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      Dexmedetomidine reduces the incidence of fentanyl-induced cough: A double-blind, randomized, and placebo-controlled study

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          Abstract

          Objectives.

          The incidence of fentanyl-induced cough (FIC) during induction of general anesthesia varies around 40% and is undesirable. It increases intracranial, intraocular, and intra-abdominal pressures. This prospective, randomized, double-blind, placebo-controlled study evaluated the effect of dexmedetomidine (DEX) pretreatment on the incidence and severity of FIC.

          Methods.

          Altogether 300 patients undergoing elective surgical procedures were randomly allocated into three groups (I, II, III; n = 100) and administered intravenously, over 10 min, 10 mL isotonic saline, DEX 0.5 μg/kg in 10 mL isotonic saline, or DEX 1 μg/kg in 10 mL isotonic saline, respectively. All groups subsequently received a fentanyl (4.0 μg/kg) intravenous push. The incidence and severity of cough were recorded for 1 min after fentanyl administration.

          Results.

          The incidence of FIC was 61%, 40%, and 18% in groups I, II, and III, respectively ( P < 0.05 for treatment groups II and III versus control group I). There was no significant difference in the severity or onset time of cough, or hemodynamic variables, among the three groups.

          Conclusions.

          Intravenous DEX (0.5 μg/kg or 1 μg/kg) immediately before the administration of intravenous fentanyl (4.0 μg/kg) significantly reduced the incidence of FIC.

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          Most cited references 28

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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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            Single-dose dexmedetomidine attenuates airway and circulatory reflexes during extubation.

             A Boyaci,  A Mizrak,  Z Tosun (2005)
            The alpha agonist dexmedetomidine, a sedative and analgesic, reduces heart rate and blood pressure dose-dependently. We investigated whether it also has the ability to attenuate airway and circulatory reflexes during emergence from anaesthesia. Sixty ASA I-III patients received a standard anaesthetic. Five minutes before the end of surgery, they were randomly allocated to receive either dexmedetomidine 0.5 microg/kg (Group D) (n=30) or saline placebo (Group P) (n=30) intravenously (i.v.) over 60 s in a double-blind design. The blinded anaesthetist awoke all the patients, and the number of coughs per patient was continuously monitored for 15 min after extubation; coughing was evaluated on a 4-point scale. Any laryngospasm, bronchospasm or desaturation was recorded. Heart rate (HR) and systolic and diastolic blood pressure (SAP, DAP) were measured before, during and after tracheal extubation. The time from tracheal extubation and emergence from anaesthesia were recorded. Median coughing scores were 1 (1-3) in Group D and 2 (1-4) in Group P (P<0.05), but there were no differences between the groups in the incidence of breath holding or desaturation. HR, SAP and DAP increased at extubation in both groups (P<0.05), but the increase was less significant with dexmedetomidine. The time from tracheal extubation and emergence from anaesthesia were similar in both groups. These findings suggest that a single-dose bolus injection of dexmedetomidine before tracheal extubation attenuates airway-circulatory reflexes during extubation.
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              Dexmedetomidine as an anaesthetic adjuvant in patients undergoing intracranial tumour surgery: a double-blind, randomized and placebo-controlled study.

              Dexmedetomidine (DEX) has been shown to provide good perioperative haemodynamic stability with decreased intraoperative opioid requirements. It may have neural protective effects, and thus may be a suitable anaesthetic adjuvant to neurosurgical anaesthesia. Fifty-four patients scheduled for elective surgery of supratentorial brain tumour were randomized to receive in a double-blind manner a continuous DEX infusion (plasma target concentration 0.2 or 0.4 ng ml(-1)) or placebo, beginning 20 min before anaesthesia and continuing until the start of skin closure. The DEX groups received fentanyl 2 microg kg(-1) at the induction of anaesthesia and before the start of operation, the placebo group 4 microg kg(-1), respectively. Anaesthesia was maintained with nitrous oxide in oxygen and isoflurane. The median times from the termination of N2O to extubation were 6 (3-27), 3 (0-20) and 4 (0-13) min in placebo, DEX-0.2 and DEX-0.4 groups, respectively (P<0.05 anova all-over effect). The median percentage of time points when systolic blood pressure was within more or less than 20% of the intraoperative mean was 72, 77 and 85, respectively (P<0.01), DEX-0.4 group differed significantly from the other groups. DEX blunted the tachycardic response to intubation (P<0.01) and the hypertensive response to extubation (P<0.01). DEX-0.4 group differed in the heart rate variability from placebo (93 vs 82%, P<0.01). DEX increased perioperative haemodynamic stability in patients undergoing brain tumour surgery. Compared with fentanyl, the trachea was extubated [corrected] faster without respiratory depression.
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                Author and article information

                Journal
                Ups J Med Sci
                UPS
                Upsala Journal of Medical Sciences
                Informa Healthcare
                0300-9734
                2000-1967
                March 2012
                15 February 2012
                : 117
                : 1
                : 18-21
                Affiliations
                Department of Anesthesia , The Second Xiangya Hospital of Central South University, Changsha, China
                Author notes
                Correspondence: Jun-Mei Xu, MD PhD, Department of Anesthesia , The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, 410011, China. doctorjmxu@ 123456163.com
                Article
                UPS_A_629749_O
                10.3109/03009734.2011.629749
                3282237
                22335390
                © Informa Healthcare

                This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

                Categories
                Original Articles

                Medicine

                dexmedetomidine, cough, opioid-induced muscular rigidity, fentanyl

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