What happened after the PCI?

A middle-aged male with h/o CABG x 3, previous stents, and aortic valve and aortic root replacement presented primarily with headache, but also told the medics that he had chest pain (for 6 hours) because he "knew they would respond faster than if he said headaches."  The chest pain was right sided rib and shoulder pain, worse with inspiration, sharp, and sometimes 7-8/10.  But the headache was much worse.   Chest pain was not relieved by sublingual NTG.

He has noticed worsening exertional dyspnea, such that he feels he can only walk about a block before experiencing "chest tightness. 

Here is his ED ECG (compare with the 2 month previous ECG below it):

--Is there a new Q-wave (tiny r-wave) in III?  

--There is new ST elevation in III, with new STE also in aVF.  

--There is reciprocal ST depression in aVL.  

--There is STE in V1, suggesting RV MI, but this was present on the old one.  

--There is some ST depression in V5 and V6.  

--This is almost certainly an acute inferior MI, though does not meet mm "criteria" for STEMI 

--The beginnings of T-wave inversion suggest an open artery.

Previous ECG from 2 months prior:

Previous, does not have the same ST deviations

CT head was negative for acute bleed.  The patient was managed medically with ASA 325 mg, heparin, and Plavix, and nitroglycerine, but his pain did not improve.  A troponin I returned at 7.7 ng/mL (diagnostic of MI).

A repeat ECG was recorded:

There is slightly more STE in III and reciprocal STD in aVL

Cardiology was consulted for NSTEMI that needs the cath lab now (objective evidence of ischemia and ongoing pain).  The cath lab was activated.


Cath results:

It was a complex cath and anatomy.  The RCA was diffusely diseased and had an acute on chronic occlusion that was opened.

A Post Cath ECG was obtained an hour later:

What is going on?

I ran across this case and this ECG while reading through a series of ECGs and it alarmed me.  The inferior ST elevation is now gone, but there is new DIAGNOSTIC ST elevation in V1-V3.  Look closely: the ST elevation is greatest in V1 and V2, and does not extend out to V4.

Why?  Because this "anterior" MI is due to STEMI of the right ventricle (RV), not of the LV.  

Case Progression

The cardiologist quickly went to evaluate the patient, who found that the chest pain was unchanged and that the patient was hemodynamically stable.  A formal echo showed some RV dysfunction and normal LV anterior wall.

This was presumed to be an isolated acute RV infarction and due to the patient stability and the difficulty of the coronary anatomy, no intervention was undertaken.  Presumably, the procedure induced a thrombus in the RV marginal branch.



This was recorded 3 hours post cath:

The RV infarct appears to be resolving spontaneously.

5 hours post cath:

More resolution of ST elevation, with some T-wave inversion.  This is good evidence of spontaneous reperfusion of the RV marginal branch

Next day:

The troponin I peaked at 29, fell to 20, then rose again just a little to 21.5 ng/mL due to the brief RV STEMI.


The patient did well.

Learning points:

1. NonSTEMI often need immediate cath lab activation. as I have often discussed.
2. STEMI in V1-V3 is anterior, but not necessarily due to LV anterior STEMI.  It may be due to RV STEMI, which is also anterior.  
3. When the RCA is the vessel involved, new anterior ST elevation is likely to be RV STEMI
4. When the ST elevation is greatest in V1-V3 vs. V2-V4, RV STEMI is more likely than LV




Detailed cath results:

1) 2 vessel CABG [Left internal mammary (LIMA) to LAD, and Saphenous Vein Graft (SVG) to left posterolateral artery (L-PLA)]

months ago.

3) The SVG to the L-PLA is occluded. The LIMA to the Mid-LAD is widely

patient.

4) The RCA was patent on the cath of xxxxxxx. The occluded RCA currently

likely represents acute on chronic obstruction in light of the patients

clinical presentation and the collaterals to the R-PDA.

5) Balloon angioplasty only due to noncompliance with clopidogrel, 

reducing the sub-total occlusion to diffuse 30-40% stenosis. The R-PDA is

occluded proximally and was probe with a wire.

Coronary Angiograms 

LMCA: 60% calcified mid to distal LM stenosis.

LAD: Multiple stents in the LAD system. Sub-totally occluded LAD after the

first major septal and diagonal. D1 has an instent 70% take-off stenosis.

LCx: Co-dominant system. 80% circ take-off stenosis. Scattered 30% stenosis

throughout the circ system. The L-PLA that received the SVG has a 70%

stenosis on the native vessel just at the proximal insertion of the graft.

Only a small remnant of the SVG is visible at the insertion site consistent

with occlusion.

RCA: Stent noted in proximal portion. Sub-total occlusion proximally. A

R-PDA fills faintly by L to R collaterals.

Lesion on Prox RCA: 99% stenosis.

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You've all heard about SMACC 2013 and SMACC Gold, the best EM and Critical Care conferences in the world.

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View the incredible program here:

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18 hours of intermittent chest pressure

A male in his 60's with no previous cardiac history complained of substernal chest pain intermittently for 18 hours.  It has more recently become constant.  He was diaphoretic.  He called 911 and had this prehospital ECG recorded:

I saw this when he arrived, and was worried about the slight ST depression in V2 and the size of the T-waves in V5 and V6, as well as the minimal terminal T-wave inversion in aVL and a bit of ST depression there.

We recorded this immediately:

The same findings are here, without any evolution.

BP was 140/80.

His pain continued and would be relieved from 8/10 to 6/10 with sublingual nitroglycerin.  We gave aspirin and clopidogrel for high suspicion of ACS.


Had I looked for it (which, foolishly, I did not), I would have found this previous ECG from 9 months prior:

There are definite changes compared to this one

Had I seen this, I would have immediately diagnosed definite ACS and started high dose IV nitroglycerin.

As it was, we did give sublingual NTG, and sent a troponin and, while the pain continued, recorded this ECG 42 minutes later:

The T-waves in V5 and V6 have less amplitude.  This caught my eye. 

Not having seen the old one yet, and seeing no diagnostic evolution, I just kept a high index of suspicion.  But I was pretty sure that, with the duration of pain, that if this chest discomfort was indeed due to ACS, that the first troponin would be at least slightly elevated.

The first troponin then returned at 0.20 ng/mL (normal up to 0.030 ng/mL).  The diagnosis was clear.  High dose nitro was started with no relief.

We activated "Pathway B", a system we have worked out which is intermittent between cath lab activation and no activation, and which covers patients with NonSTEMI but whom the emergency physician believes need to go to the cath lab immediately.

Patients with objective evidence of ongoing ischemia that is not relieved by anti-platelet, anti-thrombotic, and anti-ischemic therapy should go directly to the cath lab.

The cardiologist agreed, and the patient went straight up for angiogram:

The red arrow shows the very tight, hazy, acute thrombotic 95% stenosis of a very large Obtuse Marginal (this vessel is in the right position to either be a high takeoff OM, a high takeoff 1st diagonal, or a ramus intermedius, which is a vessel that is sometimes seen between the circumflex and the LAD).  The black arrows point out its entire course, which now has TIMI III flow.

Here is the post cath ECG:

The V2 ST depression is gone, and the V2 T-wave has much higher amplitude (posterior reperfusion T-wave).  The T-waves in V5 and V6 are normalized.  There is now T-wave inversion in aVL.  There is much artifact in inferior leads. 

Here is the next day ECG:

There is deep T-wave inversion in I and aVL, with reciprocally large T-waves in III and aVF, and some terminal T-wave inversion in V5 and V6.

Next day echo showed Lateral and inferolateral wall motion abnormality.
Troponin I peaked at 28 ng/mL


Learning points:

1. Aggressively investigate suspicous ECG abnormalities in the context of typical chest discomfort and unrelieved symptoms
2. Compare with the old ECG!
3. Some NonSTEMI need the cath lab now!  (objective evidence of ischemia and refractory symptoms)
4. Notice that, in ACUTE posterior infarction, there is not necessarily any increase in R-wave amplitude in V1-V3.  In this case, there was a decrease.

EP Report back on this case: a very fast narrow complex rhythm followed by a very fast wide complex

This was a very interesting case:

A Very Fast Regular Narrow Complex, Followed by an Equally Fast Regular Wide Complex

It had a very fast narrow complex rhythm, then a very fast wide complex rhythm, then converted to sinus with a very short PR interval.

We surmised that there must be accelerated AV conduction AND an accessory pathway.

The EP results are back, and:

1. Accelerated AV conduction
2. Left lateral accessary pathway.  It was ablated.

A Hybrid of de Winter's T-waves and Diffuse Subendocardial Ischemia: Left Main Ischemia

A very elderly woman who was highly functional complained of jaw pain and called 911.  Her BP was 80/40 with a puls of 45.  Here is her prehospital ECG:

There is ST elevation in aVR,  but also in aVL, V1 and V2.  There is diffuse, marked ST depression, in II, III, aVF, V3-V6.  The computer appropriately read ****Acute MI**** 

The ST elevation vector is superior and anterior, not to the right as one would expect with the typical "ST elevation in aVR MI", which would be reciprocal to diffuse ST depression (I, II, V3-V6).

This ST elevation vector is also not only towards aVL, as one would expect of the typical high lateral STEMI.  It also has a rightward/upward component toward aVR, and an antero-superior component toward V1 and V2.

The ST depression vector is also not typical of the "diffuse subendocardial ischemia" pattern which typically is towards leads II and V5, in the antero-lateral-inferior direction towards the apex of the heart.

[When there is diffuse subendocardial ischemia, the entire subendocardium is affected, causing ST depression vectors around the entire myocardium: inferior, lateral, posterior, anterior and apical (but not superior as this has little ventricular myocardium).  The additive effect of all this is an ST depression vector towards the apex.]

Thus the ST elevation vector is superior and anterior, and suggests STEMI of the very high part of the anterior and lateral wall and of the septum.  Does the remainder of the ST depression signify subendocardial ischemia or posterior STEMI?

This is all academic because such a high risk ECG and case requires immediate cath lab activation if such an elderly patient is in favor of aggressive therapy to save her life.  If you don't have a cath lab, then thrombolytics are also indicated, even by the rules (2 consecutive leads, V1 and V2, are involved).  The medics activated the cath lab before arrival in the ED.

The patient arrived in the ED talking and not in clinical shock, but with a low BP and low pulse.  There was no SOB or pulmonary edema.  This ECG was recorded:

Now there is no ST elevation in V2, but there is a hyperacute T-wave.  This is a de Winter's T-wave and diagnostic of near occlusion of the LAD.  V3 also has ST depression with a hyperacute T-wave very suggestive of de Winter's T-waves.  The ST depression persists.

The change from STE to de Winter's in V2 suggests some minimal flow in the artery.

The bedside cardiac ultrasound is shown here, in a slightly off-center parasternal short axis view:

This shows a dense anterior wall motion abnormality.  The posterior wall appears to be contracting effectively.

She was given atropine and this improved both her pulse and blood pressure.

Angiogram:

Black arrows are very narrowed left main, red arrow is LAD with flow, and yellow arrow is circumflex with flow.

Interpretation: 95% left main thrombus with TIMI-2 flow, with thrombus extending to the ostial LAD and the circumflex.

The patient was not a CABG candidate.   Angioplasty and stenting of this very high risk lesion (estimated mortality without therapy = 100%; estimated mortality with = 50%.  This is because, in order to treat a left main lesion, one must temporarily completely occlude it, which is very high risk).  Here is the ECG a couple days later:

Minimal signs of ischemia (mild ST depression)

Outcome:

Her heart did very well.  

However, the trouble with the very elderly is that they are frail, and all that antiplatelet and anticoagulant therapy can lead to other complications and she died.   In order to protect her identity, I cannot go into the details.

Smith SMACC-Gold Lecture in on the Intensive Care Network: Subtle ischemia, or NonSTEMI that need the Cath Lab Now

This is the 30 minute lecture I gave at Social Media and Critical Care (SMACC)  on the Gold Coast of Australia in March.

It is called "Subtle ECG signs of Ischemia," but I prefer to call it "NonSTEMI that need the Cath Lab Now."

What a great event SMACC was!

Don't miss SMACC-Chicago, June 23-26, 2015.

We will have a pre-conference ECG workshop (AM) and critical cardiac workshop (PM) on the 23rd!!

Here is the lecture: http://vimeo.com/108865066

http://intensivecarenetwork.com/subtle-ecg-signs-ischemia-smith/

Chest Pain and a Very Abnormal ECG

A male in his 60's with no history of coronary disease presented with chest pain.  Here is his ED ECG:

He had several previous ECGs this year and they were all identical.

What do you notice?  What should you do?





















There is bizarre ST depression, T-wave inversion, prolonged QT, and large U-waves (vs. VERY long QT).

This should make you worry about hypokalemia or about acquired long QT syndrome.  I saw this ECG in a stack and noticed that caregivers had been only worried about ischemia.  The patient was appropriately evaluated for ischemia (with a negative workup) but other etiologies of this ST depression had not been considered, and the long QT and U-waves had not been noticed.  This is partly because the computer interpretation did not notice the U-waves.  The computer did measure the QT accurately as 488 ms.  However, it should EITHER have noticed the U-waves, OR included them in the QT interval. If it had, the QTc would have been over 600 ms.

Seeing this, I thought it would be hypokalemia, but the K was normal.  So I looked at the medications and found that the patient was on methadone at a dose of 260 mg daily.

Doses of 60 mg daily are associated with a longer QT and with U-waves.

Methadone may cause torsade de pointe due to these effects.  See this case of Polymorphic VT with long QT (Torsade) due to Methadone.

The patient's physicians were contacted and he was taken off methadone.

Learning points:
1. U-waves are not only caused by hypokalemia, but also by drugs that block postassium channels.
2. The computer does not accurately measure QT and QU intervals.
3. Just because an ECG findings is stable, seen on old ECGs, does not mean it is safe.

Some Cardiologists still are not familiar with Sgarbossa Criteria.....

This case shows how you have to advocate for your patient. You have to be the expert.  I talk to a lot of emergency physicians who have trouble convincing their interventionalist colleagues of various ECG findings.  

Many cardiologists and even interventionalists, are not aware of many of the newer findings of STEMI equivalent, including the Sgarbossa criteria, and especially are unaware of the modified Sgarbossa criteria.  

My partners and I are fortunate that at our institution there is a long history of ECG expertise in our cardiology department.  We also have a very cooperative system in which all concerns of the emergency physicians are addressed.

It is very important to establish these relationships so that when difficult cases arise, the patient gets the best care.

Case presentation

A male in his mid 40's presented with 20 minutes of chest pain.  He had no previous cardiac disease.  Here is his first ECG:

There is sinus rhythm with LBBB.  There is subtle concordant STE in lead aVF, almost 1 mm.  There are about 2 mm of discordant STE in III.  Since the S-wave is only 3 mm, this is proportionally excessively discordant ST elevation.

One may not be convinced of STEMI with less than 1 mm of concordant STE and 2 mm of discordant STE, but it should certainly catch your attention.

Within minutes, the patient had a ventricular fibrillation arrest and was resuscitated.  This is the post-resusitation ECG:

There is sinus tach and LBBB still.  Now there is huge concordant ST elevation in III, also in aVF, and huge reciprocal concordant ST depression in aVL.  There is concordant STE in V3 and excessively proportionally discordant ST depression (greater than 30% ratio) in V5 and V6.

This second ECG is diagnostic of STEMI.

The physician activated the cath lab in the middle of the night.

When the interventionalist heard that the patient had LBBB, he was furious and stated that you cannot diagnose STEMI in the presence of LBBB (even though there was a cardiac arrest).

When he arrived and saw the ECG, he insisted that all ECG findings were due to post-resuscitation changes.  (Aside: while it is true that cardiac arrest can cause strange ST elevation, one can easily differentiate it from actual coronary occlusion by obtaining serial ECGs.  If due to cardiac arrest only, it should quickly start to normalize).  

He insisted that "You inappropriately called in the cath team.  The only STEMI by criteria is 2mm ST elevation in 2 consecutive leads with normal QRS AND it is the cardiac arrest that created these ECG abnormalities." 

The emergency physician insisted that it was STEMI and instructed on the Sgarbossa criteria.  

He did take the patient to the cath lab and found a 100% acute RCA occlusion.

He still insisted that there are no ECG findings in of STEMI in patients with LBBB except for New LBBB.

She gave him some papers to read.  We now know that new LBBB has very weak correlation with acute occlusion, and that + Sgarbossa criteria is very specific for occlusion, and that the modified Sgarbossa criteria are much more sensitive.

Here is a calculator from mdcalc.com: http://www.mdcalc.com/sgarbossa-criteria-for-mi-in-left-bundle-branch-block/

Learning point: You need to be the ECG expert and advocate for your patient
The emergency physician's confidence in her diagnosis could have been undermined by the interventionalist.  She could have doubted herself and relented.  But she had learned about LBBB and Sgarbossa criteria well enough to be confident.  She also was aware that consultants are fallible, and have various occasional weaknesses.  So she was able to be persistent in advocating for the patient, and to do so diplomatically, so that the interventionalist would not resist.


Imagine how resistant the interventionalist would have been if the patient had no cardiac arrest, but rather chest pain only.

Is it Wellens' Syndrome?

A middle-aged African American man with history of tobacco use, HTN, and chronic renal disease, but no known coronary disease, presented with chest pain. 

Symptoms in the 24 hours prior to presentation: On the evening prior to admission, he had an episode of sharp stabbing chest pain while talking to his wife, which improved after 30 minutes. This recurred on the morning of the date of presentation.  He did not seek care for these episodes of pain.

On the evening of presentation, the chest pain recurred at work, with increased pain radiating to his shoulder and neck in the afternoon, associated with diaphoresis and SOB.  He was given ASA and nitro by medics with improvement.  He was pain free on arrival.

Here is his initial ED ECG:

1. Computerized QTc is 391.  There is a bit of ST elevation in V2 and V3, and the T-wave turns sharply downward, with a trace of terminal T-wave inversion in V3.

I was slightly concerned for the subtle beginnings of Wellens' waves in V2 and V3, so recorded this one 37 minutes later:

2. Now the QTc is 411 and there is definite terminal T-wave inversion in V3, and some also in V4 and V5.  Importantly, there is none in V2.

At this point, I was worried that this was "Wellen's syndrome" and initiated medical treatment for ACS.

Wellens' is a syndrome and not an ECG finding.  If you only look at the ECG, there will be many false positives.  In order for the diagnosis to be fairly specific, there must be:

1. Chest pain (not some other atypical symptom) of at least 20 minutes duration
2. Complete resolution of pain at the time of the ECG
3. Presence of normal R-waves in the precordial leads (not Q-waves, not LVH)
4. Pattern A or Pattern B (see bottom of post) T-wave inversions in V2-V3, and also possibly, in decreasing order of prevalence, V3, V4, and V5.
5. Evolution of the pattern [though de Zwaan and Wellens' did not describe evolution (probably because they did not do serial ECGs nearly as often as we do today), in my experience Wellens' always evolves: biphasic T-waves (Pattern A) become deep symmetric (Pattern B) and they also extend out to V4, then V5, then V6.]

The patient remained pain free, and this was recorded 27 minutes after the 2nd ECG (64 after the first):

3. QTc is 402.  The terminal T-wave inversion is gone

At this point, without any more evolution, I considered that this might not be Wellens' syndrome, which in a persistently pain free patient usually continues to evolve, and not resolve.

I thought I might have been deceived by a Wellen's mimic.

So I decided to look back at ECG 2 and realized that I had, indeed, been deceived.

What is the real diagnosis?











This is typical benign T-wave inversion.  It is impressive that it can change from one ECG to the next.  This BTWI was dynamic: in some ECGs, there is terminal T-wave inversion and in others, there is not

Left Ventricular Hypertrophy is the other common mimic of Wellens' syndrome.  Here is a representative case.

Here is another case of benign T-wave inversion, with a detailed discussion.

In both ECGs, V3 and V4 have the classic look of BTWI, which particularly involves very tall T-waves, and almost no S-wave, in the leads with biphasic T-waves.

Beware, however, because unstable angina can also have dynamic t-wave inversion that mimics Wellens' waves, which appear and disappear.  See this case.

For the classic evolution of Wellens' waves over 26 hours, see this case.

Case continued

This 4th ECG was recorded 46 minutes after the 3rd ECG (110 minutes after the first):

4. No major difference

The patient remained asymptomatic, but his ECG is dynamic:

5.  Recorded 4 hours after arrival, and 2 hours after ECG #4.

He ruled out (all contemporary troponins less than 0.03 ng/mL).  In spite of this, because of his ECG, he underwent an angiogram.  It was completely normal.



Here is one week later:

6. Now there is no trace of terminal T-wave inversion!!

Typical Wellens'


Here is classic Wellens', with evolution:

Initial ECG, and two subsequent ECGs hours apart in True Wellens'.  Notice the evolution extending farther out to more lateral precordial leads, and also from biphasic (Wellens' Pattern A) to deep symmetric (Wellens' Pattern B).  [Later writers mistakenly gave a label of Type 1 to Pattern B and Type 2 to Pattern A]

Here is Wellens' original image:

Here is another post on Benign T-wave inversion: Wellens' syndrome - NOT!


Learning points:
1. Not all that looks like Wellens' is Wellens'
2. Wellens' is a syndrome, not an ECG finding.
3. If it is truly Wellens,' it will evolve and there will almost always be postive troponins.
4. Even if the whole syndrome is present, as in this case, there are false positives. Benign T-wave Inversion (BTWI) is one.
5. BTWI can be dynamic.
6. Unstable angina (troponins all negative) can also have dynamic T-wave inversions that appear and disappear
7. There are identifying features of BTWI.  I list them below:

BTWI is a normal variant associated with early repolarization.  K. Wang recently studied it.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)  
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves). 
5. The leads with T-wave inversion (left precordial) usually have some ST elevation 
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion.