Hello, I came across this paper today and I think it is very important regarding the dangers of the fentanyl analogs.
Basically rapid administration of fentanyl can cause "wooden chest syndrome", which is a failure of diaphragm and upper airway muscles.
This effect is not mediated by mu opioid receptors (anesthesiologists deal with this via anti-nicotinic parylitics). This occurs at dosage levels that would not produce death by respiratory depression alone. Morphinan opioids do not produce this effect at recreational dosage levels.
This effect occurs 1-2 minutes after injection and lasts for 8-15 minutes. This can synergize with the respiratory depression effects of fentanyl, making what would be considered a sub-lethal dose into a lethal dose.
Worst thing is this effect is not responsive to naloxone or other mu opioid antagonists. It also complicates recussitation via cpr.
This effect looks to be mediated by both alpha 1 adrenergic receptors and nicotinic acetylcholine receptors. Unfortunately, pre medication with antagonists of either receptor would increase respiratory depression.
The best way to avoid this syndrome seems to be slow administration of the dose, as it is both dose and rate dependant.
This is another good reason to avoid fentanyl containing preparations as it seems unique to this class of opioids (though i would not assume it doesn't happen with other ultra strong opioids such as the nitazenes, until data indicates otherwise).
From article:
Noradrenergic mechanisms in fentanyl-mediated rapid death explain failure of naloxone in the opioid crisis
I'm stickying this thread because I think it has extreme harm reduction value.
Basically rapid administration of fentanyl can cause "wooden chest syndrome", which is a failure of diaphragm and upper airway muscles.
This effect is not mediated by mu opioid receptors (anesthesiologists deal with this via anti-nicotinic parylitics). This occurs at dosage levels that would not produce death by respiratory depression alone. Morphinan opioids do not produce this effect at recreational dosage levels.
This effect occurs 1-2 minutes after injection and lasts for 8-15 minutes. This can synergize with the respiratory depression effects of fentanyl, making what would be considered a sub-lethal dose into a lethal dose.
Worst thing is this effect is not responsive to naloxone or other mu opioid antagonists. It also complicates recussitation via cpr.
This effect looks to be mediated by both alpha 1 adrenergic receptors and nicotinic acetylcholine receptors. Unfortunately, pre medication with antagonists of either receptor would increase respiratory depression.
The best way to avoid this syndrome seems to be slow administration of the dose, as it is both dose and rate dependant.
This is another good reason to avoid fentanyl containing preparations as it seems unique to this class of opioids (though i would not assume it doesn't happen with other ultra strong opioids such as the nitazenes, until data indicates otherwise).
From article:
Noradrenergic mechanisms in fentanyl-mediated rapid death explain failure of naloxone in the opioid crisis
I'm stickying this thread because I think it has extreme harm reduction value.
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