窒息时的血流动力学和动脉血气反应：无脉电活动的犬类模型

The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity.

作者信息

DeBehnke D J, Hilander S J, Dobler D W, Wickman L L, Swart G L

机构信息

Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee 53226, USA.

出版信息

Resuscitation. 1995 Oct;30(2):169-75. doi: 10.1016/0300-9572(95)00873-r.

DOI:10.1016/0300-9572(95)00873-r

PMID:8560107

Abstract

OBJECTIVE

Asphyxiation is a time-honored animal model for producing pulseless electrical activity cardiac arrest. To date, there has not been a detailed description of the hemodynamic and arterial blood gas response to asphyxiation in a large number of animals. Our objective was to describe a single laboratory's experience with a standardized canine model of asphyxial pulseless electrical activity arrest.

METHOD

Design--Data from 4 separate research protocols using a standardized asphyxial model were retrospectively reviewed. Setting--Resuscitation research laboratory. Participants--169 mixed-breed dogs. Interventions--Each animal was anesthetized and instrumented for hemodynamic monitoring. The endotracheal tube was clamped and hemodynamic data was monitored. Following loss of aortic fluctuations by thoracic aortic catheter, animals remained in pulseless electrical activity for up to 20 min. Hemodynamic data was measured continuously and arterial blood gases were sampled intermittently.

RESULTS

Following endotracheal tube clamping, there was a characteristic increase in heart rate and systolic blood pressure. The heart rate peaked at 2-3 min following clamping, while the systolic blood pressure peaked at 7 min. Both heart rate and systolic blood pressure then steadily decreased until loss of aortic fluctuations. Loss of aortic fluctuations occurred 11.4 +/- 2.4 min following clamping. Following loss of aortic fluctuations, the heart rate steadily decreased. Arterial blood gases during asphyxiation and pulseless electrical activity arrest showed profound hypoxemia with hypercarbia (pH 7.03 +/- 0.07; Pco2 93 +/- 19; Po2 12 +/- 7 at loss of aortic fluctuation).

CONCLUSIONS

In this canine asphyxial model of pulseless electrical activity, a characteristic hemodynamic pattern of mild tachycardia-hypertension-bradycardia-hypotension was produced. Arterial blood gases reflect a profound hypoxemia and respiratory acidosis.

摘要

目的

窒息是一种用于制造无脉电活动心脏骤停的长期动物模型。迄今为止，尚未有对大量动物窒息时血流动力学和动脉血气反应的详细描述。我们的目的是描述一个实验室使用标准化犬类窒息性无脉电活动骤停模型的经验。

方法

设计——回顾性分析来自4个使用标准化窒息模型的独立研究方案的数据。地点——复苏研究实验室。参与者——169只混种犬。干预措施——每只动物均接受麻醉并安装血流动力学监测仪器。夹闭气管插管并监测血流动力学数据。在经胸主动脉导管检测到主动脉波动消失后，动物保持无脉电活动状态长达20分钟。持续测量血流动力学数据并间歇性采集动脉血气样本。

结果

夹闭气管插管后，心率和收缩压出现特征性升高。夹闭后2 - 3分钟心率达到峰值，而收缩压在7分钟时达到峰值。随后心率和收缩压均稳步下降，直至主动脉波动消失。夹闭后11.4 ± 2.4分钟出现主动脉波动消失。主动脉波动消失后，心率持续下降。窒息和无脉电活动骤停期间的动脉血气显示出严重低氧血症伴高碳酸血症（主动脉波动消失时pH 7.03 ± 0.07；Pco2 93 ± 19；Po2 12 ± 7）。