1987Acta Physiologica ScandinavicaRequires access

CO2 sensitivity in humans breathing 1 or 2% CO2 in air

Ingrid Ellingsen, G Sydnes, Anton Hauge, John‐Anker Zwart, Knut Liestøl, Gunnar Nicolaysen

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Abstract

Ventilation increases when the concentration of CO2 in the inspired gas is increased, thereby limiting the increase in alveolar and arterial PCO2. The extent of this compensation at low levels of inspired CO2 has been debated. In five healthy humans, we have measured arterial PCO2, arterial pH and ventilation during exposure to 1 and 2% CO2 in the inspired gas. Each exposure lasted at least 7 min and arterial blood was sampled over at least 30 s during the last minute of each period. The ventilation was measured in the sixth and seventh min. The protocol included the sequences: control-test-control and test-control-test with 'test' representing CO2 loading and 'control' 0% CO2, respectively. We found that arterial PCO2 increased and pH decreased at both levels of inspired CO2. The mean increase in arterial PCO2 was 0.09 and 0.25 kPa, at CO2 1 and 2%, respectively. Three subjects were exposed to 1% CO2 in the inspired gas for 28 min flanked by similar control periods. In each period arterial blood samples were taken at 2- or 3-min intervals. Arterial PCO2 remained elevated for at least 20 min during the CO2 loading. The sensitivity to CO2 (ratio of increase in ventilation to increase in arterial PCO2) was within the range described by others at higher levels of inspired CO2. Arterial PCO2 increased by about 10% of the imposed load. We conclude that the increase in ventilation provides only incomplete compensation for exposure to CO2: arterial CO2 is increased and arterial pH decreased also at very low levels of inspired CO2.

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Ventilation increases when the concentration of CO2 in the inspired gas is increased, thereby limiting the increase in alveolar and arterial PCO2. The extent of this compensation at low levels of inspired CO2 has been debated. In five healthy humans, we have measured arterial PCO2, arterial pH and ventilation during exposure to 1 and 2% CO2 in the inspired gas. Each exposure lasted at least 7 min and arterial blood was sampled over at least 30 s during the last minute of each period. The ventilation was measured in the sixth and seventh min. The protocol included the sequences: control-test-control and test-control-test with 'test' representing CO2 loading and 'control' 0% CO2, respectively. We found that arterial PCO2 increased and pH decreased at both levels of inspired CO2. The mean increase in arterial PCO2 was 0.09 and 0.25 kPa, at CO2 1 and 2%, respectively. Three subjects were exposed to 1% CO2 in the inspired gas for 28 min flanked by similar control periods. In each period arterial blood samples were taken at 2- or 3-min intervals. Arterial PCO2 remained elevated for at least 20 min during the CO2 loading. The sensitivity to CO2 (ratio of increase in ventilation to increase in arterial PCO2) was within the range described by others at higher levels of inspired CO2. Arterial PCO2 increased by about 10% of the imposed load. We conclude that the increase in ventilation provides only incomplete compensation for exposure to CO2: arterial CO2 is increased and arterial pH decreased also at very low levels of inspired CO2.

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Available abstract

Ventilation increases when the concentration of CO2 in the inspired gas is increased, thereby limiting the increase in alveolar and arterial PCO2. The extent of this compensation at low levels of inspired CO2 has been debated. In five healthy humans, we have measured arterial PCO2, arterial pH and ventilation during exposure to 1 and 2% CO2 in the inspired gas. Each exposure lasted at least 7 min and arterial blood was sampled over at least 30 s during the last minute of each period. The ventilation was measured in the sixth and seventh min. The protocol included the sequences: control-test-control and test-control-test with 'test' representing CO2 loading and 'control' 0% CO2, respectively. We found that arterial PCO2 increased and pH decreased at both levels of inspired CO2. The mean increase in arterial PCO2 was 0.09 and 0.25 kPa, at CO2 1 and 2%, respectively. Three subjects were exposed to 1% CO2 in the inspired gas for 28 min flanked by similar control periods. In each period arterial blood samples were taken at 2- or 3-min intervals. Arterial PCO2 remained elevated for at least 20 min during the CO2 loading. The sensitivity to CO2 (ratio of increase in ventilation to increase in arterial PCO2) was within the range described by others at higher levels of inspired CO2. Arterial PCO2 increased by about 10% of the imposed load. We conclude that the increase in ventilation provides only incomplete compensation for exposure to CO2: arterial CO2 is increased and arterial pH decreased also at very low levels of inspired CO2.

Key concepts: Arterial pH, Arterial blood, Ventilation (architecture), Anesthesia, Blood pressure, Chemistry, Respiratory compensation, Respiration

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