Carbon dioxide is produced as a by-product of the Kreb's cycle that links the metabolism of glucose, lipids and amino acids to oxidative phosphorylation and the aerobic generation of energy within cells. Carbon dioxide is excreted by the lungs. The partial pressure of carbon dioxide (PCO2) in arterial blood (PaCO2) can be viewed in reasonably simple mathematical terms as the equilibrium between its production and elimination, modified by the balance between arterial and venous carbon dioxide content (Figure 7.1). It is less subject to the confounding elements seen in oxygen physiology, namely the effects of shunt and the oxy-haemoglobin dissociation curve.

The basic physiology of carbon dioxide elimination has been considered in Chapter 1. In essence, since inspired carbon dioxide concentration is minimal and carbon dioxide production relatively constant over short periods of time, the PaCO2 depends on alveolar ventilation, regulated largely via central chemoreceptors sensitive to PaCO2 and pH that influence both respiratory frequency and tidal volume. This usually results in normocapnia and a PaCO2 between 4.5 and 6.0 kPa. Nevertheless, this balance may be stressed, and even overwhelmed, in unusual physiological states such as extreme exercise, although this is often limited by the onset of fatigue. In pathophysiological states, carbon dioxide production may be increased, elimination may be impaired, or frequently both aberrations may co-exist.