EKG of the Week – Week 24 ANSWERS
Man, this one was a touch tricky, right? So let’s start with the EKG:
Rate: 22 (I cheated, I looked at the rate at the top)
Rhythm: Tricky, let’s circle back to this in a bit
Axis: Up in 1, Down in aVF, looks like left axis
Intervals: Uhhh… Is there a PR interval? not really…
Morphology: I don’t see any obvious signs of a STEMI.
So what’s going on with this EKG? Spoiler alert: it’s concerning for third degree heart block.
The P waves march out and are operating independently of the ventricles. What does that mean? Let’s take a quick look at this picture from life in the fast lane:
So in this picture, which is labeled way better than I could do, you can see that the P waves are firing at a rate of roughly 100 bpm and the ventricles are firing at roughly 40 bmp and they aren’t talking to each other. Notice how the PR interval is vastly different between each P-QRS complex.
Let’s go back to our EKG. The p waves definitely march out. Do the QRS complexes? It’s pretty close. It’s not perfect, but close enough that it’s either a very strange block (maybe a 4:1?) or complete heart block.
(SIDE NOTE: in patients with BRADYCARDIA and HYPERGLYCEMIA: please consider a calcium channel blocker overdose! Bradycardia makes sense, right? The heart is dependent on calcium to pump, if you block the calcium, it cannot pump as well. But why Hyperglycemia?? Well, the CCB isn’t specific to the heart. It also affects the pancreas. The pancreas requires calcium to release insulin, but it can’t, because of the calcium blockade . No insulin = hyperglycemia. For more, see: https://lifeinthefastlane.com/ccc/calcium-channel-blocker-toxicity/)
OK, now what? let’s not forget about the bradycardic, hypotensive patient you have on the bed barely protecting her airway.
Considerations (in no particular order)
1) Hypotension
2) Bradycardia
3) Airway
What do you want to do? Here’s what we did. I’m not saying that this was the perfect way to manage the patient, but I’ll do my best to explain every step we took.
Thought: You CANNOT intubate a patient with a BP that low. They are so dependent on their catecholamine surge, that as soon as you push RSI drugs, they will code. Codes are fun, but try to prevent them.
This is a little blurb from http://www.christem.com/eruditionem/2014/1/28/intubating-the-hypotensive-patient.html on tips for intubating the hypotensive patient. It’s a pretty quick read and it’s pretty interesting. Honestly, you probably know most of the info already, but it gets you in the mindset for critically ill resuscitations:
“Then if it is apparent that there is a loss of vasomotor tone, you should replace the lost endogenous catecholamines with temporary vasopressors. I suggest blousing aliquots of phenylephrine 100 mcg Q 1 minute unless the MAP has precipitously dropped, then start with 300mcg. Once you have stabilized their MAP see if you have to keep pushing phenylephrine, if you do they need a drip, if you don’t, congratulations you have successfully intubated a sick hypotensive patient without killing them.
If you are slick with the echo probe and see the LV or RV is down consider epinephrine 10mcg boluses instead and an epi infusion if needed.”
For me, I’m a push dose epi guy. I know some people like push dose phenylephrine and when you’re on the STICU, they hand out sticks of it like they’re candy. However, I just like working with epi, it makes sense in my brain. Current interns, you should know how to mix up your own push dose epi. I used it a ton of times overnight in the BICU. Incoming interns: you take a box of code dose epi (1:10,000) and a 10 cc saline flush. Get rid of 1 cc of saline from the flush, then add 1 cc of the code dose epi to that flush. Mix well. You now have a concentration of 10 mcg/ml. I like to give little 10-20mcg bumps to get the BP up and get them through intubation.
Other Thought: We tried to give the patient some atropine and see if that would increase her heart rate. It came back up to 70 for about 10 seconds and then went right back to 20. We gave up on atropine and started her on an epi drip (put 1 mg in a 1L bag on NS and start at 5 mcg/min, titrate up as needed) to get her BP up.
We tried to transcutaneously pace her, but she needed 110 milliamps of electricity and that really hurts. So we had to give up on that. Once the epi drip started, her BP came up enough and she was able to be intubated. Once intubated, a transveinous pacemaker was placed and she was paced to a rate of 70. Here’s a pretty good video of a nurse walking you through the transveinous pacer (https://www.youtube.com/watch?v=dunUZxJvQEA)
The patient was taken by cards to the Cath lab and a pacemaker was placed.
Cool twist: What was going on with her VBG?
So it turned out that the patient had a UTI that put her into DKA and for some reason led to complete heart block. It wasn’t a CCB OD like we thought. But still pretty cool.