Systemic and global cerebral oxygen extraction (O2 Ext) in acute carbon monoxide (CO) toxicity

Deborah M. Lopez, Jacqueline Weingarten-Arams, Lewis Singer, Edward Conway

Research output: Contribution to journalArticle

Abstract

Introduction: Carbon Monoxide is a colorless and odorless gas produced by incomplete combustion of carbon containing compounds. CO affects most notably those organs with high metabolic rates such as the central nervous system. CO causes a left shift of the oxyhemoglobin dissociation curve. Limited adult animal studies have suggested that systemic O2 Ext is decreased in the presence of CO toxicity. The purpose of this study is to evaluate systemic and cerebral O2 Ext in a pediatric model of CO toxicity. Methods: 15 Yorkshire piglets were anesthetized with pentobarbital. Tracheostomy, femoral arterial, pulmonary arterial and retrograde jugular venous bulb pressure catheters were inserted. Following a one hour rest period, baseline data was collected. CO was administered via the endotracbeal tube to achieve and maintain a level of 60% carboxyhemoglobin (COHb). Arterial, mixed venous and internal jugular blood samples were drawn within five minutes of each other. Blood samples were measured with the Radiometer OSM 3 Hemoximeter. O2 Ext was calculated via standard formula. Measurements were stratified by the corresponding COHb level: mild toxicity = 0-10%, moderate = ≥ 10-40% and severe ≥40%. Results: 158 sets of blood samples were obtained. Mean values are summarized below. Systemic versus cerebral O2 Ext were analyzed via two tailed t-test and were significant at all levels of COHb with * p ≤ 0.01. COHB% O2 delivery (ml O2/min) CO (L/min) Systemic O2 Ext Cerebral O2 Ext 0-10 102.6 1.14 0.40 0.28* >10-40 95 1.17 0.43 0.36*, # >40 56.8 1.40 0.41 0.33*, # In addition, cerebral oxygen extraction significantly increased as the percentage of COHb escalated with no change in systemic oxygen extraction. (ANOVA, # p = 0.05) Conclusion: Cerebral oxygen extraction increased with increasing COHb level. Contrary to adult animal studies, systemic oxygen extraction remained unchanged despite increasing COHb levels. Cardiac output remained the same and as expected oxygen delivery decreased with increasing level of COHb.

Original languageEnglish (US)
JournalCritical Care Medicine
Volume27
Issue number1 SUPPL.
StatePublished - 1999

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Carboxyhemoglobin
Carbon Monoxide
Oxygen
Neck
Oxyhemoglobins
Venous Pressure
Tracheostomy
Pentobarbital
Thigh
Cardiac Output
Analysis of Variance
Carbon
Catheters
Central Nervous System
Gases
Pediatrics
Lung

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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Systemic and global cerebral oxygen extraction (O2 Ext) in acute carbon monoxide (CO) toxicity. / Lopez, Deborah M.; Weingarten-Arams, Jacqueline; Singer, Lewis; Conway, Edward.

In: Critical Care Medicine, Vol. 27, No. 1 SUPPL., 1999.

Research output: Contribution to journalArticle

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abstract = "Introduction: Carbon Monoxide is a colorless and odorless gas produced by incomplete combustion of carbon containing compounds. CO affects most notably those organs with high metabolic rates such as the central nervous system. CO causes a left shift of the oxyhemoglobin dissociation curve. Limited adult animal studies have suggested that systemic O2 Ext is decreased in the presence of CO toxicity. The purpose of this study is to evaluate systemic and cerebral O2 Ext in a pediatric model of CO toxicity. Methods: 15 Yorkshire piglets were anesthetized with pentobarbital. Tracheostomy, femoral arterial, pulmonary arterial and retrograde jugular venous bulb pressure catheters were inserted. Following a one hour rest period, baseline data was collected. CO was administered via the endotracbeal tube to achieve and maintain a level of 60{\%} carboxyhemoglobin (COHb). Arterial, mixed venous and internal jugular blood samples were drawn within five minutes of each other. Blood samples were measured with the Radiometer OSM 3 Hemoximeter. O2 Ext was calculated via standard formula. Measurements were stratified by the corresponding COHb level: mild toxicity = 0-10{\%}, moderate = ≥ 10-40{\%} and severe ≥40{\%}. Results: 158 sets of blood samples were obtained. Mean values are summarized below. Systemic versus cerebral O2 Ext were analyzed via two tailed t-test and were significant at all levels of COHb with * p ≤ 0.01. COHB{\%} O2 delivery (ml O2/min) CO (L/min) Systemic O2 Ext Cerebral O2 Ext 0-10 102.6 1.14 0.40 0.28* >10-40 95 1.17 0.43 0.36*, # >40 56.8 1.40 0.41 0.33*, # In addition, cerebral oxygen extraction significantly increased as the percentage of COHb escalated with no change in systemic oxygen extraction. (ANOVA, # p = 0.05) Conclusion: Cerebral oxygen extraction increased with increasing COHb level. Contrary to adult animal studies, systemic oxygen extraction remained unchanged despite increasing COHb levels. Cardiac output remained the same and as expected oxygen delivery decreased with increasing level of COHb.",
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N2 - Introduction: Carbon Monoxide is a colorless and odorless gas produced by incomplete combustion of carbon containing compounds. CO affects most notably those organs with high metabolic rates such as the central nervous system. CO causes a left shift of the oxyhemoglobin dissociation curve. Limited adult animal studies have suggested that systemic O2 Ext is decreased in the presence of CO toxicity. The purpose of this study is to evaluate systemic and cerebral O2 Ext in a pediatric model of CO toxicity. Methods: 15 Yorkshire piglets were anesthetized with pentobarbital. Tracheostomy, femoral arterial, pulmonary arterial and retrograde jugular venous bulb pressure catheters were inserted. Following a one hour rest period, baseline data was collected. CO was administered via the endotracbeal tube to achieve and maintain a level of 60% carboxyhemoglobin (COHb). Arterial, mixed venous and internal jugular blood samples were drawn within five minutes of each other. Blood samples were measured with the Radiometer OSM 3 Hemoximeter. O2 Ext was calculated via standard formula. Measurements were stratified by the corresponding COHb level: mild toxicity = 0-10%, moderate = ≥ 10-40% and severe ≥40%. Results: 158 sets of blood samples were obtained. Mean values are summarized below. Systemic versus cerebral O2 Ext were analyzed via two tailed t-test and were significant at all levels of COHb with * p ≤ 0.01. COHB% O2 delivery (ml O2/min) CO (L/min) Systemic O2 Ext Cerebral O2 Ext 0-10 102.6 1.14 0.40 0.28* >10-40 95 1.17 0.43 0.36*, # >40 56.8 1.40 0.41 0.33*, # In addition, cerebral oxygen extraction significantly increased as the percentage of COHb escalated with no change in systemic oxygen extraction. (ANOVA, # p = 0.05) Conclusion: Cerebral oxygen extraction increased with increasing COHb level. Contrary to adult animal studies, systemic oxygen extraction remained unchanged despite increasing COHb levels. Cardiac output remained the same and as expected oxygen delivery decreased with increasing level of COHb.

AB - Introduction: Carbon Monoxide is a colorless and odorless gas produced by incomplete combustion of carbon containing compounds. CO affects most notably those organs with high metabolic rates such as the central nervous system. CO causes a left shift of the oxyhemoglobin dissociation curve. Limited adult animal studies have suggested that systemic O2 Ext is decreased in the presence of CO toxicity. The purpose of this study is to evaluate systemic and cerebral O2 Ext in a pediatric model of CO toxicity. Methods: 15 Yorkshire piglets were anesthetized with pentobarbital. Tracheostomy, femoral arterial, pulmonary arterial and retrograde jugular venous bulb pressure catheters were inserted. Following a one hour rest period, baseline data was collected. CO was administered via the endotracbeal tube to achieve and maintain a level of 60% carboxyhemoglobin (COHb). Arterial, mixed venous and internal jugular blood samples were drawn within five minutes of each other. Blood samples were measured with the Radiometer OSM 3 Hemoximeter. O2 Ext was calculated via standard formula. Measurements were stratified by the corresponding COHb level: mild toxicity = 0-10%, moderate = ≥ 10-40% and severe ≥40%. Results: 158 sets of blood samples were obtained. Mean values are summarized below. Systemic versus cerebral O2 Ext were analyzed via two tailed t-test and were significant at all levels of COHb with * p ≤ 0.01. COHB% O2 delivery (ml O2/min) CO (L/min) Systemic O2 Ext Cerebral O2 Ext 0-10 102.6 1.14 0.40 0.28* >10-40 95 1.17 0.43 0.36*, # >40 56.8 1.40 0.41 0.33*, # In addition, cerebral oxygen extraction significantly increased as the percentage of COHb escalated with no change in systemic oxygen extraction. (ANOVA, # p = 0.05) Conclusion: Cerebral oxygen extraction increased with increasing COHb level. Contrary to adult animal studies, systemic oxygen extraction remained unchanged despite increasing COHb levels. Cardiac output remained the same and as expected oxygen delivery decreased with increasing level of COHb.

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