I suppose a severe aspirin OD as well as some opiates thrown in would fit but (this is probably one of those area dependent things because ASA is fairly rare as a household analgesic here) why would you withhold O2 from a hypoxaemic, hypo-ventilating pt on the off chance (there is no evidence of ASA) she may have taken a six month supply of dad's cardiprin as well? What about the temp? An ASA OD severe enough to cause resp alkalosis but with no elevate temp?
Ventilate sure, if you can without fighting her. But it was already described as not tolerable.
I would not intubate her because of the unreliable history and the already difficult toxicity issues. In my risk/benefit analysis, adding a RSI to a pt who is fairly maintaining the airway prehospital vs complicating the management later doesn't pay. If she wasn't breathing, I would be more inclined to the benefit side, but also consider the hypervent may be a compensatory mechanism to the metabolic acidosis and when you control the rate at 12-20 you are knocking that mechanism out.
To use an experience on how well there can be respiratory compensation, I saw a GCS 3 renal failure patient who had dialysis removed as part of withdrawel of efforts, with textbook Kussmal's resps compensate for 9 days before expiring. My conclusion is that respiratory compensation can be considerable and sometimes beneficial.
I think I was more worried about a combined alkalosis/acidosis from potential mixes when I wrote that up and it just came out focsed on ASA.
Respiratory alkalosis can be caused by more than ASA. But I figure if she was taking the OTC stuff, potentially some alcohol, and the prescription meds that her multifunction oxidases were well saturated along with her conjugation enzymes and she could not excrete if she wanted.
I also figure that chances are good she took something other than the opioids for chronic pain.
If there is some ASA involved and she is progressing to mixed resp/metabolic acidosis with pulmonary odema (?junky lungs), then isn't intubation indicated?
She may at some point be intubated, but it is not an automatic indication, as well in ASA OD, the tox experts I have read feel intubation actually probably harms. But like I said, this is going to be complex. Renal fnction will have to be assessed before diuretics are considered for the edema. I think in this case it is probably caused by the rapid HR and decreased LV filling backing it all up.
Aside from the ASA: I suppose "shallow vents" is subjective, but I picture a person with severely reduced tidal volume, with an elevated end tidal, and reduced SpO2. Surely ventilating them is a good idea. Hypoventilation is bad regardless of whether or not its the primary problem, or on top of metabolic acidosis.
I don't disagree, but in this case, with the toxic issues as well as the harm caused by fighting a noncompliant patient, ventilating and intubating are not one in the same. As I said, the risk/benefit this early in management does not play out well in my mind.
Opiate induced hypoventilation Vs Metabolic acidosis induced hyperventilation. Is there going to be a winner? Or are you going to see an unpredictable merging of affects?
With a RR of 40+/min I think acidosis is winning. I understand that with the increased ATP demands vs. the amount being produced, it is not a good long term solution. But if you "control" ventilation and the systemic or local organ PH is still rising, which without serial labs, will probably be detected prehospitally as coma or arrest, what then? Run the ACLS algorythm and consider hypoxia as a reversible case addressed? How far or who is going to be quick on the bicarb trigger on this one if she does code? (other than me)
I'm still not sold on the naloxone. Her MAP is now 67 after only a litre of fluid. I wanted about 1400, and I'll say now she can have another 1400 (although we'd better keep an eye on these 'junky' lungs of hers). I don't see the benefits of waking up a hypoxic patient (and so probably non-compliant and mildly violent) in resp distress and pain in the hopes that her hypotension (which is now rising to more acceptable levels) is caused by the opiates,
I don't think her hypotension is caused by opiates, I think it is caused by a myriad of other things, one of which being alpha1 blockade and the inability to mitigate its effects in the short term because of failure to metabolize the prozac or now possibly TCA doing it. By eliminating the opioid effect, it can potentially (no promises) act in a vasoconstrictive manner than is potentially not acievable by the other a1 agonist meds. Otherwise with gross systemic afferent arteriole dilation, you are going to need way more than 2800ml of fluid to help. Especially if she is in renal failure or has ATN.
while taking away my MICA backup's ability to tube her if they feel she's indicated as it stands, or if she goes down hill. I think she can wait the 5-10 mins it will take for a rendezvous with MICA and then I'd be more open to narcing her if they decide not to tube. There have been a few jobs like this floating around where naloxone has been considered ill-advised on account of polypharmacy and aspiration.
I am not overly impressed with narcan myself usually, but I think in this case the problem isn't so much the opioid loss of respiratory control, but the polypharm that already exists. The more you add to it, the tougher it becomes.
