الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
S
edation in the intensive care unit Patients is assumed to reduce discomfort from care interventions, increase tolerance of mechanical ventilation, prevent accidental removal of instrumentation, and reduce metabolic demands during cardiovascular and respiratory instability. Long-term sedation may have serious adverse effects, such as prolonged mechanical ventilation, coma, delirium, delusional memories and posttraumatic stress disorder, impaired cognitive function, prolonged hospitalization, increased costs, and mortality. Daily sedation stops, sedation protocols, spontaneous breathing trials and early mobilization may help reduce these complications. Optimal sedation strategy in the critically ill should achieve effective analgesia, targeted sedation and reduced risk of delirium and agitation.
Decreasing the duration of mechanical ventilation and length of stay in the ICU can have a significant effect not only on the recovery period of a patient but also financially. Studies have confirmed that agitation can have a deleterious effect on patients by contributing to ventilator dysynchrony and an increase in oxygen consumption, situations that can lengthen the duration of mechanical ventilation. The use of sedatives is essential in the ICU.
Patients receiving assisted mechanical ventilation (MV) commonly require sedation to optimize tolerance to the endotracheal tube and to better adapt to the ventilator, thus decreasing stress response, anxiety and discomfort. Use of sedation to optimize the patient-ventilator interaction can help avoid prolongation of MV and intensive care unit (ICU) length of stay as well as an increased need for tracheostomy.
For several decades, γ-aminobutyric acid receptor agonists (including propofol and benzodiazepines) have been the most commonly used sedatives for critically ill patients, including those receiving assisted MV. During assisted MV, patient-ventilator interaction is influenced both by machine settings and by the patient’s respiratory pattern, timing and drive. These are directly affected by sedatives, whose effects vary, depending both on the drug used and on the dose administered.
This study showed that dexmedetomidine can help reduce duration of mechanical ventilation and number of days in the ICU. Because dexmedetomidine facilitates a cooperative sedation, weaning from mechanical ventilation can be started sooner, and patients are able to cooperate with physical therapy while communicating their needs. Both of these factors are important in recovery, which can be hastened when a patient is alert. Dexmedetomidine is as effective as propofol and midazolam for sedation of critically ill patients. In this study, patients receiving dexmedetomidine were calm, in stable hemodynamic status, and able to participate in the weaning process more quicker than were patients given midazolam or propofol.
Dexmedetomidine, when compared to conventional sedatives and opiates, has been demonstrated to be associated with both sedative and analgesic sparing effects, reduced delirium and agitation, minimal respiratory depression and predictable and desirable cardiovascular effects. In the intensive care setting, dexmedetomidine has been effectively used in postoperative analgesia and sedation of high risk and complex surgical patients, and during transition from other conventional sedatives. Critically ill patients requiring ventilation for more than 24 hours and patients who experienced emergent agitation and or delirium have also been successfully managed with a dexmedetomidine regimen.
Dexmedetomidine infusion has dose dependent central nervous system and cardiovascular system effects with bradycardia and hypotension as the commonest side effects. It produces a state of sympatholysis, central sedation with significant synergy with other sedatives and analgesics. Withdrawal or addition of conventional sedatives and analgesics can be used to fine tune the desired sedation target and achieve optimal analgesia. There is no need to stop dexmedetomidine infusion prior to extubation. Withdrawal of dexmedetomidine was not associated with any nervous or cardiac manifestations of withdrawal.