Overview
∗ Dr. Barker is a member of the Scientific Advisory Board of Masimo Corporation (Irvine, CA) and is also a community member of their Board of Directors. He is not an employee or a paid consultant of Masimo or any other company involved in pulse oximetry.
No monitor of oxygenation has had as much impact on the practice of anesthesiology as the pulse oximeter. Unknown in the operating room (OR) before the 1980s, the pulse oximeter is now a minimum standard of care for all patients who receive anesthetics, whether general, regional, or local. Its operation requires no special skill or training, and its use is noninvasive and therefore almost risk free. The pulse oximeter gives continuous, real-time estimates of arterial hemoglobin saturation, which can warn of hypoxemia from many causes, including loss of airway patency, loss of oxygen supply, and increases in venous admixture. As illustrated in Figure 11-1 , pulse oximetry provides a monitor of the second of four stages of the oxygen transport process. This important advance goes beyond the first stage of inspired gas monitoring, but it does not ensure the third stage of adequate oxygen delivery to vital organs.
v ¯
O 2 , mixed venous oxygen saturation.
This chapter reviews the historic development of pulse oximetry, its underlying physical and engineering principles, and recent improvements such as artifact reduction and multiwavelength processing. An understanding of these principles will enable the reader to predict sources of measurement error. Pulse oximeter accuracy, response, clinical applications, limitations, and future potential are also discussed.
Hemoglobin Saturation and Oxygen Transport
The pulse oximeter provides a noninvasive estimate of arterial hemoglobin saturation, a variable directly proportional to the oxygen content of arterial blood. Two definitions of hemoglobin saturation are in current use. The older definition, called functional saturation, or SaO 2 , is related to the concentrations of oxyhemoglobin (O 2 Hb) and deoxygenated, or “reduced,” hemoglobin (RHb) as follows:
SaO 2 = [ ( O 2 Hb ) / ( O 2 Hb + RHb ) ] × 100 %
Additional species of hemoglobin are often present in adult blood, including carboxyhemoglobin (COHb) and methemoglobin (MetHb). This leads to the definition of fractional hemoglobin saturation , or O 2 Hb%, which is the ratio of oxyhemoglobin to the total concentration of all hemoglobin species:
O 2 Hb % = [ O 2 Hb / ( O 2 Hb + RHb + COHb + MetHb ) ] × 100 % = ( O 2 Hb / Hb ) × 100 %
In this formula, Hb is the total hemoglobin, the sum of all species present. Fractional saturation is sometimes called oxyhemoglobin fraction or oxyhemoglobin percent . Fractional arterial hemoglobin saturation is related to the arterial oxygen content, CaO 2 , by the following formula:
CaO 2 = ( 1.37 × Hb [ O 2 Hb % / 100 ] ) + ( 0.003 × PaO 2 )
Here PaO 2 is the arterial oxygen tension in millimeters of mercury. The first expression in brackets in Equation 11-3 represents the oxygen bound to hemoglobin, which under normal conditions (Hb = 15 g/dL and O 2 Hb% = 98) equals approximately 20 mL oxygen per 100 mL blood. The second expression represents oxygen dissolved in plasma, which equals 0.3 mL per 100 mL for a PaO 2 of 100 mm Hg. Plasma-dissolved oxygen usually does not play a significant role in oxygen transport. Equation 11-3 shows that arterial oxygen content is directly proportional to both total hemoglobin (Hb) and fractional saturation. O 2 Hb% and PaO 2 are related by the oxyhemoglobin dissociation curve, shown in Figure 11-2 . Under normal conditions, this relationship predicts a hemoglobin saturation for adults of 50% at a PaO 2 of 27 mm Hg, 75% at a PaO 2 of 40 mm Hg (the typical venous blood value), and 90% at a PaO 2 of 60 mm Hg. This normal dissociation curve is shifted to the right by acidosis, hypercarbia, hyperthermia, and increases in 2,3-diphosphoglycerate (2,3-DPG) concentration. Note that for PaO 2 values greater than 90 mm Hg, O 2 Hb% is nearly independent of PaO 2 . This saturation property of hemoglobin has important implications in the clinical interpretation of pulse oximeter data, discussed below.
The amount of oxygen delivered to the tissues by the arterial blood (O 2del ) is simply the product of the arterial oxygen content (CaO 2 ) and the cardiac output, or
O 2 del = CaO 2 × Cardiac output × 10
The factor of 10 appears because CaO 2 is measured in milliliters per deciliter, whereas cardiac output is measured in liters per minute. The quantity of oxygen consumed per minute is then the difference between the arterial oxygen delivery (O 2del ) and the venous oxygen return (O 2ret ):
VO 2 = O 2 del − O 2 ret = ( CaO 2 − CvO 2 ) × Cardiac output × 10
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