Hypoxia in the context of human physiology means an oxygen (O2) deficiency, or a lower than normal partial pressure of O2 (PO2; also called the O2 tension), in the tissue in question. The term strongly implies inadequate O2 availability to bodily tissues. The brain, liver and kidney, which extract the greatest amount of O2 from the blood to supply their energy requirements, are the first affected by falling O2 levels in the body. Skin, muscle and bone are less vulnerable because of their lower energy requirements. O2 does not directly supply the energy but is necessary to liberate the energy required for cellular metabolism from sugar (glucose).
Aerobic (‘with O2’) metabolism is much more efficient in the production of biological energy than anaerobic metabolism (‘without O2’) and is the key to complex life on Earth. For example, in the presence of O2, 1 molecule of glucose can produce 38 molecules of the energy storage compound adenosine triphosphate (ATP), whereas in the absence of O2, 1 molecule of glucose produces only 2 molecules of ATP (via the production of lactic acid). Thus, anaerobic conditions (hypoxia) drastically reduce the available energy.
Dry air, at a barometric pressure of 760 mm Hg, has a PO2 of 159 mm Hg. When inspired, dry air becomes saturated with water vapour at body temperature. By this dilution the PO2 drops to 149 mm Hg. Alveolar gas has a lower PO2 than inspired air because it is further diluted by carbon dioxide (CO2) and contact with de-oxygenated blood, to around 105 mm Hg. O2 freely diffuses into the capillaries in the lung so that normal arterial blood levels are in the region of 100 mm Hg. As the blood moves through the tissue capillaries, O2 moves by diffusion down partial pressure gradients to the cells, where it is consumed (Figure 16.1). After passage through the tissues the PO2 falls to approximately 40 mm Hg in mixed venous blood coming back into the lungs.
The amount of O2 stored in the body is limited, as are the high-energy phosphate bonds used to store energy. A person breathing air at sea level would hold approximately the following amounts of O2, not all of which is available for use in vital organs such as the brain or heart:
In the lungs——450 ml
In the blood——850 ml
Dissolved in body fluids——50 ml
Bound to myoglobin in muscle——200 ml
Total = 1550 ml
The result is that, unlike diving mammals, we do not have much reserve capacity and cannot stop breathing for long before severe hypoxia intervenes (Table 16.1). During a breath-hold, we are protected from hypoxia because our breakpoint is usually determined by the rising carbon dioxide tension. Hyperventilation prior to breath-holding reduces arterial carbon dioxide tension and extends our breakpoint, but at the risk of unconsciousness from hypoxia.
Basal O2 consumption is of the order of 200 ml/minute, but in swimming and diving much higher consumption is possible (up to 3 litres/minute [lpm]). This explains why hypoxia develops so rapidly if respiration has stopped while exercise continues.
The delivery of O2 at the cellular level requires an adequate inspired PO2 (PIO2), adequate lung function and adequate cardiac output. Further, because most O2 in the blood is carried bound to haemoglobin, it also requires adequate functional haemoglobin levels. At arterial PO2 (PaO2) below 60 mm Hg, the amount of O2 given up to the tissue is greatly reduced.
Although impairment of aerobic metabolism is probably the ultimate mechanism of death in most fatal diving accidents, hypoxia as a primary event is uncommon in conventional scuba diving (breathing air or nitrox). It is much more likely with mixed gas and rebreathing equipment.
The diving disorders mentioned here are discussed more fully in their specific chapters.