"You will kill the patient doing that!!!"

Also, don't suction more then 10 seconds or the patient will suffocate because you've sucked all of their oxygen out. (That one is from class.)

The Intermediate/Paramedic equivalent is this:

You must preoxygenate your patient for two minutes before you intubate. You then have EXACTLY THIRTY SECONDS to successfully tube the patient. If you don't do it in thirty seconds, reoxygenate for another two minutes OR YOUR PATIENT WILL SUFFOCATE AND DIE A HORRIBLE DEATH AT YOUR HANDS.
 
Non cardiogenic shock as in septic shock, for example, as opposed to "I have a knife in my belly" shock? It doesn't sound unreasonable for the first, somewhat horrific for the second!

The Cardiogenic Shock protocol allows for a modest fluid bolus for presumed rt sided failure, to increase preload. Non Cardiogenic Shock covers basically any other condition that presents with symptomatic hypotension, such as sepsis, the inbleed, multitrauma, dehydration, neurogenic, etc. Vasovagal syncope usually self corrects, so fluids would be unwise in that situation. Obviously, the 3&3 is intended for the trauma pt. N.C.S. is a catch-all for all non-cardiac causes of hypotension.
 
The Intermediate/Paramedic equivalent is this:

You must preoxygenate your patient for two minutes before you intubate. You then have EXACTLY THIRTY SECONDS to successfully tube the patient. If you don't do it in thirty seconds, reoxygenate for another two minutes OR YOUR PATIENT WILL SUFFOCATE AND DIE A HORRIBLE DEATH AT YOUR HANDS.

It's been proven that w/ a healthy adult in their 30's give or take, that they can knock out their respiratory drive, and then wait for several minutes or more before they de-sat. The elderly peri-arrest pt with limited physiological reserve will de-sat much quicker, but certainly not to a great degree in those magical thirty seconds, especially if they were pre-oxygenated either w/ ETI, a King, or good BVM w/cric pressure. IIRC, the oxygen dissociation curve begins to gain momentum below 80% or so, and is more or less a freefall below 60%.

Edit: Found it!

http://www.ccmtutorials.com/rs/oxygen/page06.htm
 
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It's been proven that w/ a healthy adult in their 30's give or take, that they can knock out their respiratory drive, and then wait for several minutes or more before they de-sat. The elderly peri-arrest pt with limited physiological reserve will de-sat much quicker, but certainly not to a great degree in those magical thirty seconds, especially if they were pre-oxygenated either w/ ETI, a King, or good BVM w/cric pressure. IIRC, the oxygen dissociation curve begins to gain momentum below 80% or so, and is more or less a freefall below 60%.

Edit: Found it!

http://www.ccmtutorials.com/rs/oxygen/page06.htm

We discussed that in class. Here's a simple test. Put a pulse-ox on your finger. Hold your breath for as long as you can. See how much the number changes. :P

Still, the National Registry says thirty seconds or else.
 
The Cardiogenic Shock protocol allows for a modest fluid bolus for presumed rt sided failure, to increase preload. Non Cardiogenic Shock covers basically any other condition that presents with symptomatic hypotension, such as sepsis, the inbleed, multitrauma, dehydration, neurogenic, etc. Vasovagal syncope usually self corrects, so fluids would be unwise in that situation. Obviously, the 3&3 is intended for the trauma pt. N.C.S. is a catch-all for all non-cardiac causes of hypotension.

A blanket 3 liters for would be unwise for hemorrhagic issues. That said, it's probably not a bad deal for neurogenic, sepsis ect.

Titrating fluid to target goals (pulses, LOC) is the current thinking, and that may well require 3 liters.
 
It's been proven that w/ a healthy adult in their 30's give or take, that they can knock out their respiratory drive, and then wait for several minutes or more before they de-sat. The elderly peri-arrest pt with limited physiological reserve will de-sat much quicker, but certainly not to a great degree in those magical thirty seconds, especially if they were pre-oxygenated either w/ ETI, a King, or good BVM w/cric pressure. IIRC, the oxygen dissociation curve begins to gain momentum below 80% or so, and is more or less a freefall below 60%.

Edit: Found it!

http://www.ccmtutorials.com/rs/oxygen/page06.htm

Agreed limiting your ETI attempts based on physiologic signs (SpO2 and HR primarily) makes FAR more sense than an arbitrary 30 seconds. Who's to say you don't start to get hypoxia prior to 30 seconds? Also HOW you preoxygenate a patient makes a difference. Best is an anesthesia bag, however allowing a patient to breathe through a BVM actually works fairly well, they're simply able to entrain some room air in addition to the O2.
 
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A blanket 3 liters for would be unwise for hemorrhagic issues. That said, it's probably not a bad deal for neurogenic, sepsis ect.

Titrating fluid to target goals (pulses, LOC) is the current thinking, and that may well require 3 liters.

I know, the protocol says "up to two liters."
 
I'd like to remind everyone of the hemoglobin dissociation curve, ie by the time that the patient has de-saturated you're pretty far down in PO2. So the goal shouldn't be "try intubating till the sats drop" because then that's pretty late.

Sure 30 seconds is a bit random, but you need to build a safety factor into what is being taught because there will always be those people who when aiming for 30 seconds take a minute. If everyone thinks they can really go 2 minutes, some will take 3 etc.

Speaking of killing patients, intubating Aspirin overdoses is a good way to kill your patient.
 
I'd like to remind everyone of the hemoglobin dissociation curve, ie by the time that the patient has de-saturated you're pretty far down in PO2. So the goal shouldn't be "try intubating till the sats drop" because then that's pretty late.

Sure 30 seconds is a bit random, but you need to build a safety factor into what is being taught because there will always be those people who when aiming for 30 seconds take a minute. If everyone thinks they can really go 2 minutes, some will take 3 etc.

Speaking of killing patients, intubating Aspirin overdoses is a good way to kill your patient.

The problem is the curve is so individualized to a patient there's no way to apply it in the clinical setting. I've had patients desat as soon as I stuck the blade in their mouth (far less than 30 seconds) and some that never moved off 100% through a 2+ minute intubation. The rest if medicine uses 92% as a cut off, which equates to VERY mild, reversible hypoxemia. Your safe as long as your using this.

Intubating ASA overdoses is not what kills them. SIMV at a rate of 10, tidal volume of 500mls and thinking an EtCO2 of 40 is hunky dory is what kills them.
 
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I'd like to remind everyone of the hemoglobin dissociation curve, ie by the time that the patient has de-saturated you're pretty far down in PO2. So the goal shouldn't be "try intubating till the sats drop" because then that's pretty late.

Sure 30 seconds is a bit random, but you need to build a safety factor into what is being taught because there will always be those people who when aiming for 30 seconds take a minute. If everyone thinks they can really go 2 minutes, some will take 3 etc.

Speaking of killing patients, intubating Aspirin overdoses is a good way to kill your patient.

I would hope that it would be understood that a pt w/ a low sat, or no reading if down for a while would necessitate some pre-oxygenation and a quick tube. The reason I brought up the curve was to show that when you get below 90, and definitely below 80, you're behind the 8-ball and shouldn't be tooling around. This goes for any sick pt, not just someone needing intubation. I've had a COPD pt go from 82% to the 50's in the half a minute or so I took to drop the tube, confirm it, etc. The junctional braycardia didn't help matters either.
 
picked up a CHF'er at a local SNF the other day, lungs were real wet. the RN said their pt had flash pulm edema and their BIPAP wasnt workin. i told her we were going to put the pt on our CPAP, at which time the RN informed me that CPAP wouldnt do anything for the pt, and i HAD to intubate her right now! and according to her i was wasting my time with SL nitro

mind you this pt was currently sitting up, self supporting in bed (they didnt have the forethought to raise the head of the bed), CAOx4, and while in resp distress, able to answer all questions appropriatly. oh, she was also had an SPO2 of 97% on the NRB they had her on.

if i had done everything that nurse wanted me to do, that pt probably would be dead.
 
picked up a CHF'er at a local SNF the other day, lungs were real wet. the RN said their pt had flash pulm edema and their BIPAP wasnt workin. i told her we were going to put the pt on our CPAP, at which time the RN informed me that CPAP wouldnt do anything for the pt, and i HAD to intubate her right now! and according to her i was wasting my time with SL nitro

mind you this pt was currently sitting up, self supporting in bed (they didnt have the forethought to raise the head of the bed), CAOx4, and while in resp distress, able to answer all questions appropriatly. oh, she was also had an SPO2 of 97% on the NRB they had her on.

if i had done everything that nurse wanted me to do, that pt probably would be dead.
 
The issue with aspirin OD is the patient will be breathing fast and deep to compensate for their metabolic acidosis. The problem with intubation isn't just that people don't set the vent right (though that doesn't help). It is that:

1: We can't use positive pressure to ventilate for these patients as well as they are doing for themselves, if you matched tidal volumes and rates with what they are doing in these cases you'd be doing quite a bit of barrotrauma.

2: Even the brief amount of time the patient is apenic during the intubation will increase their CO2 to a level that can be quite dangerous.

(The pathophys is that ASA is in the uncharged form more at lower PH, and thereby able to diffuse through cell membranes into the cells from the blood where they are doing the most damage. Keeping the patient alkalotic helps prevent this)

So what I've been hearing on my tox month at the poison control center is for ASA OD is:

1: Avoid intubation if at all possible.
2: Consider awake intubation, ideally using local anesthetic.
3: Don't paralyze the patient (part of number 2)
4: Pre-treat with massive doses of Na bicarb (think 8-10 amps)
5: Consider something like ketamine which will cause less respiratory supression.

Now this is the thinking for tox trained ED physicians, most of these you won't be able to do in the field. But the lesson is that people shouldn't be thinking "it's fine to intubate these patients, I just need to set my vent fast enough." You can still kill people even if you do that.
 
So what I've been hearing on my tox month at the poison control center is for ASA OD is:
1: Avoid intubation if at all possible.

I agree with this point. However, these patients will get intubated and placed on PPV, as they can not sustain the level of respiration we're talking about without failure becoming imminent at some point. Depending on where in the clinical course we contact them determines whether they get intubated by EMS or not.

It is entirely possible to ventilate these patient appropriately and not cause barrotrauma, but perhaps not on most vents EMS has access to.
 
My patient, not my actions. called for UR, Not breathing, CPR going, Arrive, do our medical thing, get pt into the truck, drive to hospital, about 5m out we successfully capture and pace the pt all the way into the code room. As we are giving the report to the RN, a tech walks over and yanks the leads off the pt, asystole, worked him for 4 more minutes, pronounced.

We worked that guy for almost 30m and everyone, ALS, BLS, PD and Fire did a damn good job. I thought the cop was going to tear the techs head off and shove it you know where
 
My patient, not my actions. called for UR, Not breathing, CPR going, Arrive, do our medical thing, get pt into the truck, drive to hospital, about 5m out we successfully capture and pace the pt all the way into the code room. As we are giving the report to the RN, a tech walks over and yanks the leads off the pt, asystole, worked him for 4 more minutes, pronounced.

We worked that guy for almost 30m and everyone, ALS, BLS, PD and Fire did a damn good job. I thought the cop was going to tear the techs head off and shove it you know where

I am not sure how this ties in to the post, but if you worked a guy for 30 minutes, and there was no response, were you expecting a different outcome?
 
In my personal experience, we had a close encounter with disaster when I had a preceptee who had drawn up 2 mLs of Dopamine instead of Ativan for a seizing patient. I should have been checking the vial behind her, but I didn't...the only reason we caught it is because we talked about how thick the Ativan was and how difficult it is to pull up into the syringe. The preceptee said, "No it isn't, it was easy." So we checked the vial and it was dopa. That's when I almost died. She had the syringe in the IV line about to push it when we figured it out.[/QUOTE]


:0 Just think of all the blood pressure that patient would have had....just before he coded! wow
 
My patient, not my actions. called for UR, Not breathing, CPR going, Arrive, do our medical thing, get pt into the truck, drive to hospital, about 5m out we successfully capture and pace the pt all the way into the code room. As we are giving the report to the RN, a tech walks over and yanks the leads off the pt, asystole, worked him for 4 more minutes, pronounced.

We worked that guy for almost 30m and everyone, ALS, BLS, PD and Fire did a damn good job. I thought the cop was going to tear the techs head off and shove it you know where

Wait... He pulled the leads off? So? Do you mean the pads off? How the hell does someone pull pacer pads off while it's pacing?
 
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