Hypoxia: Methods of Oxygen Delivery

There are various devices or apparatus for the therapeutic administration of O2 (see also Chapter 49). Selection of the appropriate mode of administration depends on a number of factors:

  1. Desired inspired O2 concentration.
  2. Need to avoid CO2 accumulation.
  3. Available O2 (i.e. efficiency and economy).
  4. Need to assist or control ventilation.
  5. Acceptance of the method by the patient.

Various methods for the administration of O2 are shown in Table 16.2 (see Chapter 49). Most plastic masks deliver less than 60 per cent of the fraction of inspired O2 unless a reservoir bag is incorporated, and this increases the risk of CO2 retention.

Modes of oxygen therapy
Table 16.2 Modes of oxygen therapy

Hypoxia: Management

First aid management involves the basic principles of resuscitation, establishing an airway and ensuring that there is ventilation of the lungs and that the oxygenated blood is circulating; 100 per cent O2 should be administered as soon as possible. Further management depends on the aetiology of the hypoxia.

First aid: Airway – Head extended, lower neck flexed, jaw forward; foreign material, secretions removed.Breathing – If breathing, 100 per cent oxygen by mask; if not breathing, mouth-to-mouth or mouth-to-nose respiration followed by intermittent positive pressure resuscitation with 100 per cent oxygen when available.Circulation – If pulse absent, cardiac massage.

In many cases there may be an overlap of different causes of tissue hypoxia, and all patients should receive a high inspired O2 concentration.

Recompression or hyperbaric oxygenation may be indicated as a temporary measure to allow the foregoing regimens time to have an effect (see Chapters 6, 13 and 19).

Hypoxic hypoxia

These patients should be given supplemental inspired O2 or ventilated with 100 per cent O2 at whatever pressure is needed to ensure adequate arterial O2 levels. Once these goals have been achieved, the pressure and percentage of O2 can be progressively reduced while arterial gases or tissue O2 is monitored by transcutaneous oximetry.

Stagnant hypoxia

The aim of therapy is to increase perfusion to the affected areas. This may require restoration of total circulatory volume, as well as vasodilator drugs, and hyperoxygenation as a temporary measure.

Anaemic hypoxia

Blood loss from trauma may require blood transfusion with packed red blood cells after crystalloid or colloid resuscitation. Synthetic blood substitutes show promise but have yet to be introduced to clinical practice.

In the case of carbon monoxide poisoning, hyperbaric oxygenation may be lifesaving during the early critical period.

Histotoxic hypoxia

This form of hypoxia can be treated only by removing the toxic substance and using hyperoxygenation as a temporary measure.

Hypoxia and Deep Diving

Animal experiments at great pressures are regularly undertaken to determine the limits of human exposure and thus ocean penetration. Ventilatory capacity is limited by restricted gas flow or increased work of breathing, both resulting from the effects of increased gas density or from pulmonary damage caused by the cooling effects on the lungs.

Hypoxia may be expected, as a result of such factors as an increased ‘diffusion dead space’ (caused by slowed diffusion of alveolar gases or incomplete mixing of fresh inspired gases and alveolar gases despite adequate inspired O2 pressure and overall pulmonary ventilation).

The Chouteau effect (a disputed concept) is apparent clinical hypoxia despite normal inspired O2 tension that, at least in goats, is rectified by a slight increase in the inspired O2 tension (i.e. normoxic hypoxia). It has been explained by both an alveolar-arterial diffusion abnormality and a non-homogenous mixing of alveolar gas at very high pressures. Saltzman2 has an alternative explanation, suggesting that at greater than 50 ATA there is decreased O2 uptake, with decreased pH and increasing acidosis. Thus, there is a block in the utilization or transport of O2.

Hypoxia and Breath-Hold Diving

In a simple breath-hold, with no immersion or preceding hyperventilation, the breaking point (the irresistible urge to breathe) is initiated mainly by a rise in CO2 level, and to a lesser extent by a fall in arterial O2.

In breath-hold diving, hypoxic blackout is sometimes called breath-hold syncope or shallow water blackout. Because ‘shallow water blackout’ was first used in 1944 to describe loss of consciousness from the use of closed-circuit diving suits, it is best avoided in the breath-holding context. ‘Hypoxic blackout’ is a reasonable alternative.

There are two causes of this disorder – hyperventilation and ascent – and because they may occur concurrently, they are often confused. The hyperventilation effect is independent of depth and may be encountered in 1-meter-deep swimming pools, often by children trying to swim greater distances underwater.

Breath-hold divers who train to extend their breath-hold and also dive deep (e.g. free diving competitors, spear fishing) risk hypoxia of ascent, with loss of consciousness and subsequent drowning.

With hypoxia there is little or no warning of impending unconsciousness. With increased experience the breath-hold diver can delay the need to inhale by various techniques, without improving the O2 status. Breath-hold time can be extended (but not with increased safety) by, for example, feet-first descent, training (adaptation), swallowing, inhaling against a closed glottis and diaphragmatic contractions.

One way of avoiding this hypoxia is to inhale 100 per cent O2 before the breath-hold.

Hyperventilation

In 1961, Craig observed that swimmers who hyperventilated could stay longer underwater but then lose consciousness with little or no warning1. They were often competing, against others or themselves, and often exercising. The hyperventilation extended their breath-holding time because it washed out a large amount of CO2 from the lungs, often to half the normal levels.

The build-up of CO2 is the main stimulus forcing the swimmer to surface and breathe. After hyperventilating it takes much longer for this level (the ‘breaking point’) to be reached. Under these conditions, the diver may extend the breath-hold to the point that PaO2 drops to a level inadequate to sustain consciousness. Increased exercise exacerbates this effect by increasing O2 consumption.

The combination of these two effects (hyperventilation and exercise) can be deadly. One can demonstrate this dangerous combination in the following experiment: When the swimmer is concentrating on some purposeful goal, such as trying to spear a fish or retrieve a catch, he or she is more likely to ignore the physiological warning symptoms of an urge to breathe (resulting from the rise in CO2 level in the blood) and delay the breaking point.

The dangers of hyperventilation and breath-hold diving are diagrammatically illustrated in Figure 16.3. It illustrates that, with earlier hyperventilation, the time to reach the irresistible urge to breathe (the breaking point) is prolonged. This extra time may allow the PaO2 to fall to dangerous levels (hypoxic danger zone).

A diagrammatic representation of changes in arterial oxygen and carbon dioxide levels with breath-holding.
Figure 16.3 A diagrammatic representation of changes in arterial oxygen and carbon dioxide levels with breath-holding. Point A, without preceding hyperventilation; point B, with preceding hyperventilation. PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen.

Ascent

Ascent hypoxia was first described in military divers losing consciousness as they surfaced with low O2 levels in their rebreathing equipment.

In breath-hold divers, with descent the pressure rises proportionately in the alveolar gases, thus increasing the available O2, CO2 and nitrogen. Some O2 can be absorbed and used, some CO2 absorbed and buffered, and some nitrogen absorbed and deposited in tissues.

Thus, if a diver having 100 mm Hg O2 and 40 mm Hg CO2 in the alveolar gases was immediately transported to 2 ATA, the lungs would halve their volume; the O2 would be 200 mm Hg, and the CO2 80 mm Hg. Both would pass into the pulmonary capillary blood, the O2 to be used and the CO2 to be buffered. The alveolar PO2 and PCO2 therefore would decrease rapidly. By the time these values were both back to ‘normal’ levels, with O2 at 100 mm Hg and CO2 at 40 mm Hg, the diver would appear to be in a satisfactory respiratory status – until he or she ascended. With an expansion of the lungs to twice their size at depth, the pressures in both gases would halve; i.e. the O2 would drop to 50 mm Hg (approaching a potentially dangerous hypoxia level) and the CO2 to 20 mm Hg – if the ascent was immediate.

Because ascents do take time, more O2 will be consumed, extracted from the lungs during the ascent, and the CO2 will increase toward normal as a result of the gradient between the pulmonary blood and alveoli.

The drop in O2 is then able to produce the loss of consciousness, the ‘syncope’ or ‘blackout’, commonly noted among spear fishers. This condition is referred to as hypoxia of ascent. In deeper dives it becomes more likely, and with some very deep dives, the loss of consciousness may occur on the way to the surface in the top 10 metres (probably an explanation for the ‘7-metre syncope’ described by French workers).

Other causes of hypoxia in breath-hold diving include salt water aspiration and the drowning syndromes (see Chapters 21, 22 and 24).

Hypoxia and Diving Equipment

Hypoxia secondary to inadequate inspired O2 results from the failure or improper use of the diving equipment. Apart from running out of air on open-circuit scuba, this disorder occurs mainly with the use of closed-circuit or semi-closed-circuit rebreathing apparatus.

Of the following six causes only the first two mechanisms are possible with open-circuit scuba:

1. Exhaustion of gas supply.
2. Low O2 concentration.
3. Inadequate flow rates.
4. Increased O2 consumption.
5. Dilution hypoxia.
6. Hypoxia of ascent.

Exhaustion of gas supply

The ‘out of air’ situation remains a major cause of diving accidents, despite contents gauges, reserve supplies and training (Case Report 16.1).


CASE REPORT 16.1

Two commercial divers were engaged in making a 110-metre mixed gas dive from a diving bell. The purpose of the dive was to tie in a 6-inch riser. While one diver was in the water at depth working on the riser, the diving bell operator excitedly informed topside that the bell was losing pressure and flooding. The surface operator, who was disconcerted by this information, opened valves to send gas to the bell. Communication with the bell operator was lost.

The diver who was in the water working on the riser was instructed to return to the bell, which he did. When the diver arrived at the bell, he found the bell operator unconscious and lying on the deck of the bell. The diver climbed out of the water into the bell, took off his Kirby-Morgan mask, and promptly collapsed. When topside personnel realized that they had completely lost communications with the bell, they made ready the standby divers. The first standby diver was dressed, put on his diving helmet and promptly collapsed unconscious on deck. At this point the bell with the diver and the bell operator was brought to the surface with the hatch open and without any decompression stops. The divers were extricated from the bell and recompressed in a deck decompression chamber. Both the diver and the bell operator died in the deck decompression chamber at 50 metres, of fulminating decompression sickness.

Examination of the rack (the collection of gas cylinders to be used during the dive) showed that the rack operator had mistakenly opened a cross-connect valve that should have been ‘tagged out’ (labeled to indicate that it should not be used). This valve permitted 100 per cent helium to be delivered to the diving bell and the standby divers, instead of the appropriate helium-oxygen breathing mixture.

Diagnosis: acute hypoxia and fulminant decompression sickness.


Low oxygen concentration in the gas supply

Accidental filling of an air cylinder with another gas, such as nitrogen, may result in unconsciousness. Low-percentage O2 mixtures (10 per cent O2 or less), designed for use in deep or saturation diving, would lead to hypoxia if breathed near the surface.

Rusting (oxidization) of scuba cylinders can reduce the O2 content, and It has led to at least one fatality and several ‘near misses’ (Case Report 16.2).


CASE REPORT 16.2

MB, a civilian diver, was asked to cut free a rope that was wrapped around the propeller of a diver’s charter boat. Because of the very shallow nature of the dive (3 metres maximum), he used a small steel cylinder not often used by divers. After he entered the water, his diving partner noticed that he was acting in a strange manner and swam to him. At this point the diver was lying on the bottom and was unconscious but still breathing through his single hose regulator. The diving partner rescued the unconscious diver and got him on deck. His fellow divers prised the mouthpiece from him and gave him cardiopulmonary resuscitation, and the diver promptly regained consciousness.

On analysis, the gas in the cylinder was found to be 98 per cent nitrogen and 2 per cent oxygen. There was sea water present in the interior of the cylinder, together with a considerable amount of rust.

Diagnosis: acute hypoxia resulting from low inspired oxygen(see Chapters 6 and 47) concentration.


Inadequate flow rates

Many rebreathing diving sets have a constant flow of gas into the counterlung (see Chapters 4 and 62 for an explanation of this equipment). A set designed to use various gas mixtures has a means of adjusting these flow rates. The flow rate should be set to supply enough O2 for the diver’s maximum requirements, in addition to that lost through the exhaust valve. The higher the O2 concentration of the gas, the lower the required flow rate will be, and vice versa.

If an inadequate flow rate is set for the O2 mixture used, then the inert gas (e.g. nitrogen) will accumulate in the counterlung. Low concentrations of O2 will then be inspired by the diver (Case Report 16.3). Other causes include blockage of the reducer by ice, particles among others.


CASE REPORT 16.3

AS was diving to 20 metres using a 60/40 oxygen-nitrogen mixture in a semi-closed-circuit rebreathing system. After 15 minutes he noted difficulty in obtaining enough gas. He stopped to try and adjust his relief valve and then suddenly lost consciousness. Another diver noticed him lying face down on the bottom. The second diver flushed the unconscious diver’s counterlung with gas and took him to the surface, after which the set was turned to atmosphere, so that the diver was breathing air. The diver started to regain consciousness but was initially still cyanosed. He became aware of his surroundings and did not require further resuscitation. Equipment investigation revealed that carbon dioxide absorbent activity was normal, but reducer flow was set at 2 lpm instead of the required 6 lpm. This would supply inadequate oxygen for the diver’s expected rate of utilization.

Diagnosis: hypoxia resulting from inadequate gas flow rate.


Increased oxygen consumption

Most rebreathing sets are designed for maximum O2 consumption between 1 and 2.5 lpm depending on the anticipated exertion. Commonly, the maximum O2 uptake is assumed to be 1.5 lpm. Several studies have shown that divers can consume O2 at higher rates than these. Values of more than 2.5 lpm for 30 minutes and more than 3 lpm for 10 to 15 minutes have been recorded without excessive fatigue underwater.

This increased exertion may be tolerated because of the cooling effect of the environment and/or greater tissue utilization with increased amount of O2 physically dissolved in the plasma. This indicates that it is possible for a diver to consume O2 at a greater than the often quoted rate under certain conditions. In rebreathing sets, a hypoxic mixture could then develop in the counterlung in response to accumulation of nitrogen (i.e. dilution hypoxia).

Dilution hypoxia

This term applies mainly to O2 rebreathing sets. Dilution hypoxia is caused by dilution of the O2 in the counterlung by inert gas, usually nitrogen. The unwanted nitrogen may enter the system by three methods:

  1. From the gas supply.
  2. From failure to clear the counterlung of air before use, thus leaving a litre or more nitrogen in it.
  3. Failure to clear the lungs before using the equipment; e.g. if a diver breathes into the set after a full inhalation, he or she may add up to 3 litres of nitrogen to the counterlung. This may also occur if the diver surfaces and breathes from the atmosphere, to report activities or for some other reason.

Dilution hypoxia is more likely if O2 is supplied only ‘on demand’ (i.e. when the counterlung is empty), rather than having a constant flow of gas into the bag. As the diver continues to use up the O2, the nitrogen remains in the counterlung. CO2 will continue to be removed by the absorbent, thereby avoiding dyspnoea. Thus, the percentage of O2 in the inspired gas falls as it is consumed. There is approximately 1 litre of nitrogen dissolved in the body, but the amount that would diffuse out into the counterlung to cause dilution hypoxia would be a small contribution.

Hypoxia of ascent

By one of the foregoing mechanisms, the percentage of O2 being inspired may drop to well below 20 per cent. An inspired O2 concentration of 10 per cent can be breathed quite safely at 10 metres because the partial pressure would still be adequate (approximately 140 mm Hg).

Hypoxia develops when the diver ascends sufficiently to reduce this PO2 to a critical level (Case Report 16.4). The disorder is therefore most likely to develop at or near the surface.


CASE REPORT 16.4

RAB was diving to 22 metres while using a semi-closed-circuit rebreathing set with a 40/60 oxygen-nitrogen mixture. After 36 minutes he was instructed to ascend slowly. At approximately 3 to 4 metres he noted some difficulty in breathing but continued to ascend and then started to climb on board, but he appeared to have some difficulty with this. When asked whether he was well he did not answer. He was cyanosed around the lips, and his teeth were firmly clenched on the mouthpiece. On removal of his set and administration of oxygen, he recovered rapidly but remained totally amnesic for 10 minutes. Examination of his diving equipment revealed that both main cylinders were empty and the emergency supply had not been used.

Diagnosis: hypoxia of ascent.

Hypoxia: Classification

Hypoxia (‘anoxia’) has been classified into four types:

  1.  Hypoxic.
  2. Stagnant.
  3. Anaemic.
  4. Histotoxic.

Hypoxic hypoxia

This designation covers all conditions leading to a reduction in arterial O2 (Figure 16.2). A better term would be ‘hypoxaemic hypoxia’. This is the common form of hypoxia seen in diving. Causes of hypoxaemia, with examples related to diving, are discussed in the following paragraphs.

Mechanisms of hypoxaemia (hypoxic hypoxia).
Figure 16.2 Mechanisms of hypoxaemia (hypoxic hypoxia). (a) Inadequate oxygen supply. (b) Alveolar hypoventilation. (c) Perfusion of non-ventilated alveoli causing venous admixture. (d) Ventilation-perfusion inequality. (e) Diffusion defect. PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen; PIO2, inspired oxygen tension.

INADEQUATE OXYGEN SUPPLY

This condition results from a decrease in O2 pressure in the inspired gas, which may in turn be caused by an incorrect gas mixture or equipment failure. CO2 retention is not a feature of this type of hypoxaemia.

ALVEOLAR HYPOVENTILATION

This condition occurs when the amount of gas flowing in and out of functioning alveoli per unit time is reduced. It may result from increased density of gases with depth or decreased compliance with the drowning syndromes, among other causes. The extreme example is breath-holding diving. There is associated CO2 retention.

VENTILATION-PERFUSION INEQUALITY AND SHUNT

Perfusion of blood past alveoli that are not being ventilated causes non-oxygenated blood to move into the systemic circulation. This blood is referred to as a ‘right-to-left shunt’ because blood is shunted from the right side of the heart through the lungs but without picking up O2 or releasing CO2. The degree of arterial desaturation depends on the proportion of the cardiac output that is shunted (the shunt fraction). Lesser degrees of mismatching of perfusion and ventilation may be seen in near drowning, salt water aspiration syndrome, pulmonary O2 toxicity and pneumothorax. Inequality of ventilation and perfusion may also occur in pulmonary DCS sickness and pulmonary barotrauma, as well as in deep divers using helium, in whom it is a consequence of lung cooling.

The arterial CO2 response is variable with ventilation-perfusion disorders, with high levels in severe cases, but mild hypocapnia (low partial pressure of CO2 [PCO2]) is more usual if ventilation in the perfused lung is increased by hypoxic drive.

DIFFUSION DEFECT

This defect results from slowed diffusion of O2 through a thickened alveolar-capillary barrier. This may occur after near drowning and as a result of pulmonary O2 toxicity. CO2 retention is not characteristic of this type of hypoxaemia because CO2 diffuses through the barrier much more rapidly than O2.

There is obviously great overlap among the different mechanisms by which the various conditions produce hypoxaemia.

Stagnant (ischaemic) hypoxia

Reduced tissue blood perfusion leads to hypoxia as a result of the continued metabolism of O2 in the presence of a reduced supply, and it may be either regional or general. The extreme form is circulatory arrest. Syncope of ascent is a transitory manifestation resulting from inadequate cardiac output (see Chapters 6 and 47).

Reduced cardiac output may also be present in serious DCS when local ischaemia results from gas bubbles obstructing venous return. In addition, reduced cardiac output may be caused by gas emboli arising in both DCS and pulmonary barotrauma.

Many marine venoms induce stagnant hypoxia, and localized ischaemia is the cause of many of the symptoms and signs of these envenomations.

Anaemic hypoxia

This designation refers to any condition characterized by a reduction in haemoglobin concentration in the blood or alterations in the O2-carrying capacity of haemoglobin. One cause is traumatic haemorrhage, with restoration of the blood volume with fluids.

Carbon monoxide poisoning (see Chapter 19), in which the formation of carboxyhaemoglobin reduces the O2-carrying capacity of the blood, is most often a consequence of contamination of compressed air.

The capacity of haemoglobin to carry O2 is also reduced in the presence of alkalaemia, e.g. low PaCO2, and hypothermia.

Histotoxic hypoxia

This term refers to the situation in which adequate O2 is delivered to the tissues, but there is a failure of utilization within the cell. Carbon monoxide poisons the enzyme cytochrome oxidase, which is a vital link in the use of O2 to provide energy for normal cell function. Histotoxic hypoxia has also been postulated as a mechanism for inert gas narcosis (see Chapter 15) and O2 toxicity (see Chapter 17).

Hypoxia: Clinical Features

The physiological consequences of hypoxia in general medicine are well known and are not discussed here.

The symptoms and signs of hypoxia become obvious when the PaO2 drops below about 50 mm Hg. This corresponds to an inspired concentration at sea level of 8 to 10 per cent. If the fall in PO2 is rapid, then loss of consciousness may be unheralded. With slower falls, an observer may note lack of coordination or poor job performance. Euphoria, overconfidence and apathy are also been reported. Memory is defective and judgement impaired, leading to inappropriate or dangerous reactions to the emergency that may also endanger others. The diver may complain of fatigue, headache or blurred vision.

There are rarely any symptoms to warn the diver of impending unconsciousness from hypoxia.

Hyperventilation may develop in some cases, but it is usually minimal if the arterial CO2 tension (PaCO2) is normal or low.

There are marked individual differences in susceptibility to hypoxia. When combined with hypocapnia or hypercapnia, hypoxia will impair mental performance earlier than if the diver is normocapnic; mental performance may not be severely impaired until the alveolar-arterial PO2 falls below 40 mm Hg. Hypoxia may precipitate or exacerbate other pathological conditions, such as coronary or cerebral ischaemia.

Cyanosis of the lips and nail beds may be difficult to determine in the peripherally vasoconstricted ‘cold and blue’ diver. Generalized convulsions or other neurological manifestations may be the first signs. Masseter spasm is common and may interfere with resuscitation. Eventually, respiratory failure, cardiac arrest and death supervene.

Diagnostic errors may arise because some of the foregoing manifestations are common to nitrogen narcosis, O2 toxicity and CO2 retention. The attending physician should also consider cerebral arterial gas embolism and decompression sickness (DCS), should the previously described features develop during or after ascent by a diver breathing compressed gases.

Hypoxia: Introduction

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 oxygen cascade.
Figure 16.1 The oxygen cascade. On the left is shown the cascade with partial pressure of oxygen (PO2) falling from the level in the ambient air down to the level in mitochondria, the site of utilization. On the right is shown a summary of factors influencing oxygenation at different levels in the cascade. (Redrawn from Nunn JF. Applied Respiratory Physiology. 3rd ed. London: Butterworth; 1987.)

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.

Effects of hyperventilation on the breath-holding time and alveolar gas pressure at the breaking point in resting and exercising man

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.