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