Now he got in touch with the acccepting rn in the er for this patient and per my partner, she stated that he was admitted in the ICU for a metabolic issue, Hyperkelemia.
I went to the medical examiner's office as a paramedic student once, and he made what seemed at the time to be a very controversial statement, "Nobody dies from aspiration". As a group of students we fundamentally failed to grasp his meaning, and got in a long and pointless argument that inevitably ended when the pathologist-medical examiner lost their interest. Both sides left thinking that they had won, but only one was right.
Hyperkalemia may be the admitting diagnosis, but hyperkalemia doesn't just appear by itself. It's caused by something else.
JPINFV has pointed out a number of potential causes. One I'd consider here is that the patient has developed renal insufficiency / acute renal failure, resulting in fluid retention, volume overload, and an inability to excrete potassium. This could cause a CHF exacerbation and some degree of shock and lactic acidosis.
Now what I saw with this patient, assessments, presentation, and understandings. That just doesnt make sense to me. With the increased, rapid, shallow, slightly irregular respirations would prodominently cause respiratory alkalosis, not acidosis-that really needs to occur to cause a severe enough hyperkelemia.
They're only going to get hypocapnic if they have enough perfused lung surface, and enough ventilation to that perfused region to have a net increased excretion of CO2 over time.
They can be as dyspneic and tachypneic as they want, but if there's minimal gas exchange occurring they're not going to blow off CO2.
If the CO2 is low, i.e. there is some degree of respiratory alkalosis, this may be compensating (partially or completely) for an underlying metabolic acidosis. It doesn't have to be the primary disturbance.
You don't need to have respiratory acidosis to have hyperkalemia. A metabolic acidosis will also cause a K+ shift.
I dont doubt that the patient had some metabolic issues secondary to the impending respiratory failure; prolonged pheumonia and CHF. But what I got on my assessment with 12-lead, ETCO2, D-stick, and just pure patient presentation alone, I would lean towards a respiratory alkalosis, poss. HYPOKELEMIA.
We really don't have the tools to assess this on the ambulance. There are 12-lead changes that point to hyperkalemia, e.g.
But even ED physicians are batting at around a 40% sensitivity for detecting hyperkalemia (>5.0 mmmol/L) on ECG changes, and only 60% or so at detecting critical hyperkalemia (>6.5 mmol/L). (Wrenn et al.) [Granted this study is just two docs looking at ECGs, but it gives us an idea of rough figures]. So the ECG's useful, but it isn't always going to tell us the story.
In this study, specificity was around 85%, so there were quite a few patients who weren't hyperkalemic who were labelled as such by the physicians.
Wrenn KD, Slovis CM, Slovis BS. The ability of physicians to predict hyperkalemia from the ECG. Annals of Emergency Medicine 20(11):1229–1232
Im dont doubting that there is a sig. diffusion issue going on. But, im calling BS on that.
BS on what? That your partner's lying / misinformed, that the RN is lying/misinformed, or that the physician or laboratory are lying / misinformed and have incorrectly measured the sample's K+?
If you have a PRIMARY metabolic issue such as hyperkelemia that is severe enough to over take the resp. failure issue, I would lead to believe that the patient would be pretty close to a polymorphic v-tach with some a influx in the interface and electrolyte levels; especially with the increased minute volume and collected increased oxygen demand.
See the ECG changes above, and take a look at some case reports. People can survive with high K+ for quite a while. How do you know that the patient is close to a polymorphic VT before it happens, especially in the field? This patient may have been. The classic electrolyte disturbance associated with this is hypomagnesemia.
Yes, hes old, yes hes severly sick, but that clinical dianoses is crap. And not to treat the underlined issue (respiratory) first with ALS intervention and I dont mean quick intubation, more or less a positive pressure splint of the airways, is foolish.
It's hard to know from a distance based on an internet vignette, but it sounds like CPAP would have been a good idea here.
Now, how could a patient be severly hyperkelemia in presence of respiratory alkalosis.
Because they're acidotic? Because the kidney's are nuked and they're retaining K+ at a greater rate than alkalosis is shifting the K+ intracellualrly? Because they've taken too much K-dur? Ischemic gut? Too much spirinolactone? Not so-benign-anymore prostatic hypertrophy? Renal failure? Overusing their beta-agonist due to the pneumonia / being stupid?
Furthermore, it didnt look like there was a sig. build of of bi-carb and the body was compensating with the increased respiratory drive to aid in blow-off, such as kuasmalls.
Don't take this the wrong way, but think about this a little bit.
It presented in clear cut, good ole, pulmonary edema-impending resp. failure.
But pulmonary edema also isn't a disease in and of itself. It's a sign of a disease. It can be due to volume overload, it can be due to a loss of plasma protein, failure of the LV, mitral valve issues, diffuse injury to the alveolocapillary membrane, lymphatic obstruction, emboli in the pulmonary vasculature, hypertension, inhalation injury, etc.
Like many of our patients, this one had a complex condition / history that was better revealed upon further evaluation by more skilled practitioners in the hospital with the aid of better diagnostic equipment. This is ok -- not every piece of information is available to us in the field, and not all of these problems need fixing right away, or can be fixed in the ambulance.
I do agree that the CPAP sounded like a good idea.
