Correlation between the levels of SpO₂ and PaO₂

Sir,

Sarkar et al. in 2017, in their recent article,[1] have very nicely elucidated various mechanisms of hypoxemia, and I would like to congratulate them for this endeavor.

In continuation, I would like to offer the following hypothesis which correlates well between the levels of hemoglobin saturation (SpO₂) and partial pressure of oxygen in the arterial blood (PaO₂).

We keep on looking arterial blood gas (ABG) reports and keenly watch multi-monitors in Intensive Care Units (ICUs) and wards. As standard teaching, we have a certain image and interpretation of high and low SpO₂ and PaO₂ reports.[2]

The sigmoid shape of the oxy–hemoglobin (Hb) dissociation curve reflects the cooperative interaction between Hb and oxygen (O₂) molecules. The oxy–Hb dissociation curve is initially steep and then flattens out (sigmoid shape). The most important aspect of the curve is that as the oximeter reading falls below 90%, the PaO₂ drops very rapidly and O₂ delivery to the tissues is reduced and leads to irreversible brain damage and cardiac arrest.

The understanding of sigmoidal-shaped oxy–Hb dissociation curve comes very handy in these situations [Figure 1]. O₂ saturation varies with the PaO₂ in a nonlinear relationship and is affected by temperature, pH, 2,3 diphosphoglycerate, and PaCO₂ (partial pressure of carbon dioxide in the arterial blood).[3] Above 90 mmHg of PaO₂, the curve becomes almost flat, and there is a small rise in SpO₂ in spite of big increments in PaO₂. The flat upper part acts as a buffer in the sense that the PaO₂ can drop to about 60 mmHg and yet the Hb will still remain highly saturated (90%) with O₂. The steep lower part also has big advantage in that if the tissues require more O₂, substantial amounts of O₂ can be removed from Hb without greater drops in PaO₂.[4] For example, Hb would be still 50% saturated although PaO₂ has dropped to 26.6 mmHg (P50).

Figure 1.

Oxy–hemoglobin dissociation curve

From last 30 years, while working in critical care wards, I always used to wonder if any formula can be devised which, while waiting for ABG results, can rapidly help a clinician to reach to a PaO₂ level just by looking at SpO₂ values, and I have come up with certain observations/calculations. For the first 10% reduction in SpO₂ from 100% to 90%, decrease PaO₂ by 4 mmHg for every single percent reduction in SpO₂ with a resultant PaO₂ falling from 100 to 60 mmHg [Table 1]. For the next 10% reduction in SpO₂ from 90% to 80%, decrease PaO₂ by 1.5 mmHg for each percent reduction in SpO₂ which will result in PaO₂ falling from 60 to 45 mmHg. Finally, for SpO₂ levels below 80%, divide it by 2, that is half the value of SpO₂, and we get the requisite PaO₂ level.

Table 1.

Calculation for PaO₂ assessment

This hypothesis can have some pitfalls, for example, cyanide poisoning and certain hemoglobinopathies, but still, a fair and working assessment may be drawn from this calculation. Two proven measurements further support this hypothesis:

1. As per classical teaching, at mixed venous point, the SpO₂ of deoxygenated blood returning to the heart is taken as 75% with a saturation of 40 mmHg.[1,3] With the present calculation, O₂ saturation would come out to be 75/2 = 37.5 mmHg, which, in clinical parlance, is not much further away from 40 mmHg

2. The hypothesis is further supported by the value of P50, which is 26.6 mmHg, and again, which is almost half of 50%.

This formula, which is not an exact mathematically proven entity, can be of extreme help to ICU residents and consultants. For example, if the monitor is showing a SpO₂ of 70%, we can almost consider a value of PaO₂ to be around 35 mmHg and take appropriate measures for the patient.

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