CO2 retention is a pathophysiological process in which too little carbon dioxide is removed from the blood by the lungs. The end result is hypercapnia, an elevated level of carbon dioxide dissolved in the bloodstream. Various diseases may lead to this state; disturbed gas exchange may lead to impaired excretion of the gas. In addition, breathing air with a high carbon dioxide concentration may also lead to hypercapnia.
The principal result of the increased amount of dissolved CO2 is acidosis (respiratory acidosis when caused by impaired lung function); other effects include tachycardia (rapid heart rate) seizures, coma, respiratory arrest and death.
CO2 retention is a problem in various respiratory diseases, particularly chronic obstructive pulmonary disease (COPD). Patients with COPD who receive excessive supplemental oxygen can develop CO2 retention, and subsequent hypercapnia. The mechanism that underlies this state is a matter of controversy. Some authorities point to a reduction in the hypoxic "drive", a condition called carbon dioxide narcosis. When carbon dioxide levels are chronically elevated, the respiratory center becomes less sensitive to CO2 as a stimulant of the respiratory drive, and the PaO2 provides the primary stimulus for respirations. Administering excess supplemental oxygen can potentially suppress the respiratory center. However, it is unclear whether such a hypoxic drive exists in the first place. An alternative explanation is that, in patients with COPD, the administration of oxygen leads to an increase in the degree to which diseased alveoli are perfused with blood relative to other, less-diseased alveoli. As a result, a larger fraction of blood passes through parts of the lung that are poorly-ventilated, with a resulting increase in the CO2 concentration of the blood leaving the lungs.
As CO2 levels increase, patients exhibit a reduction in overall level of consciousness as well as respiratory effort. Severe increases in CO2 levels can lead to respiratory arrest.
CO2 retention is the hallmark of type II respiratory failure. While in type I any degree of hypoxia is compensated for by hyperventilation (and a decrease in CO2), this mechanism fails in type II. Mechanical ventilation (through intubation, CPAP or BIPAP) may be indicated, or infusion of doxapram.
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... Signs and symptoms that need to be observed are hyperventilation, shortness of breath and tachycardia (rapid heart beat), headache and excessive sweating, mental impairment and finally, unconsciousness ... This hypercapnia comes about due to malfunction of the soda lime CO2 absorbent canisters and can be avoided by decreasing the exercise rate, watching out for the operating limits of the canister, checking for leaks at the start of the dive and not reusing the absorbent. ...
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