Mechanism of action
Dexmedetomidine is a selective a2-adrenoceptor agonist. I like to think of it as an intravenous version of clonidine. As a sedative, dexmedetomidine is unique in that it:
1. Does not suppress the respiratory center
2. Acts as an analgesic adjunct, reducing the dose of opioids required
Despite having recently been made available as a generic medication in the US, dexmedetomidine has the highest drug cost when compared to propofol or midazolam.
Dexmedetomidine commonly causes bradycardia and hypotension at rates that are similar to those of propofol. I’ll avoid its use if the patient is already severely hypotensive or bradycardic.
As I discussed in episode 27, dexmedetomidine may occasionally be associated with drug fever.
In most cases I recommend starting dexmedetomidine at 0.5 to 0.8 mcg/kg/hr. If the patient has a high RASS score and adequate cardiovascular reserve, a higher starting dose may be used.
Although some references discuss a loading dose of 1 mcg/kg IV over 10 minutes, I can’t remember the last time I recommended this. The risk of bradycardia from dexmedetomidine may be significantly higher when a loading dose is used. The risk is almost never worth the few minutes of faster sedation that a loading dose provides.
Without a loading dose, the peak effect of dexmedetomidine is within 15 to 30 minutes. Because of this I don’t adjust the rate of dexmedetomidine any more frequently than every 30 minutes. Faster adjustments can lead to overshooting the RASS target and hypotension.
My institution’s maximum rate for dexmedetomine is 1.4 mcg/kg/hr. Very rarely, we may exceed this maximum when other sedatives are not indicated, as I discussed in episode 18 in the section on high dose dexmedetomidine infusions.
Overall cost savings
Dexmedetomidine use is cited as allowing for reduced overall ICU costs due to a lower incidence of delirium when compared with midazolam. Such analyses appear to be manufacturer funded.
I wouldn’t expect that simply using dexmedetomidine in place of midazolam would allow such savings to be realized.
In the study this cost-savings is based on, patients received frequent and generous amounts of fentanyl and breakthrough midazolam.
Fentanyl was allowed to be given 0.5-1 mcg/kg IV every 15 minutes prn pain.
Midazolam was allowed to be given 0.01-0.05 mg/kg IV every 10 minutes prn until the target RASS was achieved.
Such adjunctive medication use is no doubt an essential part of the study protocol and this would need to be duplicated as well if one were to hope to realize the same level of cost savings as reported in the manufacturer’s analysis.
In addition to continuous sedation, dexmedetomidine can be used to facilitate weaning from the ventilator.
The lack of respiratory depression from dexmedetomidine is a significant advantage in this scenario. An ideal patient for such use would be someone who’s anxiety and agitation would otherwise prevent them from successfully weaning from the ventilator.
In this case I would start with a lower dose of 0.4 mcg/kg/hr, and attempt weaning after about 2 hours at this dose.
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