Per manufacturer (Hospira), bradycardia, defined as HR 30% reduction from baseline, was reported in 14% of cases. It is eliminated through hepatic metabolism and largely excreted in urine.
Dexmedetomidine is highly lipophilic with rapid distribution and elimination (t1/2 = 2-2.5 hrs). Through its sympatholytic mechanism, it exhibits direct AV and SA nodal inhibitory effect and heightened vagal tone via the baroreflex-mediated parasympathetic activation. The most common side effects of dexmedetomidine are hypotension and bradycardia which are dose dependent. Dexmedetomidine decreases anxiety, and delirium by acting on the locus coeruleus and has the added benefit of having a narcotic sparing effect and furthermore has no respiratory suppression. The routine use of continued infusion of dexmedetomidine can lead to asystole if instigated by common vagal stimulation of the trachea during mechanical ventilation.ĭexmedetomidine is a highly selective central alpha 2 receptor agonist with favorable effects when used for sedation in mechanically ventilated patients. Despite the presence of confounding factors, such as other sedatives and chronotropic medications, it was concluded the main reason for the potentiated vagal response was the presence of dexmedetomidine infusion. Each episode was resolved without intervention. The five patients were mechanically ventilated while receiving dexmedetomidine infusion and experienced periods of brief asystole triggered by vagal stimulation induced by airways suctioning or coughing. These patients were each receiving dexmedetomidine infusion while on invasive mechanical ventilation leading to periods of asystole that resolved after stopping dexmedetomidine infusion in all five patients.
#PRECEDEX DRIP SERIES#
This is a case series of five adult patients obtained from the medical intensive care unit in a community teaching hospital between May 2019 through August 2020. The bradycardia was certainly from another cause.Five adult medical, critically ill patients developed bradycardia leading to asystole while receiving dexmedetomidine infusion. 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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