The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity
| Autor: | Swen J. Hilander, Gary L. Swart, Daniel J. DeBehnke, Laurie L. Wickman, Daniel W. Dobler |
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| Rok vydání: | 1995 |
| Předmět: |
Time Factors
Systole Hemodynamics Blood Pressure Emergency Nursing Hypoxemia Hypercapnia Asphyxia Electrocardiography Dogs Heart Rate Tachycardia Heart rate Bradycardia Intubation Intratracheal Animals Medicine Hypoxia Aorta Monitoring Physiologic Retrospective Studies medicine.diagnostic_test business.industry Carbon Dioxide medicine.disease Heart Arrest Oxygen Disease Models Animal Respiratory acidosis Blood pressure Regional Blood Flow Anesthesia Hypertension Pulseless electrical activity Emergency Medicine Arterial blood Hypotension medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | Resuscitation. 30:169-175 |
| ISSN: | 0300-9572 |
| DOI: | 10.1016/0300-9572(95)00873-r |
| Popis: | 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. Methods: 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; Pco 2 93 ± 19; Po 2 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. |
| Databáze: | OpenAIRE |
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