Fig: Midazolam
When compared to placebo, Dexmeditomidine decreased the required for
intravenous propofol or intravenous midazolam to achieve and/or maintain
optimal sedation in post-surgical patients in an intensive care unit. On
the other hand, Dexmeditomidine patients were significantly more likely
to achieve and maintain optimal sedation without the requirement of
rescue sedation. Additionally, dexmedetomidine’s effect on total
morphine dosage was effective, with Dexmeditomidine recipients requiring
less than placebo recipients, as was its effect on the PMI, with
Dexmeditomidine recipients exhibiting greater apparent calm and being
easier to awaken, as well as a greater tolerance for the endotracheal
tube, ventilators, and the ICU.
Adult patients undergoing AFOI or undergoing a variety of diagnostic or
surgical procedures requiring MAC tolerated intravenous Dexmeditomidine
well. Midazolam rescue sedation rapidly reduces during Dexmeditomidine
administration. Although Dexmeditomidine is generally indicated for
infusions lasting fewer than 24 hours, intensive care patients may
require longer sedation. Dexmeditomidine has been shown to be useful in
the intensive care setting for longer-term sedation of mechanically
ventilated patients in recent published studies; findings from
subsequent trials will be eagerly awaited. Dexmeditomidine has also been
examined as an adjunct to general anesthesia in bariatric and
cardiovascular surgery, among other operations; however, their
discussion is beyond the scope of this article.
There are currently no pharmacoeconomic studies on intravenous
Dexmeditomidine as the primary sedative in mechanically ventilated
patients in a critical care setting or for procedural sedation in
non-intubated patients where the infusion duration was less than 24
hours. In a cost-cutting study of mechanically ventilated patients
treated for more than 24 hours, Dexmeditomidine was found to have much
lower ICU expenses than midazolam. This was mostly due to decreasing
expenditures associated with ICU stays and mechanical ventilation. The
cost-effectiveness of Dexmeditomidine over a period of up to 24 hours
must be established through comprehensive pharmacoeconomic research.
Excessive intravenous Dexmeditomidine administration was often well
tolerated in mechanically ventilated intensive care patients and for
procedure sedation in non-intubated subjects (section 5). Users of
Dexmeditomidine frequently experience hypotension and bradycardia as
adverse effects. In mechanically ventilated patients in a critical care
setting, Dexmeditomidine users suffered greater hypotension than placebo
users, while Dexmeditomidine users experienced more bradycardia.
Frequently, the symptoms of hypotension and/or bradycardia resolve
without the need for medication. According to US prescribing guidelines,
Dexmeditomidine infusion can be lowered or discontinued, intravenous
fluids increased, lower extremities elevated, and pressor agents
utilized if intervention is necessary. Anticholinergic medicine should
also be considered for patients with bradycardia. Dexmeditomidine may be
particularly beneficial for certain patients, as seen by the studies’
findings of lowered blood pressure and heart rate (e.g. mechanically
ventilated patients in an intensive care setting who are at high risk of
postoperative cardiac complications). Transient hypertension was
observed in clinical trials.
The loading dosage of Dexmeditomidine should be provided over a
ten-minute period. When delivered rapidly through intravenous or bolus,
Dexmeditomidine has been associated with clinically severe episodes of
bradycardia and sinus arrest. As a result, dexmedetomidine’s usage in
critically ill patients in need of rapid sedation could be reduced (e.g.
agitated patients who are attempting to self-extubate) (e.g. agitated
patients who are attempting to self-intubate).
Dexmeditomidine was not associated with respiratory depression. Due to
the absence of respiratory depression, Dexmeditomidine may be used in
some patient groups, such as the extremely obese. The absence of
respiratory depression observed in Dexmeditomidine-treated mechanically
ventilated patients may also translate into improved weaning and
extubation durations. Although there were no significant differences in
weaning and extubation times between Dexmeditomidine and placebo
participants, these studies were not designed to examine these outcomes.
It would be interesting to see additional research focused on these
results.
To summarize, intravenous Dexmeditomidine offers effective sedation in
patients requiring mechanical breathing while simultaneously providing
effective procedural sedation in the critical care unit. Additionally,
it reduces the requirement for rescue sedation with intravenous propofol
or intravenous midazolam. Dexmeditomidine sedation is also an effective
alternative for people who are easily arousable and manageable.
Intravenous Dexmeditomidine is generally well tolerated for mechanically
ventilated patients and for procedure sedation in non-intubated
patients. Delirium following surgery is less likely with Dexmeditomidine
than with midazolam or propofol, and there is no indication that this
medicine causes respiratory depression. While Dexmeditomidine
administration is associated with hypotension and Bradycardia, these
adverse effects frequently resolve spontaneously. Intravenous
Dexmeditomidine can be administered as a short-term (less than 24 hours)
primary sedative for patients who are mechanically ventilated in
intensive care and non-intubated adult patients.