Blood gas tests may be performed, typically by radial artery puncture, in the setting of acute breathing problems or other acute medical illness.<unk>  is generally defined as an arterial blood carbon dioxide level over 45 mmHg (6 kPa). Since carbon dioxide is in equilibrium with carbonic acid in the blood,<unk>  drives serum pH down, resulting in respiratory acidosis. Clinically, the effect of<unk>  on pH is estimated using the ratio of the arterial pressure of carbon dioxide to the concentration of bicarbonate ion, . Tolerance +Tolerance to increased atmospheric CO2 concentration %CO2 ininspired air Expected tolerance for useful activity on continued exposure to elevated CO2 Duration Major limitation 0.028 lifetime atmosphere, year 1780 0.04 lifetime current atmosphere 0.5 lifetime no detectable limitations (Note: refer to modern research in Carbon dioxide#Below 1% which shows measurable effects below 1%.) 1.0 lifetime 1.5 > 1 month mild respiratory stimulation 2.0 > 1 month 2.5 > 1 month 3.0 > 1 month moderate respiratory stimulation 3.5 > 1 week 4.0 > 1 week moderate respiratory stimulation, exaggerated respiratory response to exercise 4.5 > 8 hours 5.0 > 4 hours prominent respiratory stimulus, exaggerated respiratory response to exercise 5.5 > 1 hours 6.0 > 0.5 hours prominent respiratory stimulus, exaggerated respiratory response to exercise, beginnings of mental confusion 6.5 > 0.25 hours 7.0 > 0.1 hours limitation by dyspnea and mental confusion CO2 toxicity in animal models Tests performed on mongrel dogs showed the physiological effect of carbon dioxide on the body of the animal: after inhalation of a 50% CO2 and 50% air mixture, respiratory movement increased for about 2 minutes, and then, it decreased for 30 to 90 minutes. Hill and Flack showed that CO2 concentrations up to 35% have an exciting effect upon both circulation and respiration, but those beyond 35% are depressant upon them. The blood pressure (BP) decreased transiently during the increased respiratory movement and then rose again and maintained the original level for a while. The heart rate slowed slightly just after the gas mixture inhalation. It is believed that the initial BP depression with the decreased heart rate is due to the direct depressant effect of CO2 upon the heart and that the return of blood pressure to its original level was due to the rapid rise of . After 30–90 min, the respiratory center was depressed, and hypotension occurred gradually or suddenly from reduced cardiac output, leading to an apnea and eventually to circulatory arrest. At higher concentrations of CO2, unconsciousness occurred almost instantaneously and respiratory movement ceased in 1 minute. After a few minutes of apnea, circulatory arrest was seen. These findings imply that the cause of death in breathing high concentrations of CO2 is not the hypoxia but the intoxication of carbon dioxide.
Hypercapnia
Hypocapnia
Acidosis
Alkalosis
Metabolic alkalosis
Hypoxemia
Metabolic acidosis
Hypoventilation