It’s genetic disorder that effects sodium ion channel functionality, primarily in the myocardium. It’s prevalence is not known since it was only identified in 1992. It certainly might explain some cases of sudden cardiac arrest in patients with no cardiac history. What’s also interesting, although I don’t know that it applies in this particular case, is that Cocaine is one of the drugs that increases the likelihood of a dysrhythmia. That might explain some heretofore unexplained deaths among young people. That part is speculation though.
The only real treatment right now is implantation of an AICD. It’s hereditary so, if one member of a family is found to have it, parents, siblings, and any children should be examined for it.
In our case we hadn’t yet applied the limb leads, so we didn’t catch the presenting rhythm.
The keys to this are the abnormal ST segments in V1 and V2. There is an incomplete right bundle branch block, but certainly the morphology (at least to me) wasn’t typical. It makes more sense in retrospect than it did at the time of presentation.
We really weren’t sure what to make of them, with posterior AMI being on our list, but not very high thereon.
Our treatment, as outlined in the original post, was symptomatic only. 250ml bolus of Saline, Oxygen, monitor and transport.
The nicest thing about this call was that we very likely actually saved someone’s life. There are a lot of ifs involved, but it’s possible that this wouldn’t have been picked up if he hadn’t agreed to go to the hospital, or if we had gone to a different hospital, or any number of other variables.
Now that I’ve seen this both on an ECG and in person, I’m going to be more aware of the possibility in younger syncope patients.
Thanks to everyone that commented. Most of you got it right, which shouldn’t and doesn’t surprise me. Special thanks to Tom for posting a comment on Facebook. More thanks to Ambulance Driver for posting a link on his blog. I’ve had so many hits the past two days that I’m in blog heaven.