Closed-circuit systems with a constant inflow and consumption of oxygen will allow retention of other gases entering the circuit either with the fresh gas or from the patient. This affects the patient in two quite distinct ways. First, essentially inert gases such as nitrogen and argon may accumulate to such an extent that they dilute the oxygen in the system. Secondly, small concentrations of more toxic gases may arise within the breathing system.

Nitrogen enters the circuit from the patient at the start of anaesthesia. Body stores of dissolved nitrogen are small, but air present in the lungs may contain 2–3 litres of nitrogen, which will be transferred to the circuit in the first few minutes. If nitrogen is not intended to be part of the closed-circuit gas mixture, the patient must ‘denitrogenate’ by breathing high concentrations of oxygen before being anaesthetised, or higher fresh gas flow rates must be used initially to flush the nitrogen from the closed circuit.

Argon is normally present in air at a concentration of 0.93%. Oxygen concentrators effectively remove nitrogen from air, and so concentrate argon in similar proportions to oxygen, resulting in argon concentrations of around 5%. In a study of closed-circuit breathing in volunteers using oxygen from an oxygen concentrator, argon levels in the circuit reached 40% after only 80 minutes.² Cylinders of medical grade oxygen and hospital supplies from liquid oxygen evaporators contain negligible argon, so the risk of significant accumulation is low.

Methane is produced in the distal colon by anaerobic bacterial fermentation and is mostly excreted directly from the alimentary tract. Some methane is, however, absorbed into the blood, where it has low solubility so is rapidly excreted by the lung, following which it will accumulate in the closed circuit. There is a large variation between subjects in methane production and, therefore, the concentrations seen during closed-circuit anaesthesia. Mean levels in the circle system in healthy patients reached over 900 ppm, well below levels regarded as unacceptable in other closed environments, but sufficient to cause interference with some anaesthetic gas analysers.³

Acetone, ethanol and carbon monoxide all have high blood solubility, so concentrations in the closed circuit remain low, but rebreathing causes accumulation in the blood. Levels achieved are generally low,³ but acetone accumulation may be associated with postoperative nausea.⁴ Closed-circuit anaesthesia is not recommended in patients with increased excretion of acetone or alcohol, such as uncontrolled diabetes mellitus, recent alcohol ingestion or during prolonged starvation.¹

Definition of a ‘safe’ level of atmospheric CO₂ over long periods has concerned submarine designers for some years. The respiratory response to inhalation of low concentrations of CO₂ (< 3%) is similar to that at higher levels (page 69), but compensatory acid–base changes seem to be quite different.

Respiratory changes.^9,10 Atmospheric CO₂ levels of 1% cause an elevation of inspired Pco₂ of 1 kPa (7.5 mmHg), which results in an average increase in minute ventilation of 2–3 l.min⁻¹. However, the degree of hyperventilation is highly variable between subjects, and presumably relates to their central chemoreceptor sensitivity to CO₂ (page 69). Measurements of arterial blood gases in submariners show that the elevated minute volume limits the increase in arterial Pco₂ to an average of only 0.14 kPa (1 mmHg). After a few days, the increase in ventilation declines, and minute volume returns towards normal, allowing arterial Pco₂ to increase further to reflect the inspired Pco₂. The time course of the decline in ventilation is too short to result from blood acid–base compensation (see below), and is believed to reflect a small attenuation of the central chemoreceptor response. On return to the surface, ventilation may be temporarily reduced following withdrawal of the CO₂ stimulus.

Calcium metabolism.^9,11 Elevation of arterial Pco₂ causes a respiratory acidosis, which is normally, over the course of one or two days, compensated for by the retention of bicarbonate by the kidney (page 359). The changes in pH seen when breathing less than 3% CO₂ appear to be too small to stimulate measurable renal compensation, and pH remains slightly lowered for some time. During this period, CO₂ is deposited in bone as calcium carbonate, and urinary and faecal calcium excretion is drastically reduced to facilitate this. Serum calcium levels also decrease, suggesting a shift of extracellular calcium to the intracellular space.¹¹ After about three weeks, when bone stores of CO₂ are saturated, renal excretion of calcium and hydrogen ions begins to increase and pH tends to return to normal. Abnormalities of calcium metabolism have been demonstrated with inspired CO₂ concentrations as low as 0.5%.

Some other effects of low levels of atmospheric CO₂ during space travel are described below (page 307).

A summary of manned space missions and the atmospheres used is shown in Table 19.1. Spacecraft have an almost totally sealed, closed-circuit system of atmospheric control, and early Soviet space vehicles aimed to be completely sealed environments. Their designers had such confidence in the structure that emergency stores of oxygen were considered unnecessary until Soyuz 11 depressurised on re-entry in 1971, tragically killing all three cosmonauts. American Apollo missions leaked approximately 1 kg of gas per day in space, even with a lower atmospheric pressure (Table 19.1).

Table 19.1 Summary of manned space missions and their respiratory environments

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