CO2 and the diver

Our body produces CO2, as a consequence of cellular metabolism, in stoichiometric equilibrium with the oxygen used (i.e., for every molecule of oxygen consumed, one molecule of CO2 is generated); it results that the partial pressure of CO2 (PCO2) in arterial blood is about 40 mmHg while that in venous blood, where the products of metabolism accumulate, is about 46 mmHg. An average adult produces about 200 ml of CO2 per minute, and if this is not adequately eliminated through respiration, PCO2 in arterial blood increases by about 3 to 6 mmHg/minute.

In a healthy adult, alveolar ventilation is regulated to maintain a PCO2 in the alveoli and arterial blood of around 40 mmHg.

The increase in PCO2 is the primary stimulus for respiration by acting on the brain’s chemical receptors (located in the medulla oblongata) and those in the aortas. These receptors react to the increase in arterial PCO2 and to the reduction of pH (acidosis); CO2 is mainly transported as bicarbonates in the plasma, and a change in its concentration is reflected in a change in the concentration of these bicarbonates, and consequently, in a reduction in pH. Aortic receptors mainly react to the decrease in oxygen concentration in the blood.

Typically, in atmospheric air, the PCO2 is 0.23 – 0.30 mmHg at a nominal pressure of 760 mmHg. Suppose a diver breathes a contaminated mixture with higher CO2 values. In that case, the respiratory ability to control PCO2 is impaired, and the respiratory rate intensifies considerably to keep arterial PCO2 within the limits of 40 mmHg. This high respiratory rate cannot be sustained for long periods, soon leading to exhaustion of the respiratory muscles and collapse of the lungs’ ventilatory capacities. Even a modest % of CO2 in the respiratory mixture can generate unacceptable levels of PCO2 at depth.

Some symptoms have been associated with PCO2 levels:

  • Headaches and tunnel vision             60 < PCO2 < 66 mmHg
  • Nausea and panic                              PCO2 > 61 mmHg
  • Altered mental status                         51 < PCO2 < 52 mmHg

In general, it is essential to avoid even minimal CO2 contamination in the respiratory mixture because, for example, inhaling even just 2% of CO2 requires a 61% increase in respiratory rate to keep arterial PCO2 within 40 mmHg; in immersion, this respiratory rate can be excessive, and consequently the level of CO2 in the body can rise to critical levels causing even sudden loss of consciousness. 

Underwater, the respiratory system is mechanically stressed by the increase in hydrostatic pressure and the increase in the density of the breathed gas; consequently, respiratory effort increases, and alveolar PCO2 can increase as a result of two main mechanisms:

CO2 retention – results from a tendency to hypoventilation, which causes an inequality between the metabolically produced CO2 and the eliminated CO2 by respiration. This problem is most evident among more experienced divers who have developed this habit over time.

CO2 accumulation – is a typical problem of closed-loop breathing systems where a malfunction of the CO2 filtration systemcan cause an increase in PCO2 in the respiratory mixture. At a lower level, such accumulation can occur in other dead spaces, such as a snorkel that is too long or a helmet (for commercial divers) that is not well-ventilated.

Although the increase in CO2 in the blood is a stimulus to breathing, with a self-regulatory mechanism, a sudden increase in PCO2 can circumvent this mechanism by causing a sudden loss of consciousness. 

At rest, a diver can tolerate PCO2 in the respiratory mixture up to 30 mmHg (equivalent to a concentration of 4% at the nominal pressure of an atmosphere). When physical activity increases, this tolerance decreases. Under extreme exertion, such as when swimming against a strong current, the metabolic production of CO2 can reach 3 liters/minute, and toxicity can develop if it is not quickly eliminated through breathing.

The ventilation capacity decreases with the square root of the density of the breathed gas. At a depth of 90 meters, this reduction can reach 75% of that at sea level. At this point, the expiratory flow cannot be further increased, and the diver becomes unable to ventilate properly, causing further accumulation of CO2.

Increased arterial PCO2 also increases the risk of oxygen toxicity by causing cerebral vasodilation that increases blood flow through the neuronal tissue, resulting in increased partial pressure of oxygen in the brain. It has also been observed that at hyperbaric pressures, CO2 also causes an increase in the production of nitric oxide, which causes further cerebral vasodilation with a further increase in the partial pressure of oxygen. The problem becomes more pronounced when breathing mixtures with high PCO2, as in the case of Nitrox for the open circuit or a high oxygen pressure set-point in a closed circuit respirator.