Saturday, May 19, 2018

A middle aged man with ST depression and a narrow window of opportunity

Written by Pendell Meyers

I received a text at 18:13 of an ECG taken several minutes prior, with no clinical information and only the question "De Winters?"

Here is the ECG:

What would you tell the treating team???

I responded at 18:14 PM:

"I think it's posterior STEMI (OMI) instead of de Winter. Cath lab immediately is indicated."

I clarified further:

"De Winter would need hyperacute T waves (not present here), and would indicate acute occlusion of the territory in the affected leads; so if there was de Winter in anterior leads, that would mean the anterior wall is the one involved. Here we have isolated posterior STD, with no hyperacute T wave, so that's OMI of the posterior wall. Posterior wall may have hyperacute T's if posterior ECG is recorded."

Let's go back in time and see the full case play out.

A middle aged man with HTN, DM, and CAD (with two prior stents) presented for chest pain, shortness of breath, and palpitations that started several hours ago (2-3 hours) while walking his dog. He was triaged at 17:34, had normal vital signs except tachycardia, was not in cardiogenic shock, and had this ECG obtained:

There is atrial fibrillation with rapid ventricular response at about 150bpm. There is massive ST depression in leads V2-V3, with smaller amounts of STD in V4-5, I, II, III, and aVF, with obligatory reciprocal STE in aVR. The J point in V6 is isoelectric, which would be unusual in the case of widespread supply/demand mismatch ischemia because there would normally also be STD in V6; the fact that V6 is isoelectric implies that there is relative STE in this lead.

When there is rapid AF and diffuse STD with elevation in aVR, the differential does include rate-related demand ischemia (supply/demand mismatch), as well as non-occlusive ACS in the setting of three vessel disease or left main disease, as well as OMI.

However, the fact that the STD is so much greater in V2-V3 than the other leads with STD suggests that it is in fact primary STD (posterior elevation) with superimposed widespread STD from supply/demand mismatch in the setting of rapid AF.

Also, remember that the rule of thumb "STEMI (or OMI) does not produce tachycardia unless the patient is in cardiogenic shock" does not apply to patients who have an arrhythmia which bypasses the normal physiologic determiners of heart rate, such as atrial fibrillation or flutter. Any patient with underlying AF who has an acute severe illness of almost any etiology may have rapid ventricular response due to catecholamine surge or other responses to illness. So this rule of thumb does not apply to our patient in this case.

The treating team was concerned for OMI vs. rapid AF with rate related ischemia, so they very appropriately administered aspirin and IV rate controlling medications over approximately 20 minutes and collected repeat ECGs.

At 18:08, the rhythm changed and the rate decreased to about 110bpm, but the patient complained of ongoing chest pain and dyspnea. Here was the ECG at that time:

The rhythm is not entirely clear because there are not definite P-waves, but it is certainly regular and therefore not atrial fibrillation. Now the diffuse STD is resolved, leaving very focal STD from V1-V5, maximal in V2-V3 consistent with classic, obvious posterior STEMI (a very obvious case of OMI).

The treating physicians saw the focal STD in the anterior leads and were considering posterior STEMI vs. possible de Winter's pattern. They texted me at 18:13 and my opinion was posterior STEMI.

At 18:15 a Code STEMI was called, and the cardiology team responded immediately. Unfortunately they believed that the STD was more likely to be caused by rate-related ischemia from rapid AF. They advised the ED team to give nitrates and cardizem drip.

Because they were not convinced, the ED team performed a posterior EKG while the cardiologists were at beside, approximately 15 minutes after the last ECG:

It appears that leads V2 through V6 have all been moved to a posterior location, though it is unclear exactly where they were placed on the chest, or which leads are supposed to represent V7-V9. Regardless, it is irrelevant because ALL leads show diagnostic STE, confirming posterior STEMI. 

Somehow the cardiologists were still not impressed by this posterior ECG. They cancelled the Code STEMI and asked the ED team to administer nitro drip and let them know what the troponin shows.

At 18:41, the first troponin T (drawn at 17:40) returned significantly elevated at 0.44 ng/mL. The patient had ongoing pain.

Code STEMI was called a second time.

The cardiology team responded and this time agreed to take the patient to the lab. He had a delay of 87 minutes from the first, appropriate Code STEMI (18:15) to arrival in the cath lab at 19:42.

Here is what they found:

Normal RCA.
The left main coronary artery branches into a very small LAD (the vessel going vertically down the image) which has a 50% ostial stenosis, and a LCX which is 100% occluded at the ostium.

Arrows at the site of LCX occlusion.

Another view, showing the relatively small LAD in the upper half of the image, and the empty territory of the occluded LCX in  the lower half.

Arrows show the site of LCX occlusion.

A wire has crossed the ostial LCX lesion and you can now see the large vessels distal to the occlusion.

Arrows show the site of the (prior) LCX occlusion.

The epicardial vessels are now open, revealing an enormous territory supplied by the occluded LCX. As you can see, an Impella (cardiac output assist device) has also been placed, as the patient has gone into cardiogenic shock on the table.

Arrows highlight the territory that had been occluded.

 The patient became progressively more dyspneic, hypoxic, and hypotensive during the procedure, despite opening the artery as shown above. An Impella was placed for assisting cardiac output, and the patient was intubated.

Remember, the angiographic result does not ensure that the actual downstream myocardium is receiving blood supply. Only the clinical symptoms and ECG can show whether there is true reperfusion on a cellular level.

So what do you expect to see on his repeat ECG? You are looking to see if he shows signs of reperfusion vs. "No Reflow Phenomenon" (in which the ECG changes progress as if there was no reperfusion at all, because there is either no reperfusion at the level of the cells, or reperfusion was too late and the infarct is already irreversible). See the diagram below for the patterns of reperfusion vs. continued occlusion.

 Here is the patient's post-intervention ECG:

What do you make of this? Why are the anterior T-waves so big now?

This ECG shows posterolateral reperfusion. The large T-waves in V1-V3 are reciprocal to massive negative reperfusion T-waves in the posterior leads (remember: the diagram above assumes you are looking at leads directly over the site of the infarct). The inverted T-wave in V6 and I is indicative of lateral reperfusion. So this ECG is evidence that the infarct was not yet complete at the time of cath, and that there was truly successful reperfusion on a cellular level as well as the angiographic level.

Despite reperfusion, the patients troponin T peaked at over 32 ng/mL at just under 24 hours from presentation (extremely high troponin, indicative of enormously large territory of infarction). It is impossible to convert this directly to troponin I, however our experience suggests a roughly 10:1 conversion between troponin I:T, so for those of you using contemporary troponin I assays, this patient would be predicted to have a troponin I of over 300 ng/mL.

Unfortunately the patient's course was complicated by acute renal failure requiring dialysis, and the patient ultimately passed away 7 days later of a combination of complications.

It is plausible that he may have had a better outcome if his duration of acute coronary occlusion had been reduced, but we can't know for sure. But we can make sure to learn from his case and deliver reperfusion therapy as rapidly as possible to those with diagnostic ECGs.

Learning Points:

You must advocated for your patients with OMI, because the STEMI guidelines and some current practice patterns do not. Even though this particular case does have STD diagnostic of "posterior STEMI," this is not actually recognized formally as an entity in our current ACC/AHA 2013 STEMI guidelines, despite the fact that it is recognized in other ACC/AHA documents). There are no formal recommendations for posterior STEMI in the 2013 STEMI guidelines, not even millimeter thresholds for STE in V7-V9 as are given in other documents.

Posterior OMI may manifest on the classic 12-lead ECG as STD proportionally maximal in leads V2-V4.

Diffuse supply/demand mismatch ischemia, such as during atrial fibrillation with rapid ventricular response, may manifest widespread STD, but this will usually be proportionally maximal in V4-V6. Additionally, I have never seen a case of widespread STD from supply/demand mismatch with STD in lead V1 (whereas V1 is involved in posterior STEMI). Changes due to diffuse supply/demand mismatch without ACS should resolve within 10-30 minutes of resolution of the condition causing abnormally increased demand.

A delay of even just 1 hour may have been the difference between life and death in some cases such as this. Whether the patient meets STEMI criteria is irrelevant; what matters is whether the patient has an acutely occluded coronary artery that could be opened emergently in order to improve the outcome of acute MI.

The diagnosis of OMI (or STEMI) does not rely on troponin, and should be made based on clinical findings and the ECG if possible. Furthermore, troponin T level of 0.44 ng/mL does not differentiate between early-mid OMI and supply/demand mismatch from rapid atrial fibrillation with underlying structural heart disease. Our troponin assay, for example, usually does not even start to elevate from zero until at least 2-4 hours after onset of acute coronary occlusion. This period of time is in fact the most valuable for the patient, as they have the most at risk but salvageable myocardium. The whole idea of "STEMI" or "OMI" is to prevent the cells affected by acute coronary occlusion from becoming measurable troponin if possible.

The ECG predicts reperfusion on a cellular level better than the angiogram, possibly even better than the patient's symptoms. Without understanding the progression of ECG findings in continued acute occlusion vs. reperfusion, you may not understand whether your patient has had successful intervention, and more importantly you may not know when the patient has re-occluded.

Posterior leads may help convince others of diagnostic STD maximal in V2-V3, but are not mandatory for diagnosis.

Friday, May 11, 2018

A young man with lightheadedness and bradycardia, and an impatient AV node.

A healthy 20 y.o. man presented with lightheadedness. 

The symptoms began about 2 weeks prior and were exertional. He stated that he plays on a college basketball team and he noticed over the previous 2 weeks that every time he exercised with the team he felt lightheaded. 

There was no actual history of syncope. He had had no associated chest pain, shortness of breath or palpitations. He had had no symptoms at rest or associated with positional changes. No history of similar symptoms previously. No history of heart or lung disease. There was no family history heart problems, sudden death, drowning, deafness. He did not take any medications.

Here is his ECG:
What do you think?
The treating physicians diagnosed complete AV block.

There is a narrow complex bradycardia at a rate of about 42.  It is hard to determine if there is a P-wave before the first complex, as that complex is at the edge of the tracing.  

The 2nd complex definitely does NOT have a P-wave in front, nor does the 3rd or 4th.  However, the 5th has a P-wave which is followed very shortly (at less than 120 ms) by a QRS.  The 6th has a slightly longer PR interval, and the 7th and 8th longer still.  

The longest of the PR intervals is the 7th.

What is this rhythm?  Is there AV block?  

No!  At least we see no evidence of block here.  There is no P-wave which does not conduct.  This is AV dissociation.  But not all AV dissociation is due to AV block.  In this case, it is "Isorhythmic Dissociation."  The sinus node and the AV node just happen to be discharging at the same rate, and also coincidentally are happening at about the exact same time.  

The AV node is too impatient to wait for the sinus beat to conduct.

Let's look at it again with annotation:
The P-wave in complex 7 probably conducts (red line is PR interval).
But I cannot prove this!
The black lines in complexes 6 and 8 are exactly the same length as the red line in the 7th.
You can see that the QRS initiates before the end of the black line in 6 and 8.
Thus, the AV node is firing before the impulse from the sinus node had a chance to arrive.
So the AV node was too impatient to wait for AV conduction.

For complexes 2, 3, and 4, the P-wave is hidden in the QRS.
Complex 5 has a preceding P-wave, but the very short PR interval makes it obvious that the QRS fired before that sinus impulse had a chance to conduct.
Beyond rhythm, the ECG is completely normal for a young man, with early repolarization (see classic J-waves in II, aVF, V4-V6)

Could there be AV block?  Yes, it is possible, and we cannot disprove AV block based on this ECG. But we have no reason to think there is AV block.

If the AV node is firing, why are there no retrograde P-waves?  Because the sinus node fires before the impulse from below can reach the atrium.  The ascending impulse from the AV node meets the descending impulse from the sinus node and they block each other.

How could we demonstrate absence of AV block?    Just have the patient do a bit of exercise to increase his sinus rate to a rate faster than the AV node rate.  

Another ECG was recorded later in the ED:
There is a slightly faster sinus rate now, almost 50, and now all P-waves are conducting.
This shows that the J-waves were indeed J-waves, not hidden P-waves

Clinical course:

The patient was admitted because of concern for intermittent complete AV block.

A walk test showed appropriate responsiveness of the sinus node with good AV conduction.

An echo was normal.

Learning Point:

1. Complete AV block is only one etiology of AV dissociation.  Isorhythmic dissociation is another.

2. Isorhythmic Dissociation is a benign condition.

Here is a very nice article on AV dissociation: 

Here is a nice article on Isorhythmic Dissociation:

Here is a nice example of Isorhythmic Dissociation with a Laddergram:

Here are other examples of Isorhythmic Dissociation:

Sudden weakness with bradycardia and bizarre T-waves

Here are other posts on AV dissociation and AV block

AV Dissociation Lecture by K. Wang (28 minutes)

A Mystery Rhythm, Explained by K. Wang's Ladder Diagram.

Atrial Flutter. What else?? (AV dissociation with block)

Tuesday, May 8, 2018

Palpitations of unusual etiology

Written by Pendell Meyers, with edits by Steve Smith

A male in his 60s with history of HTN and previous complaint of palpitations but with a negative holter monitor workup, presented to our ED with palpitations for the past hour, associated with lightheadedness and presyncope.

He was hemodynamically stable and well appearing, but was symptomatic with palpitations and lightheadedness.

Here is his 12-lead on arrival:
What do you think?

There is a regular, seemingly wide complex tachycardia at 224 beats per minute. The computer QRS duration is calculated at 178ms, but I believe the true QRS duration is much shorter, and in most leads no greater than 100ms. The QRS morphology is similar to RBBB with LPFB. However, the RBBB morphology in V1 is not the classic rSR' [first wave (r-wave) smaller than the second (R'-wave)]. Instead, the first R-wave in V1 is taller than the second (the R'-wave).  This "sign" has been described as an indicator of ventricular origin. However, the initial deflection of the QRS complex has undeniably rapid and organized (steep slope) conduction, strongly suggesting that the conduction pattern is utilizing the intrinsic conduction system of the Purkinje fibers.

For a QRS complex to have narrow QRS duration, organized initial conduction, and morphology consistent with RBBB + LPFB, it must either:

1) be supraventricular with RBBB and LPFB


2) originate in the left anterior fascicle itself

The differential at this point includes SVT with RBBB and LPFB, anterior fascicular VT, and good old regular VT, all plus or minus hyperkalemia to be safe.

Here are some helpful ECG core content diagrams for review of the differential of a wide complex QRS, as well as tachycardias in general:

Back to the case:

The treating physicians recognized the morphology as likely fascicular VT, and suspected that it may be one of the verapamil sensitive variants. As a review, posterior fascicle VT is thought to be fairly consistently responsive to verapamil; anterior fascicle VT is thought to be a similar entity to posterior fascicle VT but it seems less consistently responsive to verapamil. The working diagnosis of anterior fascicle VT thus prompted consideration of verapamil. Vagal maneuvers and/or trial of adenosine also would have been acceptable choices at this point.

The team first confirmed good LV function with bedside US (this is important before giving verapamil, as it is contraindicated by our guidelines in the setting of structural heart disease and heart failure). They then gave 10 mg verapamil IV. There was no response. They they tried 12 mg adenosine with no response. The patient was then sedated with etomidate and cardioverted with 200J, with immediate return to sinus rhythm.

Here is the post-cardioversion ECG:

This shows sinus rhythm with RBBB. There is no LPFB present on this ECG. So the RBBB seen on the presentation ECG is already present at baseline, however the LPFB was not. This feature does not help distinguish between SVT with RBBB and LPFB vs. fascicular VT originating in the left anterior fascicle, because it is still possible to have a rate-related LPFB in the setting of SVT with preexisting RBBB.

The patient underwent an electrophysiology study, during which Bundle Branch Reentrant Ventricular Tachycardia (BBRVT) was reproduced and successfully ablated. He received an AICD, also underwent a cath showing non obstructive disease and cardiac MRI without abnormalities.

Bundle Branch Reentrant Ventricular Tachycardia is a rare arrhythmia involving components of the infra-His conduction system (including the three fascicles themselves) as necessary components of a reentrant pathway. As you would expect, there are different ways to combine these circuit limbs, all of which would create different reentrant loops and different QRS morphologies.

Tchou and Mehdirad have been credited with describing three categories of BBRVT (see diagram below). Because our patient's QRS morphology includes RBBB and LPFB, this may be consistent with Type B, which appears to use one of the LBB fascicles anterogradely and the other retrogradely to comprise the reentry loop. If the circuit were to progress anterogradely down the LAF and retrogradely up the LPF, it would theoretically have the appearance of RBBB with LPFB, matching our patient.

There are other matching possibilities, however, including Type C with additional rate-related LPFB. At some point, enumerating these possibilities becomes purely academic because they do not have implications for prospective clinical management.

If these reentrant tachycardias are particularly sensitive to any medications, I am not yet aware of it. I cannot find any evidence stating that BBRVTs typically respond to any particular medication with any reliability. The few publications that do comment on pharmacologic therapy in the acute arrhythmic phase seem to agree that pharmacologic therapy is usually ineffective. Because they exist in the conduction system below the AV node, I would not expect that they should respond to AV nodal blockade such as adenosine.

This is in contrast to posterior fascicular VT, which is verapamil responsive, and to right ventricular outflow tract VT, which is responsive to adenosine.

Apparently BBRVT is highly associated with structural heart disease and cardiomyopathy in most cases, but more rarely has been described in the absence of structural heart disease (which our patient seems to fall into, except for his baseline RBBB). This further highlights the importance of considering bedside US for LV function before considering verapamil in these cases.

Image obtained from:

See these other cases of fascicular VT to compare and contrast with this case:

Posterior Fascicle VT
Another Posterior Fascicle VT
Originating in the posterior fascicle, therefore shows morphology of RBBB + LAFB
Usually verapamil sensitive

Anterior Fascicle VT
Originating in the anterior fascicle, therefore shows morphology of RBBB + LPFB
Sometimes verapamil sensitive, somewhat less so than posterior fascicle VT

Right Ventricular Outflow Tract VT
Originating in the RV outflow tract, therefore shows morphology similar to LBBB with inferior frontal plan axis (positive QRS complexes in inferior leads)
Usually adenosine responsive

Unfortunately, as EM physicians we rarely know the exact electrophysiologic diagnosis prospectively. What we can see prospectively is whether the QRS morphology matches one of the established patterns:

RBBB + LAFB Morphology: 
DDx includes classic VT vs. SVT+RBBB+LAFB vs. posterior fascicle VT vs. BBRVT vs. (probably other even more rare and obscure rhythms); if you believe it is one of the ventricular causes but not classic VT, then posterior fascicle VT seems to be one of the most common, and it is typically verapamil sensitive. Electricity works.

RBBB + LPFB Morphology: 
DDx includes classic VT vs. SVT+RBBB+LPFB vs. anterior fascicle VT vs. BBRVT vs. (who knows what else); if you believe it is one of the ventricular causes but not classic VT, then anterior fascicle VT is possible and may be verapamil sensitive, but it may not be; the pharmacologic solutions are unknown in this category. Electricity works.

LBBB + inferior axis (positive in inferior leads) Morphology: 
DDx includes classic VT vs. SVT+LBBB vs. RVOT VT vs. BBRVT vs. (probably others). If you believe it is one of the ventricular causes but not classic VT, then RVOT VT is possible and is typically adenosine sensitive (and adenosine is already indicated for a stable patient with monomorphic wide complex tachycardia). Electricity works.


Bundle Branch Re-entry Ventricular Tachycardia Storm During the Recovery Phase of Transient Complete Heart Block 

Bundle branch reentry ventricular tachycardia.     1995 Jul;18(7):1427-37. 

Learning Points:

For learners, please remember that one should assume classic VT until proven otherwise by a combination of clinical experience with ECG and clinical findings.

With experience and training, one can recognize wide QRS complexes which are likely to represent VT originating within the conduction system itself. Unfortunately, this category still includes a wide variety of arrhythmias which differ in their mechanisms and effective medications. Perhaps the only universal truth is that they are all susceptible to electrical cardioversion.

Posterior fascicle VT is typically thought to respond to verapamil.

Anterior fascicle VT may respond to verapamil, but seems less responsive than posterior fascicle VT.

RVOT is typically thought to respond to adenosine.

BBRVT is a rare arrhythmia which originates inside the ventricular conduction system and acts similarly to other fascicular VTs we have discussed on this blog. However, there do not appear to be any clear patterns of response to pharmacologic therapy.

Sunday, May 6, 2018

Is There a Delayed Activation Wave???

This 50-something otherwise healthy male presented with one hour of epigastric and lower chest pain.

Here is his initial ECG:
What do you think?
The QRS is 90 ms and the QTc is 400 ms.

There is ST Elevation (STE) in II, III, aVF, with reciprocal ST depression in aVL.  There is also ST depression in V2 and V3.  V2 and V3 almost always have some amount of normal ST elevation, and since posterior MI is associated with inferior MI, you must make notice of this and think it is probably an inferior posterior MI.

However, II, III, and aVF have what appear to be J-waves at the end of the QRS.  If these are J-waves, then couldn't the inferior ST elevation be due to early repol?

1. When there is ST depression in aVL, early repol as a cause of inferior STE is VERY unlikely
2.  These do NOT appear to be J-waves.

Instead, these are spikes at the end of the QRS in II, III, and aVF.  There is also an unusual wave at the end of the QRS in I and V6 .

These are what J-waves look like:
This is inferior and lateral early repolarization.
The waves in II, V5, and V6 are typical J-waves.
There is typical slurring of the J-point (end of QRS, beginning of ST segment) in lead III
Note absence of ST depression anywhere.
Note that there is some ST elevation in V2 and V3, which is normal (ST depression in these leads is very abnormal)

So the above first ECG is nearly diagnostic of inferior and posterior MI.

One of our fine interns, Daniel Lee, who is also an ECG whiz, found this paper from 2013 and brought it to my attention:
The delayed activation wave in non-ST-elevation myocardial infarction.  
He also wrote about it in this post:

In this paper, they describe a new "N-wave" in NonSTEMI that helps in determining the infarct artery.   When present, the infarct artery is more likely to be the circumflex.  They do not study whether this wave differentiates between MI and non-MI, between STEMI and NonSTEMI, or between OMI and NOMI.

The N-wave was defined as:
(1) a notch or deflection in the terminal QRS complex of the surface ECG
(2) the height of notch or deflection is at least 2 mm (the point of deflection was measured with reference to the PR segment);
(3) a continuous change of the notch (the point of deflection shifted at least 2 mm with
reference to the PR segment in at least 2 leads within 24 hours, even disappeared or merged with the S-wave) 
(4) with a prolongation of QRS duration in these leads.

Here is an ECG with N-waves, from the article:

Are these N-waves in our ECG?  They do not appear to be wide enough, but they still might be.

Case continued:

The first troponin I returned at 0.087 ng/mL (elevated).  Another ECG was recorded:
Hardly any changed, though the computer now measures the QRS at 116 ms.

Approximately 45 minutes after this, the patient's pain became much worse.  Another ECG was recorded:
Obvious inferior, posterior, lateral STEMI
What is the infarct artery?
This is hard to tell.
Of all inferior STEMI, 85% are due to RCA.
When there is ST depression in lead I, that percentage is higher.

When there is no STE in I, the percentage is lower, maybe 65% (such that the % of circumflex is higher at about 35% rather than 15%)

If these spikes are indeed delayed activation waves, then this feature would further favor the circumflex artery.

The cath lab was activated.

A 100% occlusion on of the circumflex, proximal to the first obtuse marginal, was found, opened, and stented.

This case produces more questions than answers

1. Are "Delayed Activation Waves" a real phenomenon?
2. If so, were the waves in this case actually "Delayed Activation Waves" (N-waves)??
3. Can delayed activation waves be used to differentiate non-ischemic ST elevation from ischemic ST elevation?
4. Can they be used to differentiate OMI from NOMI?

Friday, May 4, 2018

Look at these "T"-waves

An alcoholic presented with confusion.  He had this ECG recorded:
What do you think?
Computer measures the QT at 505 ms, and QTc at 533 ms
The measure appears to be correct.

V3 reminds me of this ECG:

Are These Wellens' Waves??

What is going on?

These waves which you think are T-wave are really very large U-waves.  

The clues are:
1) the down-up morphology
2) the apparent very long QT

The K returned at 2.1 ng/mL.
The pH was 7.55 and bicarb was 47, with chloride less than 68.  The patient has a severe hypokalemic metabolic alkalosis from vomiting.

(By the way, the pCO2 was 55.  An appropriate compensation for metabolic alkalosis is 0.9 x bicarb + 15.  So 47 x 0.9 = 43.  Add 15 and you get an expected pCO2 of 58.  A pCO2 of 55 is just a bit below predicted.) 

The importance of this is:
Anything that increases ventilation (hypoxia, agitation, anxiety) can lead to dangerous alkalemia.  
If the pCO2 were to be lowered to normal (= 40), then the pH would rise to 7.70 (very dangerous).

Here are subsequent ECGs:

This one at K = 2.4
The down up morphology remains
The computer measures the QT at 565 ms, QTc at 591 ms
This measurment also appears to be correct
(except that now we know it is measuring the QU-interval, not the QT)

Large U-waves, with long QU-interval, also puts patients at high risk of polymorphic VT

And 6 hours later at K = 2.6 mEq/L:
Now the apparent T-waves are really T-waves (not U-waves), and the QT is 479, QTc 500

Learning Points:

1. When the QT interval is impossibly long, the "T-waves" are probably U-waves.  In this case, the QT was long, but not impossibly so.  Nevertheless, one should think of U-waves.

2.  When there are down up T-waves, and the apparent QT is long, they are probably U-waves.

3.  Large U-waves are associated with a high risk of VT.  (I will write more on this later)

Wednesday, May 2, 2018

Cardiac arrest #3: ST depression, Is it STEMI? or is he an ACCESS Trial Candidate?

A patient with unwitnessed arrest received a shock from the AED (presumably ventricular fibrillation).  He underwent extensive resuscitation, was transported in full arrest, and arrived still in V Fib.

He was receiving chest compressions on the LUCAS device.

We placed a Transesophageal echo, as we do on all arrests.

Just after TEE was placed, he was shocked into an organized rhythm.

This is the TEE:

There is now an organized rhythm, at which time we stopped compressions and monitored cardiac activity continuously during the entire resuscitation.

Here I annotate the image to orient you:

The white arrow is the left atrium; you can see that the probe in the esophagus is directly adjacent to the left atrium
The red arrow is the LV and it has reasonably good function.
The yellow arrow is the RV

A 12-lead ECG was recorded:
This shows slow atrial fibrillation.
There is massive ST Depression in V2-V5.

There is ST Elevation in aVR.
Is it a Left Main Occlusion? (no, but it may be Left Main ACS)
Is it posterior MI?

Importantly, the ST depression is MAXIMAL in V3 and V4 (by ECG features alone, this is more likely to be posterior STEMI, NOT in V5 and V6, which would be more likely to be diffuse subendocardial ischemia).
However, in the setting of cardiac arrest, there is a higher pretest probability of diffuse subendocardial ischemia:
1. Cardiac arrest is more likely in the setting of LM, LAD, or 3-vessel ACS or CAD
2. The low flow state of cardiac arrest is likely to result in subendocardial ischemia regardless of the etiology of arrest.

We activated the cath lab.

There is an ongoing randomized clinical trial at our hospital called the ACCESS trial (ACCESS to the Cardiac Cath Lab in Patients Without STEMI Resuscitated From Out-of-hospital VT/VF Cardiac Arrest, Identifier: NCT03119571)

In the ACCESS trial, patients with a shockable rhythm who do NOT have a STEMI are randomized to emergent cath vs. later angiography, as indicated.

Thus, we are only supposed to activate the lab for "True STEMI."  Others would get randomized.

However, if you read the ACCESS trial inclusion criteria closely, patients who have a "STEMI-Equivalent" are NOT supposed to be randomized; they are supposed to (appropriately) go to emergent angiography.
Inclusion Criteria:
  • Adult presumed or known to be 18-75 years old
  • Resuscitated from OOHCA
  • Initial cardiac arrest rhythm of pulseless VT/VF (including patients treated with an AED)
  • No ST-segment elevation MI (No STEMI) (or STEMI-equivalent syndrome) on ED 12-lead ECG (as interpreted by a physician)
Exclusion Criteria:
  • Initial non-shockable out-of-hospital cardiac arrest rhythm (pulseless electrical activity or asystole)
  • Valid do not resuscitate orders (DNR),
  • Blunt, penetrating, or burn-related injury, drowning, electrocution or known overdose,
  • Known prisoners
  • Known pregnancy,
  • ST-segment elevation on ED 12-lead ECG (as interpreted by a physician)
  • Absolute contraindications to emergent coronary angiography including,
  • known anaphylactic reaction to angiographic contrast media,
  • active gastrointestinal or internal bleeding, or
  • severe concomitant illness that drastically shortens life expectancy or increases risk of the procedure.
  • Suspected or confirmed intracranial bleeding
  • Refractory cardiac arrest (prior to randomization)
  • Patients meeting ACCESS Trial eligibility criteria initially seen in an outside hospital and then transferred to an ACCESS Trial participating hospital

We recorded another ECG some 15-20 minutes later to determine if the ECG abnormalities were all due to post ROSC, as the low flow state of cardiac arrest can lead to severe ischemia and profound ECG abnormalities (see post on April 25, 2018):
Still Atrial Fib.  Still with profound ST depression.
Now you can also see some STE in lead III with reciprocal STD in aVL.
So this is likely to be infero-posterior MI, but still could be due to subendocardial ischemia (Diffuse STD with STE in aVR).

The patient went for angiography.

LMCA: The LM has a 70% stenosis in the mid portion of the vessel.  This was a chronic stenosis.

LAD: Type III LAD is noted.
The LAD is a large caliber vessel.
The LAD has 70% disease in the ostial, proximal segment of the vessel. (This was also chronic, not an acute thrombotic event.)  

The LADD 1 is a large caliber vessel.

LCx: Ostial-Proximal LCX has 100% disease. This is Chronic as it fills via a grade 3 RT to LT collaterals that fills the dominant LCX.  OM1 fills via Lt to LT collaterals

RCA: RCA has Normal take off.  Small non dominant.  The Mid segment of the RCA has 100% disease between 2 RV marginal.

So the patient has profound 3-vessel disease, without apparent culprit.  Thus, there was no intervention.  The etiology of arrest is uncertain.  The ECG findings are due to the ischemia of the low flow state.

If this is hemodynamically significant, it could lead to ischemia in a low flow state)

Here is a post cath ECG, after the effects of the low flow state have resolved:
This shows Q-waves and reperfusion T-waves in inferior leads.
There are Large Precordial T-waves -- Posterior Reperfusion T-waves
So this ECG supports an infero-posterior MI due to hypoperfusion (type II STEMI)

Diffuse ischemia from LM stenosis and low flow was likely contributory

Echocardiogram confirms infero-posterior MI:

Regional wall motion abnormality-lateral/inferolateral, akinesis.

Regional wall motion abnormality- basal inferior.


This was a primary ventricular fibrillation, not due to ACS, but (as with the case on April 24), causing severe ischemia due to low flow in the presence of severe coronary stenoses.  The arrest might have been caused by demand ischemia (patient exerting himself in the setting of severe CAD with severe stenoses.)

The ST depression appears to have been transmural, subepicardial ischemia because the posterior wall requires collateral flow from the RCA for its perfusion, and the low flow in the RCA does not allow for enough perfusion.

So, again, this was not ACS.  In retrospect, there was not a need for emergent angiogram as there was no culprit and no intervention.

But it would be impossible to know this prospectively.

Learning Points:

1.  STEMI-equivalents due to ACS (more appropriately called OMI -- Occlusion Myocardial Infarction) should be brought emergently to the cath lab.

2.  In the post arrest situation, it may be very difficult to ascertain whether a finding is due to OMI or due to the low flow state with fixed stenoses.

3.  It is often only possible to make that determination after the emergent angiogram.

4.  Use bedside transesophageal echo (TEE) for all cardiac arrest cases. It makes cardiac monitoring perfect and continuous.(1, 2)

We use TEE on all cardiac arrest cases and in cases of shock who are intubated.  We will report our over 100 cases soon, but the preview is that it is incredibly helpful in managing these patients, and surprisingly easy to use.


1.  Blaivas M. Transesophageal echocardiography during cardiopulmonary arrest in the emergency department.  Resuscitation 78(2):135-40; August 2008.
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Monday, April 30, 2018

Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations -- A Case from Salim Rezaie (R.E.B.E.L. EM)

This case is posted by Salim Rezaie (@srrezaie)

Chest Pain, “Negative” Stress Tests, POCUS, & ECG Equations

It has some peer review by me at the end, so we're co-posting!!

Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations

by Salim Rezaie

I was working a busy shift in the ED, like many of us do, and the next patient I was going to see was a 57 year old male with no real medical problems complaining of chest pain.  I remember thinking as I walked into the room this guy looks ashen and diaphoretic….he doesn’t look well.  He is a paramedic telling me how he has been having off and on chest pain for the past several months.  He just had a stress test two months ago that was “negative”.  Today he was working on his pool and developed the same chest discomfort as he had been having off and on the past several months, but today, the pain would just not go away.  In his mind, he thought this might be an ulcer and just needed some Pepcid to help. He got put on the monitor and an ECG was run…
The patient involved in this case has given permission to share the story, and relevant images with the knowledge that this information will be used for the purposes of education.

This was read by the ECG machine as normal sinus rhythm and age undetermined septal infarct.  Looking closer at leads V2 and V3 I can imagine that I am seeing some ST-segment elevation.  

Given he was diaphoretic, I was thinking this was an evolving anterior STEMI.  So I asked for a second ECG and quickly ran to get the ultrasound machine so I could do a bedside POCUS to look for wall motion abnormalities.  

The 2nd ECG was done, but I didn’t get to see it until much later, as a Code Blue was called overhead.  Here is the 2nd ECG by the way…

Again the ECG machine read this as normal sinus rhythm with age undetermined septal infarct, but as you can clearly see there is more ST-segment elevations in leads V2 and V3 when compared to the 1stECG. This is still not an anterior STEMI by definition (no mm criteria met), but it is diagnostic of a coronary occlusion.

I ran back to the room and saw a cyanotic patient, unresponsive getting CPR.  The crash cart was called for and as we were waiting for the crash cart, the patient was intubated without difficulty.  Defibrillation pads were placed on the patient and after one round of CPR (≈2minutes), ventricular fibrillation was seen on the monitor.  The patient was successfully defibrillated with 200J on a biphasic machine…There was asystole on the monitor for about 5 – 10 seconds and then sinus tachycardia with ROSC.

It’s hard to have a great concept of time, but going back and reviewing the chart, all of this transpired within 10 minutes of the patients arrival to the ED.  I finally did get to do the Post-ROSC POCUS at the bedside and sure enough the patient had an antero-septal wall motion abnormality. Lucky for both of us, cardiology happened to be in the department and saw the bedside POCUS.  The patient was quickly taken to the cath lab and found to have a 100% proximal LAD lesion (“The Widow Maker”).  He ended up getting 2 stents.
I went to follow up with the patient the next day and he is doing quite well.  Extubated in less than 24 hours.  

I asked Dr. Smith to give some expert peer review as well: 

Teaching Point #1: Uselessness of “Negative” Stress Tests
Many emergency providers have taken care of patients with true acute coronary syndrome or even primary cardiac arrest despite having had a recent “negative” stress test.  I know I have.  Overreliance on “negative” stress tests can be a common reason for misdiagnosis or delays in patient care.  It is important to remember that coronary artery disease can arise from atherosclerotic lesions that are only mildly stenotic with unstable plaques that rupture and not picked up by standard stress testing. There is a huge misconception about “negative” stress tests in the health care industry and by laypersons. The sensitivities and specificities for stress testing are often reported between 65 – 90% depending on which study you read.  Here are two trials that stress this exact fact:
Trial #1 [1]:This was a retrospective chart review of 164 patients with either a “negative” stress test (122 patients) or a “normal” indeterminate stress test (42 patients) over the past 3 years.  34 patients (20.7%) from the total cohort were determined to have significant coronary artery disease in the next 30 days. Significant coronary artery disease was defined as myocardial infarction identified by positive cardiac markers, subsequent positive stress test of any type, cardiac catheterization requiring intervention, CABG, or death due to medical cardiac arrest.  Here is the troubling part…8/34 (23.5%) had their most recent stress test within 1 month prior to admission 7/34 (20.6%) had their stress test between 1 – 3 months, and 11/34 (32.4%) had their stress test between 6mo – 1 year.  Of the total cohort of 164 patients, 13 patients (7.9%) had an AMI.
Trial #2 [2]:This was a prospective evaluation of 186 patients who had been referred for coronary angiography for suspected stable angina.  All patients had a normal ECG at rest, none had undergone coronary revascularization, or have diabetes mellitus. 50% of women and 25% of men who had reversible perfusion defects on coronary angiography had completely normal exercise electrocardiographic findings.
Teaching Point #1 Bottom Line: Stress testing is used to identify critical stenosis causing obstruction to coronary blood flow, however in the setting of acute myocardial infarction the underlying pathophysiology is plaque rupture and thrombus formation.  Coronary lesions may not have been significant enough to be detected on stress testing.  Therefore a prior “negative” stress test should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
Teaching Point #2: Use POCUS (or as I like to call it Stethoscope 2.0)
For obvious reasons I was not able to get a live recording of this patient’s bedside ultrasound, but thought it would be useful to put up some images and videos describing ultrasound and coronary anatomy as this clenched the diagnosis. So first, let’s start with an ECG and the coronary anatomy and then move on to echo and coronary anatomy.

Image from Marwick TH et al [3]

Teaching Point #2 Bottom Line: Use POCUS liberally, as this will save patients' lives.  I have started putting an ultrasound machine right next to me when I am on shift.  When I go to evaluate patients I am ultrasounding as many hearts and lungs as I can.  I cannot even begin to tell you the number of times, this has changed my disposition or expedited the care my patients received, including the above patient getting to the cath lab.

Teaching Point #3: Steve Smiths Early Repolarization vs “Subtle” Anterior STEMI Equation
Steve Smith over at Dr Smith’s ECG Blog has created a calculation that differentiates early repolarization vs subtle anterior STEMI.  The key is the ratio of the T-wave amplitude to the R-wave amplitude.  In anterior STEMI, the R-wave amplitude is smaller and early repolarization has a shorter QT interval.  One HUGE CAVEAT, is that this equation should not be used in patients with LVH or LV aneurysms as this can cause false positives.
The Calculation:(1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
Don’t worry, you don’t have to memorize this.  It’s now on MD Calc

The Evidence [4]: A retrospective study of patients  with “subtle” (non-obvious) anterior STEMI and early repolarization at 2 hospitals had ECGs compared.  355 anterior STEMIs were reviewed and 143 of them were non-obvious and compared with 171 early repolarization ECGs.  The generalized findings were: in “subtle” anterior STEMI the R-wave amplitude was lower in leads V2 – V4 and the QTc was longer when compared to early repolarization. Also a value of >23.4 predicted STEMI while a value of ≤23.4 was predictive of early repolarization.  The overall sensitivity, specificity, and accuracy of this equation was 86%, 91%, and 88% respectively.  This had a positive likelihood ratio of 9.2 and negative likelihood ratio of 0.1.

Getting ECG Nerdy:
60 Milliseconds (= 1.5 small boxes) after the J Point in V3

QTc not shown in ECG #1 above was 416ms
R Wave Amplitude in V4

So for the above patient…

(1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
(1.196 x [2.7mm) + (0.059 x [416ms]) + (0.326 x [4.5mm]) = 26.3 which is suggestive of an anterior STEMI, not early repolarization
Teaching Point #3 Bottom Line:  When you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting.
Clinical Bottom Line & Things I Learned from the Case:
  1. A prior “negative” stress test, even if recently done, should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
  2. In patients having chest pain, use POCUS liberally, as this will save patients' lives
  3. If you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting
Expert Peer Review
Stephen W. Smith, MD
Hennepin County Medical Center (HCMC
Minneapolis, MN
Blog:Dr. Smith’s ECG Blog

I can see the ECGs better now, and also see the computer read.  

There is a Q-wave in lead V2.  Since normal variant ST elevation never has Q-waves in V2 – V4, it must be assumed to be LAD occlusion (OMI – Occlusion Myocardial Infarction) even without using the formula.  

One might think this... there is a QS-wave in V2, therefore this is old MI.  And the computer read is “age undetermined septal infarct.”  But I have a rule for Old MI with persistent ST elevation (LV aneurysm morphology). The rule is based on the fact that acute MI has large T-waves compared to the QRS, and old MI has small T-waves.

ECG Differential May Include: Old anterior MI with Persistent ST Elevation (LV aneurysm morphology)

My rule for differentiating acute STEMI from LV aneurysm really only reliably distinguishes between:
  1. Acute STEMI on the one hand
  2. Subacute STEMI or LV aneurysm on the other
What is the Rule?
  • First, there must be ST Elevation
  • Second, the ECG differential diagnosis must be LV aneurysm (old MI with persistent ST Elevation) vs acute STEMI
  • This rule should not be used for early repol vs acute STEMI.  Conversely, if the differential is LV aneurysm vs acute STEMI, then you should NOT use the early repol formula
When should LV Aneurysm be on the ECG differential diagnosis?
Primarily when there are well-formed Q-waves, with at least one QS-wave, in V1 – V4.  A QS-wave is defined by absence of any R-wave or r-wave of at least 1mm.  (If there is an R-wave or r-wave, we call the whole wave a QR-wave, Qr-wave, or qR-wave, depending on the relative size of the Q-wave vs. R-wave.)

The Rule: If there is one lead of V1 – V4 in which theT/QRS ratio is greater than 0.36, then acute STEMIis the likely diagnosis, though subacute STEMI is also possible.  Since both require the cath lab, if the ratio is greater than 0.36, and the clinical situation is right (i.e. unexplained chest discomfort), then cath lab activation is indicated.  I both derived and validated this formula, for which the cutoff has good sensitivity and specificity.
  • Derivation: Accuracy of Formula = 93.2% (Smith SW T/QRS Ratio Best distinguishes Ventricular Aneurysm from Anterior Myocardial Infarction. Am J Emerg Med 2005. PMID: 15915398)
  • Validation: Sensitivity 91%, Specificity 81% (Electrocardiographic criteria to differentiate acute anterior ST-Elevation Myocardial Infarction from Left Ventricular Aneurysm. Am J Emerg Med 2015. PMID: 25862248)
  • False negatives had pain duration greater than 6 hours.  Thus, it may classify those patients with prolonged chest pain as LV aneurysm when they are really subacute STEMI.
Here is More Data on Stress Tests:
  • Nerenberg et al. Impact of a Negative Prior Stress Test on Emergency Physician Disposition Decision in ED Patients with Chest Pain Syndromes. Am J Emerg Med 2007. PMID: 17157680
  • Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 [Abstract]
    • There were about 600 visits in 300 patients who had a negative stress imaging test within 3 years.  There were 20 MIs, most in patients whose negative stress had been within the last year.  We show that a recent negative stress imaging test is poor evidence that someone who returns to the ED with chest pain is not having an MI.
  1. Walker J et al. coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
  2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
  3. Marwick TH et al. Techniques for Comprehensive Two Dimensional Echocardiographic Assessment of left Ventricular Systolic Function. Heart 2003. PMID: 14594869
  4. Smith SW et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment elevation Myocardial Infarction. Ann Emerg Med 2012. PMID: 22520989
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