PHARMACOKINETICS Administration and AbsorptionĪlthough only licenced for intravenous (IV) use, multiple routes of administration of dexmedetomidine have been described, including oral, intranasal, intramuscular, buccal and as an additive in neuraxial and peripheral nerve blocks. Dosing varies depending on the application however the most common dosing regimen for conscious sedation involves an infusion of 0.2 – 1.4 μg-kg -1-h -1 with or without an initial loading dose of 1 μg-kg -1 over 10 minutes. It is presented as a clear, colourless solution of 100 μg-ml -1 dexmedetomidine hydrochloride, which is usually diluted 2 with normal saline to a concentration of either 4 μg-ml -1 or 8 μg-ml -1. 1 STRUCTURE, PRESENTATION AND DOSINGĭexmedetomidine is the active dextro-isomer of medetomidine, an imidazole compound used as a veterinary sedative and analgesic. Please see the recent tutorial on the use of dexmedetomidine in the ICU (ATOTW 454) for its use in critical care sedation. This tutorial will cover basic and practical pharmacology as well as its clinical applications in the perioperative context. It exerts sympatholytic, analgesic and sedative effects which make it an attractive option for the maintenance of sedation in the intensive care unit (ICU) and for the conscious sedation of adults and children during diagnostic or surgical procedures. Dexmedetomidine has a developing role as an adjunct in regional and neuraxial anaesthesia.ĭexmedetomidine is a highly selective a2-adrenoceptor agonist.Dexmedetomidine can be used as an analgesic adjunct in cases in which opioid-sparing regimes are desirable (eg, bariatric surgery).Due to its sympatholytic, analgesic and sedative effects, dexmedetomidine is an attractive option for premedication and procedural sedation in both adult and paediatric populations.Side effects are dose dependent and include bradycardia and hypotension. Dexmedetomidine exerts its effects via inhibition of noradrenaline release in noradrenergic neurons.Dexmedetomidine is a highly selective a2-adrenoceptor agonist with multiple applications in anaesthesia and intensive care medicine.The bradycardia was certainly from another cause. However 50 mcg/kg/hr is again, nothing for this patient. The propofol isn't "maxed out" either, maybe it is by your unit's policy. It must have been running at 0.3 ml/hr! They probably didn't even get any in there IV lol! It just gets funnier the more I think about it. You can give 15 mcg of fentanyl to a 80 y/o little old lady and she won't blink from it. This patient, having OD'd on narcotics, was so used to them from home that 15 mcg/hr is probably juuuust keeping them from DTs. The only time you'll see a change in hemodynamics when administering fentanyl is if the hemodynamics are being held where they are due to a stress response from patient being in pain. These explanations for the bradycardia are essentially zebras when there was much more likely a horse which caused it.įentanyl does not cause a vasovagal response. I don't believe it was either of the drips. Could fentanyl effect the heart rate with no changes to the blood pressure? I learn and remember things betterįentanyl is preferred because of its ability to attentuate hemodynamic stability but it can stimulate a vasovagal response. I suspect, in this situation, her heart rate had nothing to do with the drips.Įveryone was telling me that it was the fentanyl but didn't understand it. Pt had continued transient asymptomatic bradycardia. Left the fentanyl drip on with ranges of 50 to 75mcg/kg/hr. The next day the discontinued the propofol and precedex drip.
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