change.
--A bedside ultrasound showed poor LV function.
--The patient was given midazolam to prepare for electrical cardioversion
--The BP dropped to 50-60 systolic after midazolam.
--He was shocked multiple times with biphasic synchronized cardioversion at 200 J.  The rhythm reportedly converted, then reverted to VT each time.
       --The patient was greatly distressed by the shocks, in spite of midazolam.
--The patient was intubated and given another 12 mg of adenosine without change.
--Another 150 mg bolus of amiodarone was given.
--Mg 4 g IV was given
--Ultimately, lidocaine 100 mg bolus x 2 was given
--Patient converted to a bradycardic rhythm:

Potassium was 4.1 mEq/L

Slow junctional rhythm.
Notice very tall R-waves in V2-V4, consistent with old posterior MI
ST depression in V2-V4 is consistent with acute ischemia or old MI

A previous ECG showed similar R-waves, consistent with the old "lateral" MI and chronic total occlusion of the circumflex.

Transcutaneous pacing was successfully initiated.

When pacemaker temporarily stopped, patient was in sinus rhythm on the monitor.

Shortly after, this ECG was recorded:
Sinus rhythm
Less ST depression
Same tall chronic R-waves

An echocardiogram was done:

Decreased left ventricular systolic performance moderate .
Regional wall motion abnormality-inferior .
Regional wall motion abnormality-inferolateral .
Regional wall motion abnormality-anterolateral .
The estimated left ventricular ejection fraction is 30-35 %.

Clinical Course
Later, recurrent VT was terminated again with lidocaine.

--Lidocaine is a parenteral type Ib antidysrhythmic.  Therefore, the patient was started on started on oral mexiletine, another type Ib antidysrhythmic.
--There was discussion of placing an implantable cardioverter-defibrillater.
--The VT was thought to be due to scar from old myocardial infarction.
--There was a plan to also keep K above 4.0 and Mg above 2.0.

Is this incessant VT?

While it certainly is incessant (it is not converting with multiple therapies), "incessant VT" is a term usually used for sustained VT that is not causing any hemodynamic compromise.  It is defined by at least 2 VT/VF episodes requiring intervention over a 24-hour period.  So this is not standard incessant VT, as this patient was not stable.

Treatment of Unstable Sustained Monomorphic VT (SMVT)

For initial conversion:

--Adenosine will not work for this VT
    (Adenosine does work for some VT associated with structurally normal hearts, especially right ventricular outflow tract VT -- see this case.  These cases generally are in healthy people, are not usually unstable, and are not very wide).

---If you think it is SVT with aberrancy, adenosine is safe in VT and may be worth a try.  In this case, the probability of SVT was very low.

--Synchronized electrical cardioversion is indicated, using safe and effective sedatives.  If the patient is very unstable with altered mental status, cardioversion may be done without sedation.
          --Occasionally, the machine's algorithm cannot differentiate the QRS from the T-wave, and cannot synchronize, and therefore the shock does not fire at all.  In such a case, synchronization must be turned off.
         This patient received midazolam and the shocks greatly disturbed him and he feared there would be more.  Midazolam is also NOT safe.  It causes hypotension and respiratory depression.  Etomidate (causes annoying myoclonus) or ketamine (may result in emergence dysphoria) are safer.  However, any sedative can cause some hemodynamic compromise and respiratory depression, no matter its reputation.

If the VT does not convert, or converts and recurs, then medication will be needed:

--Always replete K to above 4.0 mEq/L and Mg to above 2.0 mEq/L.

--Amiodarone bolus and infusion can be very effective and is a good first line agent.  150 mg over 10 minutes followed by infusion of 1 mg/min.  The bolus can be repeated to a maximum total dose of 2.2 g over 24 hours.  There are potential adverse events, including hypotension.  In particular, the diluent can cause hypotension when amio is given too rapidly, and amio has some beta blocking effects.

--Lidocaine is less likely to be effective, but also with fewer adverse events. So it is well worth a try.  Loading must be given in several boluses, as it is an intracellular drug and takes a few minutes to redistribute from serum.  For a standard sized person, give an initial 100 mg over 2 minutes, then 50 mg q 5 minutes x 3 for a total of 4 boluses in 15 minutes.  If VT recurs, then an infusion of 1-4 mg/min.

--Beta blockers may work and are frequently used due to the high catacholamine state (which may be exacerbated by shocks with inadequate sedation).  However, of course, they are potentially hazardous in patients with poor LV function.  I have always been too nervous to give metoprolol to these patients; I have used esmolol.  Our electrophysiologist wrote this:
     "Beta blockers can be used in stable patients if other agents fail, and we don’t want people to take message that they should not use it at all. The key is beta blockade and blocking sympathetic activation is important in these situations of incessant VT where other therapies fail. Actually sometimes we deeply sedate patients to take away sympathetic stimulation and that by itself helps. In fact, some big centers in extreme cases do cervical sympathectomy as last ditch effort."  He added that he finds that esmolol often causes more hypotension than metoprolol. After administration of beta blockade, attempt DC Cardioversion again.

--Pace termination.  If these therapies fail, our electrophysiologist writes:  If the VT had not terminated after lidocaine, "I probably would have taken him to cath lab for temporary pacemaker and 'pace-termination' before considering procainamide (of course depending on hemodynamics at the moment)."

--Procainamide may work if the above do not, but is especially hazardous with decreased LV function and should be given very slowly, if at all.  Give 20 mg/min to a total of 15 mg/kg until the arrhythmia terminates, the BP drops, or the QRS is prolonged by more than 50%.  Procainamide slows the VT rate and though it often causes hypotension, it can sometimes be hemodynamically beneficial if the slower rate allows for more ventricular filling time.  Maintenance infusion if necessary.

--IV sotalol (100 mg IV over 5 minutes) was found to be more effective than lidocaine (100 mg IV over 5 minutes) when administered to patients with spontaneous hemodynamically stable sustained monomorphic VT in a double-blind randomized trial within a hospital setting.  However, if the QT is prolonged after you've already given a QT prolonging drug like amiodarone, it is relatively contraindicated.  And you can't measure the QT while the patient is still in VT!
Ho DS, Zecchin RP, Richards DA, Uther JB, Ross DL. Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet. 1994;344:18–23.

AHA guidelines:

[PDF] 2010 American Heart Association

guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science  (Full text)

Learning Points:

1. Learn to identify VT
2. Adenosine will not work for this VT.
3. Cardiovert unstable VT at 200 J biphasic
4. If no conversion, or if reversion, use amiodarone
5. If amio does not work, try lidocaine
6. Consider beta blockade.
7. Consider pacing termination
8. Only then consider procainamide, as it is particularly hazardous.

Stable VT

Here is a great review of the literature on stable VT at EM Docs:


Quick summary: For stable VT, Procainamide may be a first choice for those with good LV function, but any of amiodarone, lidocaine, or sotalol may work.  Obviously, electricity is likely to work as well, and (just like with unstable VT) this is usually my first choice, saving medications for VT refractory to electricity, or recurrent.

Other literature

Incessant VT (stable persistent or recurrent VT) responds best to amiodarone, lidocaine may also work, but in this randomized crossover study, amiodarone performed better than lidocaine:

In this study of refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation, the event rate decreased with increasing doses of amiodarone: median values were 0.07, 0.04, and 0.02 events per hour for the 125-, 500-, and 1000-mg dose groups (mg per hour, with 150 mg boluses for breakthrough VT), respectively, representing a significant decrease from baseline event rates.  There was a 26% rate of hypotension as an adverse effect.

Cardiac Arrest

Amiodarone and lidocaine in cardiac arrest or to prevent recurrent arrest

Some randomized studies show higher rates of ROSC and hospital admission for out-of-hospital cardiac arrest treated with amiodarone: (amio vs. lidocaine) (amio vs. placebo)

In this study, both were superior to placebo for witnessed arrest, but neither was superior to each other:

Preventing Recurrent Arrest after VF:
On the other hand, in this study, lidocaine was very effective in preventing recurrent ventricular fibrillation after ROSC:  Here is the abstract:

Resuscitation. 2013 Nov;84(11):1512-8. doi: 10.1016/j.resuscitation.2013.05.022. Epub 2013 Jun 3.
Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest.

Antiarrhythmic drugs like lidocaine are usually given to promote return of spontaneous circulation (ROSC) during ongoing out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation/tachycardia (VF/VT). Whether administering such drugs prophylactically for post-resuscitation care after ROSC prevents re-arrest and improves outcome is unstudied.
We evaluated a cohort of 1721 patients with witnessed VF/VT OHCA who did (1296) or did not receive prophylactic lidocaine (425) at first ROSC. Study endpoints included re-arrest, hospital admission and survival.
Prophylacic lidocaine recipients and non-recipients were comparable, except for shorter time to first ROSC and higher systolic blood pressure at ROSC in those receiving lidocaine. After initial ROSC, arrest from VF/VT recurred in 16.7% and from non-shockable arrhythmias in 3.2% of prophylactic lidocaine recipients, 93.5% of whom were admitted to hospital and 62.4% discharged alive, as compared with 37.4%, 7.8%, 84.9% and 44.5%, of corresponding non-recipients (all p<0 .0001="" 0.34="" a="" adjusted="" admission="" analysis="" and="" arrest.="" arrhythmias="" associated="" association="" beneficial="" confidence="" covariates="" discharge="" for="" from="" higher="" hospital="" however="" improved="" in="" incidence="" independently="" interval="" lidocaine="" lower="" nonshockable="" odds="" of="" only="" outcome="" pertinent="" propensity="" prophylactic="" rate="" ratio="" re-arrest="" recurrent="" reduced="" s="" score-matched="" sensitivity="" span="" survival="" to="" vf="" was="" with="">

Administration of prophylactic lidocaine upon ROSC after OHCA was consistently associated with less recurrent VF/VT arrest, and therapeutic equipoise for other measures. The prospect of a promising association between lidocaine prophylaxis and outcome, without evidence of harm, warrants further investigation.


Lecture by Peter J. Schwartz

Schwartz, PJ. Cutting Nerves and Saving Lives.  Heart Rhythm 6(6):760-763, 2009-06-01

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