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It comes down to awareness. If someone is on 100 mcg/kg/min of propofol, their higher CNS is essentially shut off, so they aren't experiencing anything. Of course they may show objective signs of sympathetic discharge as a result of a noxious physiologic stimulus such as an injury or a ETT moving around in their trachea, but that is not the same as feeling pain.Not to continue dragging this off topic, but that's not something that I was aware of. Do you have any links or can you point me in the right direction to read more about this? When I have patients who are sedated/unresponsive I don't want them to be in pain (hence, the prophylactic pain management), but I also don't want to be giving them pain meds if the science states that it's not necessary. Pain management is a pretty important topic to me, so any info you have or any direction you can point me in I'd be interested in!
What happens though, is that we give some fentanyl or morphine to these folks and their HR and BP drop and we think "his tachycardia went away because he's feeling less pain now", when in reality his tachycardia went away because we just increased his depth of sedation by adding another GABA agonist, and also interrupted the reflex loop that was causing the sympathetic stimulation. Opioids act on receptors in the ascending spinal cord tracts to interrupt the afterrent side (as well as the efferent side, esp when you use large doses) of the reflex loop, which propofol and benzodiazepines don't do.
Again, there are good reasons to use opioids for sedation, but not really to make someone more "comfortable".
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