Dexmedetomidine is able to sedate patients to a state similar to non–rapid eye movement sleep. It also has some advantages over propofol because it causes less respiratory depression or decreases in upper airway tone.
I am unfamiliar with central apnea with the use of dexmedetomidine in patients without underlying central apnea patho- physiology. Anecdotal (my personal) experience doesn’t support Central apnea.
Dear Dr. Alicino, as stated by you and Dr. Smith, central apnea is not expected with dexmedetomidine however, in my country we say "There are no illnesses but there are patients". Each patient may respond in a different manner to every drug. Moreover any comorbidities as OSA may trigger apnea in a patient receiving dexmedetomidine.
You are correct in your statement although you are answering a question of your own mak not the question posed in this thread. A severe sleep apnic at a dinner party will obstruct during an after dinner nap. But that has nothing to do with this question.
I know of no central sedative free of apnea - patient factors and dose play a major role and therefore close monitoring is necessary when sedatives are used for anesthesia care
Dex is an alpha 2 agonist works on LC and mimics natural sleep even with high doses 2-4 mck/kg/h. Apnea should not occur . in my experience at least with children we used this novel sedative agents for thousands of procedural sedation and so far did not experience central apnea.
now regarding the airway tone with dex the reflexes of upper airway muscle dilators are close dex induced sedation as measured recently in patients with down syndrome with obstructive sleep apnea . This means dex will not improve the upper airway tone but in the mean time will cause airway collapse compared to natural sleep.
Christopher Smith, I answered the question above as it is posted; that in higher dose ranges apnea occurs. Research shows that Dex has less propensity to cause respiratory depression and that it better preserves airway tone but it does not mean that it DOES NOT (caps for emphasis, am not shouting :) ) cause apnea. As I have said, I have seen it happen.
The point is, as a Clinician (not as a researcher), apnea is a possibility for all hypnotic-sedative drugs; how many times have research data failed us in our expectations?
Your point was clear, as I previously stated. The question asked “central apnea” Your answer was broader. I agree with your points: 1. OSA patients May obstruct (severe OSA - Will obstruct).
2. Bench Research does not always inform clinical practice (Forgive me for paraphrasing)
One Germaine point is that we can more easily treat OSA apnea (clinically) than central apnea. If dexmedetomidine was causing central apnea, WE (anesthesia community) would probably not be using it clinically. IMHO.
interesting I have seen central apnea with rapid bolus of ketamine (2 mg/kg) in neonates but have never seen apnea in neonates, infants or adolescent who received dex in our practice.
We introduced dex relatively recently in our ITU and HDU areas,after a trial period and development of a fairly strict dosing protocol,and havent seen any instances of apneoa thus far.
Whilst this is not to say it could not possibly occur,it does emphasize that a tightly controlled dose regime may mitigate risks either from central or other causes.
Not a major concern when used within therapeutic ranges (effect-site concentrations between 0.5 and 2.5 ng/mL - Hannivoort model - DOI 10.1097/ALN.0000000000000740). There are always concern about interaction with other drugs but even when remifentanil is added it looks that there are no problems (doi: 10.1097/ALN.0000000000002882).