Wednesday, May 27, 2015

Chest pain and Very Large T-waves

A middle aged male had chest pain.  There was suspicion of acute MI.

The initial ECG was texted to me:
The QTc is 423 ms.  There is a large amount of ST elevation and Massive T-waves in V2 and V3, worrisome for LAD occlusion.  However, there is also excellent R-wave progression.


A repeat ECG was done a short time later:
No definite change.  Computerized QTc is 399 ms.


The potassium was 4.5 mEq/L.

Both of these ECGs are very worrisome for STEMI, but not diagnostic even though the second one meets criteria for STEMI (greater than 2 mm at the J-point in 2 consecutive leads).  Early repolarization can look like this, however.

So the formula for differentiating acute LAD occlusion from Early repolarization was applied:

See sidebar for calculator:
The exclusions are CRITICAL (in red)


Applying the formula to ECG 1, we get 22.025.  This is about 97% sensitive for LAD occlusion at a cutoff of 22.0, and 92% sensitive at a cutoff of 23.4.

If we apply to ECG 2 (which has MORE ST elevation), we get 19.63 (very low).

This ECG is so worrisome that I would not be entirely convinced that this is not MI.  But I would not activate the cath lab without more information if it is a strain on resources (nighttime, weekends, for instance).

A formal echocardiogram with contrast was done and showed no anterior or apical wall motion abnormality.

The patient ruled out for MI.

Learning Points:

1. When the differential is LAD occlusion vs. Benign Early Repol, the formula may help you to rule out STEMI

2.  If it is STEMI, there will be a Regional Wall Motion abnormality.  If the equation indicates Early repol and you don't want to overuse scarce resources, then obtain an emergency high quality ultrasound to look for a wall motion abnormality.



Tuesday, May 26, 2015

New 40 minute lecture on T-wave Inversion



T-wave Inversion

I just found one mistake at minutes 7:00 to 7:30: 

The QRS axis is 90 degrees and the T-wave axis minus 30, for a QRST angle of 120 degrees.


Sunday, May 24, 2015

Look at II, III, aVF in this case, and the outcome.....

I just posted this case:

Isolated "Inferior" ST Segment Depression: Not a Sign of Inferior Ischemia


Today I post another case that nicely demonstrates the significance of inferior ST depression.

A middle-aged female presented to the ED with chest pain. It had been intermittent all day.

Here was her first ED ECG with active pain:
There are abnormal ST segments in "inferior" leads, and very subtle STE in aVL, with T-wave inversion.  There are "down-up" T-waves in the inferior leads, which are almost always due to ischemia. 
(Up-down T-waves are sometimes due to hypokalemia - the upright "T" wave is actually a U-wave in these cases.  This is usually in leads V2 and V3.  See these cases for examples)

Isolated ST depression in II, III, and aVF should be considered to be reciprocal to subtle ST elevation in aVL and to indicate that there is occlusion of the Diagonal, Obtuse Marginal, or even the LAD.

Initial troponin I was 0.65 ng/mL.

After she was initiated on ASA/Plavix/Heparin and Nitro, her chest pain resolved. 

Time 40 minutes:
The ST depression is resolved.  "Inferior" T-waves are now fully upright, consistent with reperfusion in the territory of aVL.  Now there are Wellens' waves in anterolateral leads, consistent with reperfusion in the proximal LAD.  This strongly suggests that while the patient was having chest pain, the proximal LAD was occluded.

She remained pain free all night.

It is wise to put these patients on continuous 12-lead ST segment monitoring, as re-occlusion can occur without any chest pain.

Next morning:
Evolution of T-wave inversion confirms Wellens' waves.  There is no doubt that this will be a proximal LAD lesion


Echo showed anteroapical wall motion abnormality.  Troponin I peaked at 2.5 ng/mL.

Angiogram showed 99% thrombotic stenosis with TIMI-II flow in proximal LAD.  It was stented.

Comment:

At time zero, during maximal chest pain, she had a full proximal LAD occlusion.  After NTG, it opened enough for adequate perfusion, chest pain relief, and T-wave inversion.

Note how subtle this occlusion was: it is only seen by some subtle ST depression in II, III, and aVF and subtle STE in aVL.

Note also that the ischemia was in the LAD territory, but the ST depression was "inferior."








Friday, May 22, 2015

Isolated "Inferior" ST Segment Depression: Not a Sign of Inferior Ischemia

I have long maintained that ST segment depression does not localize and the isolated ST depression in "inferior" leads is actually reciprocal to less obvious ST elevation in lead aVL or in "anterior" leads.

A reader alerted me to a 2010 paper that addressed this issue.  They looked at all ACS cases in a CCU over a 12 year period, chose those with isolated "inferior" ST depression without any ST elevation, and found that only 10% had inferior ischemia.  Most had LAD or first diagonal culprits, and most were due to occlusion or high grade thrombotic stenosis (i.e., cath lab indicated).

(The one example they showed was an LAD occlusion that would also have been identified by the LAD occlusion rules and formula).

Here is a link to the paper (unfortunately, no full text):

Isolated inferior wall ST segment depression as an early sign of acute anterior wall myocardial infarction

Here is a case of a first diagonal occlusion that demonstrates this fairly well:
This one does have minimal but significant ST elevation in aVL, so perhaps not the perfect example.


Here are some other  cases that demonstrate this.




Tuesday, May 19, 2015

Is there ST Segment Depression here?

A middle aged male with a history of Hypertension, Diabetes, Hyperlipidemia, and CHF due to severe concentric LVH presented with severe substernal chest pain and SOB.   The blood pressure was 170/120.

There were B-lines on chest ultrasound, diagnostic of pulmonary edema.

Here is his initial ED ECG:
Sinus rhythm.  There is high voltage diagnostic of LVH.  With a large S-wave in V2 and V3, there should be baseline ST elevation of LVH in these leads.  However, the J-point in V2 and V3 is isoelectric.  This is abnormal.  This is highly suggestive of relative ST segment depression.


So the previous ECG was sought:
Here we see the expected ST baseline ST elevation of LVH in V1-V3.  It is proportional and appropriate.

This confirms that the presentation ECG shows relative ST depression, consistent with ischemia.  There was worry for subendocardial ischemia vs. posterior STEMI.  The elevated blood pressure makes one lean heavily towards subendocardial demand ischemia.

A review of the chart showed there was an angiogram from one year prior with no significant obstructive lesions, mild plaque only.  This does not rule out ACS as the etiology of ischemia, but makes it far less likely.

The patient was placed on a high dose nitro drip, and his BP dropped to 150/90.  His symptoms resolved.

Another ECG was recorded 40 minutes after the first:
The relative ST depression is resolved.


The patient had a mild rise in troponin to 0.084 ng/mL which was deemed due to demand ischemia, not ACS.  Of course there could possibly be ACS, but I think it is unlikely.

Learning Point:

1. An isoelectric J-point may represent ST segment depression in a patient with baseline ST elevation, and in a patient who should, due to QRS abnormalities such as LVH, have baseline ST elevation.






Sunday, May 17, 2015

ST elevation and depression: is it ischemia? The entire clinical context is critical.

This patient has a history of cardiomyopathy (EF 10%) and IVCD and heart failure and presented with altered mental status.   BP was 87/52, pulse 90, saturations 100%, and respirations 14.   An ECG was recorded:
There is sinus rhythm.  The P-wave in V1 has a huge negative component, diagnostic of left atrial enlargement.  The PR interval is 360 ms (the computer read it as 227 ms).  The QRS = 134 ms, so it is an IVCD (intraventricular conduction delay), but is not LBBB because of Q-waves in I and aVL.

There is a large amount of ST elevation in V3-V5, and ST depression in V6.  But there are also very deep S-waves in V3-V5 and a very tall R-wave in V6.  The highest ST/S ratio is about 10% (normal).  

There was an ECG from 4 months prior:
Atrial fib.  QRS = 118 ms.  Voltage was high then too, but ST segments were not.  So the ST elevation is new.

The physicians were worried about this and showed it to me.

I said that this is very unlikely to be ischemia because of:

1) the severe cardiomyopathy
2) the high voltage
3) relative clinical stability in a patient with a baseline EF of 10%
4) presentation without chest pain

I recommended a bedside echo and further eval. This was done and showed very poor LVF and no WMA.


Electrolytes and Venous Gas results returned:

Na = 117 mEq/L
K = 2.7 mEq/L
Chloride = 68 mEq/L  (this indicates metabolic alkalosis)
CO2 = 46 mEq/L
Anion Gap = 3 mEq/L (so there is no serious metabolic acidosis)
Venous pH = 7.58 (normal = 7.33), corresponds to an arterial pH of 7.65 (very alkalemic)
HCO3 = 45
Venous pCO2 = 47 (normal = 47), which corresponds to an arterial pCO2 of about 40 mmHg.

This actually represents a superimposed respiratory alkalosis: when the HCO3 = 45, the patient should compensate with a decrease in minute ventilation, such that the arterial pCO2 should be about 57 (0.9 x HCO3 + 15), and venous pCO2 should be slightly higher, around 62-64 mmHg, not 47 mmHg.

For a comprehensive presentation on Acid Base disturbances, see my 55 minute lecture on the topic.

So the patient has profound metabolic disturbances [hypokalemic metabolic alkalosis without any respiratory compensation (and thus a superimposed resp alkalosis)], and this explains the ECG findings.  After some treatment, this ECG was recorded 23 hours after the first:
It is normalizing


At 36 hours, after more electrolyte correction:
Looking more and more like the old ECG


At 3.5 days, there was some tachycardia:
This was diagnosed as SVT, but it is, in reality, sinus tachycardia.  See image below with arrows.

Annotated
Arrows point to P-waves. Note the P-wave morphology, and PR interval, are the same as in the slower sinus rhythms.


Learning Points:

Cardiomyopathy, especially with metabolic derangement, can result in profound PseudoSTEMI patterns.

Sunday, May 10, 2015

Paced rhythm. Are there hyperacute T-waves? See the T-wave evolution, even in paced rhythm.

This was sent to me by John Larkin, from Australia, who has a great ECG Blog called "ECG of the Week," where he posted it, and graciously allowed me to post it here.

The ECG is from an elderly male with multiple co-morbidities including significant cognitive impairment, cardiac failure and diabetes. He presented to the Emergency Department with several hours of chest pain and has a pacemaker in-situ for an unknown indication.

Here is his ECG:
John's thoughts on the ECG are as follows:

·         Regular V-paced rhythm at 60 bpm with LAD.
·         Lead V2 has concordant ST elevation but less than 1mm
·         Lead V3 has excessive discordant ST elevation (ratio -0.33)
·         Lead V4 has excessive discordant ST elevation (ratio -0.32)
·         Lead V5 I suspect has excessive discordance but the baseline wander and native P wave superimposition makes it difficult to measure
·         The T waves in leads V2-6 are huge compared with the QRS voltages
·         Evidence of non-conducted native atrial activity

My thoughts

I was less certain of LAD occlusion because of the profound upward concavity, and I didn't think any lead met a consistent ratio of 0.25, though I think V3 did meet a ratio of 0.20.  But was very suspicious of the very large T-waves.

One should keep in mind that in our LBBB studies (we have two now, with data forthcoming on the second, and larger, validation study) an ST/S ratio of 0.20 is more sensitive though slightly less specific, than 0.25. 

But a ratio of 0.20 is still nearly 90% specific.

All this data is for LBBB and I do believe that it applies to paced rhythm.  

Follow-up

The patient was not taken for angio given their extensive co-morbidities (including GI bleed) following discussion with both cardiology and patient’s family. He did have a troponin rise and was treated with maximal medical therapy.

Although he did not have an angiogram, followup ECGs, echos, and troponin prove that he did, indeed, have an LAD occlusion.

His initial troponin I was 6.7 ng/mL.

Echo showed EF of 30% with large amount of severe segmental systolic dysfunction.

This was 130 minutes later:
Now lead V4 has a ratio of 0.25

This was recorded at 6 hours:
The hyperacute T-waves are gone.  The ST segments have nearly resolved.

This one is at 20 hours
Still more resolution of ST elevation and T-waves

T-wave starting to invert

In some data we have recently collected and will publish, we have shown that reperfusion of an occluded artery in LBBB, just like in normal conduction, results in reperfusion T-waves in many, if not most, cases.

Is this also true in paced rhythm?


This one is at 43 hours
More T-wave Inversion (reperfusion T-waves vs. evolution of completed MI)
345 hours
Much deeper T-wave inversion
454 hours
T-waves are deeper still




Learning Points

1.  Hyperacute T-waves may be seen in paced rhythm
2.  The Modified Sgarbossa criteria are likely applicable in paced rhythm as well as in LBBB
3.  The ECG often evolves T-wave inversion in reperfusion of an occluded artery in both LBBB and in Paced rhythm.






















Thursday, May 7, 2015

Paced rhythm, Modified Sgarbossa negative, but with a Wall Motion abnormality.

This case was posted by my colleagues at the Hennepin Ultrasound Blog, as Apical Wall Motion Abnormality or Electrical Asynchrony?

But there was no comment on the ECG, which is very interesting.

Case

A male in late middle age with a history atrial fibrillation, significant renal insufficiency, and implanted single chamber right ventricular pacemaker, but no known coronary disease, presented with 2 hours of sudden onset chest pain.  It felt like heavy pressure.  The pacer was placed 2 months prior, and the patient had no ECG recorded after placement to establish a baseline.

Here is his ED ECG:
There is a paced rhythm with proportionally discordant ST segments.   There are no concordant ST segments.  Thus, there is no evidence of STEMI.

Unlike Left Bundle Branch Block, there is comparatively little data on the accuracy of the Sgarbossa criteria in diagnosing acute MI (better, acute coronary occlusion) in the setting of a paced rhythm, and no data on the Modified Sgarbossa criteria.  There are two small studies showing good specificity of the traditional Sgarbossa criteria, but poor sensitivity.  There are 2 case reports (both by me and co-authors, references below) of STEMI diagnosed in paced rhythm by proportionally excessive discordant ST elevation (modified Sgarbossa criteria).   I have posted other cases in which STEMI was easily diagnosed in the setting of paced rhythm.  Here is one.  Here is another.  But we really don't know the sensitivity of concordant STE or proportionally excessively discordant STE in paced rhythm.  I suspect it is as good in paced rhythm as in LBBB.

So the ECG in this case does not meet any Sgarbossa criteria

However, this patient has very suspicious symptoms and you do not want to miss a coronary occlusion.

So a bedside echo was done; here is the parasternal long axis view:

It looks as if the apex is not moving well.



Here is the apical view:


There is clearly an apical wall motion abnormality.





And this apical view shows the WMA clearly as well.

A review of the patient's chart showed that the last formal echo had been normal, but had also been done prior to placement of the pacemaker.    Right ventricular pacing results in an abnormal sequence of activation and so there may appear to be a wall motion abnormality.

So the ECG shows no indication of occlusion, but the echo shows a new wall motion abnormality that can be completely due to the pacemaker.

The patient has a relative contraindication to coronary angiogram (renal insufficiency).

It was decided not to take the patient to the cath lab.  Troponins were negative and the pain resolved.

Formal ultrasound done later had the same findings.



This ECG was recorded 4 hours after the first:
The T-waves are slightly taller, but there are no abnormal ST segments.

Learning points:

1. Use the modified Sgarbossa criteria in paced rhythms.  The specificity is good. The sensitivity is unknown but probably similar to sensitivity in LBBB, which I believe to be as good as ST elevation in normal conduction, probably about 70-75% sensitive for coronary occlusion (though the sensitivity was much higher in our case control studies, which probably do not accurately reflect clinical practice).

2. The ECG in this instance was more reliable than formal echocardiography



Here is the ECG from the first case I link to:
This shows both concordant ST elevation in V2, and proportionally excessively discordant STE in V3.  There is also concordant ST depression in V6.


One difference between LBBB and Paced rhythm is that, in paced rhythm, the QRS in V5 and V6 is almost always negative (but positive in LBBB).  Therefore, any STEMI that manifests in V5 and V6 in LBBB will usually manifest by concordant ST elevation in these leads, whereas in paced rhythm, it must be excessively discordant ST elevation.



References

1. Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular-paced rhythm.(full text pdf) GUSTO-I investigators. Am J Cardiol. 1996;77:423–4.

2.  Maloy KR, Bhat R, Davis J, Reed K, Morrissey R.   Sgarbossa criteria are highly specific for acute myocardial infarction with pacemakers. (full text link)  West J Emerg Med. 2010;11(4):354-357.

modified Sgarbossa rule. (full text link) Ann Emerg Med. 2012;60(6):766-776.

4. Schaaf SG, Tabas JA, Smith SW. A patient with a paced rhythm presenting with chest pain and
hypotension. JAMA Intern Med. 2013;173(22):2082-2085.

5. Ukena C, Mahfoud F, Buob A, Böhm M, Neuberger H-R. ST-elevation during biventricular pacing. Europace 2012;14(4):609-611.

6. Karumbaiah K, Omar B. ST-elevation myocardial infarction in the presence of biventricular paced rhythm. J Emerg Med. 2013;45(2):e35-e40.

7. Walsh B.  Smith SW.  A Patient with a Biventricular Paced Rhythm Presenting With Chest Pain.  Challenges in Clinical Electrocardiography. JAMA Internal Medicine.  April 6, 2015.

Wednesday, May 6, 2015

40 Minute Lecture with Many Cases: Complications of Acute Coronary Syndrome.


This lecture starts with 13:45 minutes of didactics, then goes on to 26 minutes of 11 case presentations.  There are many ECGs and echocardiograms.









Sunday, May 3, 2015

Severe LVH and PseudoSTEMI

An elderly male with end stage renal disease had hypotension (50's systolic) and syncope (LOC, and loss of radial pulses) during dialysis. He quickly regained consciousness.  There was no chest pain or SOB.  The patient has an implanted cardioverter defibrillator (ICD) due to previous cardiac arrest; it did not shock. His BP was 106/59 in the ED, with a pulse of 90.

He had a history of out of hospital cardiac arrest due to ventricular fibrillation and also recurrent ventricular fibrillation/polymorphic ventricular tachycardia, for which he received the Implantable defibrillator.

Previous echo had shown severe concentric LVH.

He also had a h/o CAD with PCI to mid LAD 2011.

Here is his ED ECG:
There is sinus rhythm with a wide QRS at 138 ms.  It is very similar to LBBB, but because of Q-waves in aVL, it does not meet formal criteria.  However, it is surely an intraventricular conduction delay, and all of the rules of appropriate discordance apply.   Applying these rules, there is no concordant ST elevation.  There is discordant ST elevation in V1-V3, and this was very concerning to the clinicians.  It is not, however, out of proportion (ST/S ratio not greater than 0.25).  The highest ST/S ratio is no more than 0.12, within normal limits.  There is also high voltage.



Here is the most recent ECG from 6 months prior:
Sinus rhythm. QRS is 107 ms (much shorter).  There is high voltage.   There was much less ST elevation at this time, and the increased ST elevation concerned the clinicians.  But the QRS is now wider too (new conduction delay) and the heart rate is also much slower and both of these can greatly affect the ST elevation.  A faster heart rate generally exaggerates ST elevation in LVH, LBBB, and paced rhythm.  Finally, the T-wave inversion in V4-V6 is deeper than typical for LVH.  There is a very long QT.

Anterior STEMI is very unlikely here, even though the patient has a history of LAD CAD:

1) there is no chest pain or SOB
2) there is history of severe concentric LVH
3) there is appropriate and proportional discordance
4) the increase in ST elevation compared to the previous ECG can be explained by heart rate.


Nevertheless, there was still concern for anterior STEMI, so a bedside echo was appropriately done:

Here is the parasternal long axis:


This shows severe LV hypertrophy and good wall motion


A short axis echo was done:


This shows severe concentric hypertrophy and no wall motion abnormality.



This allayed fear of possible STEMI and a formal echo was done which also showed no wall motion abnormality.  It confirmed severe concentric hypertrophy with a diastolic septum measurement of 1.76 cm (normal up to 11 mm)


The first troponin returned at 0.50 ng/mL (normal, less than 0.030).  This patient frequently has troponins in the 0.12 - 0.16  range.


This ECG was recorded 8 hours later.
ST elevation persists, now with more upright T-waves



The next troponin was 0.41 ng/mL.

The syncope and hypotension was thought to be due to volume depletion from over-dialysis.  The patient did well.


Learning Point

1. Severe concentric hypertrophy can result in many ECG abnormalities that mimic STEMI and NonSTEMI.
2. LVH may evolve into conduction delay (IVCD).  The rule of appropriate discordance may come into play in IVCD and also in LVH.
3. Heart rate can affect ST segments, particularly in LVH, LBBB, and paced rhythm
4. Bedside echo can help in differentiating ischemic ST elevation from STE secondary to LVH or other etiologies.

Thursday, April 30, 2015

A Case of Clinical Unstable Angina in the ED

A woman in late middle age with a history of a mild stenosis of the RCA seen on CT coronary angiogram 4 years prior presented 2 hours after the onset of nondescript substernal chest discomfort that radiated to both axillae.

Her daughter was worried and brought her to the ED.  This is her initial ECG:
There is a suggestion of inferior MI: the T-waves in II, III, and aVF are slightly large.  There is T-wave inversion in aVL, which is a soft sign of inferior MI.

She received nitroglycerin, and the discomfort was relieved, but she attributed the relief to the removal of a tight-fitting garment.

A repeat ECG was unchanged after pain relief.

I was worried about her, but with pain resolution and a non-diagnostic ECG, there was no indication for cath lab activation at night.

The first troponin was undetectable.

Nevertheless, I was still worried about her and gave her aspirin, ticagrelor, and heparin, and admitted her to the hospital.

After admission, serial troponin I later climbed, peaking at 1.6 ng/mL.

A formal Echo the next AM showed an inferior wall motion abnormality.  A repeat ECG in the morning was recorded:
This shows resolution of the enlarged T-waves, confirming that there had been inferior ischemia.

I was sure there would be a tight RCA lesion that would need stenting.

However, the angiogram showed a chronic total occlusion of the RCA, with the inferior wall supplied by collaterals.  No stent was deployed.

The angiographer explained it this way: "she could have had some small left to right collateral channels that closed off, and then she recruited more collaterals to reperfuse."  Perhaps as a result of nitroglycerin.

Nevertheless, until angiography was done, this was presumed ACS of the RCA (or possibly circumflex) until proven otherwise.

Learning Point

1.   Inferior hyperacute T-waves can be extremely subtle

2.   Even if they do not lead you to cath lab activation, such T-waves, along with lead aVL and the convincing history, may persuade you in spite of an undetectable troponin, to give maximal medical therapy (aspirin, ticagrelor, and heparin) for ACS.

3.  The territory of a chronic total occlusion which is supplied by collaterals is particularly vulnerable.

Monday, April 27, 2015

A Middle-Age Male with Chest Pain that Recurs in the ED

A middle aged male with some coronary risk factors presented to the ED after an episode of typical sounding chest pain that was resolved upon arrival.

He was in the ED for an hour when he developed chest pain again and had this ECG immediately recorded:
There is sinus rhythm at a rate of about 60.  There is ST elevation at the J-point that does not quite meet "STE criteria" of 2 mm for these 2 leads.   There is no convexity, ST depression, or Q-waves that would tell us that this ST elevation is clearly pathologic.  

So we can use the formula that differentiates STE from LAD occlusion from that due to early repolarization (normal variant).  The computerized QTc = 400, STE60V3 = 2.5, RV4 = 19; so the formula value = 20.39, and this is consistent with normal ST elevation. 

So the ECG is normal, right?

Some Background

What I neglected to tell you is that when the patient had arrived pain free, he had this ECG recorded:
Here there is subtle terminal T-wave inversion in V2, and a bit in V3, typical of early Pattern A Wellens' waves.

See this case for Wellens' original images of Pattern A and Pattern B Wellens' waves.

So the first ECG is not normal; it is "pseudonormal."

It triggered the recording of serial ECGs (sorry, not available) which showed increasing ST elevation diagnostic of LAD occlusion.

So this was Wellens' syndrome, a state of spontaneous reperfusion of the LAD, manifesting with "reperfusion T-waves" and R-wave preservation after an episode of closure of the LAD.  Thus, the patient presents pain free after an episode of angina.

The importance of Wellens' syndrome is that the artery can close off again at any moment, in which case the inverted T-waves will become upright again and look normal.  This is called "pseudonormalization".

The first ECG was recorded so soon after re-occlusion of the artery that this ECG shows no signs of occlusion other than pseudonormalization, which requires comparison with the previous.

See these other cases of less subtle pseudonormalization (there are 7 cases here, the best are the last two)


Saturday, April 25, 2015

Syncope and a Possible Type 2 Brugada Morphology

A young man had 10 seconds of syncope without a prodrome.  He had had it once before.  Exam was normal.

This ECG was recorded:
There is rSr' in both V1 and V2, with a "saddleback" in lead V2, and the "beta" angle is wide.  It meets, or at least nearly meets, criteria for type 2 Brugada.


Having just written on this topic, I knew that this could be the result of lead placement that is too high.

V1 and V2 should be placed at the 4th intercostal space.  Placing them at the 3rd can result in false positives for Brugada.

I asked the tech if she was sure she had placed them correctly.

She returned saying that she had placed them one interspace too high, and handed me this ECG recorded at the right interspace:

The rSr' is gone and the saddle is gone as well.


Learning point:

Beware lead placement in the diagnosis of right ventricular conduction delay (rSr") and in the finding of Brugada pattern ECG.

One hour lecture on Subtle ECG findings of Acute LAD Occlusion (plus some inferior/lateral/posterior)

This is my most popular lecture, which Scott Joing of www.hqmeded.com just recorded for me in his amazing video recording studio.

When I give this lecture real-time, I usually do it in a workshop and have more time - enough time to stop and let people get a good look at the ECG and try to find the critical elements for themselves before going on to explain them.  That makes for a significantly longer lecture.

But if you want to have time to scrutinize any ECG, just pause the video to look at the ECG for a while before you play my explanation.








Friday, April 24, 2015

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

A middle-aged male had a V Fib arrest.  He had not complained of any premonitory symptoms (which is very common).   He had a history of CAD with CABG.  Here was his initial ED ECG:
There is atrial fibrillation with a rapid ventricular response.  There is profound ST depression especially in I, II, V2-V6.
ST depression is common BOTH after resuscitation from cardiac arrest and during atrial fib with RVR.

The patient was cardioverted.  Here is the post cardioversion ECG:
ST depression, with ST elevation in aVR persists.

Does this patient have ACS?  Should he necessarily go to the cath lab?

Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion.

One must wait a short time (perhaps 15 minutes?), and repeat the ECG, to see if the apparent ischemia persists.

This was done.  A third ECG was done about 25 minutes after the first:
This shows resolution of all apparent ischemia.

The patient thus did not need immediate angiography.

An echocardiogram showed:

Left ventricular hypertrophy concentric .
The estimated left ventricular ejection fraction is 58 %
Aortic stenosis, mild, 9.0 mmHg mean gradient. 1.50 cm^2 valve area.

Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.

The patient underwent angiography later (the next day) and there was no culprit lesion.  He did not have ACS.

He recovered and had an ICD implanted.

Learning Points:

1. Ventricular fibrillation is not only caused by acute coronary syndrome.   There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies.  We found that 38% of out of hospital ventricular fibrillation was due to STEMI.  The remainder were due to other etiologies, (including NonSTEMI ACS).  But approximately 50% were due to non-ACS etiologies.

2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.

3.  One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.

4. Not all patients with ventricular fibrillation necessarily need emergent angiography.  Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.


Reference:

Scott NL. Mulder M. Bart B. Smith SW.  Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580). Academic Emergency Medicine 17(s1):S194; May 2010