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Cerebral oxygen saturation: graded response to carbon dioxide with isoxia and graded response to oxygen with isocapnia.

Mutch WA, Patel SR, Shahidi AM, Kulasekara SI, Fisher JA, Duffin J, Hudson C - PLoS ONE (2013)

Bottom Line: The end-tidal oxygen versus cerebral saturation followed log-linear behaviour and best fit a hyperbolic relationship (R(2) = 0.85±0.10).The cerebral saturation during normoxic hypocapnia was equivalent to normocapnic hypoxia of 60 mmHg.Hypocapnia reduces cerebral saturation to an extent equivalent to moderate hypoxia.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia and Perioperative Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. wacmutch@shaw.ca

ABSTRACT

Background: Monitoring cerebral saturation is increasingly seen as an aid to management of patients in the operating room and in neurocritical care. How best to manipulate cerebral saturation is not fully known. We examined cerebral saturation with graded changes in carbon dioxide tension while isoxic and with graded changes in oxygen tension while isocapnic.

Methodology/principal findings: The study was approved by the Research Ethics Board of the University Health Network at the University of Toronto. Thirteen studies were undertaken in healthy adults with cerebral oximetry by near infrared spectroscopy. End-tidal gas concentrations were manipulated using a model-based prospective end-tidal targeting device. End-tidal carbon dioxide was altered ±15 mmHg from baseline in 5 mmHg increments with isoxia (clamped at 110±4 mmHg). End-tidal oxygen was changed to 300, 400, 500, 80, 60 and 50 mmHg under isocapnia (37±2 mmHg). Twelve studies were completed. The end-tidal carbon dioxide versus cerebral saturation fit a linear relationship (R(2) = 0.92±0.06). The end-tidal oxygen versus cerebral saturation followed log-linear behaviour and best fit a hyperbolic relationship (R(2) = 0.85±0.10). Cerebral saturation was maximized in isoxia at end-tidal carbon dioxide of baseline +15 mmHg (77±3 percent). Cerebral saturation was minimal in isocapnia at an end-tidal oxygen tension of 50 mmHg (61±3 percent). The cerebral saturation during normoxic hypocapnia was equivalent to normocapnic hypoxia of 60 mmHg.

Conclusions/significance: Hypocapnia reduces cerebral saturation to an extent equivalent to moderate hypoxia.

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Related in: MedlinePlus

As in Figure 1 for the same subject but for the hypoxic end-tidal sequences.These data were obtained after two of the gas cylinders supplying the MPET were changed from a 10% oxygen mixture to a 6% mixture.
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pone-0057881-g002: As in Figure 1 for the same subject but for the hypoxic end-tidal sequences.These data were obtained after two of the gas cylinders supplying the MPET were changed from a 10% oxygen mixture to a 6% mixture.

Mentions: Thirteen studies were undertaken. The first subject was excluded as end-tidal gas targeting was not adequate with a series of missed or poorly realized targets. Data are reported for the other 12 studies, and the subject demographics are listed in Table 1. The mean±SD baseline end-tidal carbon dioxide and oxygen tensions were 37±2 mmHg and 110±4 mmHg respectively. The time course of the experimental target sequence for one subject is shown in Figure 1 and 2. The mean±SD changes in end-tidal carbon dioxide tensions under baseline isoxic conditions are presented in Table 2. End-tidal clamping of oxygen tension was within ±4 mmHg for the group as a whole. The end-tidal carbon dioxide targets were within ±2 mmHg of their desired values for all measurement periods, but only 4/12 subjects were able to achieve a 15 mmHg decrement from their baseline values. A significant increase in blood pressure and heart rate was seen with increases in carbon dioxide tension (group×time interactions for repeated measures ANOVA p<0.001 for both variables). The changes in end-tidal oxygen tensions under baseline isocapnic conditions are presented in Table 3. In 2/12 subjects end-tidal targeting to 500 mmHg was not achieved, and one subject did not effectively achieve a target end-tidal oxygen tension of 50 mmHg. Significant decreases in pulse oximetry (SpO2) were seen at end-tidal tensions of oxygen of 60 and 50 mmHg, (group×time interactions for repeated measures ANOVA p<0.001). An individual example of the changes in cerebral saturation under the study conditions is depicted in Figure 3. The relationship between cerebral saturation and end-tidal carbon dioxide is presented in Table 4 for the group data. The mean calculated change in cerebral saturation/mmHg change in carbon dioxide tension was 0.48±0.09 percent/mmHg increase in carbon dioxide tension. The relationship between end-tidal carbon dioxide concentrations and cerebral saturation was well described in all subjects by a linear relationship (mean±SD R2-value 0.92±0.06). The relationship between end-tidal oxygen concentration and cerebral saturation was best graphed on a log-linear scale and in most cases best fit by a rectangular hyperbolic function (mean R2-value 0.85±0.10). Because of the hyperbolic curve fit we additionally analyzed the mean calculated change in cerebral saturation/mmHg change in oxygen tension as two linear data sets: end-tidal oxygen tensions from 50 – 100 mmHg and 100–500 mmHg. For the hypoxic-normoxic range the mean calculated change in cerebral saturation was 0.14±0.04 percent/mmHg increase in oxygen tension. For the normoxic-hyperoxic range the change was 0.009±0.003 percent/mmHg increase in oxygen tension - only 7 percent of the response at the lower range of oxygen tensions.


Cerebral oxygen saturation: graded response to carbon dioxide with isoxia and graded response to oxygen with isocapnia.

Mutch WA, Patel SR, Shahidi AM, Kulasekara SI, Fisher JA, Duffin J, Hudson C - PLoS ONE (2013)

As in Figure 1 for the same subject but for the hypoxic end-tidal sequences.These data were obtained after two of the gas cylinders supplying the MPET were changed from a 10% oxygen mixture to a 6% mixture.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3585256&req=5

pone-0057881-g002: As in Figure 1 for the same subject but for the hypoxic end-tidal sequences.These data were obtained after two of the gas cylinders supplying the MPET were changed from a 10% oxygen mixture to a 6% mixture.
Mentions: Thirteen studies were undertaken. The first subject was excluded as end-tidal gas targeting was not adequate with a series of missed or poorly realized targets. Data are reported for the other 12 studies, and the subject demographics are listed in Table 1. The mean±SD baseline end-tidal carbon dioxide and oxygen tensions were 37±2 mmHg and 110±4 mmHg respectively. The time course of the experimental target sequence for one subject is shown in Figure 1 and 2. The mean±SD changes in end-tidal carbon dioxide tensions under baseline isoxic conditions are presented in Table 2. End-tidal clamping of oxygen tension was within ±4 mmHg for the group as a whole. The end-tidal carbon dioxide targets were within ±2 mmHg of their desired values for all measurement periods, but only 4/12 subjects were able to achieve a 15 mmHg decrement from their baseline values. A significant increase in blood pressure and heart rate was seen with increases in carbon dioxide tension (group×time interactions for repeated measures ANOVA p<0.001 for both variables). The changes in end-tidal oxygen tensions under baseline isocapnic conditions are presented in Table 3. In 2/12 subjects end-tidal targeting to 500 mmHg was not achieved, and one subject did not effectively achieve a target end-tidal oxygen tension of 50 mmHg. Significant decreases in pulse oximetry (SpO2) were seen at end-tidal tensions of oxygen of 60 and 50 mmHg, (group×time interactions for repeated measures ANOVA p<0.001). An individual example of the changes in cerebral saturation under the study conditions is depicted in Figure 3. The relationship between cerebral saturation and end-tidal carbon dioxide is presented in Table 4 for the group data. The mean calculated change in cerebral saturation/mmHg change in carbon dioxide tension was 0.48±0.09 percent/mmHg increase in carbon dioxide tension. The relationship between end-tidal carbon dioxide concentrations and cerebral saturation was well described in all subjects by a linear relationship (mean±SD R2-value 0.92±0.06). The relationship between end-tidal oxygen concentration and cerebral saturation was best graphed on a log-linear scale and in most cases best fit by a rectangular hyperbolic function (mean R2-value 0.85±0.10). Because of the hyperbolic curve fit we additionally analyzed the mean calculated change in cerebral saturation/mmHg change in oxygen tension as two linear data sets: end-tidal oxygen tensions from 50 – 100 mmHg and 100–500 mmHg. For the hypoxic-normoxic range the mean calculated change in cerebral saturation was 0.14±0.04 percent/mmHg increase in oxygen tension. For the normoxic-hyperoxic range the change was 0.009±0.003 percent/mmHg increase in oxygen tension - only 7 percent of the response at the lower range of oxygen tensions.

Bottom Line: The end-tidal oxygen versus cerebral saturation followed log-linear behaviour and best fit a hyperbolic relationship (R(2) = 0.85±0.10).The cerebral saturation during normoxic hypocapnia was equivalent to normocapnic hypoxia of 60 mmHg.Hypocapnia reduces cerebral saturation to an extent equivalent to moderate hypoxia.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia and Perioperative Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. wacmutch@shaw.ca

ABSTRACT

Background: Monitoring cerebral saturation is increasingly seen as an aid to management of patients in the operating room and in neurocritical care. How best to manipulate cerebral saturation is not fully known. We examined cerebral saturation with graded changes in carbon dioxide tension while isoxic and with graded changes in oxygen tension while isocapnic.

Methodology/principal findings: The study was approved by the Research Ethics Board of the University Health Network at the University of Toronto. Thirteen studies were undertaken in healthy adults with cerebral oximetry by near infrared spectroscopy. End-tidal gas concentrations were manipulated using a model-based prospective end-tidal targeting device. End-tidal carbon dioxide was altered ±15 mmHg from baseline in 5 mmHg increments with isoxia (clamped at 110±4 mmHg). End-tidal oxygen was changed to 300, 400, 500, 80, 60 and 50 mmHg under isocapnia (37±2 mmHg). Twelve studies were completed. The end-tidal carbon dioxide versus cerebral saturation fit a linear relationship (R(2) = 0.92±0.06). The end-tidal oxygen versus cerebral saturation followed log-linear behaviour and best fit a hyperbolic relationship (R(2) = 0.85±0.10). Cerebral saturation was maximized in isoxia at end-tidal carbon dioxide of baseline +15 mmHg (77±3 percent). Cerebral saturation was minimal in isocapnia at an end-tidal oxygen tension of 50 mmHg (61±3 percent). The cerebral saturation during normoxic hypocapnia was equivalent to normocapnic hypoxia of 60 mmHg.

Conclusions/significance: Hypocapnia reduces cerebral saturation to an extent equivalent to moderate hypoxia.

Show MeSH
Related in: MedlinePlus