Korean Circ J.  1971 Jun;1(1):39-47. 10.4070/kcj.1971.1.1.39.

Hemodynamic Effects of Acute Carbon Monoxide Poisoning

• Han YS
• Park HM

• KMID: 1659312
• DOI: http://doi.org/10.4070/kcj.1971.1.1.39

Abstract

Hemodynamic effects of acute carbon monoxide poisoning were studied in mongrel dogs. In this study dogs were divided into two groups, namely the control and the experimental. Carbon monoxide poisoning in the experimental group was induced by the breathing of about 2% CO gas mixture for 15 minutes, and this group was further divided into two, in which the arterial CO saturation was below 50%, 30 minutes after the CO gas breathing for 15 minutes (group I) and above 50% (group II). The heart rate was markedly decreased in the both experimental groups, particularly in the group I. The cardiac index showed a relative increase in the group II compared to that of the control, and the stroke volume also showed a relative increase in the both experimental groups, being more marked in the group II. Thus the increase in the cardiac output in the group II was caused mainly by the increase in the stroke volume. The femoral artery mean pressure was decreased both in the control and the experimental groups, being more marked in the group II. There was no appreciable difference in the femoral venous pressure between the control and the experimental groups. The total peripheral resistance was decreased 30 minutes after CO gas breathing in both experimental groups, particularly in the Group II. The pulmonary artery mean pressure showed a decrease in the control and the experimental groups, and there was no prarticular difference between these two groups. The changes in the total pulmonary resistance were rather similar to those of the total peripheral resistance.

MeSH Terms

Animals
Carbon Monoxide Poisoning*
Carbon Monoxide*
Carbon*
Cardiac Output
Dogs
Femoral Artery
Heart Rate
Hemodynamics*
Pulmonary Artery
Respiration
Stroke Volume
Vascular Resistance
Venous Pressure
Carbon
Carbon Monoxide