As opposed to completely rehashing the previous post, here is the link if you need to read it: Sick dude.
It was fairly obvious to me, as well as to most of you I am sure, what this gentleman’s problem was from the outset. He was lots of things, but most notably, hypotensive, bradycardic, hyperkalemic, and hypoglycemic. Without having a serum K+, and just by looking at his ECG, I guessed a K+ around 7.
What I found to be interesting was the lack of the pacemaker firing, even though the LP15 sensed something on all the ECGs.
Frankly, I think the LP15 is making it up, because I don’t see a darned thing where it says there should be pacer spikes. When you get over my masterful skills in cutting and pasting, if you happen to see any spikes, please point them out.
But, his heart rate is 50, why isn’t the pacemaker working? Shouldn’t the pacer be set at a rate of 70 or so?
Why is he so hyperkalemic? He doesn’t look that sick to be this sick.
There are a bunch of things going on in my head here, while everyone else is devising a plan to move this guy to our stretcher. I know what my treatment for him is going to be, but I want to know why he is this sick to start with. Let me give you a more detailed list of meds:
- Ranitidine 150mg b.i.d.
- Doxazosin 4mg b.i.d.
- Norvasc 5mg q.d.
- Atenolol 50mg b.i.d.
- Lasix 40mg q.d.
- Warfarin 0.5mg q.d.
- Neurontin 600mg q.d.
- Potassium chloride 20 mEq packet q.d.
- ASA 325mg am
- Lisinopril 40mg q.d.
- Lipitor 40mg q.d.
- Plavix 75mg q.d.
- Metolazone 2.5mg q.d.
- Nitroglycerin 0.4mg tablet PRN
- Metformin 850mg b.i.d.
Lisinopril is an ACE inhibitor, and potassium is, well, potassium. Common risk factors for hyperkalemia are renal insufficiency, potassium supplementation, ACE inhibitor usage, and excessive consumption of a potassium diet. I didn’t enquire into the patient’s diet for the past few days, though admittedly I probably should have.
I was pretty confident we were dealing with hyperkalemia.
So we have a pretty good idea why he is hypotensive (vomiting and diarrhea) and hypoglycemic (vomiting, diarrhea, and lack of food intake), but why isn’t the pacer working?
From “Hyperkalemia induced failure of atrial and ventricular pacemaker capture” Int J Cardiol 2005 Nov 2;105(2):224-6.;
“a mild to moderate increase in serum potassium causes an increase in myocardial excitability, but further increase leads to impaired myocardial responsiveness, including that to pacing stimulation. Hyperkalemia has been reported to cause failure of atrial capture due to pacemaker exit block.”
Fair enough. So we have a fairly good idea why the pacer isn’t working. The gentleman became nauseous and experienced diarrhea, causing his hypoglycemia and hypotension, which led to renal insufficiency, which led to increased potassium retention and decreased urine output, which led to hyperkalemia, which led to his pacemaker failure, which led to his bradycardic rhythm, which led to him feeling like crap, which led to the 911 call, which led to me being in his house, which led to the case, which led to the blog. And on and on and on.
What I did for this gentleman was administer a large fluid bolus, almost 2 liters, of Dextrose 5%. Having a fairly good idea what was wrong with this gentleman, I decided that immediate transport to the closest hospital, as opposed to his preference, which was a good 45 minutes away, was in order.
I returned to Local Hospital several hours later, and discussed the case with the nurse who was taking care of the patient. She gave me the lab report, the most pertinent of which are below:
- RBC 3.95
- WBC 16.7
- K+ 7.7
- Lactic acid 11.2
- Hemoglobin 12.2
- Hematocrit 37
- Na 118
- Creatinine 16.4
- BUN >150
Most notably, this guy’s kidneys ain’t working.
Nurselady informed me the doctor had ordered calcium, bicarb, glucose and insulin. He was not given kayexalate due to his diarrhea. I didn’t ask about the doses of each. He was given a Foley, and 4 more liters of fluid through his IV.
In two hours, he had a urine output less than 50 milliliters.
Renal failure for sure.
I’ve always known the most important thing we can do for our patients is to get them to a hospital. But knowing why they are as sick as they are is also important to me, and I imagine to a large portion of EMS in general.
I will do some more awesome cutting and pasting with the 12-leads for the next post.
Yeesh.
When the lactate is almost as high as the hemoglobin, you are sick!
I have to admit, I don’t know too much about lab values, “just enough to get me in trouble,” as my mother would say.
Are you seeing anything that I haven’t pointed out, or is there something you would have done differently? I’m always interested in other opinions.
Lactic acid is, basically, a “how sick” test. Over 2 is abnormal, and > 4 gets you in the ICU. When the level is > 10, you bring the chaplain in with you to talk to the family!
He needed that large bolus and the dextrose bad, and likely kept him from arresting on you. Possibly the dextrose provoked some endogenous insulin release as well, and dropped the K+ somewhat.
We give a bunch of drugs for hyper-K+ in the ED, but the key one for EMS is calcium. It’s the only one that works in the prehospital time-frame, and you can see the effects on the ECG very quickly. Don’t know what your protocols are, but our medics have to call for calcium. For a patient with wide-complex bradycardia and teneted T-waves, I hope med control would agree to a gram or 2.
“For a patient with wide-complex bradycardia and tented T-waves, I hope med control would agree to a gram or 2.”
I would hope so, too. But the reality is that med control rarely approves anything these days. They much prefer us to bring the patients to them instead of starting treatment enroute.
Brooks, that is a workable scientific statement. I shall remember it.
One of the worse types of patients to manage prehospital or in the hospital for that manner. I would take about any type of patient over a hyperkalemic, renal failure patient any day.
I’m curios to know what the LP was seeing also. My first thought when I saw it was you bumped the sync button but, that probably would have been marking the T waves also. Very interesting.
I haven’t used the sync on the 15 yet, only on the 12. If I remember correctly, the 12 put a triangle on the peak of the R wave.
He was sick, that’s for sure. Thankfully, the hospital was close, and they are competent people there.
There is a lesser known sign that the GE Marquette 12SL algorithm has when faced with hyperkalemia known as Littmann’s Sign. This is when it double counts QRS complexes due to peaked T-waves. It would be interesting to know if this happened in this case as the LP15 uses the Glasgow algorithm.
According to the user manual, the LP15 uses the Glasgow algorithm.
Yes, I read the manual.
Don’t judge me.
FIFTEEN MEDICATIONS!
“I’ve always known the most important thing we can do for our patients is to get them to a hospital. But knowing why they are as sick as they are is also important to me, and I imagine to a large portion of EMS in general.”
You, as a paramedic, are going to have no better clue as to what is going on with the patient than any doctor that treats him.
Whoever it is that prescribed those meds to him — or whatever group involved that did not pay attention to what everybody else was prescribing — has made your job impossible. Don’t kid yourself that you could have a clue.
What you’ve outlined are bullets aimed toward specific symptoms that allow complex interactions laid on increasingly complex interactions laid on so-called “side-effects” which, in reality there is no such thing; there are only effects. Your patient was effect laid upon effect laid on effect, ad nauseum.
This patient’s physiology may as well have been a pinball!
How could you possibly determine “WHY” the patient was sick? The WHAT of it was renal failure, but believe me, that ending diagnosis could easily have been the result of the incredibly uncoordinated, scattershot medications issued.
A respected Internist friend of mine makes it quite clear. He says when he gets a new patient, he reduces their total medication load to two to three at most. Why? Because he says, no one can track or predict interactions beyond that number.
Darn you, Bouthillet!
Hahahaha!
Haters gonna hate. Or as I say to Kelly, “You hurt my feeling.”
Excellent grand rounds case study, CCC. I flatter myself that I came to the same conclusion you did, absent actually putting a value on the potassium and my treatment protocol would have been the same as yours absent the D5 because they don’t provide us with D5 any more.
I appreciated firetender’s comment on polypharmacy. My doctor does not permit any patients of his to be presribed by any other doctor. He requires that all prescriptions be called into him and he will prescribe it – so he can always know what his patients are receiving and catch any potential problems.
I’m also intrigued by firetender’s comment on the paramedic not knowing any more than the doctor what is going on but I wonder whether, if we did have a clue, if we could actually get anyone to listen to us or if they’d just start over trying to figure it all out.
Kudos for a great scenario:
I wonder if anyone thought about Metformin toxicity be a large part of this Pt’s problem?
Having seen a similar pt with most of the same meds and signs & symptoms, that coded several times over a 24 hr period. Pt survived with mass infusion of fluids continuous dialysis for 48 hrs to flush system and slow return of renal function over a 7 day period.
Our pt went from 17 meds prior to episode to 4 post release from hospital & is doing very well 1 yr later.
Ed;
Thanks for the input. I never thought of metformin toxicity, but found this: http://www.ncbi.nlm.nih.gov/pubmed/18571361
Very interesting.