Straightforward...or is it?

[Fox800]

Awesome discussion going on in here. I'm a bit short for time but I'll come back and address all of the questions a little later, the parents are coming to visit from out of town.

Initially we were concerned about a PE on top of an opiate OD. The main thing that didn't fit in my mind was the high ETCO2 reading.

The ER MD was also concerned about a PE, that was the main thing going through his mind as they started patient care.

Called the ER a few hours later, the patient was indeed septic with pneumonia, on top of the opiate OD.

 

[Veneficus]

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.

 

[Melclin]

Ventilate sure, if you can without fighting her. But it was already described as not tolerable.

Yeah, thats why I make mention of our closed circuit. Its much easier to tolerate and spontaneously breathe through than a BVM (hence my reluctance about a BVM) and one can also discern spontaneous resps/assist vents, as well as monitor RR and get a rough idea of Vt trends. In the end, I suspect its probably still considerably less desirable in the eyes of the baked pt than lying undisturbed in a comfy puddle of drool.

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.

Fair point.

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.

Do you have to control the rate? Why cant you maintain the hypervent?

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 wasn't aware that compensation like that could go on for so long. Very interesting.

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.

Gotcha.

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.

True. Was it you that had a mentor or lecturer that said something in the order of, "No one ever died from not having a plastic tube in their throat"? I think about that one liner often lately. I feel like I'm a bit quick on the intubation trigger in scenarios. Doesn't matter terribly since I won't be doing it for 4-5 years, but good to consider all the same.

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)

If she arrests then yeah bicarb is up front. Def. Its not even that big a leap, it'd be per guidelines.. sort of.

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.

I'm ganna have to get my hands on a copy of Goodman and Gilman's. Its becoming increasingly apparent to me that my pharm book learning is grossly inadequate.


10char

 

[Veneficus]

Do you have to control the rate? Why cant you maintain the hypervent?

What is the point? She is compensating for metabolic acidosis with increased rate. What would bagging at that rate really do? The body only needs roughly 11% O2 to survive, Room air is usually around 21%

You could increase the partial pressure of o2, but I think if you are going to maintain the rate, what would be the point? If you were going to slow the rate, to say 20-30, you are still degrading the natrual compensation.

True. Was it you that had a mentor or lecturer that said something in the order of, "No one ever died from not having a plastic tube in their throat"? I think about that one liner often lately. I feel like I'm a bit quick on the intubation trigger in scenarios. Doesn't matter terribly since I won't be doing it for 4-5 years, but good to consider all the same.

Yes, it was one of my anesthesia lecturers.

If she arrests then yeah bicarb is up front. Def. Its not even that big a leap, it'd be per guidelines.. sort of.

I think it is the proper clinical decision if you are making them and not being a protocol junky. But you know how the game works in many US systems, bicarb is way down the list. Sometimes even needing an order.

I'm ganna have to get my hands on a copy of Goodman and Gilman's. Its becoming increasingly apparent to me that my pharm book learning is grossly inadequate.

That is a great book.

But it also is how you se your knowledge. You can know there is A1 blockade, but you can also reason in this case there is some opioid induced dilation. Of course you can try to saturate A1 agonists, but you might also get something from removing the opioid. If you were really desperate to increase the BP, you could even pace the pt or add some digoxin But I wasn't thinking that radical. Volume will still be needed.

 

[Melclin]

What is the point? She is compensating for metabolic acidosis with increased rate. What would bagging at that rate really do? The body only needs roughly 11% O2 to survive, Room air is usually around 21%

You could increase the partial pressure of o2, but I think if you are going to maintain the rate, what would be the point? If you were going to slow the rate, to say 20-30, you are still degrading the natrual compensation.

But it also is how you se your knowledge. You can know there is A1 blockade, but you can also reason in this case there is some opioid induced dilation. Of course you can try to saturate A1 agonists, but you might also get something from removing the opioid. If you were really desperate to increase the BP, you could even pace the pt or add some digoxin But I wasn't thinking that radical. Volume will still be needed.

Well put.

Cheers, as always, for taking the time with me

You, Ventmedic (surly though she was) and Usafmedic45 should apply to my uni for a stipend seeing as though you guys are responsible for a considerable portion of my education

 

[boingo]

It would seem this patient could benefit from mechanical ventilation. Her work of breathing requires a huge amount of o2 and energy, both could be better used elsewhere. She is also failing to oxygenate/ventilate, some PEEP would likely come in handy, although with her BP we need to be careful.

 

[Veneficus]

Well put.

Cheers, as always, for taking the time with me

You, Ventmedic (surly though she was) and Usafmedic45 should apply to my uni for a stipend seeing as though you guys are responsible for a considerable portion of my education

Anytime,

you are always welcomed to encourage your uni to pay my way down there to come and speak. I'd be more than happy to make an appearance for travel and lodging.

 

[MrBrown]

Doors open .... hmm looks well clear, clear to ground, illegal Mexicans running away one o'clock low, well clear, skids coming on, load coming off ....

*Brown leaps out and hands Oz his orange "PARAMEDIC" jumpsuit and David Clark headset,

Come quick Oz, now that Brown missed this one he has a chance to redeem himself, she's a go-er, an RTA, persons trapped, Ambulance on scene ....

Ambulance, Medivac airborne