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.





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.


A 50-something woman with atypical chest pain

This was provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club   

A 50-something female presented with atypical chest pain described as stabbing, with no radiation 
PMHx : DM poorly controlled 
VITAL signs stable 

Here is the initial ECG with the question "should the cath lab be activated?"
This is suspicious for ischemia because of the T-wave inversion in aVL.
However, this is very nonspecific and one would not activate the cath lab!


Another ECG was recorded 20 minutes later:
This has more obvious T-waves and T-wave inversion in aVL
Here is my response:
"This 2nd one is an extraordinarily subtle but real change!!" (i.e., this is diagnostic of MI).  "These often resolve with nitro, so I would try that first. It depends on your resources: if activating at night tires out your team for the next day, you try to avoid if possible.
But this pain and ECG may not resolve, in which case you must activate."

In other words, this is diagnostic of inferior MI, but not of STEMI, and may not need emergent cath lab activation.

If the pain and ECG findings resolved with nitroglycerine, it will need at least maximal medical therapy and continuous 12-lead ST segment monitoring

See these cases for the importance of ST segment monitoring:
http://hqmeded-ecg.blogspot.com/search/label/ST%20Segment%20Monitoring

A third ECG was recorded at 45 minutes:
Now it is unequivocally diagnostic of inferior MI, even though it does not meet millimeter criteria for inferior STEMI.
The cath lab must be activated.

Here are all 3 ECGs, one after another, so you can see the changes:




The cath lab was not activated, but a 4th ECG was recorded at one hour:
Now it meets STEMI criteria.
Cath lab was activated
What else do you notice?









There is also new ST elevation in V1.  So this is a right ventricular MI also

Echo: Basal inferior wall hypokinetic, pseudonormal LV filling pattern

Initial Troponin T: less than 0.01 ng/mL initial
Troponin T after 2 hours: 0.49 ng/mL


Troponin T after 4 hours: 1.6 ng/mL (this is a large MI)

Cath showed a 100% proximal RCA occlusion.


Learning Points:

1. T-wave inversion in aVL may be the first sign of inferior MI
2. Pay attention to slightly enlarged T-waves
3. When you see these subtle, nonspecific abnormalities, make certain you get serial ECGs!
4. Any patient with ongoing potentially ischemic chest pain should get serial ECGs!




What is this? A Perplexing ECG.

A 46 year old woman had syncope.  

Before seeing the patient or reading the chart, the physician viewed the ECG and was perplexed:
What is going on??


















Then he found out she had a heart transplant.  Now can you tell what is going on?





It turns out that both the native heart and the transplanted heart are beating.  The native heart is paced by the transplanted heart.  The sequence is given in the legend of the annotated version below.

How does this work mechanically??


Both left ventricles pump blood into their respective aortas, then these two aortas converge immediately after their origins.  Thus, the hearts work in parallel, but the native heart beating slightly later than the transplanted one, and synchronized by the pacemaker. 

In this case, the patient had pulmonary hypertension.  If she had had a normal orthotopic transplant, the new right ventricle would not have been able to pump against the high pulmonary resistance.  Therefore, the native right ventricle pumps into the pulmonary artery, while the atria are connected (right with right and left with left).

The transplanted heart is over the native heart, with the apex directed rightward and upward (lead I, II and III are indeed negative). 

Annotated ECG:

Here I have drawn vertical lines at the beginning of each QRS:

The start of the native QRS is the first line
The start of the transplanted, paced QRS is the second line.

1. Transplanted heart P-wave 
2. Transplanted heart (abnormal) QRS (axis negative because heart is upside down!)
3. Native heart atrial spike (having sensed on the transplanted ventricle); no clear P-wave. 
4. Native heart ventricular spike followed by 
5. Native heart QRS.