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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 CO
2 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.
CO2 retention with its attendant dangers of death from convulsions and hypoxia (low oxygen level) is primarily of concern to the scuba diver due to "skip breathing". Other mechanisms of CO2 retention are breath-hold diving, breathing in a sealed environment, faulty regulator, exercise at extreme depth and using contaminated air.
Symptoms include rapid respiration in 4-6%, rapid pulse rate, shortness of breath in 7-10% and convulsions and unconsciousness in 11-20%.
The CO2 level in the blood is unchanged by the ambient pressure (i.e., the depth) per se, since the partial pressure of carbon dioxide in a scuba diver's blood is a function only of metabolism and the rate and depth of breathing—the same factors that determine blood CO2 concentration on land.
All of the CO2 developed during breathing from open circuit equipment underwater is normally expelled from the apparatus in the exhaled breath as bubbles. The partial pressure of CO2 produced by the body does not increase with depth as do other gases in breathing mixes, such as nitrogen, oxygen, carbon monoxide and hydrocarbons.
Abnormal carbon dioxide accumulation in the blood can occur from too high a level of metabolism, such as from exercise at depth, or from inadequate breathing. If the diver takes shallow breaths or skip breathes, a larger proportion of the CO2 is not completely expelled and is re-inhaled on the next breath. The medical term for high carbon dioxide in the blood is hypercapnia; when the level is high enough it can cause "CO2 toxicity," which can lead to shortness of breath, headache, confusion and drowning (depending on how severe).
Elevated CO2 levels play a significant role in oxygen toxicity and in nitrogen narcosis. The acceptable CO2 level for diving operations is 1.5% surface equivalent (10.5 mmHg); the acceptable level for hyperbaric oxygen therapy operations is one that allows a vent schedule of 4 scfm per person displacement.
Closed circuit equipment
With the increased usage of rebreather diving, mainly by the military—but recently by more and more civilian divers, there is the possibility of hypercapnia (high CO2 levels), among other medical considerations.
This hypercapnia comes about due to malfunction of the soda lime CO2 absorbent canisters and can be avoided by decreasing the exercise rate, remaining within the recommended operating limits of the canister, checking for leaks at the start of the dive, ensuring that the absorbent is well packed with no possibility of tunneling (formation of clear passages through the absorbent allowing gas to bypass the reactive material) and not reusing the absorbent on multiple days.
- Schaefer, KE; Dougherty Jr, JH; Wilson, JM; Frayre, RL; Knight, DR (1982). "CO2 Retention And ECG Changes In Exercise During Prolonged Hyperbaric N2-O2 Breathing.". Naval Submarine Medical Research Laboratory Technical Report. NSMRL-956 (ADA125403). Retrieved 2013-05-11.