Hypoxaemia During One-Lung Anaesthesia

Highlights
- Development of hypoxaemia (i.e. arterial oxygenation <90%) caused by OLV may be explained by considering oxygen storage, dissociation of oxygen from haemoglobin, the relationship between ventilation and perfusion, and factors that reduce the effect of hypoxic pulmonary vasoconstriction. (View Highlight)
- Atelectasis in the ventilated dependent lung occurs as a result of:
compression caused by the weight of the mediastinum;
compression by abdominal contents after diaphragmatic muscle relaxation;
increased closure of small airways with old age, reduced elastic recoil, and the lateral decubitus rather than the erect position. (View Highlight)
- During OLV, there is a reduction in arterial oxygen partial pressure and also permissive hypercarbia and respiratory acidosis. These physiological changes lead to rapid dissociation of oxygen from haemoglobin (Bohr effect) (View Highlight)
- When the patient is breathing spontaneously, ventilation, under negative pressure, is greater in the dependent lung than in the non-dependent lung (except at the very bottom of the dependent lung). Similarly, perfusion in the dependent lung is greater than that in the non-dependent lung. Thus, the ventilation–perfusion relationship is normal and is similar to that observed if the patient is sitting in the standard upright position (View Highlight)
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Fig 1. Schematic diagrams showing ventilation–perfusion relationship in the lateral decubitus position during: (a) spontaneous ventilation, with two lungs, (b) positive pressure ventilation to both lungs, and (c) positive pressure ventilation to the dependent lung. (View Highlight)
- The relationship of ventilation and perfusion changes when the patient is paralysed. In this situation, positive pressure ventilation is directed preferentially to the non-dependent lung, whereas perfusion remains greater in the dependent lung than in the non-dependent lung (Fig. 1b). Thus, compared with spontaneous ventilation, positive pressure ventilation leads to an increase in areas of lung with low ventilation–perfusion ratios. The volume of dead space, that is to say, ventilated lung with no perfusion, also increases during positive pressure ventilation; this effect contributes to hypercarbia. (View Highlight)
New highlights added August 13, 2023 at 5:15 PM
- Hypoxic pulmonary vasoconstriction in the extra-alveolar pulmonary arterioles supplying the unventilated lung is an essential physiological response to minimize shunt and hence hypoxaemia during OLV. This effect occurs when there is a reduction in alveolar partial pressure of oxygen to between 4 and 8 kPa (View Highlight)