Monday, September 19, 2016

Non-Vagal Syncope and Saddleback Morphology in V2

This is another case provided by Mustafa Alwan, an internist from Jordan and very talented ECG enthusiast.  He posted it on Facebook EKG Club, and I am reposting with his permission.

Case
This is a 26 year old male who presented after having had 2 episodes of syncope in 1 day.  Both episodes started with palpitations, then dizziness.  He had no family history of sudden death.    

Vital signs: normal 

Initial ECG :
This is suggestive of Type 2 Brugada morphology because of the Saddleback in lead V2
At first glance, the beta angle looks wide.
 
See this post for a review of Type 2 Brugada.
The method is to draw a line from the peak of the R'-wave down along the downslope of the R'-wave, as shown.  At a point which is 5 mm below the peak, you draw a line across and if the distance to the S-wave is greater than 3.5 mm, it is a wide beta angle.   This is equivalent to a 35 degree angle, or 0.61 radians (calculated as the inverse tangent of 3.5/5, or 0.7).


Dr. Ken Grauer, the ECG master who runs this site: http://ecg-interpretation.blogspot.com/, measured the beta angle here: 

So the beta angle is not wide enough to meet type 2 Brugada morphology criteria


For those wanting more — go to minute 21:19 in Ken's ECG Video on Brugada Syndrome. Here is the link to this specific point in the video — https://youtu.be/h1MhtLMF-7M?t=21m19s 

Type 2 Brugada morphology (in contrast to syndrome) is really quite common, and if you rely on the morphology alone, without the other criteria for syndrome (see below), you will have a lot of false positives.


Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2 morphology)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
syndrome
(e) Type 1 Brugada pattern in relatives.


This patient only had (c), and no other criteria.

So this ECG did not even meet the criteria for Type 2 Brugada morphology (because the beta angle was too small).  These criteria were developed in a comparison of Brugada syndrome patients with athletes who have an Rsr' saddleback, and they were about 90% sensitive and 90% specific, so they weren't perfect.  

Presumably because this patient had 2 episodes of non-vagal syncope, he was admitted for observation and the admitting cardiologist referred him for Ajmaline challenge test (a sodium channel blocker) in the electrophysiology (EP) lab.

Here is the resulting ECG:
Now there is clearly Brugada morphology.


Commentary

Does this establish Brugada syndrome?  

One cannot clearly state that there is, or is not, Brugada syndrome due to response to Ajmaline or other Na channel blockers.  One can only risk stratify for future arrhythmic events.

The considerations for ICD implantation are far beyond the scope of this article and all such patients should be evaulated by an electrophysiologist.

Not all emergency and primary care physicians, and even some general cardiologists, recognize these important issues:

This paper (full text) discusses the risk of arrhythmia in patients who have spontaneous vs. drug induced (e.g. ajmaline) type 1 morphology.  If the patient only has a history of syncope (like our patient), the risk of future arrhythmic events is 0.6%-1.9%.  If the patient with only drug-induced Brugada morphology is asymptomatic (unlike this patient), the risk of future arrhythmia is extremely low.

They reference this paper which shows that ICD implantation has a high rate of inappropriate shock and that the ICD's record a low annual rate of dysrhythmia.  

Moreover, the authors of this study, (Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome) found that the best cutoff for the beta angle is wider than 35 degrees.  It is 58 degrees, which corresponds to a triangle base width of 8 mm (not 3.5 mm!!).

Here are the latest recommendations from this 2014 publication (full text: HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes): 

Unfortunately, the situation of our patient is not reflected here:
Symptomatic with drug induced Type 1 ECG, but no family history

Here are the full recommendations:
Class I
  • 1.
    The following lifestyle changes are recommended in all patients with diagnosis of BrS:
    • (a)
      Avoidance of drugs that may induce or aggravate ST-segment elevation in right precordial leads (for example, visit Brugadadrugs.org),
    • (b)
      Avoidance of excessive alcohol intake.
    • (c)
      Immediate treatment of fever with antipyretic drugs.
  • 2.
    ICD implantation is recommended in patients with a diagnosis of BrS who:
    • (a)
      Are survivors of a cardiac arrest and/or
    • (b)
      Have documented spontaneous sustained VT with or without syncope.
Class IIa
  • 3.
    ICD implantation can be useful in patients with a spontaneous diagnostic type I ECG who have a history of syncope judged to be likely caused by ventricular arrhythmias.
  • 4.
    Quinidine can be useful in patients with a diagnosis of BrS and history of arrhythmic storms defined as more than two episodes of VT/VF in 24 hours.
  • 5.
    Quinidine can be useful in patients with a diagnosis of BrS:
    • (a)
      Who qualify for an ICD but present a contraindication to the ICD or refuse it and/or
    • (b)
      Have a history of documented supraventricular arrhythmias that require treatment.
  • 6.
    Isoproterenol infusion can be useful in suppressing arrhythmic storms in BrS patients.
Class IIb
  • 7.
    ICD implantation may be considered in patients with a diagnosis of BrS who develop VF during programmed electrical stimulation (inducible patients).
  • 8.
    Quinidine may be considered in asymptomatic patients with a diagnosis of BrS with a spontaneous type 1 ECG.
  • 9.
    Catheter ablation may be considered in patients with a diagnosis of BrS and history of arrhythmic storms or repeated appropriate ICD shocks.
Class III
  • 10.
    ICD implantation is not indicated in asymptomatic BrS patients with a drug-induced type 1 ECG and on the basis of a family history of SCD alone.
     But what about symptomatic patients with drug-induced type 1 ECG??




Sunday, September 18, 2016

A Patient with Vomiting and Abdominal Pain

This patient complained of prolonged vomiting and abdominal pain.
With this history, the ECG is pathognomonic.
What is it?




















First, there are narrow J-waves that are similar to Osborn waves.  The temperature was normal.  I am not certain, but I believe these are just exaggerated J-waves with nonspecific etiology.

More importantly, there are large U-waves best seen in leads V3 and V4.    You can also see that lead II has no visible T-wave but only a large U-wave.  (If you look at V3 directly above lead II, you see both a T-wave and U-wave.  If you follow that down to lead II below, you see no T-wave corresponding to the T-wave in V3, only a large U-wave.  This is also true for V5 and V6.)  Thus, what appears to be a long QT interval in these leads is really the QU interval.

This is nearly pathognomonic for hypokalemia.  The K was 2.4 mEq/L.  Magnesium was normal.


Wednesday, September 7, 2016

An Alcoholic Patient with Syncope

A middle-aged male had sudden syncope.  There was head injury and he was intoxicated with alcohol, but he stated "I've been way more intoxicated than this; I have no idea why I passed out."

He denied any kind of chest discomfort or dyspnea or jaw or shoulder pain or epigastric discomfort.

He was completely asymptomatic.

He had a head CT that was normal, a breath alcohol of 0.10% and had this ECG recorded:

What do you think?















As is very common, the computer did not adequately measure the QT interval.  The computer did find a long QT, but greatly underestimated it.
(See this post, which also links to others: Syncope and Bradycardia)

I showed this ECG to the residents and they could not identify the abnormality.  To me, it shouts in my face "long QT!"  This demonstrates how important experience is to Gestalt, and how, if one does not have that experience, one must force oneself to systematically read the ECG.

You must look at every ECG, and if the QT looks long, then measure it yourself.  A good rule of thumb is that if the QT is more than half the RR interval, then measure it and correct for heart rate.  Importantly, at high heart rates (short RR interval), the half-the-RR rule of thumb tends to label too many QT’s as abnormal. At low heart rates (long RR interval), the rule of thumb tends to label too many as normal.

I measured the QT at 530 ms, which results in a Bazett corrected QTc of 620 ms, and that is how I interpreted the ECG at the time:




Here is the old ECG for comparison:
Normal



Since the patient is alcoholic and has a long QT, one must consider hypomagnesemia and hypokalemia.  One must also consider medications, and as it turns out, the patient was on 2 psychiatric drugs which can prolong the QT.

Also, I always give any alcoholic 2 g of Mg if they are sick enough to get an IV, so we administered 2 g Mg.

He was also given IV fluids for possible dehydration.

Another ECG was recorded before the Mg was administered:

Again the QT is not correctly measured by the computer
I get 500 ms, not 467.
The correct QTc would then be approximately 610 ms.

There are also very large inferior T-waves, consistent with inferior hyperacute T-waves.
The patient continued, however, to be asymptomatic, serial ECGs showed no change, and bedside echocardiography showed no wall motion abnormality.
Therefore, I attributed these T-waves to the long QT and not to ischemia




The Mg level returned at 1.3 mEq/L (low but not terribly low, reference 1.4 mEq/L)) and K returned at 3.4 mEq/L (low but not terribly low).  2 g of Mg were administered, and then the patient was admitted, after which he received another 2 g of Mg.

The next AM, the Mg was 2.2 mEq/L and this ECG was recorded:
Near normal QTc


The patient was taken off the QT prolonging medications.

The next AM (1.5 days later) a final ECG was recorded:
The patient still has large T-waves, but the QT is normal

Assessment

Whether this patient had Torsades de Pointes (due to long QT) as the etiology of his syncope is uncertain, but such a prolonged QTc certainly puts him at high risk.  The longer the QTc, the higher the risk, and that risk gets significant when the QTc is greater than 500 ms and becomes very high risk at 600 ms.

Neither the ED treating resident, nor the inpatient team, saw this long QT.  The inpatient team was skeptical of my manual measurement.  They were going to attribute the syncope entirely to dehydration and alcohol intoxication.  I had to personally consult the cardiologists to redirect the evaluation, even though my formal interpretation stated that the QTc was 620 ms.

Physicians want to believe the computer's inaccurate measurements!

Learning Points:

1.  The computer will not consistently accurately measure a very long QT.
2. Look at every ECG and visually estimate the QTc by using the half the RR interval rule of thumb.
                    --If it appears long, manually measure it yourself!  
3. Correct for heart rate using Bazett’s formula: QTc = QT / √RR  (QT divided by square root of the preceding RR interval)
4. A prolonged QT can make T-waves look very large and unusual
5. Check for QT prolonging medications or drugs.  See these two posts.
6. Check Mg and K, and give Mg to patients who drink ethanol daily.
7. Even obvious very long QT may go unrecognized without systematic interpretation.

Sunday, September 4, 2016

40-something with severe CP. True + vs. False + high lateral MI. ST depression does not localize.

This was sent by Jason Winter of the Facebook Page Clinical Electrocardiology 

This post presents one new case, then reviews some interesting aspects of high lateral MI and of ST Depression in "inferior" leads.  Down below are 3 more cases and a discussion of how to differentiate false positive isolated STE in aVL from True positive.

Case

A 47 year old male called 911 for severe chest pain.  He was clammy and looked unwell.  He had a previous MI with cardiac arrest 2 years prior.  

This is his prehospital ECG:
There is very subtle ST elevation in I and aVL, with very subtle ST depression in III and aVF.
Is this due to coronary occlusion?



















Jason asked me if I thought it is due to occlusion (without either of us knowing the outcome), and this was my answer:

This is a posterolateral MI.  Probably due to occlusion of the circumflex or one of its obtuse marginal branches.

Why did I say this?

1.  The inferior ST depression is reciprocal to high lateral subtle STE
2.  There is a down-up T-wave in aVF.   Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL.
3.  ST segment in V2 has minimal ST elevation and is very flat, and the one in V3 is actually subtly downsloping.  This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL.  Together they strongly suggest a circumflex lesion.


The medic activated the cath lab but was refused by the interventionalist, who did not believe that this ECG represented acute coronary occlusion.

Later, the patient was taken to the cath lab.  The artery was occluded. It was opened and stented.  I could not get details on which artery, but I'm sure it was the circumflex.

Important Learning Point:

"STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet.  Therefore it is not a STEMI.  But what we truly care about is coronary occlusion, for which STEMI is just a surrogate that is only about 75% sensitive for occlusion.

"Inferior" ST Segment Depression

It is important to understand that "inferior" ST Depression is not due inferior wall ischemia.  Data from stress testing proves that the ST depression of ischemia does not localize.  See this article:

Relation between the electrocardiographic stress test and degree and location of myocardial ischemia

When there is ischemic ST depression localized to the "inferior" leads, it is more likely to be reciprocal to ST elevation that localizes to the high lateral wall (aVL), even though that ST elevation may be nearly invisible.  The ST depression may be the most visibly obvious sign of STEMI.

Here is a case that demonstrates this very well:

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


Here is the most viewed post of all time on Dr. Smith's ECG Blog, with nearly 100,000 views:

Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.



True Positive ST elevation in aVL vs. False Positive ST elevation in aVL


Case 1.  

A woman in her 60s with no prior history of CAD presented with 3 hours of sharp, centrally located chest pain with radiation to the anterior neck, with associated nausea. She had known HTN and DM.  She appeared to be in distress.  She was given sublingual NTG with improvement, but there was not complete resolution.

Here was here initial ECG:
There is ST elevation in I and aVL, with inferior reciprocal ST depression in all of II, III, and aVF, and a down-up T-wave in aVF (a sign that is very specific for ischemia).  There is also ST depression in V3-V6.  This ECG is diagnostic of ischemia.



It is important to compare this one with the false positive case #3 at the bottom; that one is a case which could fool you.




There was an old ECG for comparison:
One year prior with no ST segment abnormalities

A bedside cardiac ultrasound was done by the emergency physician.  Here is the parasternal short axis view:


There is an anterior and lateral wall motion abnormality.

This still helps to show the wall motion abnormality:
Arrows point to area of wall motion abnormality

















The Cath Lab was activated, and here are the results:

1. LM: No significant stenosis.
2. LAD: luminal irregularities with a 40% stenosis at the take-off of a D3. D3 has a 95% tubular ostial stenosis. (Culprit, stented)
3. LCX: Luminal irregularities, no significant stenosis. Two OM branches without significant stenosis.
4. RCA: dominant. Luminal irregularities without significant stenosis.  Supplies a small RPDA and RPLA.

After cath lab activation, her initial troponin returned at 0.124 ng/mL (99% level = 0.030 ng/mL)

This was the post-cath ECG:
After reperfusion: aVL shows resolution of ST elevation and inverted (reperfusion) T-wave.  There is also some terminal T-wave inversion in anterior precordial leads


A large Diagonal artery may supply both the lateral wall and part of the anterior wall.



Case 2: Another subtle lateral MI, from this post:
A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain.  Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG.  The patient had never had pain like this before.  The pain improved from 9/10 to 3/10 after NTG.  Here is the initial ED ECG:
There is subtle ST elevation in I and aVL with subtle reciprocal ST depression in III.  Look at aVF.  There is a downsloping reciprocal ST segement followed by an upright T-wave ("down-up" T-wave).  This morphology is highly suspicious for ischemia.   There are also symmetric anterior T-waves with very poor R-wave progression.  T-waves in V4-V6 are taller than normal (compare to ECG in case 3 below)

This ECG, especially along with the very typical history, was very worrisome, but not absolutely diagnostic of, ischemia.  Several serial ECGs showed no change, even after the pain finally resolved to 0/10 after NTG.

He was given aspirin,
clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was called and notified that this patient was very high risk and needed close attention.  He readily agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063
ng/ml (upper limit of normal = 0.025 ng/ml).  Repeat ECG remained unchanged.
--He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on medical therapy with plan for angiogram in the morning.
--Just before admission to the hospital, the patient admitted to recurrent pain and appeared uncomfortable.  Therefore, the
cath lab was activated urgently.
--The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or subtotal occlusion.
--At
cath, there was a 95% proximal LAD stenosis with TIMI-II flow, proximal to a large diagonal.  A stent was placed and the patient became pain free.


Case 3: False positive
And here is a similar one that is NOT MI.  How do we tell the difference?
There is ST elevation in I and aVL, with reciprocal ST depression in lead III.   

Just so you don't think I'm cheating by using a retrospectoscope, this was sent to me without any outcome, and I read it as "no MI" with a high degree of certainty.  This is because:
1. The remainder of the ECG is normal.  No poor R-wave progression, no other ST depression, no symmetrical T-waves, no large T-waves, no down-up T-waves, typical early repol in anterior leads
2. The reciprocal ST depression is in lead III only.  Not in leads II and aVF.
3. There are distinct J-waves in the two leads with ST elevation.  This is highly suggestive of early repolarization in these leads.
4. The T-waves in I and aVL are not large (this was also true with the MI case 1 at the top, but that case had many other suspicious findings (many leads with ST depression and no J-waves)
5. There is ST elevation in V2-V4 that is clearly due to early repol.  Early repol in aVL should be accompanied by early repol in the "anterior" leads.

Lessons:
When there is ST elevation in aVL, with reciprocal ST depression in III:
1. Look for:
    a. J-waves
    b. Other ST depression
    c. Large T-waves
    d. Symmetric T-waves
    e. Down-Up T-waves
2. Compare with an old ECG
3. Use ED Echo if available 
4. Use formal Echo 
5. A positive troponin is helpful (a negative one is not)
6. Angiogram if necessary.  You don't want to miss an occlusion.






























Thursday, September 1, 2016

Syncope, Hypotension, and a Large Right Ventricle -- What is the ECG Diagnosis?

Case

A 60-something woman had syncope and was unconscious for a few minutes.  It was not a seizure.  EMS found her lethargic and short of breath but without chest pain.  Pulse was 103, BP 100/60, and O2 saturation on room air 98%.

She was brought to the ED, where her SpO2 was 93%, BP 88/48, pulse 100.

On arrival in the ED, she underwent an immediate bedside cardiac ultrasound:


What do you see?
















There is a very large RV and very poor LV filling; the LV ejection fraction is nearly 100%.  It is easy to jump to the conclusion that this patient has a pulmonary embolism (hypotension, tachycardia, low O2 saturations, syncope, large RV).

An ECG was recorded:
What do you see?














At first glance, this ECG also suggests pulmonary embolism.  It shows an S1Q3T3.  One might think this is then highly specific for pulmonary embolism.  However, S1Q3T3 has a very limited (+) and (-) likelihood ratio for PE; it is seen in only 8.5% of patients with PE and 3.3% of patients who are evaluated for PE but do not have it.  See this post for detailed information.

This ECG has quite a bit more information: it shows sinus tachycardia with right axis deviation, a large wide R-wave in V1 (but without complete RBBB), and ST depression with T-wave inversion in V2-V6.  This is a typical ECG of right ventricular hypertrophy.

Further history

Further history revealed that the patient had poor po intake and vomiting.   Review of records revealed "chronic cor pulmonale" and a review of a previous formal echo showed:
--Pulmonary hypertension .
--Cor pulmonale, severe.
--Normal estimated left ventricular ejection fraction.
--Right ventricular enlargement Marked.

--Decreased right ventricular systolic performance severe 
--pulmonary artery pressure: 75 mmHg (normal 15-25)

People with right ventricular hypertrophy due to pulmonary hypertension may have severely decreased RV function and are very susceptible to low preload.  Any condition which lowers intravascular volume (such as vomiting and poor po intake) may lead to hypotension and syncope.

In these patients, can volume be assessed with ultrasound imaging of the inferior vena cava (IVC), as is often done in the ED?  

No!  The pulmonary hypertension will result in a "plump" IVC even with severe volume depletion.  The pulmonary hypertension requires high filling pressures (plump IVC) for adequate RV filling.

Physical exam tip: In patients who can stand up, a better measure of volume than IVC is to check orthostatic vital signs and symptoms.  In patients who are young and not on beta blockers or calcium channel blockers, the change to an upright position will result in a rise in heart rate to more tachycardic.  Older patients or those on such medications will have a drop in BP.  If symptomatic, it is pretty specific for volume depletion.   The exact numbers are more difficult to specify and beyond the scope of this post, but correction with volume repletion is very good evidence of relative volume depletion.  


Case continued

The first troponin returned at 0.090 ng/mL (normal, up to 0.030).

I had just seen this ECG in a stack and knew it was RVH.  I had not seen the history yet when the treating physicians sought me out to show me the ECG.   Due to the ST depression, echo, and troponin, they were worried about posterior MI or pulmonary embolism.   I pointed out that it represents typical findings of chronic RVH due to chronic pulmonary hypertension, not of pulmonary embolism or acute MI.   I suggested that this would be typical for an acute exacerbation of severe pulmonary hypertension due to dehydration.

Suggested evaluation: Check orthostatics, do thorough chart review and review of previous ECGs (these showed RVH) and echos (which showed RVH).  Give some fluids and check a d dimer (this was not done).

The patient did get a CT pulmonary angiogram for other reasons (suspicion of AV malformation), and  it was negative for pulmonary embolism.

Troponin peaked at 0.289 ng/mL.  The patient was rehydrated and discharged after a short stay in the hospital.

Although acute coronary syndrome (type 1 Non-STEMI) was not absolutely ruled out, the clinical presentation is typical for dehydration in the setting of pulmonary hypertension and I agree that an angiogram is not necessary.

Comment:

So this episode of volume depletion in the setting of RVH resulted in a type II MI.


Monday, August 29, 2016

2 Cases of Acute Ischemic Stroke -- What is the Etiology?

Case 1.

An elderly patient had sudden onset of severe hemiplegia.  He had no chest symptoms.  Head CT was negative.  tPA (alteplase) was started and an ECG was subsequently recorded:
There are well formed QS-waves in V2 and V3, suggestive of old MI with LV aneurysm.
Is the ST elevation due to LV aneurysm?
Unlikely: there is too much ST elevation.
V3 especially has a high T/QRS ratio, with 4 mm of T-wave divided by 7.5 mm of QRS, for a ratio of 0.55.  A value in any of leads V1-V4  greater than 0.36 makes acute STEMI far more likely than LV aneurysm.
However, there is also T-wave inversion, suggesting an open artery or prolonged (subacute) MI.


So this is either:
1.  Subacute STEMI (~24 hours old), or
2.  Old anterior STEMI (with probable aneurysm) with superimposed acute and reperfused STEMI (with inverted reperfusion T-waves).
3.  Recent (within a week or two) anterior STEMI with "no-reflow" resulting in marked persistent ST elevation.

An initial troponin I returned at 0.788 ng/mL.

If this were a subacute STEMI, already having formed well developed QS-waves, the initial troponin would be substantially higher.

Therefore, this is either #2 or #3.

When someone has a stroke and has old QS-wave MI, or especially a recent QS-wave STEMI on the ECG, one should be looking for LV thrombus.  LV aneurysm results in an akinetic (immobile) LV wall, which results in blood stasis which is thrombogenic.  Subacute STEMI adds inflammation to the endocardium, which enhances thrombogenicity.

Formal echo was therefore done:

1. Regional wall motion abnormality-distal septum anterior and apex akinetic
2. LV thrombus

The patient was treated medically for the MI.  (I now can't remember if the patient went for stent retrieval and, if so, the outcome.)

Subsequent troponins trended down and hit a plateau at a slightly lower level of 0.660 ng/mL.

This suggests the MI was recent (within many days to a week or so), not subacute.

This model fits best with the presentation, as a recent transmural STEMI in the LAD territory would result in a thrombogenic endocardium and LV thrombus, which is then at risk to embolize and result in stroke.

In the era before reperfusion therapy (early 1980's), all anterior STEMI were routinely put on heparin drips to prevent the occurrence of LV thrombus with its attendant stroke risk.

Diagnosis: Recent completed anterior wall STEMI with subsequent akinetic anterior wall, thrombus formation, and subsequent embolism with large middle cerebral artery ischemic stroke.  And that entire diagnosis could be gleaned from the clinical presentation and the ECG.


Case 2

This elderly patient had sudden onset of left-sided hemiplegia.  He had this ECG recorded before going for a head CT:

ECG:
There are wide, well-formed Q-waves in inferior leads, diagnostic of subacute or old inferior MI.
Not all LV aneurysms have persistent ST elevation, especially in the inferior location.
Additionally, inferior aneurysms usually do NOT have QS-waves (as they do with anterior MI); rather, they have QR-waves, as here.
So absence of QS-wave does not rule out inferior LV aneurysm.  
 


He also had this ED bedside echo done prior to head CT.  Here is the parasternal short axis:


What do you see in addition to a dense inferior wall motion abnormality?  (Answer is below)

Clinical course:

The head CT showed no bleed and tPA was given.

Here is one image from the head CT.  What do you see?

What do you see?










There is a hyperdense MCA sign in the left Middle Cerebral Artery [radiodenseity (white) in upper right part of brain].  Hyperdense MCA sign is seen more commonly in cerebral embolism (though most embolism is from atrial fibrillation) than in carotic artery thrombosis, as the thrombus is mature and more radiodense at the time of stroke onset.  So this is further evidence that there is a cardio-embolic source.  Since the patient is not in atrial fibrillation, that embolic source is likely to be a mural thrombus.  Since the patient has a dense inferior wall motion abnormality to go along with the large Q-waves, this is the likely source.


Bedside Ultrasound Legend:

Here is a still shot at the 1 second mark of the above ultrasound, where the ultrasound is pointed closer to the apex than the base:


Here I have circled the finding of the ultrasound:
There is a myocardial rupture with pseudoaneurysm of the inferior wall, with thrombus filling the pseudoaneurysm.



Clinical course:

CT angiogram stroke protocol revealed thrombus in the right internal carotid artery and middle cerebral artery.  The patient received tPA (alteplase) very quickly, then went for a stent retrieval. Unfortunately, the clot could not passed with the stent retrieval system, consistent with a mature thrombus.  It could not be retrieved.  The patient was started on long term anticoagulation.

Here the interpretation of the subsequent formal ultrasound (this formal US is not shown):

Regional wall motion abnormality, inferoposterior, akinetic with rupture and thrombus filled left ventricular pseudoaneurysm.

Clinical course:

The tPA did not cause catastrophic bleeding in this patient with a myocardial rupture, as the thrombus in the pseudoaneurysm was quite mature.  The stroke completed, as this mature thrombus is resistant to thrombolysis and could not be retrieved.

Learning Points

LV aneurysm can be diagnosed by ECG.  In the context of stroke, it strongly suggests cardioembolic source.



Thursday, August 25, 2016

An Unusual Tachycardia

This Case was sent by Atif Farooqi and Scott Weingart, from Stony Brook.

This is a 70-something with history of CABG who presented with 30 minutes of SOB and palpitations.

Here is his ECG:
What is it?












Atif wrote this:
"My first thought was perhaps a bidirectional V Tach, though the pt is not on digoxin and otherwise has no discernable reason to be in BVT.  Scott was considering maybe an intermittent aberrant conduction, though we thought it odd for it to be strictly alternating beats.


Here is my answer:
Atif,
Interesting EKG!
I think it is SVT with every-other-beat-aberrancy. 
--Every QRS comes right on time, perfectly regular, so it can't be Bigeminy. 
--Every other beat is RBBB, which is the most common type of aberrancy because the right bundle has a longer refractory period than the left.
--The inbetween beats are of normal duration (100 ms).  The axis does not alternate.  There is no alternating RBBB and LBBB.  So it can't be bidirectional tachycardia (neither bidirectional VT nor bidirectional SVT).
--There are no P-waves.
So this is AVNRT with alternating aberrancy (Scott was right!).

Additionally, both the aberrant and the normally conducted beats have significant ST depression.

Bidirectional Tachycardia implies alternating frontal plane axis, from -60 to +120, or alternating LBBB and RBBB.

Bidirectional tachycardia can be Bidirectional Ventricular Tachycardia, as with Digoxin toxicity.  The etiology may be:
1. alternating location of origin of the VT ectopic focus, or
2. alternating routes of depolarization from a single ectopic focus

Bidirectional VT may also result from aconite toxicity, as in this case I reported, which has alternating RBBB and LBBB.

Bidirectional Tachycardia can alternatively be due to SVT with Bidirectional Aberrancy:  the aberrancy may be due to:
1. RBBB with alternating LAFB (left axis) and LPFB (right axis), or
2. Alternating RBBB and LBBB.

Here is the ECG from this case of Aconite Toxicity:
Alternating RBBB and LBBB.  Intervals are regular.





This case presented here today does NOT have alternating frontal plane axis, nor does it have alternating RBBB and LBBB, so is not bidirectional tachycardia.


Case continued:

The attending gave IV Metoprolol, (the patient was supposed to be taking oral metoprolol as an outpatient), and the rhythm changed to the following: 
This appears to be sinus, though the P-waves are not obvious.
This subsequent ECG proves that the first was SVT with aberrancy: the complexes are identical to the non-RBBB beats of the first ECG.
There is also persistent ST depression.  Hopefully now that there is no longer tachycardia, this ischemia will resolve.

It is typical for metoprolol to convert an AVNRT. 
I would have tried adenosine.





Sunday, August 21, 2016

A 25 year old with Epigastric Discomfort, Worse Supine, Better Sitting Up.

This is another case provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club  

This is a 25 year old male diabetic who presented with epigastric heaviness for 12 hours.  The discomfort was intermittent and associated with sweating and dizziness; it was increased increased by lying flat and relieved when sitting up.

Here is his initial ECG, with pain and diaphoresis:

It is really quite normal.
When I first saw it, I did not know the patient still had pain, and I responded on FB:

"This is normal.  However, the sharp downturn of the T-wave in V4-V5 suggests possible development of Wellens' waves, but is nonspecific. The T-wave flattening in limb leads is non specific."
However, with ongoing pain, these are unlikely to be vestigial Wellens' waves.

He was given NTG and Morphine and pain was improved.

An interventionalist was consulted.  
He performed an echocardiogram which showed no wall motion abnormality.  

The first Troponin T returned at 0.017 ng/mL, slightly elevated but indeterminate.  

The interventionalist diagnosed pericarditis and prescribed an NSAID.

[This ECG shows no evidence of either pericarditis or of STEMI.  The diagnosis must have been based on the positional nature of the pain.]

Dr. Alwan smartly recorded more ECGs.   Here is the second one recorded 4 hours later:
No significant change


6 hours after the first ECG, and 2 hours after the 2nd, a third ECG was recorded:
Now there is new ST elevation, the change being diagnostic of LAD occlusion.
This is not an ECG one would see with pericarditis, which manifest inferolateral ST elevation.

Even if this were the first and only ECG, the differential diagnosis would be early repol vs. LAD occlusion, and the formula could be used:

STE60V3 = 2.5 mm
 computerized QTc = 437
(notice how it lengthened from the earlier values of 372 and 402 ms!)
R-wave amplitude V4 = 9 mm
formula = 25.839 (greater than 23.4 is all but diagnostic of LAD occlusion)

The patient was taken for angiogram.  Here is the report:

Here is the post reperfusion ECG
Typical reperfusion T-waves, identical to Wellen's waves (Wellens' waves represent reperfusion!)


Learning Points:

1.  Young People can have myocardial infarction
2.  Though positional pain lowers the likelihood that chest pain is MI, it does not eliminate it!
3.  Always get serial ECGs.
4.  Pay attention to even slightly elevated troponin levels.  This could have been myocarditis, but that is a diagnosis of exclusion, after a negative angiogram.


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