A 40-something with Chest Pain

A 40 something presented with chest pain.  Here is the ECG:

QTc 415 ms.  What is it?

   

The QRS is normal size and duration.  So any ST elevation has to by primary, not secondary to LVH, LBBB, etc.

Is it early repolarization?  Pericarditis?

There is ST elevation in V1-V3, maximal in V2 at barely more than 1 mm (measured at J-point, relative to PQ junction).  The T-wave in V2 is nearly peaked.  It does not have the typical wide and fat appearance of an ischemic hyperacute T-wave.

But it has two features that should alert you to LAD occlusion:

1. Look at inferior leads: there is downsloping ST depression with a down-up T-wave in III and aVF.  These are highly suspicious for reciprocal changes of LAD occlusion.

2. QRS distortion, which does not happen in early repol or in pericarditis.  This is when there is an absence of BOTH and S-wave AND a J-wave in EITHER V2 or V3.  This ECG only barely has an S-wave in V3 (the S-wave only goes 0.5 mm below the PQ jct.).

Best Explanation of Terminal QRS Distortion in Diagnosis of Electrocardiographically Subtle LAD Occlusion

A repeat ECG was done 10 minutes later:

QTc 419 ms

Compare V1-V3 side-by-side from the two ECGs:

There is subtle evolution of the T-waves.  They become less peaked, more broad.
There is less S-wave in V3 than before.

The patient was taken to the cath lab and a 100% acute thrombotic LAD occlusion was found.  K was normal.

Is this STEMI? Pattern Recognition is Key

This was sent to me, asking what I thought of it:

A very elderly woman presented with weakness and diarrhea. There was no chest pain or dyspnea.  

An ECG was recorded because weakness is a common symptom of MI, especially in elderly women. 

What is your interpretation?

I was told the computer interpretation was "Acute STEMI".

My response was: "LVH only.  No STEMI."  

How do I know?

It is hard for me to explain exactly how I know this except that I have seen it so often and recognize the pattern.  But I'll try.  

Features suggesting  STEMI: 

One could easily believe this is inferior-posterior STEMI, as there is ST elevation in lead III with reciprocal ST depression in aVL, and there is ST depression in V2 and V3 with a tall R-wave (the mirror image of a posterior Q-wave).  

However: 

1. There is high voltage, especially in I, V2, and V3.  aVL meets "criteria" for LVH of 11-12 mm amplitude.  (As with most ECG features, however, morphology is more important than criteria)

2. The T-wave inversion might be mistaken for NonSTEMI, but then the locations are contradictory:  The "inferior" ST elevation would imply active coronary occlusion of the inferior wall, while the T-wave inversion would suggest anterolateral NonSTEMI with reperfusion.

3. The ST elevation in III is not accompanied by any STE in II or aVF.  In fact, II has some ST depression.  This means that, in the frontal plane, the ST vector is directly to the right at 180 degrees.  (In the axial plane it is also posterior, resulting in anterior ST depression)

4. ST elevation in III is a scooped-out saddleback, and that is because the ST segment is long and flat, and thus the T-wave is not hyperacute; rather, it has a narrow base.  Contrast it with this wide-based T-wave in a true inferior STEMI:

Lead III
This is STEMI.  There is no true saddleback because the T-wave is wide-based (it is particularly fat and bulky resulting in an absence of upward concavity).

[Although I have found that precordial ST elevation associated with Saddleback is almost never due to MI, I have not assessed it in inferior leads and am not sure of its significance.]

But doesn't all ST elevation with reciprocal ST depression in aVL mean Acute MI?

No! Absence of ST depression in aVL all but rules out pericarditis and early repolarization as the etiologies of inferior ST elevation.  But reciprocal ST depression in aVL is frequently found in these STEMI mimics: LVH, LBBB, inferior LV aneurysm, myocarditis.

Much of ECG interpretation depends on pattern recognition

It is up to those of us who recognize the patterns to figure out what it is that we are seeing so we can communicate it to those who don't recognize it.

I have long thought that reading ECGs is like recognizing faces (maybe I'm autistic).  I have long thought that we need to use computer facial recognition software that can learn from its mistakes, and train it to recognize these patterns.

Fortunately, I have come into contact with some software geniuses who know how to do this and we're hoping to improve ECG algorithms and make them self-teaching.

The patient did not have an MI.

This ECG is pathognomonic and you must recognize it.

This patient was found with a bottle of alcohol and altered mental status.  His breath alcohol was 0.259.  Due to bradycardia, a 12-lead ECG was obtained:

There is atrial fibrillation at a rate of 54.  The QRS is 166 ms.
Why is it slow?  What is the diagnosis?

This is pathognomonic and you must recognize this!  There is a wide QRS and peaked T-waves.   In particular, notice how flat the ST segment is before it abruptly rises into the T-wave! 

HyperKalemia was immediately recognized and the patient was given Calcium.

A followup ECG was obtained after Calcium:

The QRS is now 129 ms.

The potassium returned at 7.8 mEq/L.  His pH was 6.97.  It was caused by new onset of acute renal failure.

This patient could easily have been just assumed to be intoxicated.  He might have been brought to detox, or might have just been observed in the ED.

But because of bradycardia, a 12-lead was obtained, which gave the critical diagnosis.

Learning Points:
1.  When a patient is bradycardic, especially if irregular, one must always think of hyperK and one must get a 12-lead ECG.
2. One must recognize this pattern as hyperK
3. Calcium's effect is almost miraculous
4. Slow atrial fibrillation implies an sick AV node, or one affected by electrolytes, ischemia, or medications/drugs.  Otherwise, the ventricular response should be fast.

Anterorlateral STEMI? Old Anterior MI? But cath shows RCA thrombotic stenosis.

This case is from a frequent contributor, Brooks Walsh.  With additions and edits by me.

A 68 year-old man had been having chest discomforts intermittently for the past 2 weeks. About 18 hours prior to presentation, his pain began to worsen. He developed nausea, and 911 was called after he vomited once. EMS obtained an ECG:

There is subtle ST depression in II, III, and aVF. There is ST elevation in V2 – V5, with Q waves in V2 – V4.  This is all but diagnostic of anterior MI.
Is it acute? subacute? Old MI with persistent ST elevation?

EMS requested cath lab activation. The patient was given nitroglycerin 3 times, and his discomfort resolved completely before arrival to the ED. The ECG was repeated at that point:

The ST elevation in V2-V5 appears more pronounced, otherwise no significant changes.

Is this acute or chronic ST-segment elevation?

Concern was raised by cardiology that, given the duration of symptoms, as well as the anterior Q waves, that the ECG changes could reflect a chronic pattern of persistent ST-elevation (STE) following previous MI; aka “left ventricular aneurysm” (LVA). Emergent angiography for an NSTEMI might not serve an elderly patient well, they emphasized. Quite true!

However, there are elements of the ECG that suggest that, even if she does have an old anterior MI, she also likely has superimposed features of an acute anterior STEMI.

First:

Specifically, the anterior T-waves are relatively tall, compared with the QRS complexes. In both V2 and V3 we see that the T-wave height exceeds 36% of the total QRS amplitude. Recent results from Klein et al. strongly suggest that this indicates acute anterior STEMI, even in the presence of so-called LVA.

Furthermore, QR-waves commonly develop in the first hour of an anterior STEMI.

[It is important to note that QS-waves (in contrast to QR-waves - Q-waves followed by an R-wave) do NOT develop so quickly, and QS-waves are the waves one most commonly sees in LV aneurysm]
So, QR-waves cannot, by themselves, demonstrate a subacute or chronic presentation.

Second:

There is increasing ST elevation on the 2nd ECG.  This can only happen in acute STEMI.  

Therefore: the diagnosis is either:

1. acute STEMI with early Q-waves

2. subacute STEMI (prolonged occlusion with development of Q-waves, or

3. old anterior MI with superimposed acute STEMI

Clinical Course:

While awaiting the cath lab team, a second ECG was obtained:

Improvement in anterior STE and inferior ST-segment depression. New T-wave inversion in leads I and aVL now suggest that earlier ECGs showed ST segment “straightening” and hyperacute T waves in those leads. These dynamic changes support acute occlusion affecting the anterior wall, with possible spontaneous reperfusion.

The EM resident acquired a bedside echo:

There is an anterior wall motion abnormality, with severe hypokinesis/akinesis, but no overt dyskinesis or aneurysm.  There is no inferior WMA, or only a mild one.

Only one troponin I (Ortho clinical diagnostics) was obtained, pre-PCI: 1.4 ng/ml (0.034 ng/ml is 99^th %)

Angiography and PCI

In angiography a 100% LAD lesion was found at the take-off from the LM.  However, this contained multiple calcifications, and was quite difficult to cross, the interventionalist felt this was chronic.

By contrast, the dominant RCA had a proximal 90% occlusion, but appeared acute. 

Pre- and post-stent deployment in the prox RCA (blue arrow = lesion).

Note that the RV branch (red arrow) is patent.

Both the LAD and the RCA lesions were stented.

Post-PCI results:
A post-cath ECG was obtained.

Inferior ST depression has resolved, as has the anterior STE. T-wave inversion is seen in leads I, aVL, and V2-V6, consistent with a reperfused anterior wall.

The post-cath echo demonstrated severe hypokinesis in the distal septal, anterior, and anterolateral segments, while the RV had normal systolic function.

This is all consistent with anterior LV STEMI.

How do you explain the ECG and echo findings by a 90% thrombotic lesion in the RCA?

Anterior STEMI – But which anterior wall?

Keep in mind that the right precordial leads are actually looking at TWO anterior walls – the anterior wall of the LV of course, but also the anterior wall of the RV.

Accordingly, there are (at least) two possible explanations for the anterior ST elevation and reversion

 RV branch of the RCA?

The first is that the RV branch of the RCA was transiently occluded. Numerous case reports have shown that occlusion of the RV branch (whether due to occlusion of a non-dominant RCA¹,²,³,⁴ isolated occlusion of the RV branch⁵, or a surprisingly-common iatrogenic occlusion of the RV branch!⁶,⁷,⁸,⁹,¹⁰) can produce anterior STE without inferior STE.  In these cases of isolated RV MI, the anterior STE is produced by the ischemic anterior RV, not the antero-septal LV wall. Since the RV branch does not supply the inferior wall of the LV, STE in the inferior leads would not be expected.

However, the bedside echo, as well as the post-PCI comprehensive echo, did not reveal any RV dilation or dysfunction, making even a transient RV MI unlikely. Even though the symptoms and the ECG showed spontaneous improvement prior to PCI, it would be unusual to recover RV function so quickly and completely, even from a transient occlusion!
More importantly, an RV branch occlusion would not produce STE or T-wave inversion in aVL. Lastly, isolated RV MIs typically produce maximum STE in the right-side leads V1 and V2, whereas the maximal elevation here is more lateral, in V3-V5.

Subtotal RCA occlusion produced acute-on-old anterior MI?

Given the old compete LAD occlusion, how could the anterior wall have a “new” MI? Probably the anterior wall was being perfused by the RCA, via collaterals. After an acute RCA sub-total occlusion, the flow to the inferior wall might have been sufficient to prevent infarction of the inferior LV wall. However, the flow to the anterior wall through the collaterals might have been dramatically decreased, to the point that the anterior wall would become acutely ischemic.

In effect, this would produce an acute anterior STEMI (produced by RCA 90% occlusion) superimposed on the old anterior MI (due to LAD occlusion). This would be consistent with the ECGs (acute STE anterior and high-lateral, followed by TWI in those same leads), and with the echos (wall motion abnormalities limited to the anterior wall), virtually excluding inferior or lateral ACS.

Our explanation: All findings are explained by the presence of an old anterolateral MI which now only has collateral circulation from the RCA.   A 90% RCA occlusion remains enough to perfuse the inferior wall, but not enough to reach the anterior and lateral walls supplied by the LAD.

Without getting a detailed view of the video angiogram, this hypothesis cannot be verified.  We did not do this.

1.         Porter A, Herz I, Strasberg B. Isolated right ventricular infarction presenting as anterior wall myocardial infarction on electrocardiography. Clin Cardiol. 1997;20(11):971-973. doi:10.1002/clc.4960201115.
2.         Hsu P-C, Lin T-H, Su H-M, Lu Y-H, Lai W-T, Sheu S-H. Unexpected anterolateral ST elevation after cardiopulmonary resuscitation in a patient with right coronary artery occlusion. Resuscitation. 2009;80(6):713-714. doi:10.1016/j.resuscitation.2009.03.011.
3.         Logeart D, Himbert D, Cohen-Solal A. St-segment elevation in precordial leads* : Anterior or right ventricular myocardial infarction? Chest. 2001;119(1):290-292. doi:10.1378/chest.119.1.290.
4.         Muhammad KI, Kapadia SR. Anterior ST-Segment Elevation With Right Coronary Artery Occlusion: A Unique Case of Isolated Right Ventricular Infarction. Angiology. 2008;59(5):622-624. doi:10.1177/0003319707305464.
5.         Turkoglu S, Erden M, Ozdemir M. Isolated right ventricular infarction due to occlusion of the right ventricular branch in the absence of percutaneous coronary intervention. Can J Cardiol. 2008;24(10):793-794.
6.         Acikel M, Yilmaz M, Bozkurt E, Gürlertop Y, Köse N. ST segment elevation in leads V1 to V3 due to isolated right ventricular branch occlusion during primary right coronary angioplasty. Catheter Cardiovasc Interv. 2003;60(1):32-35. doi:10.1002/ccd.10610.
7.         Hilliard AA, Nkomo VT, Mathew V, Prasad A. Isolated right ventricular infarction — An uncommon cause of acute anterior ST segment elevation. Int J Cardiol. 2009;132(2):e51-e53. doi:10.1016/j.ijcard.2007.08.017.
8.         Kocaman SA, Uğurlu Y, Ergül E, Bozkurt E. Prominent ST-segment elevation in leads V1–V4 due to isolated right ventricular branch occlusion after primary percutaneous coronary intervention for right coronary artery. J Cardiol Cases. 2010;2(3):e135-e138. doi:10.1016/j.jccase.2010.05.008.
9.         Koh TW, Coghlan JG, Lipkin DP. Anterior ST segment elevation due to isolated right ventricular infarction during right coronary angioplasty. Int J Cardiol. 1996;54(3):201-206. doi:10.1016/0167-5273(96)02610-1.
10.       Bolt CLB van der, Vermeersch PHMJ, Plokker HWM. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty. Eur Heart J. 1996;17(2):247-250.

Atrial Fib and RVR with a run of wide complex tachycardia. Was this Ventricular Tachycardia?

An elderly male with history of atrial fibrillation presented by ambulance.  His prehospital tracing (lost, sorry) showed a 6-beat irregular run of wide complex tachycardia.  The medics were worried about a run of ventricular tachycardia (VT).

Here is his first ED ECG:

There is an irregularly irregular rhythm with QRS duration of 115 ms.
(There is also left axis deviation, probably left anterior fascicular block)
This is atrial fibrillation.
Notice there are three wide complex beats in lead II across the bottom.
Are these PVCs?  Was the 6 beat run due to VT?
What is going on?

Here is a magnification with annotation:

First, notice that beats 8 and 14 (black arrows) are identical.
Second, notice that beat 14 is simultaneous with leads V1-V3, and that beat 14 in lead V1 has an RBBB pattern.
The right bundle has a longer refractory period than the left bundle, so aberrancy is most likely to have an RBBB pattern.
What is this aberrancy in atrial fibrillation called?  Ashmann's phenomenon.

Ashmann's Phenomenon:  After a relatively long R-R interval, repolarization is delayed and there may be an aberrant beat if it comes relatively early.  In Ashmann's phenomenon, the AV node and HIS bundle have shorter refractory periods than the bundle branch, in this case the right bundle, and so the impulse traverses both the AV node and HIS bundle and then the left, but not right bundle branch.

The phenomenon is frequent with a long-short sequence:

Complex 8: The preceding R-R interval affects the refractory time of the subsequent beat.
Thus, the long R-R interval between complexes 6 and 7 (410 ms) makes the refractory period of complex 7 longer, then complex 8 comes early at 320 ms and thus complex 8 has aberrancy.

Complex 12: this is also wide, but I cannot measure a definite difference in QRS duration between it and complexes 8 and 14.  The preceding R-R interval (between complexes 10 and 11) is again long, making the refractory period of complex 11 long, resulting in aberrancy in complex 12.

Complex 14:   the long R-R interval between complexes 12 and 13 (560 ms) makes the refractory period of complex 13 longer and thus complex 14, which comes early after only 380 ms, has aberrancy.

The prehospital strip with a run of 6 beats had the same RBBB morphology.  Therefore that was NOT a run of VT, but several aberrant beats in succession.

In that rhythm strip, the beat preceding those beats did occur after a long preceding R-R interval, but the others did not.  If all the succeeding beats come very early, ("long-short" without the long), then there can be aberrancy without the preceding long R-R interval.

An Obvious LAD Occlusion that did not meet STEMI "Criteria"

This case was provided by Tom Bouthillet, who is Editor-in-Chief of EMS 12-Lead and Chief Content Architect of ECG Medical Training.

Case

An elderly male with a history of an RCA and mid-LAD stent started feeling ill with nausea and vomiting.  3 hours later he developed substernal chest pain.

Paramedics found him with a normal exam. Pain was 5/10 without radiation or diaphoresis.  This ECG was recorded:

 The computer algorithm read "nonspecific".  Computerized QTc is 439 ms. 
What do you think?  See below.  

Sinus rhythm.  There is ST elevation which is very worrisome for STEMI, especially in this high risk patient.  However, there are not 2 mm of ST elevation at the J-point, relative to the PQ junction, in two consecutive right precordial leads, which is the ACC/AHA and Universal Definition of MI criteria for males over age 40 (2.5 mm are required for males under 40; 1.5 mm for women). 

This ECG is very worrisome for LAD occlusion [in fact, when Tom and I (Smith) saw it, we had no doubt that it represented LAD occlusion], partly because the T-waves appear so bulky and wide.  This is partly because of a slightly longer QT interval and smaller T-wave amplitude.  See below:

Here is V2 from a typical early repol ECG:

The STE is 4 mm at the J-point.  The T-wave is 13 mm tall.

Compare it with V2 in the above ECG.   

Here there is 2.5 mm STE at the J-point.  The T-wave is 10 mm tall.This looks wider and more "bulky," don't you think?

What should you do when you suspect that this may be LAD occlusion?

Features to look for to differentiate subtle LAD occlusion from normal variant ST elevation in V2-V4 ("early repolorization"):
1. Early repol must have upward concavity in all of leads V2-V6 (all are concave here)
2. Early repol must not have any Q-waves in V2-V4 (there are none here)
3. There must be no "inferior" or precordial ST depression (there is none here)
4. There must be no "terminal QRS distortion" in either V2 or V3 (this means neither an S-wave that goes below the level of the PQ junction, nor a J-wave).  This is explained very well here.
5.  There should be no T-wave inversion in precordial leads, unless it is "Benign T-wave Inversion," which can only be diagnosed by someone very familiar with it.


If an ECG has all these features that qualify it for early repolarization, then one should apply the early repol vs. LAD occlusion formula below.

The differential diagnosis must be only early repol vs. LAD occlusion: LVH is likely to result in a false positive.

Formula: (1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).

STE 60 V3: ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PQ junction, in millimeters.

 A value greater than 23.4 is quite sensitive and specific for LAD occlusion.  A value less than 22.0 is extremely unlikely in LAD occlusion.  There is an applet on the sidebar of the blog which I have reproduced here.  Just fill in the values and get the result:




A couple other findings may give a clue:

1. An upright T-wave in V1
2. Less upward concavity

In our study, we found that neither of these findings were independently associated with LAD occlusion.

The formula value is 27.2, which is clearly in the LAD occlusion range above 23.4.


Another ECG was recorded at t = 21 minutes, when the patient was feeling slightly better:

QTc is 442.  T-waves are slightly smaller, but the formula value is still over 27.

Another ECG was recorded at t = 26 minutes:

QTc is 448.  No significant change.

In spite of these ECGs, and the high pretest probability, the patient was only taken to the cath lab after a long delay and absence of improvement with medical therapy.

The exact delay is uncertain, and the exact reasoning uncertain, but physicians still are inappropriately dependent on millimeter criteria for diagnosing STEMI even if the diagnosis is obvious, even though these criteria are very insensitive for acute MI (less than 50%, and about 75% sensitive for occlusion

The patient was eventually taken to the cath lab and had a 100% in-stent thrombosis occlusion of the LAD.

Learning Point:

Millimeter criteria are dangerously insensitive for acute myocardial infarction (sensitivity 48%!), though better for acute coronary occlusion (around 70%).  If you rely on them, you will miss approximately 25-30% of acute occlusions.

You can get fooled if you don't read the ECG systematically

A middle-aged woman presented with chest pain continuous since the previous day.  Here was the inital ECG:

What is it?
The treating physicians interpreted ST and T-wave abnormalities worrisome for ischemia

The patient was treated for ACS medically.  Cardiology was consulted for persistent pain in a patient with presumed ACS.

What is really going on?  See below.





















Remember to read the ECG systematically.  Don't look at the ST segments and T-waves first! Your eye is drawn to them, but resist!

Instead, read:

1. Rate
2. Rhythm
3. Intervals
4. QRS voltage, axis, duration, conduction delays and bundle branch blocks.
5. Repolarization (ST, T, U)


Here is an annotated version:

Notice there a no P-waves in front of the QRS complexes!
The black arrow points to a retrograde P-wave (atrial activity would be more accurate)
The red arrow also points to retrograde atrial activity in V3.
The blue lines point out the retrograde atrial activity in every lead.

Possible rhythms:
1.  A slow re-entrant rhythm with retrograde atrial activity
            a. AVNRT
            b. AVRT (accessory pathway)
2. Junctional tachycardia with retrograde P-waves

Why do we think it is not simply atrial tachycardia?

Because the atrial activity comes after the QRS and is inverted.

If it is atrial tachycardia, then:
1.  There would have to be a VERY long PR interval (400 ms) and
2.  The atrial activity would have to be low in the atrium for the P-wave to be inverted.

This is all possible, but much less likely than a re-entrant rhythm.

Why do the ST segments and T-waves look so abnormal?

This is just a result of a large and inverted, superimposed P-wave.  The atrial activity is simultaneous with the ST segment and T-wave.


The patient was given adenosine and converted:

There is now sinus rhythm and normal ST segments and T-waves.

This proves that it is an adenosine sensitive (re-entrant) paroxysmal supraventricular tachycardia.

In this case, failure to read rhythm first led to error.  

While there may be some underlying ST-T abnormalities, any ischemia must first be managed by managing the dysrhythmia and re-assessing with a repeat ECG.  When this was done, there was no residual ischemia.

Some points:
1.  This conversion by adenosine would work in both AVNRT and AVRT.
2.  It was a very slow rhythm for both AVNRT and AVRT, but especially for AVNRT.  A slow accessory pathway is likely.
3.  If it is an accessory pathway, should there not be delta waves?  No!  See explanation below.
4.  Does conversion with adenosine help in diagnosis of atrial tachycardia?  No!  Some atrial tachycardia is automatic and does not respond to adenosine.  Some is re-entrant and does not responds.  But some is re-entrant and does respond to adenosine.

There was a slight rise in troponins which is consistent with type II MI.  However, the rate was not so fast, and some significant coronary disease may be involved.  She will therefore get a stress test.


I received this question:

How do you tell that the retrograde P is not a T wave, and the T wave is not a P wave with a 1st degree heart block? Is it just their relative shapes?

And answered it thus:

Not at all a dumb question.  With experience, you can tell that the T-wave is deformed by another wave.  You can suspect this, and then test your hypothesis by looking in other leads to see if the T-wave is deformed at the same time in those other leads.   

One cannot say for certain that it is not an inverted P-wave with a long PR interval, but: 1) a PR interval of 400 ms is very uncommon and 2) if not retrograde, then an inverted P-wave must come from low in the atrium.  

Therefore, you have to hypothesize two unusual occurrences: 1) very long PR interval and 2) low atrial pacemaker.  And you also have to explain a fast rhythm.

All this can be explained by a low atrial tachycardia with a prolonged PR interval.  But it also has to be an atrial tach that is adenosine sensitive, and not all of them are.

Steve Smith





Absence of delta wave in WPW:

The below refers to this case: http://hqmeded-ecg.blogspot.com/2015/09/a-large-r-wave-in-lead-v1.html

Preexcitation and delta waves may not be apparent in sinus rhythm in patients with WPW who have a left-lateral bypass tract.   In this setting, the time for the atrial impulse to reach the atrial insertion of the accessory pathway is longer than the time to reach, and transmit through, the AV node.  This patient does in fact have a left lateral bypass tract and that is why it has right axis deviation and some of the characteristics of RBBB, with the majority of forces going from left to right, causing large R-wave in V1.

If there were a normal conduction through the AV node (here it is slowed - 1st degree AV block), then the impulse would have gotten through the AV node before pre-excitation and there would be no delta wave.   Some call this "concealed conduction," because on the baseline ECG you cannot see a delta wave, yet the patient can have WPW related tachycardias.

You can read more about concealed conduction here.

See this fascinating case of WPW with a normal PR interval.

A Missed STEMI. How could the Diagnosis have been certain?

A middle aged patient presented to the ED with "ischemic-sounding chest pain" of unknown duration. An ECG was recorded: 

The ST Elevation in V1-V4 by itself is not diagnostic.  The computerized QTc was 410 ms.
What feature(s) makes this ECG diagnostic of LAD Occlusion?

The emergency physician at the small referral hospital made the diagnosis of STEMI and activated the cath lab pathway, which includes faxing a copy of the ECG to the referral center.  This was done.

The referral center instructed the emergency physician to hold onto the patient and repeat the ECG in one hour.

This was done:

There is still more ST elevation.  Now it should be super obvious that this is a STEMI, and even meets STEMI "criteria" of at least 2 mm in 2 consecutive leads.

This prompted another discussion with cath lab staff (including another faxed ECG) who stated that as the ECG was improving (???? -- my italics and question marks), the patient should be kept locally in the cardiac ICU and treated as a non-ST-elevation-MI. The patient at this point had been given dual anti-platelet therapy, opiate analgesia which relieved his chest pain, and a Xa inhibitor. Initial highly-sensitive troponin T (hsTnT) returned at 150 ng/L (normal is less than 14 ng/L).  

Comment: now can there be any doubt about the diagnosis?

In the cardiac ICU, the patient had further chest pain overnight (comment: the opiates wore off) and was re-discussed with the PCI center. Advice given at that time was to start a nitro drip.

Patient went for PCI the following day (greater than 12 hours after onset of pain). This showed LAD occlusion.  Peak hsTnT > 10,000 ng/L.

Comment: This is a massive MI.  Most STEMI have a TnT greater than 1000 ng/L.  A TnT of 10,000 is a very large MI, especially if it is not after reperfusion (release at the time of reperfusion results in a high troponin spike).  In this case, there was no reperfusion and such a peak is therefore especially high and indicative of very large MI.

Transthoracic echo showed "good LV function" (this is hard to believe) with Anterior and Apical WMA. 

Post-PCI ECG is here:

This shows the typical QS-waves of completed transmural anterior MI.  The T-wave inversion is shallow compared to the T-wave inversion of reperfused MI, as T-wave amplitude correlates with amount of viable ischemic myocardium.  There is so much nonviable myocardium here that the T-wave inversion will not be deep.This ECG shows that the patient lost the entire anterior wall.  Irreversibly.

What made the first ECG diagnostic?

There is about 1.5 mm of ST elevation in V2 and V3.  This alone could be normal or due to ischemia.  Therefore, one must explain the ST elevation.  If it is normal, then the rest of the ECG should conform to normal, and that includes normal QRS, R-waves, and R-wave progression.  The presence of a Q-wave in lead V2 makes normal variant impossible.  Furthermore, there is Reverse R-wave progression.   The R-waves get smaller from V2-V4.  This never happens in normal variant ST elevation.  

Reverse R-wave progression is analogous to presence of Q-waves.   When there are Q-wave present, one should mark the ST elevation in V2-V4 as either acute occlusion or as old MI with persistent ST elevation.  This ECG is clearly not due to the latter, therefore must be acute LAD Occlusion.

Since it should be "obvious" LAD occlusion, one should not use the LAD-early repol formula.  However, if one did use the formula, and one used 2 mm for STE at 60 ms after the J-point (an underestimate), 410 ms for the QTc, and 2 mm for the R-wave amplitude in V4, one would get 25.93, which is far higher than 23.4 and indicates LAD occlusion.

Further comment:

1. Opiate analgesia.  This should never be given in ACS unless you are committed to the cath lab!  It only hides the symptoms and obscures the diagnosis.  If a patient has refractory pain from ACS, that patient needs emergent angiogram and PCI!

2. A nitro drip is fine, but only precludes emergent angiogram if it resolves the pain and the ischemic ECG findings.  By the time of the second ECG, this patient has STEMI, and so even if it resolves with medical therapy, emergent cath must be done.

3. Serial ECGs.  These should not wait one hour!  If you are doing serial ECGs, they should be every 15 minutes.  In one hour, a lot of damage can be done.

4.  Your referral center may be wrong.  If you are worried about the patient, tell them you are not comfortable keeping that patient and insist on transfer.

5.  In this case, thrombolytics are indicated.  In this patient, thrombolytics were indicated if PCI could not be done within 90-120 minutes of arrival at the outlying institution.

This ECG was texted to me last night with the question: Occlusion or Not?

This ECG was sent along with this text:

"Thoughts? Occlusion or not? - context : cardiac arrest:"

Here is my answer: 

"Yes, but probably > 6 hours old, or an acute superimposed on an old MI, but there is acute STEMI here."

Question:

"You think the ST elevation is diagnostic according to criteria?"

Answer (Quoted):

"Not according to criteria.  

But you cannot call it normal variant ST elevation when there are Q-waves like that." 

So the differential is:

"Old MI with persistent ST elevation (LV aneurysm)" 

vs. 

"Subacute MI" 

vs. 

"Old MI with superimposed STEMI."  

"I have derived and validated a formula to differentiate LV aneurysm from acute MI: if there is one lead of V1-V4 with a T/QRS ratio > 0.36, then it is 90% specific for acute.  In this case, V3 has a 5 mm T-wave and the QRS amplitude is 8.5 mm.  5/8.5 = about 0.6 which is far higher than 0.36."   Also V4.

Question:

How about ultrasound?

Answer:

"There will be an anterior wall motion abnormality (WMA) for sure, but you won’t be able to tell whether it is old or old with superimposed acute.  Either one could have WMA with thinned out wall.  Only acute has a T-wave like that."

Outcome:

"I pushed for the activation - proximal LAD 100% - I'm glad I pushed for it.  First troponin I returned at 11."

My answer:

"Just as I said: Subacute STEMI"

Aside: Ryan Tee also noted correctly that there is also a PVC in aVL with concordant ST elevation. This is a very good sign for STEMI, but it could possibly also be seen in LV aneurysm. 


Comment

One might say that any shockable cardiac arrest should go to the cath lab emergently, and there are many good arguments for that.  Most of these arguments are based on "if there is no alternative explanation."

Old MI is such an alternative explanation, as it supplies the underlying substrate (scarred myocardium) that leads to ventricular fibrillation.

Furthermore, not all hospitals actually take all shockable cardiac arrests for angiogram, but rather do so selectively for those with ECG evidence of ischemia (especially, of course, STEMI).

In this case there is a clear alternative diagnosis: old MI, and no obvious ischemia on the ECG.  

But that is only true if you do not understand the T-wave in old MI: it is not large, but rather small or slightly inverted.  

The T-waves were too large and upright in V3 and V4 to be due to old MI.  They had to be acute (or, I should say, subacute).  This is confirmed by the initial troponin of 11, which is only present in MI that has been going on for "a while" (at least 6 hours).

Brooks Walsh recently wrote this post which explains it all in much more detail.

Transient STEMI, no T-wave Evolution and no Wall Motion Abnormality

A Middle-Aged male had chest pain.  Here is his first ECG:

Obvious Anterior STEMI (note that among the findings is terminal QRS distortion (no S-wave or J-wave in V3)

No Echocardiogram was done at this point, but you can be certain that there was an anterior-apical wall motion abnormality (WMA) during this ECG.

Shortly thereafter, his pain resolved:

The STEMI is completely resolved.  Even the S-wave in V3, and the J-wave in V4, are restored.

A bedside echo was done and showed no wall motion abnormality.  Granted, this was not done with contrast or interpreted by a super expert, but an anterior STEMI should show some WMA.


The cath lab was activated and the patient went for PCI of a critical acute LAD stenosis with thrombosis.  There was TIMI-3 flow prior to the intervention.  A stent was placed.

This ECG was recorded after the procedure, 2.5 hours after the first ECG:

No significant change from the last one

A formal echocardiogram was done which was completely normal.

Serial troponin I peaked at around 1.2 ng/mL.

Another ECG was recorded about 10 hours after the first one.  

This is remarkable for no T-wave evolution.

Usually, when there is transient STEMI and positive (even though not very high) troponins, the ECG develops "reperfusion T-waves" or "Wellens' waves."

Usually, after transient STEMI, there is some residual wall motion abnormality for at least a day or so.

But not always!!!

Some argue that a normal echo in the course of an evaluation for MI means that no MI is ongoing.  But wall motion can recover extremely rapidly after spontaneous reperfusion.

Learning Point:

If the ECG findings have resolved, the wall motion may be recovered also

Question in my mind:

Does complete normalization of the ECG after reperfusion, with the absence of any T-wave evolution (reperfusion T-waves), predict full wall motion recovery?   I can find no literature on this, but I strongly suspect it is true. 

What is the clinical significance?

If the serial troponins are normal, as is often the case, and you do not record the ST elevation when it is there, you may entirely miss this case of ACS because there are no Wellens' waves and no wall motion abnormality.

The link below has some such cases:

See here for more cases and discussion of Transient STEMI, including literature.