Pulse oximeters are mandatory monitors for any anesthetic, including cases of moderate sedation. There are no contraindications.
Pulse oximeters combine the principles of oximetry and plethysmography to noninvasively measure oxygen saturation in arterial blood. A sensor con-taining light sources (two or three light-emitting diodes) and a light detector (a photodiode) is placed across a finger, toe, earlobe, or any other perfused tissue that can be transilluminated. When the light source and detector are opposite one another across the perfused tissue, transmittance oximetry is used. When the light source and detector are placed on the same side of the patient (eg, the forehead), the backscatter (reflectance) of light is recorded by the detector.
Oximetry depends on the observation that oxygenated and reduced hemoglobin differ in their absorption of red and infrared light (Lambert–Beer law). Specifically, oxyhemoglobin (HbO2) absorbs more infrared light (940 nm), whereas deoxyhemo-globin absorbs more red light (660 nm) and thus appears blue, or cyanotic, to the naked eye. The change in light absorption during arterial pulsations is the basis of oximetric determinations (Figure 6–2). The ratio of the absorptions at the red and infrared wavelengths is analyzed by a microprocessor to pro-vide the oxygen saturation (Spo2) of arterial blood based on established norms. The greater the ratio of red/ infrared absorption, the lower the arterial satu-ration. Arterial pulsations are identified by plethys-mography, allowing corrections for light absorption by nonpulsating venous blood and tissue. Heat from the light source or sensor pressure may, rarely, result in tissue damage if the monitor is not periodically moved. No user calibration is required.
In addition to Spo2, pulse oximeters provide an indication of tissue perfusion (pulse amplitude) and measure heart rate. Because Spo2 is normally close to 100%, only gross abnormalities are detectable in most anesthetized patients. Depending on a particu-lar patient’s oxygen–hemoglobin dissociation curve, a 90% saturation may indicate a Pao2 of less than 65 mm Hg. This compares with clinically detect-able cyanosis, which requires 5 g of desaturated hemoglobin and usually corresponds to an Spo2 of less than 80%. Bronchial intubation will usually go undetected by pulse oximetry in the absence of lung disease or low fraction of inspired oxygen concen-trations (Fio2).
Because carboxyhemoglobin (COHb) and HbO2 absorb light at 660 nm identically, pulse oxim-eters that compare only two wavelengths of light will register a falsely high reading in patients with car-bon monoxide poisoning. Methemoglobin has the same absorption coefficient at both red and infra-red wavelengths. The resulting 1:1 absorption ratio corresponds to a saturation reading of 85%. Thus, methemoglobinemia causes a falsely low satura-tion reading when Sao2 is actually greater than 85% and a falsely high reading if Sao2 is actually less than 85%.
Most pulse oximeters are inaccurate at low Spo2, and all demonstrate a delay between changes in Sao2 and Spo2. Other causes of pulse oximetry artifact include excessive ambient light, motion, methy-lene blue dye, venous pulsations in a dependent limb, low perfusion (eg, low cardiac output, pro-found anemia, hypothermia, increased systemic vascular resistance), malpositioned sensor, and leakage of light from the light-emitting diode to the photodiode, bypassing the arterial bed (opti-cal shunting). Nevertheless, pulse oximetry can be an invaluable aid to the rapid diagnosis of hypoxia, which may occur in unrecognized esophageal intu-bation, and it furthers the goal of monitoring oxygen delivery to vital organs. In the recovery room, pulse oximetry helps identify postoperative pulmonary problems, such as severe hypoventilation, broncho-spasm, and atelectasis.
Two extensions of pulse oximetry technol-ogy are mixed venous blood oxygen saturation (Svo2) and noninvasive brain oximetry. The for-mer requires the placement of a pulmonary artery catheter containing fiberoptic sensors that continu-ously determine Svo2 in a manner analogous to pulse oximetry. Because Svo 2 varies with changes in hemoglobin concentration, cardiac output, arterial oxygen saturation, and whole-body oxygen con-sumption, its interpretation is somewhat complex. A variation of this technique involves placing the fiberoptic sensor in the internal jugular vein, which provides measurements of jugular bulb oxygen satu-ration in an attempt to assess the adequacy of cere-bral oxygen delivery.
Noninvasive brain oximetry monitors regional oxygen saturation (rSo2) of hemoglobin in the brain. A sensor placed on the forehead emits light of spe-cific wavelengths and measures the light reflected back to the sensor (near-infrared optical spectros-copy). Unlike pulse oximetry, brain oximetry mea-sures venous and capillary blood oxygen saturation in addition to arterial blood saturation. Thus, its oxygen saturation readings represent the average oxygen saturation of all regional microvascular hemoglobin (approximately 70%). Cardiac arrest, cerebral embolization, deep hypothermia, or severe hypoxia cause a dramatic decrease in rSo2. (See the section “Neurological System Monitors.”)
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