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在使用阻抗阈值设备进行主动按压-释放心肺复苏期间,肾上腺素对颈总动脉血流和 ETCO2 的潜在负面影响。

Potential negative effects of epinephrine on carotid blood flow and ETCO2 during active compression-decompression CPR utilizing an impedance threshold device.

机构信息

Department of Emergency Medicine, Regions Hospital, Saint Paul, MN, United States.

出版信息

Resuscitation. 2012 Aug;83(8):1021-4. doi: 10.1016/j.resuscitation.2012.03.018. Epub 2012 Mar 20.

Abstract

OBJECTIVES

This study examines the effects of IV epinephrine administration on carotid blood flow (CBF) and end tidal CO(2) (ETCO(2)) production in a swine model of active compression-decompression CPR with an impedance threshold device (ACD-CPR+ITD).

METHODS

Six female swine (32 ± 1 kg) were anesthetized, intubated and ventilated. Intracranial, thoracic aorta and right atrial pressures were measured via indwelling catheters. CBF was recorded. ETCO(2), SpO(2) and EKG were monitored. V-fib was induced and went untreated for 6 min. Three minutes each of standard CPR (STD), STD-CPR+impedance threshold device (ITD) and active compression-decompression (ACD)-CPR+ITD were performed. At minute 9 of the resuscitation, 40 μg/kg of IV Epinephrine was administered and ACD-CPR+ITD was continued for 1 min. Statistical analysis was performed with a paired t-test. p values of <0.05 were considered statistically significant and all values are reported in mmHg unless otherwise noted.

RESULTS

Aortic pressure, cerebral and coronary perfusion pressures increased from STD<STD+ITD<ACD-CPR+ITD (p<0.001). Epinephrine administered during ACD-CPR+ITD signficantly increased mean aortic pressure (29 ± 5 vs 42 ± 12, p = 0.01), cerebral perfusion pressure (12 ± 5 vs 22 ± 10, p = 0.01), and coronary perfusion pressure (8 ± 7 vs 17 ± 4, p = 0.02); however, mean CBF and ETCO(2) decreased (respectively 29 ± 15 vs 14 ± 7.0 ml/min, p = 0.03; 20 ± 7 vs 18 ± 6, p = 0.04).

CONCLUSIONS

In this model, administration of epinephrine during ACD-CPR+ITD significantly increased markers of macrocirculation, while significantly decreasing carotid blood flow and ETCO(2). This calls into question the ability of calculated perfusion pressures to accurately reflect oxygen delivery to end organs. The administration of epinephrine during ACD-CPR+ITD does not improve cerebral tissue perfusion.

摘要

目的

本研究旨在探讨在阻抗阈值设备(ACD-CPR+ITD)辅助下的主动按压-释放心肺复苏(ACD-CPR)中,静脉内给予肾上腺素对猪模型颈动脉血流(CBF)和呼气末二氧化碳(ETCO2)产生的影响。

方法

6 只雌性猪(32±1kg)接受麻醉、气管插管和通气。通过留置导管测量颅内压、胸主动脉压和右心房压。记录 CBF。监测 ETCO2、SpO2 和心电图。诱发室颤并未经治疗 6 分钟。分别进行 3 分钟标准心肺复苏(STD)、STD-CPR+ITD 和主动按压-释放心肺复苏(ACD-CPR+ITD)。在复苏的第 9 分钟,给予 40μg/kg 的静脉内肾上腺素,并继续进行 ACD-CPR+ITD 1 分钟。采用配对 t 检验进行统计学分析。p 值<0.05 被认为具有统计学意义,除非另有说明,所有值均以 mmHg 报告。

结果

主动脉压、脑和冠状动脉灌注压从 STD<STD+ITD<ACD-CPR+ITD 增加(p<0.001)。在 ACD-CPR+ITD 期间给予肾上腺素可显著增加平均主动脉压(29±5 vs 42±12,p=0.01)、脑灌注压(12±5 vs 22±10,p=0.01)和冠状动脉灌注压(8±7 vs 17±4,p=0.02);然而,平均 CBF 和 ETCO2 降低(分别为 29±15 vs 14±7.0ml/min,p=0.03;20±7 vs 18±6,p=0.04)。

结论

在该模型中,在 ACD-CPR+ITD 期间给予肾上腺素可显著增加宏观循环标志物,同时显著降低颈动脉血流和 ETCO2。这使得计算的灌注压能否准确反映终末器官的氧输送受到质疑。在 ACD-CPR+ITD 期间给予肾上腺素并不能改善脑组织灌注。

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