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.