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      Effect of intravenous infusion of dexmedetomidine on perioperative haemodynamic changes and postoperative recovery: A study with entropy analysis

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          Abstract

          Background:

          Dexmedetomidine, an α2 agonist, when used as an adjuvant in general anaesthesia attenuates stress response to various noxious stimuli, maintains perioperative haemodynamic stability and provides sedation without significant respiratory depression postoperatively.

          Methods:

          Sixty patients were randomly divided into two groups of 30 each. In group A, fentanyl 2 μg/kg and in group B dexmedetomidine were given intravenously as loading dose of 1 μg/kg over 10 min prior to induction. After induction with thiopentone, in group B, dexmedetomidine was given as infusion at a dose of 0.2–0.8 μg/kg. Sevoflurane was used as inhalation agent in both groups. Haemodynamic variables and entropy (response entropy and state entropy) were recorded continuously. Postoperative sedation and recovery were assessed by sedation score and modified Aldrete's score, respectively.

          Results:

          Dexmedetomidine significantly attenuates stress response at intubation with lesser increase in heart rate (10% vs. 17%), systolic blood pressure (6% vs. 23%) and diastolic blood pressure (7% vs. 20%) as compared to the control group ( P<0.05). Intraoperatively, an average of 8% fall in systolic blood pressure and 8.16% fall in diastolic pressure in the test group as compared to 3.6% rise in systolic and 3.3% in diastolic pressure of the control group was observed. Postoperatively, the test group showed significant sedation at 2 h as compared to the control group ( P=0.00) and recovery was better in the control group for the first 2 h post extubation.

          Conclusion:

          Dexmedetomidine attenuates various stress responses during surgery and maintains the haemodynamic stability when used as an adjuvant in general anaesthesia. Also, the sedative action of dexmedetomidine delays recovery for the first few hours post extubation.

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          Most cited references14

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          The effects of increasing plasma concentrations of dexmedetomidine in humans.

          This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.
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            Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions.

            This research determined the safety and efficacy of two small-dose infusions of dexmedetomidine by evaluating sedation, analgesia, cognition, and cardiorespiratory function. Seven healthy young volunteers provided informed consent and participated on three occasions with random assignment to drug or placebo. Heart rate, blood pressure, respiratory rate, ETCO(2), O(2) saturation, and processed electroencephalogram (bispectral analysis) were monitored. Baseline hemodynamic measurements were acquired, and psychometric tests were performed (visual analog scale for sedation; observer's assessment of alertness/sedation scale; digit symbol substitution test; and memory). The pain from a 1-min cold pressor test was quantified with a visual analog scale. After a 10-min initial dose of saline or 6 microg. kg(-1). h(-1) dexmedetomidine, volunteers received 50-min IV infusions of saline, or 0.2 or 0.6 microg. kg(-1). h(-1) dexmedetomidine. Measurements were repeated at the end of infusion and during recovery. The two dexmedetomidine infusions resulted in similar and significant sedation (30%-60%), impairment of memory (approximately 50%), and psychomotor performance (28%-41%). Hemodynamics, oxygen saturation, ETCO(2), and respiratory rate were well preserved throughout the infusion and recovery periods. Pain to the cold pressor test was reduced by 30% during dexmedetomidine infusion. Small-dose dexmedetomidine provided sedation, analgesia, and memory and cognitive impairment. These properties might prove useful in a postoperative or intensive care unit setting. IMPLICATIPNS: The alpha(2) agonist, dexmedetomidine, has sedation and analgesic properties. This study quantified these effects, as well as cardiorespiratory, memory and psychomotor effects, in healthy volunteers. Dexmedetomidine infusions resulted in reversible sedation, mild analgesia, and memory impairment without cardiorespiratory compromise.
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              Intraoperative infusion of dexmedetomidine reduces perioperative analgesic requirements.

              This prospective, randomized, double-blind study was designed to assess whether intraoperative infusion of dexmedetomidine provides effective postoperative analgesia. Postoperative pain scores and morphine consumption were compared in a treated group and a placebo group, both of which received patient-controlled morphine after total abdominal hysterectomy. Fifty women were randomly assigned to two groups. Group D (n = 25) received a loading dose of dexmedetomidine 1 mug.kg(-1) iv during induction of anesthesia, followed by a continuous infusion at a rate of 0.5 mug.kg(-1).hr(-1) throughout the operation. Group P (n = 25) received a volume-matched bolus and infusion of placebo (0.9% saline). For each case, heart rate, peripheral oxygen saturation, and systolic and diastolic blood pressure were recorded intraoperatively and for 48 hr postoperatively. Patients used a patient-controlled analgesia device to receive bolus doses of morphine after surgery. Total morphine consumption, pain scores, and sedation scores were recorded for the first 48 hr (two hours in the postanesthesia care unit and 46 hr on the ward). The groups were similar with respect to mean times to extubation of the trachea. Pain and sedation scores were also similar between groups at all corresponding times throughout the 48-hr period of observation. Group D patients consumed significantly less morphine in the postanesthesia care unit and on the ward (P < 0.05 and P < 0.01, respectively). Fewer patients in Group D experienced itching or nausea/vomiting (P < 0.05). Continuous iv dexmedetomidine during abdominal surgery provides effective postoperative analgesia, and reduces postoperative morphine requirements without increasing the incidence of side effects.
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                Author and article information

                Journal
                Indian J Anaesth
                Indian J Anaesth
                IJA
                Indian Journal of Anaesthesia
                Medknow Publications & Media Pvt Ltd (India )
                0019-5049
                0976-2817
                Nov-Dec 2012
                : 56
                : 6
                : 542-546
                Affiliations
                [1]Department of Anesthesia, B. J. Medical College, Civil Hospital, Ahmedabad, Gujarat, India
                Author notes
                Address for correspondence: Dr. Chirag Ramanlal Patel, No.22, Chirag Society, Opp. Ankur Bus Stand, Ankur, Naranpura, Ahmedabad, Gujarat, India. E-mail: chiragpateld10@ 123456yahoo.com
                Article
                IJA-56-542
                10.4103/0019-5049.104571
                3546240
                23325938
                4e3f1cf6-16da-49ac-8046-e43d635eddd7
                Copyright: © Indian Journal of Anaesthesia

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Clinical Investigation

                Anesthesiology & Pain management
                perioperative haemodynamics,entropy,dexmedetomidine,recovery
                Anesthesiology & Pain management
                perioperative haemodynamics, entropy, dexmedetomidine, recovery

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