右美托咪啶对外科病人呼吸影响的重症监护

Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care

Introduction: The a2-agonist dexmedetomidine is a new class of sedative drug that is being investigated for use in ICU settings. It is an effective agent for the management of sedation and analgesia after cardiac, general, orthopaedic, head and neck, oncological and vascular surgery in the ICU [1].Cardiovascular stability was demonstrated, with significant reductions in rate–pressure product during sedation and over the extubation period.

Dexmedetomidine possesses several properties that may additionally benefit those critically ill patients who require sedation. In spontaneously breathing volunteers, intravenous dexmedetomidine caused marked sedation with only mild reductions in resting ventilation at higher doses [2]. Dexmedetomidine reduces the haemodynamic response to intubation and extubation [3–5] and attenuates the stress response to surgery [6], as a result of the a2-mediated reduction in sympathetic tone. herefore, it should be possible to continue sedation with dexmedetomidine over the stressful extubation period without concerns over respiratory depression,while ensuring that haemodynamic stability is preserved.

The present study is a retrospective analysis of the respiratory response to dexmedetomidine in 33 postsurgical patients (who were involved in a randomized, double-blind,lacebocontrolled trial [1]) after extubation in the ICU.

Methods: Patients who participated in the present study were admitted after surgery to our general or cardiothoracic ICUs,and were expected to receive at least 6 h of postsurgical sedation and artificial ventilation.

On arrival in the ICU after surgery, patients were randomized to receive either  exmedetomidine or placebo (normal saline) with rescue sedation and analgesia being provided, only if clinically needed, with midazolam and morphine boluses, respectively.Sedation was titrated to maintain a Ramsay Sedation Score [7]of 3 or greater while the patients were intubated, and infusions of study drug were continued for a maximum of 6 h after extubation to achieve a Ramsay Sedation Score of 2 or greater.

The patients were intubated and ventilated with oxygenenriched air to attain acceptable arterial blood gases, and extubation occurred when clinically indicated. All patients received supplemental oxygen after extubation, which was delivered by a fixed performance device. Assessment of pain was by direct communication with the patient.

Results are expressed as mean ± standard deviation unless otherwise stated. Patient characteristics, operative details and morphine usage were analyzed using the Mann–Whitney Utest.Statistical differences for respiratory measurements between the two groups were determined using analysis of variance for repeated measures, with the Bonferroni test for

post hoc comparisons.

Results: Of the 40 patients who participated in the study,seven patients could not be included in the analysis of respiratory function because they did not receive a study drug

infusion after extubation. Consequently, data from 33 patients are used in the analysis of respiratory function; 16 received dexmedetomidine and 17 placebo. Inadequate arterial blood

gas analysis was available in five patients (two from the dexmedetomidine group, and three from the placebo group).There were no significant differences in patient characteristics and operative details between the groups.

Requirements for morphine were reduced by more than 50% in patients receiving dexmedetomidine when compared with placebo after extubation (0.003 ± 0.004 vs 0.008 ± 0.006 mg/kg per h; P = 0.040).

There were no statistically significant differences between placebo and dexmedetomidine for oxygen saturations measured by pulse oximetry (P = 0.26), respiratory rate (P = 0.16; Fig. 1),arterial pH (P = 0.77) and PaCO2 (P = 0.75; Fig. 2) for the 6 h after extubation.

The dexmedetomidine group showed significantly higher PaO2 : FIO2 ratios throughout the 6-h intubation (P = 0.036) and extubation (P = 0.037) periods (Fig. 3). There were no adverse respiratory events seen in either the dexmedetomidine or placebo group.

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