So we were dispatched for a low-priority call, for someone who is “sick” and unable to get out of bed. Usually, when a 50-something year old male is “too sick to get out of bed,” he has either a) Man Flu, or b) Acute lazy syndrome. Usually.
My partner and I were met at the front door of a typical middle-class home in a typical middle-class neighborhood by a typical looking housewife. “My husband has diarrhea and has been vomiting all day” she says.
Sure enough, there is a guy in his 50s laying in his bed. This guy doesn’t look too good, though. He is sure enough sick. He appears pale, and sickly. He complains of general malaise and vomiting all day, accompanied by diarrhea, much like his wife says. While my partner obtains a quick set of vital signs, I ask the patient about his medical history, but he says he is too weak to talk. His wife hands me a medication list.
His medication list includes Norvasc, Lasix, Coumadin, Lisinopril, Lipitor, Plavix, Metformin, Humalin, Aspirin, and Atenolol. So his history is pretty clear. His wife mentions that he had a pacemaker implanted about 7 or 8 months ago. Sure enough, there is a conspicuous lump in his upper chest.
Partner of the day reports a blood pressure too low to hear, but she thinks she palpated 90 systolic. His room air O2 saturation is 93 percent, his pulse is weak at 50, and his blood sugar is 48.
All of that seems normal for someone with these complaints, aside from his curiously low heart rate, so we decide to attach the monitor:
I will leave the interpretation up to you, the reader. But I’m not sure what the monitor was seeing with those mythical pacer arrows at the bottom of the strip.
Partner establishes an IV of Dextrose 5% while the fire crew comes up with a plan to get this gentleman from his bed down a narrow hallway, around a corner, down 5 steps, and onto our stretcher, all while I grab a 12-lead:
This seems to me to be a pretty straight forward ECG, and I was pretty confident in my interpretation, and what the problem was with this guy. But again, I will leave the interpretation up to you all.
The patient was moved to the stretcher without a problem, and loaded into the ambulance, and we began transporting to Local Hospital. While enroute, the Lifepak spit out another 12-lead:
Again, the interpretation is up to you. The change is pretty obvious, though, which serves to reiterate the importance of leaving the ECG leads on the patient.
As somewhat of a side note, one thing I particularly appreciate with the new Lifepak 15 is the STJ Level measurement on the right side of the printout.
The handoff at the hospital was easily completed, and we left the patient in capable hands. We returned to the hospital a few hours later, and got some information on the patient from his nurse.
I’ll discuss that information, with lab results, in the next post.
That is a pretty drastic change in the QRS morphology there…! I have a question for you – is the STJ printout on the 12-lead pre-set up when your agency’s LP15′s were initially programmed, or is it something that you turn on yourself?
If it is something that you turn on, which menu is it in on the LP?
Thanks
Joffre
Joffre;
I’m pretty certain it’s a default. I looked through the LP15 User Manual, and didn’t see anything that would lead me to believe it could be turned “off or on.”
I didn’t go so far as to call our PhysioControl rep,though…
CCC
Ok, thanks – I don’t remember seeing it in the LP menu settings or in the user guide binder.
It is a pretty nice option… although you and I probably know somebody in our respective agency who would take those numbers for absolute truth without looking at the causative reasons behind the elevation/depression…
I remember on the LP12′s, the sensed pacing spikes would display realtime on the screen if you turned on the option… very nice way to keep track of the pacing rate of a patient’s pacemaker. I do miss that on the 15.
Thanks again!
Well, I’m not going to say I know the answer with 100% certainty, but there’s no doubt about the drug I’m grabbing for, even without the labs.
Missed a very similar case a few weeks ago…
I’m thinking about Sodium Bicarb, Calcium, and Albuterol. Probably also D50. Had a very similar case a few weeks ago, minus the Hypoglycemia.
Sick guy, forsure. It appears as if he has multiple things going on and the most obvious is that he has a pacemaker failure. Maybe the failure led to all of his other illnesses? I see pacer arrows, but its obvious that its not doing its job. From the first 12 lead, I was initially going to say that it appears to be hyper K+, but after looking at the second 12 lead, I would most defientely call this an anterioseptal MI w/ lateral involvement. Most likelly the LAD is occluded hince the bradycardic rate and findings on the 12 lead. Reciprocal changes in the inferior leads (which are new in 2nd 12 lead) just put the icing on the cake. ALSO, there is no doubt in my mind that he has metabolic alkalosis. (diarrhea, bradycardia, and hypoglycemic). I would activate the cath lab, and if his pressure and heart rate maintained then I would only administer fluid, 02, ASA, and any other supportive measures.
Despite the doubtless presence of The Thing We’re All Thinking Of, it may be good to remember that it does not acutely evolve with reciprocal changes.
Are you sure? They call it “the great imitator” for a reason! I’ve seen many cases with apparent “reciprocal changes” and there are many examples in the peer reviewed literature. I’d be shocked beyond belief if this is also STEMI.
Tom, I’ll defer, but I have never seen hyperk (or any electrolyte abnormality) evolve so dramatically and consistently over a few minutes. To me that would be a classic differentiation between an acute dynamic process and a stable insidious one.
The rhythm changes from RBBB morphology to LBBB morphology so I don’t think it’s an apples-to-apples comparison.
I was viewing that as a progression from ischemic depression to increasing STE. Perhaps a stretch, and certainly the lyte distortions are confusing things, but you could at least argue that it’s a consistent pattern.
@ Brandon O- It’s evolved and there are changes, that’s a significant change no matter how you want to look at it. Symptoms have been going on “all day,” so who’s to say that “acute” hasn’t been happening for the last six, seven, eight hours? I think it’s safe to say that EKG changes like this are to be expected. Not trying to be argumentative, just curious where you are going with this.
When diabetics get sick boy do they get sick ! scoop stretcher to the bus if he can’t handle the stair chair. obvious O2. check for nuero deficits before D50. see how he reacts to the sugar . ASA 324mg PO if he can chew without choking. hold off on NTG for obvious BP issues, Call MC and tell bout the funky rhythm and EKG changes and past PMHx. rhythm seams junctional, ask MC about dopamine ( If the rate doesn’t come up after d50). please be enroute by this point. Check lungs before 250cc fluid bolus due to Hx of CHF per med list. Most of all, watch the Pt. and see how he reacts to each treatment. Its easy to get carried away as a new medic and snow somebody with every med in your protocol, but don’t forget there is a ” reaction time ” to each one. It’s hard to tell the MD which med made a difference in the Pt’s condition if you slam em all home at once. get done what you can enroute without delaying Pt transport to ER. transporting early could be the difference between a pt deteriorating in your truck vs. in the ER.
The HPI (GI distress) would be consistent with electrolyte loss, combined with hypoglycemia makes me think his oral CHO intake hasn’t been sufficient for the diabetes medication. Another concern is the lasix, which will also cause potassium wasting (again in the context of diminished or absent nutrient intake). All of this would set this patient up for hypokalemia. I know this isn’t necessarily consistent with the ECG findings, but I think it needs to be considered. My hunch is that it would take some pretty significant renal insufficiency (lack of potassium excretion and inability to produce post-emetic bicarb spikes) to have a patient retaining potassium under these conditions; its a definite possibility given the inferred history of DMII and CAD but I’d hate to bank on it and be wrong.
Aa a nursing student, prehospital treatment is not something I’m familiar with so I’ll hold off on treatment options other then getting a lyte panel asap (in no way trying to imply that simply transporting this patient is a reasonable suggestion…I really wouldn’t know).
Im going to say Hyperkalemia due to the spiked T waves along with St elevation in leads V1 and V2(its very hard to see the 12 lead in my screen)
hi…i am an emt-b…i like to read about stuff everyone puts on here but since i dont have my medic license, i cant read leads yet…i was wondering if someone would be willing to give me the answer to this and tell me what is going on with this sick man…thank you
Sine waves all the way. HyperK+
Why do you call them sine waves? I would think peaked T’s but not sine waves. Alos think its interesting that the pacemaker is not capturing. Heard alot about how futile trying to pace can be in the event of hyperkalemia. Very interesting.
Judging by the patient’s symptoms, and his ecg, I would have to say that he is having an AMI. The AMI could be causing the flu like symptoms which in turn are causing the hyperkalemia. I really feel that the AMI is the main problem with the hyperkalemia as an underlying issue.