Abstract
Despite its success as a clinical monitoring tool, pulse oximetry may be improved with respect to the need for empirical calibration and the reports of biases in readings associated with peripheral vasoconstriction and haemoglobin concentration. To effect this improvement, this work aims to improve the understanding of the photoplethysmography signal—as used by pulse oximeters—and investigates the effect of vessel calibre and haemoglobin concentration on pulse oximetry. The digital temperature and the transmission of a wide spectrum of light through the fingers of 57 people with known haemoglobin concentrations were measured and simulations of the transmission of that spectrum of light through finger models were performed. Ratios of pulsatile attenuations of light as used in pulse oximetry were dependent upon peripheral temperature and on blood haemoglobin concentration. In addition, both the simulation and in vivo results showed that the pulsatile attenuation of light through fingers was approximately proportional to the absorption coefficients of blood, only when the absorption coefficients were small. These findings were explained in terms of discrete blood vessels acting as barriers to light transmission through tissue. Due to the influence of discrete blood vessels on light transmission, pulse oximeter outputs tend to be dependent upon haemoglobin concentration and on the calibre of pulsing blood vessels—which are affected by vasoconstriction/vasodilation. The effects of discrete blood vessels may account for part of the difference between the Beer–Lambert pulse oximetry model and empirical calibration.
Highlights
1 Introduction Pulse oximeter outputs can be influenced by factors other than arterial haemoglobin oxygen saturation (SaO2): blood haemoglobin concentration has been shown to affect the accuracy of pulse oximetry (Severinghaus and Koh, 1990; Vegfors et al, 1992); placing pulse oximeter probes close to large blood vessels can degrade performance (Mannheimer et al, 2004; Vegfors et al, 1992); temperature induced peripheral vasoconstriction has been associated with increased pulse oximeter readings (Hynson et al, 1992; Sessler et al, 1992; Schramm et al, 1997; Talke and Stapelfeldt, 2006; Kelleher and Ruff, 1989); non-temperature-induced peripheral vasoconstriction and vasodilation have resulted in increases and decreases respectively, in pulse oximeter readings (Talke and Stapelfeldt, 2006)
As the absorption coefficients of blood increase, pulsations in light transmission tend to increase - according to the Beer-Lambert law, and pulsations tend to decrease due to the influence of blood being located in discrete vessels
This study identifies the influence of discrete blood vessels as a mechanism that can explain some of the anomalies of pulse oximetry – namely why vasoconstriction and vasodilation, total haemoglobin concentration (tHb) and the presence of large calibre blood vessels affect pulse oximetry
Summary
Pulse oximeters determine the pulsatile component of attenuation from measurements of the pulsating intensity of red and infrared light that has passed through tissue. The ratio of pulsatile attenuations of red (AR) versus infrared (AIR) light is used to determine SpO2 (pulse oximeter estimation of arterial haemoglobin oxygen saturation). The theoretical basis of pulse oximetry is described by a Beer-Lambert model which demonstrates how ratios of optical measurements carry information about haemoglobin oxygen saturation (Webster, 1997). With this model, pulsations are attributed to the change in blood volume from diastole to systole (Mannheimer, 2007; Mendelson, 1992; Alexander et al, 1989), and SpO2 is calculated according to equation (2) (Mendelson and Kent, 1989; Webster, 1997):
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