EKG of the Week

 This EKG comes from a 65 year old female with a chief complaint of altered mental status.  She was found down at home and EMS tell you that her HR for them was 20.  You decide to run her in the trauma 2 with an intern, a second year and you running the case.  What do you want the intern to do?  What should the second year do?

Initial vitals: HR 22, BP 60/palp, RR 18, Pulse Ox 90% on RA, Temp 102F, D-Stick 531

Here is her EKG:

What are your concerns?  Let’s say her GCS is roughly a 7.  What do you want to do?  Are there any medications you want to give?  Procedures to set up for?  Can you immediately go to intubate someone with a BP of 60/palp?  I guess technically you can, but should you?  Any interventions you want to take first?  Should you pace her?  how?  Any consultants you want to call? Is it too soon?
Thought about those questions?  here’s some labs for you:
VBG: pH of 7.15, CO2 20 O2 45 HCO3 10 Lactate 4iSTAT chemistries unremarkable, K was 4 ish.
 This was a really cool case that turned out really well.  Think hard about this one!

So, to be honest, I made this one a little harder on you than it was for me with the stem.  This was billed to me as, Hey Doc, he’s in VTach in lead II.  Not to give it away, but you’re either in VTach or not.  I was leaning towards not in this case.  The big question is, is this Torsades du Pointes (TDP), a form of polymorphic VTach or not?  Let’s look at the Rhythm strip again with some marks on it, See Rhythm_1_Marked_Up:

All of the black lines on it were obtained by measuring the R-R Interval between the two red stars.  Notice how the R-R interval is consistent in all of the places I measured.  You should not be able to march out QRS complexes in TDP.  So, feeling pretty good about this being artifact over TDP.  This patient had a lot of reasons to go into TDP like taking multiple QT prolonging meds due to all those psych meds, Super high K, etc.  So, if you take nothing else away from this, when a nurse calls you about a patient, especially when you don’t plan on doing anything, GO SEE THE PATIENT.  Which is what I did.  He was hemodynamically stable, with no complaints.  His EKG from that morning had a normal QT, which is also reassuring.  I felt pretty good with my decision that this was artifact and there was nothing to do.
Cardiology was eventually consulted and agreed that it was likely artifact.  I believe their actual words were, “Please ask the patient not to use his electric toothbrush while connected to the tele monitor.”
Let’s do a quick TDP review: 
Click on this link for a classic example of TDP from life in the fast lane (https://lifeinthefastlane.com/ecg-library/tdp/):

Notice the smooth, almost wavy nature of it? Our rhythm strip was missing that.  Our was very harsh almost alternating large then small then large complexes.  Notice also how you cannot march out underlying QRS complexes?
From Life in the fast lane: 

• TdP is often short lived and self terminating, however can be associated with hemodynamic instability and collapse. TdP may also degenerate into ventricular fibrillation (VF).
• QT prolongation may occur secondary to multiple drug effects, electrolyte abnormalities and medical conditions; these may combine to produce TdP, e.g. hypokalaemia may precipitate TdP in a patient with congenital long QT syndrome.
• Recognition of TdP and the risk of TdP allows the instigation of specific management strategies (e.g. magnesium, isoprenaline, overdrive pacing, etc.)

Amal Mattu has an excellent case on artifact vs VTach: http://www.mededmasters.com/vtach-versus-artifact.html

Solution to this week’s EKG of the week!  Here was my read:
Rate: 170 (I cheated and looked off of the read)

Rhythm: Well, regular or irregular?  I’d call it regular.  Definitely tachycardic and I don’t see a P wave before each QRS…

Axis: Up in 1, down in aVF, looks Left axisIntervals: the big question here is: is the QRS wide or narrow.  QRS is 102 ms, so narrow

Morphology: seems ok to me

So we have a regular, narrow complex tachycardia.  I’m gonna borrow from our tachydysrhythmia chart: 
Narrow and Regular: Sinus Tachycardia, Atrial Tachycardia, Atrial Flutter with a fixed block (remember if you see a rate of 150 on the exam LOOK FOR FLUTTER WAVES), and AVNRT (colloquially called SVT) 
Narrow and IRREGULAR: Sinus tach with PACs (remember that non compensatory pause?), Afib, MAT, Atrial flutter with variable block
Wide and Regular: Regular SVT with BBB, Regular SVT with preexcitation, Vtach, V Paced (Check every EKG for pacer spikes)
Wide and IRREGULAR: Irregular SVT with BBB, Irreg SVT with preexcitation, VFib, Torsade de pointes

So if we look at the narrow and regular choices: Sinus Tachycardia: No p waves, right?  So not Sinus Tach. Atrial Tachycardia: We haven’t covered atrial tachycardia expressly, but MAT and Aflutter and two types of atrial tachycardia.  But, I cannot confidently pick out atrial activity, so I’m going to lean away from ATach.  For more, see (https://lifeinthefastlane.com/ecg-library/atrial-tachycardia/) AFlutter: I don’t see flutter waves.  The rate is 170, which is close to 150, but doesn’t appear to be flutter.  But bonus points for thinking about it with a rate near 150.AVNRT (SVT): This looks like SVT to me.
So I read this as SVT.  Lets take a quick side trip and refresh on what is going on with a patient in SVT:
Technically, we should be calling this AVNRT (that’s Atrioventricular Nodal Reentrant Tachycardia).  This is the most common cause of SVT.  Life in the fast lane has some excellent drawings of what is going on:

In this picture, the reentry circuit on the left is within the AV node (what is likely going on with our patient) as opposed to outside the AV node on the right which is more consistent with a process like WPW.
So what happens within the AV node??

If a PAC activates the slow pathway while the fast pathway is still refractory, BAM!  you get SVT and an EKG that looks like this patient.  For more, see : https://lifeinthefastlane.com/ecg-library/svt/
Cool!  But I didn’t become an EM physician to talk about pathophys….
Very true, so with the first patient scenario, I’d give adenosine (6mg – 12mg – 12 mg).  Remember, Adenosine is an AV node blocker and allows the heart a pause to reset and have the heart’s electrical activity go down the right pathway.
For the second patient, get out the paddles.  This patient needs electricity.  Remember to synchronized cardiovert this patient.  Do not fibrillate someone with a pulse. Please.
For me, she was resistant to the first dose of adenosine but the 12 mg put her right back into NSR.  She was admitted to the hospital for further work up as she had never been in SVT before.

This week’s EKG is a tricky one.  Start with EKG_1 and EKG_RhythmStrip.  Try to figure out what is going on with the patient and what treatment you would recommend.  Once you have decided what treatment to give, take a look at EKG_Treatment and see if you did the same thing we did and if you agree with our decision.  Hit me up with any questions.
Patient scenario: 56 yo M with no PMH p/w palpitations.  Vitals are stable.

    This week’s write up comes from an EKG Dr. Sean Griffiths saw during his thrilling month on medicine.  He wrote up the case and sent it to me.  I’d encourage you to look at the EKGs first and then read his solution to each of them.  It’s really interesting case with a solution that I had never heard of before!  Enjoy!
-Lloyd

Had an interesting EKG case that I saw on the wards and thought it would be good to share with everyone. 

Brief Hx: 72 year old male PMHx of CVA with severe personality changes, dementia, AV pacer, HRrEF, aortic stenosis, and Afib who was admitted from the ED for possible pneumonia after infiltrate seen on CXR. To give you a better idea he was the patient screaming in B Pod a few days ago and had to be put down with Haldol, Ativan, and Benadryl. 

Overnight, the night float team was paged on him several times with strange rhythms on EKG and agitation requiring more haldol. In these rhythms he would go from paced left bundle pattern, to RBBB, then SVT and then convert back to regular pacing. In the morning, the tele tech and nurse paged me several times to come look at his monitor for “weird rhythms”. 

ECG 1: 30 Oct 0827 – irregular AV paced rhythm, with LBBB pattern no concerns for ischemia by Sgarbossa criteria

ECG 2: 0828 – irregular paced rhythm with RBBB pattern, PVCs – weird but not quite sure what to think. Machine saying ****ACUTE MI*****. Patient asymptomatic.

ECG 3: 0829 – irregular paced rhythm with what looks like paced beats of LBBB then PVCs that look RBBB to me. Again very weird, by this point I’ve already decided to call cards and have them come interrogate the pacer. No signs of acute ischemia and patient asymptomatic. Machine saying ****ACUTE MI**** but neg Sgarbossa

ECG 4: 0838 – at the end of the tracing he goes into SVT with what looks like a strain pattern at a rate of slightly less than 150. This stopped after a few seconds and patient remained asymptomatic. 

Ok all that was very weird, not sure what’s going on. I called the electrophysiology fellow and told him what’s up and he agreed to go check out the pacer and call me back; which of course he didn’t call after. A few hours later I get a page about his rhythm again so I have them do an ECG and go down there to check it out. 

ECG 5 (Rhythm Strip): on this ECG there are new T wave inversions in II, III, AvF, V3-V6. At this point now I am very concerned. The patient is asymptomatic but then I started thinking about Wellens Syndrome and T wave inversions in V2-V3 in a pain free patient could be indicative of proximal LAD lesion that is in imminent need for cath. I immediately walk down to the CCU work room and ask some people there who were useless and told me this is a fellow level ECG. So I went back upstairs, paged the cards fellow, and ordered a right sided ECG for the inferior changes I saw. 

Cards calls me back and I filled them in on the findings. So what happened? He informed me that he had adjusted settings on the patient’s pacemaker and that yes these findings would be concerning in a normal person but in this person they were not concerning. So what was going on?

They are called “memory T waves”

So what are memory T waves? According to the fellow, memory T waves are a phenomenon that result from a change in the electrical conduction of the heart that causes the heart to “remember” the old T waves and retain their morphology from the pre-changed state. Clear as mud? This case example is pretty similar to mine and it gives a good definition of “cardiac memory” as it applies to paced people:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4995449/

“Cardiac memory refers to persistent T-wave changes that develop after a period of abnormal ventricular activation (wide QRS complexes) once normal ventricular activation (with narrow QRS complexes) is restored. After normal ventricular activation is restored, the T wave “remembers” and mirrors the direction of the wide QRS complexes. Therefore, cardiac memory results in positive T waves in leads that had positive wide QRS complexes and negative T waves in leads that had negative wide QRS complexes. These T-wave changes can follow resolution of any condition that triggers transient QRS widening, including transient left bundle branch block, ventricular tachycardia, intermittent ventricular pre-excitation, and ventricular pacing. Cardiac memory can persist up to weeks after normal ventricular conduction is restored.”

So after all of the running back and forth to 3W, going to the CCU, paging cards fellows and a lot of worrying if I doing the right thing it ended up being sort of nothing. The EKGs were concerning enough for cards to mess with the pacer but the result of that tinkering was not actually Wellens or some terrible pattern just “cardiac memory/memory T waves”.

Take aways:

Interns: When shit looks weird and you’re concerned, go get help. I was nervous going to the CCU to ask for help in case they would have called me a jackass but I was more concerned something actually bad was happening. Trust yourself, but not too much.

Everyone: Someone with weird T wave inversions and pacer ask about recent changes made to their pacer by their cardiologist. A quick phone call with cards who will confirm these are memory T waves could prevent a hospitalization and large work up.

Thanks guys!

Sean Griffiths

5 Attachments