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The α-2 adrenergic agonist dexmedetomidine (DEX) continues to become more widely used for sedation and general anesthesia due to its sedative and analgesic effects primarily attributed to its actions on the locus coeruleus in the brainstem and suppressed pain signal transmission in the spinal cord, respectively. Sedation with DEX mimics physiological sleep and triggers less respiratory depression. 1 , 2 DEX is also frequently used in elderly patients as it may help prevent postoperative delirium. 3 However, DEX suppresses the sympathetic

Dentists routinely use added low-dose epinephrine to prolong the duration and efficacy of dental local anesthesia. However, epinephrine may produce unwanted hypertension and tachycardia, particularly in those with cardiovascular compromise. Therefore, alternative vasoconstrictors added to dental local anesthetics would be desirable. Dexmedetomidine (DEX) is a selective α 2 -adrenoreceptor agonist used for intravenous procedural sedation and sedation of intubated patients in intensive care units. It has recently been reported that DEX

Indications for dexmedetomidine hydrochloride include sedation during artificial respiration and after extubation in patients in whom early extubation is possible under intensive care. 1 Its sedative actions resemble physiologic sleep, 2 and respiratory depression is less marked; this differs from the features of benzodiazepines and propofol, which have been used in the dental field for psychosedation. It has been reported that this agent causes cardiovascular and psychiatric/neurologic side effects such as hypertension and bradycardia. 1

Alpha-2 (α-2) adrenergic receptor agonists were first used as nasal decongestants but soon were valued for the treatment of hypertension and withdrawal symptoms. The sedative and amnesic qualities of clonidine, the prototypic representative of this drug class, fueled interest in its use as an anesthetic adjuvant. It was also quickly noted that, at sedative doses, the normal respiratory drive was unaffected when administered as an intravenous infusion. 1 – 3 Dexmedetomidine (Precedex, Abbott Laboratories), the pharmacologically active

patients are unable to respond during sedation. In recent years, dexmedetomidine (DEX), a newly developed drug, has been used clinically for sedation in intensive care units. This agent is said to have a less respiratory depressive effect compared to other existing sedative drugs. 1 , 2 The most distinctive characteristic of DEX is the high quality of its hypnotic action. Specifically, unlike existing sedatives, it has been described as inducing a state that is close to physiologic sleep, but allowing full awakening with stimulation. 3 The use of DEX for sedation

Administration of dexmedetomidine (DEX) is associated with the onset of bradycardia, biphasic blood pressure responses (brief hypertension followed by hypotension), and other cardiovascular complications. 1 – 4 Cardiovascular agonists must be appropriately used for treatment in the event of such issues. However, literature regarding ventricular tachycardia (VT) caused by cardiovascular agonists in patients under DEX-induced sedation is scarce. We present the case of a patient who received intravenous (IV) ephedrine to treat low

nausea and vomiting, and emergence delirium. 1 Many of these side effects are dose dependent. 1 , 2 It is common practice at our institution to coadminister IM ketamine with midazolam to reduce the ketamine dose, and, therefore, the incidence and severity of ketamine-related negative side effects. Dexmedetomidine, a centrally-acting α 2 adrenergic agonist with sedative and analgesic properties, is most frequently administered intravenously. However, alternative routes of administration, including oral, 3 intranasal, 4 and IM 5 have been reported

to address these concerns. 7 Dexmedetomidine (DEX) is a selective α-2 agonist used for sedation during mechanical ventilation and after ventilator weaning in intensive care unit postoperatively and for sedation during minor surgeries as well as prevention of emergence agitation due to its analgesic, anxiolytic, and sedative effects, accompanied by only mild inhibitory effects on respiration. Compared with PRO or MDZ, DEX has a smaller inhibitory effect on respiration, and its use in pediatric patients has recently increased. 8 MDZ, on the other hand

available in combination with either 1:100,000 or 1:200,000 epinephrine concentration. Because articaine exhibits lower cardio-depressant and vasodilator activity than lidocaine, 2 articaine can be combined with lower dosages of epinephrine than those used with lidocaine. However, the quantity of epinephrine used in most dental local anesthetics causes a transient minimal elevation in blood pressure as well as modest tachycardia. Dexmedetomidine (DEX), a selective α 2 -adrenoreceptor agonist, has been reported to increase the duration of analgesia in a dose

Dexmedetomidine (Dex) is a sedative and analgesic agent that acts through an α 2 -agonist effect. 1 In Japan and the United States, it is licensed as a sedative agent for intensive care unit (ICU) sedation after surgery. The effects of α 2 -agonists have been associated with reduced anesthetic requirements and attenuated blood pressure and heart rate in response to stressful events. 2 – 5 The α 2 -receptors within the spinal cord modulate pain pathways, thereby providing some degree of analgesia. 6 – 8 In addition, Dex induces a sedative