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REVIEW

Misconceptions in Reporting Oxygen Saturation

John Toffaletti, PhD^*, and Willem G. Zijlstra, MD, PhD

From the *Department of Pathology, Duke University Medical Center, North Carolina; and Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands.

Address correspondence and reprint requests to: John Toffaletti, PhD, PO Box 3015, 133 CARL Bldg., Duke University Medical Center, Durham, NC 27710. Address e-mail to: toffa002{at}mc.duke.edu.

Abstract

BACKGROUND: We describe some misconceptions that have become common practice in reporting blood gas and cooximetry results. In 1980, oxygen saturation was incorrectly redefined in a report of a new instrument for analysis of hemoglobin (Hb) derivatives. Oxygen saturation (sO₂) was redefined as the ratio of oxyhemoglobin (O₂Hb) to total Hb instead of the ratio of O₂Hb to active Hb (O₂Hb + desoxyhemoglobin). In addition, the new terms "functional saturation" and "fractional saturation" were introduced. Since the new parameter was implemented in a widely used cooximeter, its use is now widespread and has caused misunderstandings.

METHODS: In this report, we review the development of the definitions and measurements of sO₂ and related quantities and contend that the misconceptions should be resolved by standardizing instrument read-outs and clinical reports, so that sO₂, defined as the ratio of O₂Hb to active Hb, should replace FO₂Hb and be reported along with the total Hb concentration and the common dyshemoglobin fractions (%CO-Hb and % methemoglobin [metHb]).

RESULTS: The redefinition of sO₂ as the %O₂Hb or FO₂Hb did not address the confusion that might result from interchanging these two often-similar but different terms. The term fractional saturation is an inappropriate terminology and lacks clear physiological meaning. We see frequent cases of confusion: (a) the difference between the sO₂ in pulse oximetry and the FO₂Hb in cooximetry is called the "pulse oximeter gap;" (b) sO₂results are described as "method dependent;" and (c) reference ranges for these terms are substituted.

CONCLUSIONS: Although either parameter could be used by clinicians who fully understand the relatively simple difference between these parameters, we find clear evidence that there is widespread confusion of these terms, even among experts in the field. Standardization of the reporting format would help, and instrument manufacturers could contribute by standardizing the reporting format for cooximetry results.

We call attention to a misunderstanding of terms that has crept into common practice over the years in reporting blood gas and cooximetry results. It began in 1980 with the introduction of an incorrect redefinition of O₂ saturation (sO₂) in a report of a new instrument for analysis of hemoglobin (Hb) derivatives (1). Oxygen saturation (sO₂) was redefined as the ratio of oxyhemoglobin (O₂Hb) to total Hb, instead of the ratio of O₂Hb to active Hb (O₂Hb + desoxyhemoglobin [HHb]). This definition was implemented in the computer program of the instrument and its successors, which were introduced into the market. No arguments were given for this change from the original definition on the sound fundamental work of Christian Bohr around 1900 and presented in textbooks of physiology. The report (1) simply stated, "Defining saturation in terms of all Hb species present gives a more exact and meaningful interpretation of the data." Although it was almost immediately noted that significant misunderstandings would result (2), this did not provoke either a discussion or a retraction of the new definition.

The interchanging of these two similar but different definitions of sO₂ has led to confusion between the saturation reported by pulse oximetry (sO₂) and that reported by many blood gas analyzers (FO₂Hb). This has fostered the idea that the definition of sO₂ is instrument-dependent, and suggested that there are two kinds of saturation (3). These, now widespread, misconceptions have become entrenched in the clinical literature and have occasionally confused the proper clinical interpretation.

For example, a recent guideline for treating carbon monoxide (CO) poisoning, published in the Netherlands (4), stated that under these circumstances transcutaneous oximetry is unreliable, because of a consistent over-estimation of sO₂ by the pulse oximeter. Although the statement was accompanied by two references (5,6), it was based on the incorrect assumptions that the sO₂ is decreased by the presence of carboxyhemoglobin (COHb) in the blood, and that the pulse oximeter would somehow detect the presence of COHb. These are erroneous assumptions because: 1) the calculation of sO₂ is independent of COHb, 2) clinically sO₂ does not decrease in CO poisoning because there is no noticeable decrease in pO₂, and 3) the pulse oximeter is, at the wavelengths used, virtually insensitive to COHb (7).

We believe that the O₂-carrying properties of the blood can be clearly described using three well-defined quantities: O₂ capacity (BO₂), sO₂, and O₂ affinity (3). These quantities can be reliably measured in patients and provide useful information for the treatment of impending hypoxia.

Although the quantities pertaining to the O₂-carrying properties of blood are explained in most textbooks of physiology, we present here a concise summary of the definitions and measurement of BO₂, sO₂, and affinity. We also explain the relationship between the various methods and show that the definitions are independent of the measuring systems.

DEFINITIONS OF O₂ PARAMETERS AND PHYSIOLOGIC REQUIREMENTS

BO₂
The BO₂ is the maximum amount of Hb-bound O₂ per unit volume of blood. It is expressed in mmol/L or in mL standard temperature and pressure dry (STPD)/L or mL(STPD)/dL. BO₂ is determined by the concentration of active hemoglobin, which may be expressed as either the concentration of O₂Hb + HHb, or the concentration of the total Hb (ctHb) minus the concentration of any dyshemoglobin (c_dysHb) present in the blood. dysHbs are Hb derivatives, which have temporarily or permanently lost the capability of reversibly binding O₂ at physiological pO₂ (8). In most patients, COHb and metHb are the major dysHbs.

Hence, when B and c are expressed in mmol/L and the substance concentration of Hb reflects the monomer:

when B is expressed in mL(STPD)/L and c in g/L:

where βO₂ is the volume of O₂ in mL(STPD) that can be bound by 1 g of Hb.

Theoretically, βO₂ = 22394/16114.5 = 1.39 mL/g, where 22,394 is the molar volume of O₂ in mL(STPD), and 16,114.5 is the molar mass of the monomer of human HbA in g (9). This theoretical value has been confirmed experimentally (8).

To satisfy the O₂-consumption requirements of all cells, the O₂-capacity of arterial blood should be high enough to maintain adequate O₂ flow to all cells throughout the capillary bed. We note that the actual O₂ concentration in milliliter O₂ per deciliter blood (minus the small contribution of dissolved O₂) may be calculated with either the sO₂ or the FO₂Hb (fraction of O₂Hb in total Hb, defined in Eq. 7):

with FO₂Hb and sO₂ in decimal fraction of 1.00, and Hb concentrations in g/dL.

sO₂
The blood sO₂ is defined as the concentration of Hb-bound O₂ divided by the BO₂. This is equivalent to the concentration of O₂Hb divided by the sum of the concentrations O₂Hb and HHb:

where cO₂(Hb)is the concentration of O₂ bound to Hb, cO₂(free) is the concentration of O₂ dissolved in blood but not bound to any other substance and ctO₂ is the total O₂ concentration in blood. We note that, although there is a conceptual difference between cO₂(Hb)and cO₂Hb, the two quantities are numerically equal when both are expressed in mmol/L.

The arterial sO₂ should be high to maximize O₂ content, so that the blood is almost fully loaded with O₂ as it enters the capillaries.

O₂ Affinity
The O₂ affinity of the blood is usually demonstrated as a graph of the relationship between sO₂ and pO₂, commonly known as the O₂ dissociation curve (ODC). The influence of other quantities on the O₂ affinity is shown by changes in the position and/or shape of the ODC. The O₂ affinity is decreased by factors such as H⁺ ion, pCO₂, temperature (T), and 2,3-diphosphoglycerate, and increased by COHb, and metHb. The standard-ODC is the ODC at pH = 7.40, pCO₂ = 5.33 kPa (40 mm Hg), T = 37°C.

The O₂-affinity should be such that Hb reaches almost full saturation in the lungs, yet readily releases O₂ at the relatively lower pO₂ in the tissue capillaries. At a normal mixed venous sO₂ of about 70% at rest, most O₂ is released at a pO₂ of around 5 kPa (37 mm Hg), which is the driving pressure for O₂ diffusion to most tissue cells.

DEVELOPMENT OF O₂ AND Hb MEASUREMENTS

BO₂
During the first half of the 20th century, the standard method for determining BO₂ was by measuring the concentration of total O₂ of a known volume of blood that had been equilibrated with room air, using the manometric method of Van Slyke and Neill (10), after correcting for the freely dissolved O₂. In the 1960s, an internationally standardized method for measuring Hb in blood (11) became generally accepted, and also became the method of choice for the determination of BO₂. Since this method measured the ctHb, a correction for the presence of dysHb had to be included for the correct calculation of BO₂. The common dysHbs, COHb and metHb, were measured by spectrophotometry (12,13), and BO₂ was calculated using Eq. 2. Presently, ctHb and cdysHb are usually measured by an automated multiwavelength spectrophotometer, commonly referred to as a cooximeter.

sO₂
The classical procedure for measuring sO₂ was the determination of ctO₂ of a blood sample by means of VanSlyke and Neill’s manometric method (10), then repeating the measurement after equilibrating the remaining part of the sample with air at room temperature. After calculation of cO₂(free) for the 2 measurements, sO₂ was determined using Eq. 5. Even with the development of photometric procedures, the manometric method long remained the "gold standard."

Among the accurate photometric procedures for measuring sO₂ are many two-wavelength methods that use various combinations of wavelengths, multiple types of cuvettes with different path lengths, and Eq. 6 for calculating sO₂ (12–14). In current clinical practice, blood samples are typically analyzed for sO₂ simultaneously with ct_Hb and the concentration of dysHbs (15,16), performed by means of multiwavelength cooximeters capable of analyzing very small samples (14).

A less-reliable method is the calculation of sO₂ from pO₂, pCO₂, and pH on the basis of the standard ODC using a computer program added to a blood gas analyzer. While the calculation works reasonably well in normal blood, erroneous results may be obtained on patients’ blood, because of changes in the O₂ affinity of the blood due to factors not accounted for in the computer program.

sO₂ has also been measured continuously in vivo. Since the early German devices of the 1930s and Millikan’s first oximeter of 1942, several types of oximeters have been developed, using either transmitted or reflected light (14,17–19). Although these methods are fairly accurate and have been used in some physiological and clinical research (20), the procedures are too complicated for routine clinical use. Ex vivo methods for measuring sO₂, i.e., in a cuvette connected to an artery or vein, were developed, especially for use during cardiac catheterization (17–20). Currently, point-of-care devices for conveniently determining sO₂ in very small blood samples have largely replaced the use of the more complicated devices.

Introduction of the pulse principle by the Japanese engineer Takuo Aoyagi made noninvasive in vivo oximetry suitable for routine clinical application (21,22). A pulse oximeter is a two-wavelength photometer that determines arterial sO₂ (as in Eq. 6) by measuring pulsating light absorption through well-perfused tissue, such as a finger (14,21). The relationship of the pulse oximeter output signal to sO₂ is determined empirically by measurements in healthy volunteers. Therefore, sO₂ can accurately be measured only in the higher sO₂ range. sO₂ values <70% are determined by extrapolation and are less accurate. In addition, very high levels of metHb can affect sO₂ readings.

O₂ Affinity
Since determining a complete ODC is difficult (23) and the standard ODC of normal human blood is reasonably constant (14,24), the determination of one or a few points of the actual ODC of a patient is usually sufficient. Customarily, the pO₂ is determined at an sO₂ of approximately 50%, from which the p₅₀ may be determined as a measure of the O₂ affinity (25). After correcting to pH = 7.40, pCO₂ = 5.33 kPa, and T = 37°C, standard-p₅₀ is obtained. The corresponding value as read from the normal standard ODC is 3.554 kPa (27 mm Hg) (14).

Relationship of % Difference (sO₂ – FO₂Hb) and % dysHbs (FCOHb + FmetHb)
Figure 1 shows a graph of the calculated % difference (sO₂ – FO₂Hb) versus the % dysHb concentration for FO₂Hb values ranging from 100% down to 70%. These plots show that for FO₂Hb of 95% and above, the % difference (sO₂ – FO₂Hb) is almost exactly equal to the combined percent of %COHb + %metHb. At lower F (80%, 70%, etc.), the % difference (sO₂ – FO₂Hb) actually becomes slightly less than the sum of %COHb + %metHb, depending on the proportions of deoxyhemoglobin and dysHb. When the % deoxyhemoglobin equals zero (% dysHb + %O₂Hb = 100%), the % difference (sO₂ – FO₂Hb) again equals the % dysHb.

View larger version (18K): [in this window] [in a new window]   Figure 1. Plots of the % difference between sO2 and FO2Hb versus the % dyshemoglobins (%COHb + %metHb). sO2 was calculated as % FO2Hb/(100% – %dysHb).

DISCUSSION

We believe the substitution of (cO₂Hb + cHHb + cdysHb) for (cO₂Hb + cHHb) in calculating sO₂ of Hb is fundamentally incorrect. Consequently, some instruments correctly present sO₂ according to Eq. 6, whereas others incorrectly present sO₂ as the fraction of O₂Hb in total Hb (FO₂Hb):

VanSlyke’s classic manometric method for determining sO₂ defined sO₂ as the ratio of Hb-bound O₂ and O₂-capacity (Eq. 4), with this ratio dependent on pO₂. The relationship between sO₂ and pO₂ in the ODC expresses the ability of Hb to bind and release O₂ as pO₂ changes. Because the influence of the dysHbs upon the O₂-affinity is a secondary effect, analogous but opposite to that of H⁺ ion and pCO₂, their concentration should not be included in the definition of sO₂.

In an attempt to better distinguish between sO₂ and FO₂Hb, a new terminology was introduced by calling sO₂ "functional saturation" and FO₂Hb "fractional saturation." However, the addition of "functional" to "saturation" for designating sO₂ is redundant, and the term "fractional saturation" ignores the concept that "saturation" requires that the system can achieve full saturation, even in the presence of other ligands. The presence of COHb, for instance, does not prevent the remaining Hb from being fully saturated with O₂ (26). Thus, the concept of sO₂ applies to the remaining Hb and not to total Hb. A "saturation scale" by definition runs from 0 to 1, or 0 to 100% (26).

The similarity of these saturation terms actually contributes to the confusion. Moreover, their frequent use led to the fictitious concept of a "pulse oximeter gap" being the difference between these two different quantities (5). That different instruments supposedly measure different kinds of oxygen saturation suggests that the definition of sO₂ is method-dependent. The suggestion is reinforced by the use of the hybrid symbol Spo₂ for sO₂ as measured by a pulse oximeter. In cooximetry, multiwavelength spectrophotometry measures the concentration of the multiple Hb derivatives (27) from which several quantities can be calculated: ctHb, sO₂, FO₂Hb, FCOHb, FmetHb, BO₂, ctO₂ etc. When sO₂ values are reported by blood gas analyzers, cooximetry is in line with pulse oximetry. However, the substitution of FO₂Hb instead of sO₂ in the cooximetry method described by Brown (1) has led to the present widespread confusion of these terms.

Is the difference between sO₂ and FO₂Hb a concern in routine reporting of blood gas reports? For clinicians who understand the differences, either parameter could be used, especially if reported with the appropriate reference interval. Because the COHb and metHb are usually no more than about 2% of the Hb, the sO₂ and FO₂Hb typically differ by only a small amount. However, confusion arises when either (a) both parameters are used interchangeably, (b) inappropriate reference intervals are used, or (c) the concentration of dysHb becomes large. The ubiquity of pulse oximeters ensures the widespread use of sO₂, and so conformity with blood gas/cooximetry reports would be beneficial. In such reports, the sO₂ could replace the FO₂Hb when reported along with the COHb and metHb values, but we do not believe that both sO₂ and FO₂Hb should be reported together. We have observed cases where inappropriate reference intervals are used, such that the FO₂Hb was reported along with the reference range for sO₂. As shown in Figure 1, the % difference (sO₂ – FO₂Hb) increases approximately linearly as the %dysHb increases. Therefore, when either COHb or metHb levels are increased, the sO₂ and FO₂Hb become markedly different, which could more likely cause a misinterpretation of the FO₂Hb.

Being unaffected by the dysHbs, the sO₂ is physiologically more specific for monitoring pulmonary oxygenation than FO₂Hb. Thus, the sO₂ becomes a parameter that specifically monitors oxygen saturation, whereas the COHb and metHb specifically identify the amounts of dysHb present. The inadequacy of reporting either FO₂Hb or sO₂ without the COHb and metHb values was highlighted in a report of a patient with methemoglobinemia, who was introduced as "a woman with low oxygen saturation (28)." Only after working through a long differential diagnosis was the tentative conclusion reached that a dysHb might be present. If the dysHb fractions had been reported along with either the FO₂Hb or sO₂, the correct diagnosis would have been reached immediately.

Because CO increases the O₂-affinity of Hb, one could argue that a decrease in FO₂Hb coincides with a decreased O₂ availability to the tissues. However, clinicians must have sufficient understanding of O₂ physiology to differentiate whether this is caused by a decreased pO₂ and O₂content, an increased O₂ affinity of Hb due to CO (29) or other factors, or both. Both COHb and metHb increase the O₂-affinity and shift the ODC to the left. This effect is quantitatively expressed by the relationship of standard-p₅₀ and FdysHb, as given for COHb in Eq. 8 (14,29):

It follows from Eq. 8 that at FCOHb = 0.35, p₅₀ = 2.14 kPa (16 mm Hg). Consequently, in the presence of COHb, pO₂ must decrease to a considerably lower level for the release of the amount of O₂ needed by the tissues. The diffusion of O₂ to the most unfavorably situated cells becomes even more difficult, with hypoxia more likely. MetHb has a similar effect, but to a lesser degree (14). Because dysHbs influence O₂ affinity as well as BO₂, they should be reported separately, in addition to sO_2.

Although FO₂Hb has a clear analytical definition, it lacks a clear physiological meaning and is a less specific parameter than sO₂. Because FO₂Hb depends on pO₂ as well as on the dysHb fractions, a low FO₂Hb may signal a decreased sO₂, or an increased dyshemoglobin fraction, or both. One study (30) clarified several misconceptions and emphasized the importance of including the dysHb fractions with the FO₂Hb, as would also be the case with sO₂. As mentioned earlier, listing two saturation measurements on the same report could cause even more confusion.

The problems described here can be solved by standardization of both the instrument readouts and the clinical reports, so that ctHb, sO₂, FCOHb, and FmetHb are displayed separately. This requires participation and cooperation of international organizations, such as the International Federation of Clinical Chemistry, and the companies that produce the instruments.

Footnotes

Accepted for publication 11 June 2007.

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