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右美托咪定与咪达唑仑对新型冠状病毒肺炎重型患者无创通气临床效果的对比研究

[A comparative study on clinical effects of dexmedetomidine and midazolam on patients with severe coronavirus disease 2019 on non-invasive ventilation].

作者信息

Xie Wenjie, Zhong Zhentong, Li Guang, Hou Guo, Huang Kesheng, Yu Zhui

机构信息

Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, China. Corresponding author: Yu Zhui, Email:

出版信息

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2020 Jun;32(6):677-680. doi: 10.3760/cma.j.cn121430-20200305-00187.

Abstract

OBJECTIVE

To compare the therapeutic effects and safety of dexmedetomidine and midazolam on patients with severe coronavirus disease 2019 (COVID-19) who received non-invasive ventilation.

METHODS

Patients with COVID-19 who needed non-invasive ventilation in one critical care medicine ward of Wuhan Jinyintan Hospital during the team support period from the department of critical care medicine of Renmin Hospital of Wuhan University from January 23rd to February 15th in 2020 were investigated retrospectively. Ramsay score, mean arterial pressure (MAP), heart rate (HR), respiratory rate (RR), arterial oxygen partial pressure (PaO) before sedation and at 1, 12, 24 hours after sedation, sleep time were collected, and the side effects such as excessive sedation, fall of tongue, abdominal distension, aspiration, bradycardia, escalation to invasive mechanical ventilation during 24 hours were also collected. According to different sedative drugs, patients were divided into the control group (without sedative drugs), dexmedetomidine group and midazolam group. The changes of indicators among the three groups were compared.

RESULTS

Fourteen patients were injected with dexmedetomidine (loading dose of 1 μg/kg for 10 minutes, maintained at 0.2-0.7 μg×kg×h); 9 patients were injected with midazolam (loading dose of 0.05 mg/kg for 2 minutes, maintained at 0.02-0.10 mg×kg×h); 12 patients didn't use sedative drugs due to limitations of previous hospital or patients' rejection. In dexmedetomidine group and midazolam group, the Ramsay score was maintained at 2-3 points after sedation, which were higher than those of control group at different time points after sedation, and there was no significant difference between dexmedetomidine group and midazolam group. MAP of dexmedetomidine group and midazolam group decreased gradually after sedation. MAP after 1-hour sedation was significantly lower than that before sedation, and MAP after 24 hours sedation was significantly lower than that in the control group [mmHg (1 mmHg = 0.133 kPa): 109.7±11.5, 107.1±12.3 vs. 121.1±13.3, both P < 0.05]. HR decreased gradually after sedation treatment, which was significantly lower after 12 hours of sedation than that before sedation, and HR in dexmedetomidine group was significantly lower than that in control group after 12 hours of sedation (bpm: 84.0±13.9 vs. 92.8±15.4 at 12 hours; 81.0±16.7 vs 92.6±12.7 at 24 hours, both P < 0.05). PaO increased and RR decreased in all three groups after ventilation. PaO in dexmedetomidine group and midazolam group were significantly higher than that in the control group after 12 hours of sedation [cmHO (1 cmHO = 0.098 kPa): 79.0±6.5, 79.0±8.9 vs. 70.0±7.8, both P < 0.05]; the decreases of RR in dexmedetomidine group and midazolam group were significant than that in control group after 1 hour of sedation (bpm: 34.0±3.9, 33.8±4.6 vs. 39.0±3.6, both P < 0.05). There were no differences of MAP, HR, PaO and RR between dexmedetomidine group and midazolam group at different time points. The sleep duration in dexmedetomidine group and midazolam group were significantly longer than that in the control group (hours: 4.9±1.9, 5.8±2.4 vs. 3.0±1.8, both P < 0.05), but there was no difference between dexmedetomidine group and midazolam group (P > 0.05). Adverse events occurred in all three groups. In midazolam group, there were 2 cases of excessive sedation with fall of tongue and abdominal distension, including 1 case of aspiration, 1 case receiving intubation due to refractory hypoxemia and 1 case due to unconsciousness. In dexmedetomidine group, there were 2 cases of bradycardia, 1 case of intubation due to refractory hypoxemia. In control group, 4 cases underwent intubation due to refractory hypoxemia.

CONCLUSIONS

Non-invasive mechanical ventilation is an important respiratory support technology for patients with severe COVID-19. Appropriate sedation can increase the efficiency of non-invasive mechanical ventilation. Dexmedetomidine is more effective and safer than midazolam in these patients, but attention should be paid to HR and blood pressure monitoring.

摘要

目的

比较右美托咪定和咪达唑仑对接受无创通气的重症2019冠状病毒病(COVID-19)患者的治疗效果及安全性。

方法

回顾性调查2020年1月23日至2月15日武汉大学人民医院重症医学科团队支援期间,武汉金银潭医院一个重症医学病房中需要无创通气的COVID-19患者。收集镇静前及镇静后1、12、24小时的Ramsay评分、平均动脉压(MAP)、心率(HR)、呼吸频率(RR)、动脉血氧分压(PaO)、睡眠时间,并收集24小时内过度镇静、舌后坠、腹胀、误吸、心动过缓、升级为有创机械通气等副作用。根据不同镇静药物,将患者分为对照组(未使用镇静药物)、右美托咪定组和咪达唑仑组。比较三组指标的变化。

结果

14例患者注射右美托咪定(负荷剂量1 μg/kg,持续10分钟,维持剂量0.2 - 0.7 μg·kg·h);9例患者注射咪达唑仑(负荷剂量0.05 mg/kg,持续2分钟,维持剂量0.02 - 0.10 mg·kg·h);12例患者因既往医院限制或患者拒绝未使用镇静药物。右美托咪定组和咪达唑仑组镇静后Ramsay评分维持在2 - 3分,高于镇静后不同时间点的对照组,右美托咪定组和咪达唑仑组之间无显著差异。右美托咪定组和咪达唑仑组镇静后MAP逐渐下降。镇静1小时后的MAP显著低于镇静前,镇静24小时后的MAP显著低于对照组[mmHg(1 mmHg = 0.133 kPa):109.7±11.5,107.1±12.3 vs. 121.1±13.3,均P < 0.05]。镇静治疗后HR逐渐下降,镇静12小时后的HR显著低于镇静前,镇静12小时后右美托咪定组的HR显著低于对照组(12小时时bpm:84.0±13.9 vs. 92.8±15.4;24小时时81.0±16.7 vs 92.6±12.7,均P < 0.05)。通气后三组患者的PaO均升高,RR均下降。镇静12小时后,右美托咪定组和咪达唑仑组的PaO显著高于对照组[cmH₂O(1 cmH₂O = 0.098 kPa):79.0±6.5,79.0±8.9 vs. 70.0±7.8,均P < 0.05];镇静1小时后,右美托咪定组和咪达唑仑组RR的下降幅度显著大于对照组(bpm:34.0±3.9,33.8±4.6 vs. 39.0±3.6,均P < 0.05)。右美托咪定组和咪达唑仑组在不同时间点的MAP、HR、PaO和RR无差异。右美托咪定组和咪达唑仑组的睡眠时间显著长于对照组(小时:4.9±1.9,5.8±2.4 vs. 3.0±1.8,均P < 0.05),但右美托咪定组和咪达唑仑组之间无差异(P > 0.05)。三组均发生不良事件。咪达唑仑组有2例过度镇静伴舌后坠和腹胀,其中1例误吸,1例因难治性低氧血症行气管插管,1例因意识不清行气管插管。右美托咪定组有2例心动过缓,1例因难治性低氧血症行气管插管。对照组有4例因难治性低氧血症行气管插管。

结论

无创机械通气是重症COVID-患者重要的呼吸支持技术。适当的镇静可提高无创机械通气的效率。在这些患者中,右美托咪定比咪达唑仑更有效、更安全,但应注意监测HR和血压。

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