I appreciate the hat-tip, VPIMedic.
So a well sedated patient, absent a painful injury or procedure is not experiencing pain. This is the point that Halothane is really trying to make, I think. This is true.
That is indeed the main point I was trying to make. Even if there is some nociceptor activation (pain) involved, if they are indeed well-sedated, they should not be
feeling the pain.
Nociceptor activation has two basic effects: 1) it causes an autonomic (sympathetic) response which manifests clinically as tachycardia and hypertension, and 2) it causes an unpleasant conscious experience, which we call pain.
One way to limit the effect of nociceptor activation is to administer opioids which block pain impulse transmission primarily in the spinal cord, keeping the pain impulse from reaching the upper spinal cord, where the reflex sympathetic stimulation is generated, and also from reaching the brain, where the pain experience is generated. Think of giving fentanyl as "blocking the road" that pain signal has to travel up the spinal cord in order to get to the brain.
When you adequately sedate someone, you do nothing to "block the road" that goes up the spinal cord, so the impulse is able to reach the parts of the spinal cord where a sympathetic response is generated. However, sedation shuts down the parts of the brain that turn that electrical "pain" stimulus into an unpleasant experience. This explains why giving fentanyl works so well to blunt the sympathetic response to intubation. It's not that the patient
feels any less - after an adequate dose of propofol or etomidate, they weren't going to
feel the intubation anyway. But the fentanyl blocks the signal much earlier in it's travels towards the brain before it can elicit a sympathetic response.
In addition to blocking pain transmission in the spinal cord, opioids also have sedative effects in the brain (same basic mechanism as etomidate or propofol or versed, just different receptors), and also blunt the respiratory drive.
So when your vent patient on a propofol drip is still breathing against the vent and tachycardic, and you give them 100 mcg of fentanyl and they stop fighting the vent and their HR comes down, it probably isn't because they were
experiencing pain before the fentanyl, it's probably because the fentanyl further sedated them, slowed their respiratory drive, and blocked any sympathetic response that was occurring in response to inadequate sedation. You would likely have had similar results just by increasing the propofol infusion significantly, though there are obviously downsides to that.
As you can imagine, the neurophysiology of all this is actually pretty complex, but this is kind of the down-and-dirty about the differences between using opioids and sedatives for post-intubation patient comfort.
The reason you hear things lately on blogs like EMCrit about how much better "analgo-sedation" is as compared to benzo- or propofol- based sedation, has less to do with short-term patient comfort and more to do with vent weaning and long-term cognitive outcomes of patients who are on a vent for several days or longer. I'm not aware of any studies that show superior patient comfort with a narcotic-based technique, or that the outcomes are affected at all by a very short-term regimen of benzo-based sedation in the prehospital or ED setting.
A post-intubation cocktail of versed
and fentanyl or morphine is a really good way to go. It's simple, safe, and effective, and it covers all the bases and is pretty hemodynamically stable.
But if for some reason your protocols don't allow opioids, or only allow very small doses of them, do not fret about being "cruel" to your patients. As long as you can give adequate sedation (the "adequate" part is important, mind you), your patients are probably not suffering.