Drs Jon Warwick and Neil Crooks discuss hypoxic respiratory failure and the effects of cabin pressurisation on patients with respiratory conditions, considering whether or not patients with high oxygen concentrations may benefit from a lower cabin altitude during transfer
The oxygenation of blood and the removal of carbon dioxide at the alveolar capillary interface is an extremely efficient process. Total surface area for gas exchange in the adult depends on body size; the true value is a matter of debate, but there may be some 500 million alveoli with a total surface area of 150m2. The diffusion distance across the blood/gas interface is just 1 m, and in some places even thinner. Transit time for an erythrocyte to traverse the alveolar capillary (i.e. from the venous to the arterial side of the vasculature) is 1 sec, and the haemoglobin (Hb) it contains will become fully saturated with oxygen in approximately the first quarter of its journey (¼ sec) along the capillary. Blood flow in the lung (Q), and ventilation (V), must be closely matched (V/Q 0.8) for optimum gas exchange to occur, and there are various mechanisms within the lung that help to achieve this.
Arterial oxygen partial pressure (PaO2) is related to both content (CaO2) and haemoglobin saturation (SaO2, or SpO2 if measured by pulse oximetry) by the oxyhaemoglobin dissociation curve (Fig. 2). Normal PaO2 is approximately 13.3KPa, and assuming a Hb concentration of 150 g/l, and normal oxygen carrying capacity of 1.34 ml/g, this will produce a CaO2 of some 200 ml/l (or 20 ml/dl). Normal cardiac output is 5 litres/min, giving a total oxygen delivery (from left ventricle to aorta) of 1,000 ml/min.
The leading cause of hypoxic respiratory failure in patients receiving intensive care is ventilation/perfusion (V/Q) mismatch. This is true for a wide range of conditions, for example pulmonary oedema, pneumonia, sepsis, aspiration, blast injury – indeed, almost every cause of acute respiratory distress syndrome (ARDS). Following an injury or insult from whatever cause, the lung responds by becoming wet, inflamed, poorly-aerated, and stiff. These patients have areas of the lung that are inadequately ventilated in comparison to their perfusion (V/Q<<1). This low V/Q area will result in arterial blood with a depressed oxygen content. Blood from these lung areas will mix with blood from areas with normal and higher V/Q ratios, and hence normal or elevated PO2 values. What is sometimes not appreciated is that even if blood from low V/Q regions (with low PO2) mixes with blood from high V/Q regions (with high PO2), the resulting mixed arterial blood will always have a depressed PO2 and SaO2. This is because it is the oxygen contents from these different areas that become averaged in the pulmonary vein, and not an average of PO2. High V/Q regions cannot increase their oxygen content despite their elevated PO2. Oxygen content is primarily due to the oxygen bound to Hb; this is practically maximal even at a ‘normal’ PO2.
Shunt refers to that fraction of the pulmonary blood flow which effectively bypasses the gas-exchange surface. Pure shunt (V/Q=0) is clearly not correctable by an increase in FIO2, since both ventilation and perfusion are completely separated – no amount of increase in alveolar partial pressure of oxygen (PAO2) can compensate for a situation where there is no ventilation to a perfused alveolus. True shunt is usually small. In sick patients with ARDS-type respiratory failure, the depression of arterial oxygenation is principally due to V/Q mismatch rather than shunt, but since it is not easy to quantify degrees of V/Q mismatch, it is conventional to describe it in terms of the degree of true shunt which would produce the same observed gas exchange abnormality, hence the term ‘shunt-like effect’.
It is important to understand the relationship between FIO2 and PaO2 (Fig. 3). In health, with effectively zero shunt-like effect, there is an almost direct linear relationship between the two. As FIO2 increases, then PaO2 will also increase. But as shunt fraction increases in patients with V/Q inequality, then a progressively higher inspired oxygen percentage is required to achieve a given PaO2. It can be seen from Fig. 3 that as shunt fraction exceeds 25 to 30 per cent, then large changes in FIO2 can be made with only minimal improvement in PaO2. To put it another way, arterial oxygenation (measured by content, partial pressure or haemoglobin saturation) becomes progressively independent of the inspired oxygen percentage above shunt fractions of 25 to 30 per cent. In effect, the patient becomes increasingly ‘oxygen resistant’. And it follows that the more oxygen resistant a patient becomes, then the less their oxygenation will be affected by changes in ambient pressure, i.e. aircraft cabin altitude. This is the explanation why we sometimes meet patients on intensive care, receiving high inspired oxygen concentrations, whose oxygenation remains much the same despite the reduction in ambient pressure of the aircraft cabin.