CO 2 narcosis

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Abstract
Excess CO2 within brain tissue may be due to inhalation of exogenous gases having a high content of CO2 or to retention of endogenous CO2. Endogenous CO2 retention within brain tissue may result from diminished pulmonary ventilation, circulation, and other conditions associated with increased PaCO2 decreased cerebral capillary flow; or diminished CO2 transport by the blood which results from large doses of acetazoleamide. CO2 retained within brain tissue diffuses rapidly across cell membranes and lowers intracellular pH by combining with H2O to form H+ and HCO3- ions. Acidosis of brain tissue from other causes predisposes the brain to the narcotic effect of CO2. Changes in the EEG correlate with the pH levelof brain tissue and may occur in the absence of hypoxia. If the pH of the pial surface of the monkey cortex is reduced below 6.6 to 6.9 units, EEG abnormality regularly results. EEG changes correlated poorly with brain pCO2, PaCO2, and apH levels. Ischemia of the brain predisposes it to CO2 narcosis because acid metabolites are poorly removed by a sluggish circulation and brain acidity develops more rapidly than in brain tissue having intact circulation. Epileptic spike activity present in the EEG before CO2 inhalation tends to be reduced or abolished as the pHof the pial surface is lowered below 6.6 to 6.9 units. The intravenous administration of acetazoleamide (Diamox) during CO2 narcosis is potentially dangerous. The intravenous administration of sodium bicarbonate during CO2 narcosis increases blood and brain pH, in spite of an accompanying rise in arterial and brain pCO2. EEG abnormality present may show transient improvement during the alkaline shift of brain pH. When arterial pCO2 is held constant at high levels for several hours, brain pCO2 and pH and the EEG do not alter significantly. Adaptation to CO2 narcosis may be mediated by increases in the buffer base of the blood or changes in neuronal excitability. Possible explanations for individual differences in susceptibility to CO2 narcosis include pre-existing acidity of blood or brain, decreases in capillary-venous flow within the brain, and decreased CO2-carrying capacity of the blood. Oxygen administration during CO2 narcosis is dangerous because it further increases arterial and brain pCO2 levels, tends to further lower brain pH, causes cerebral vasoconstriction, and tends to inhibit the anoxic drive to the respiratory center.