Pulse oximetry in the newborn is useful for detecting critical CHD not detectable by careful clinical examination. At sea level, a cut-off value of 95% will detect most critical CHD (except for some coarctation of the aorta) with an acceptably low false positive rate. At altitude, because of the lower atmospheric pressure, the normal arterial oxygen saturation is lowered^{Reference Subhi, Smith and Duke1–Reference Hoffman3} and the variability of normal saturations (standard deviation) is increased. Consequently, we can expect more false positives and false negatives at high altitudes than at sea level. The reasons for the increased variability are varied. There are different responses to altitude among different ethnic groups.^{Reference Niermeyer, Yang, Shanmina, Drolkar, Zhuang and Moore4,Reference Huicho5} Some of these differences are related to shifts of P₅₀ (the arterial oxygen tension at which blood is 50% saturated with oxygen), due to alterations of haemoglobin configuration^{Reference Storz and Moriyama6}, cardiac output, respiration, blood pH, and 2,3 diphosphoglycerate concentrations. These differences make it difficult if not impossible to determine a cut-off arterial oxygen saturation at a given altitude while breathing ambient air for different ethnic communities.

Some cities at high altitudes such as Quito and Mexico City have large populations and excellent medical services, so that ancillary investigations by echocardiography are available. Many high-altitude cities and towns, however, have small populations⁷, limited medical services, and in general do not have echocardiography available, let alone paediatric echocardiography. They are often remote from larger cities to which travel is difficult and expensive.

How can these disadvantages be overcome? One possibility is to accept that false positives will be more common and arrange for transport of all infants who do not have saturations appropriate for the altitude to a larger city. A second might be to arrange for all deliveries to take place in towns at lower altitudes. Both of these choices involve extra expense and inconvenience.

One possible approach would be to determine the change in arterial oxygen tension while the infant is breathing 100% oxygen. How does this affect arterial oxygen tension? Arterial oxygen tension is lower than that in the alveoli. The alveolar–arterial (A-a) oxygen tension difference depends on diffusion, ventilation–perfusion (V/Q) mismatch, and venous admixture.^{Reference Rahn and Fenn8} In neonates at sea level, the A-a difference averages 28 mmHg with a standard deviation of 10 mmHg;^{Reference Nelson, Prod’Hom, Cherry, Lipsitz and Smith9} most of the difference is due to a large shunt bypassing the alveoli. When breathing 100% oxygen, diffusion and V/Q mismatch no longer contribute to the A-a difference^{Reference Rahn and Fenn8}, but venous admixture remains, possibly at the same magnitude as at sea level. Therefore, in practice, the neonate breathing 100% oxygen will have an arterial oxygen tension as much as 50 mmHg below the alveolar oxygen tension at any given altitude. The graph relating arterial oxygen tension to altitude while breathing 100% oxygen is given in Figure 1.

Figure 1.

The alveolar oxygen tension in mmHg is plotted against altitude in metres. (based on data from Rahn and Fenn^{Reference Rahn and Fenn8}. The arterial oxygen tension in mmHg is shown in the dashed curve and is based on the mean A-a difference plus two standard deviations.

The normal neonate in the week after birth has about 80% fetal haemoglobin with an oxygen dissociation curve very different from that seen with adult haemoglobin.^{Reference Oski10} However, at oxygen tensions above 200 mmHg, these differences disappear and need not be considered. At sea level, while breathing room air, the arterial oxygen tension is about 60 mmHg at 95% saturation, the cut-off for normal by pulse oximetry. When breathing 100% oxygen, the arterial oxygen tension should increase to about 630 mmHg. At 4000 m altitude, the average arterial oxygen saturation is about 90%, with a wide standard deviation up to about 5% so that a normal value of 85% would not be exceptional. This corresponds to an arterial oxygen tension of 43 mmHg.

Jones et al.^{Reference Jones, Baumer, Joseph and Shinebourne11} studied cyanotic and acyanotic infants at sea level. While breathing room air, the cyanotic infants had a mean arterial oxygen tension of 39 mmHg, with a range of near 0 to 100 mmHg. While breathing 95–100% oxygen, their mean arterial oxygen tension was 54 mmHg, and very few were over 150 mmHg. Shannon et al.^{Reference Shannon, Lusser, Goldblatt and Bunnell12} noted that supplying 100% oxygen by positive end-expiratory pressure reduced the arterial oxygen tension in cyanotic neonates but increased it from an average of 66 mmHg on room air to 207 mmHg on oxygen in those with pulmonary problems.

At high altitudes, we expect a normal neonate to have an arterial oxygen saturation of as low as 85%, with a corresponding arterial oxygen tension of 43 mmHg, but supplying 100% oxygen, even at lowered atmospheric pressures, should increase the arterial oxygen tension to >150 mmHg. Failure to achieve this increase would indicate a significant right-to-left shunt at one of three sites: (1) the heart, due to cyanotic heart disease, (2) the ductus, due to aortic coarctation or severe pulmonary hypertension, or (3) the lungs due to severe pulmonary disease. In fact, if a cyanotic neonate turns pink with increased oxygen administration, lung disease is very likely to be present. Any of these would be good indications for further investigation of the infant and would warrant transport to a larger regional centre.