Understanding Pulse Oximetry

 Introduction 

The concept of monitoring hemoglobin oxygen saturation by optical means has been known for over 40 years. It is, however, only very recently that real time oximeter monitors have become commercially available – mainly due to discovery of the pulse oximeter technique and the revolutionary development in electronic computer technology. 

The Pulse oximeter extracts the pulsatile arterial blood signal from an in vivo measurement, and therefore needs only 2 wavelengths to measure oxygen saturation – in contrast to earlier ear oximeters that used up to 8 wavelengths to filter out signals from tissue and venous blood. 

This has significantly simplified the instrument, the probes, and the oxygen saturation calculations, and made development of a small, inexpensive clinical monitor possible.

 The Pulse oximeter’s simple, convenient technique for continuous monitoring of arterial oxygen saturation fulfills the clinician’s goal of patient monitoring – to provide early warning of undetected hypoxemia during anesthesia, post-operative recovery, and intensive care. The simplicity of this monitor has also made it possible to review home care of chronically in patients.

Oxygen saturation measurement can now be done continuously and noninvasively using the Radiometer Pulse oximeter.  

Conventions and symbols

 Three different conventions are currently used for representing clinical chemical, physiological quantities and instrumentation nomenclature:
The Pappenheimer convention adopted by the American Physiological Society use SaO₂ as the symbol for arterial oxygen saturation. 

The symbol used by the IFFC¹⁾ and by IUPAC²⁾ for arterial oxygen saturation is sO₂(aB). 

The ASTM³⁾ISO⁴⁾ are currently considering whether to recommend the SpO₂ symbol for pulse oximeter measurement of arterial oxygen saturation.

 Theory

Oxygen is essential to all life. Body cells must have oxygen for their metabolism, where after they must dispose of their waste product – carbon dioxide. Oxygen uptake occurs in the lungs and is carried to tissues by the blood in two forms: combined with hemoglobin (HbO₂) and dissolved in plasma.
Approximately 1 – 2 % of the oxygen is dissolved in plasma, whereas the remaining approximately 98 % is carried by hemoglobin. Hemoglobin contains four iron atoms, each capable of binding one molecule of oxygen. The actual number of oxygen molecules that can be bound to the hemoglobin molecule depends on the partial pressure of oxygen, pO_2, as well as the configuration of hemoglobin. Normally, the pO₂ in the lungs is such that hemoglobin becomes almost saturated with oxygen and becomes oxyhemoglobin. As oxygen is consumed by the cells, the pO₂ declines, thereby stimulating the hemoglobin to release its oxygen and change back into reduced hemoglobin, 

Hemoglobin exists in two principle forms: oxygenation (HbO₂) and reduced or deoxygenated, (Hb). The oxygen saturation, SaO₂, is defined as the ratio of the concentration of oxyhemoglobin (cHbO₂) to the concentration of HbO₂ + Hb (cHbO₂ + cHb). Although strictly speaking a fraction, oxygen saturation is commonly expressed as a percentage and defined as: 

 The amount of oxygen carried in blood is primarily dependent on the amount of oxyhemoglobin in the blood, and only to a lesser extent on the dissolved oxygen in blood and plasma.

The relationship between the partial pressure of oxygen, pO₂, and oxygen saturation is commonly expressed as the oxyhemoglobin dissociation curve, Fig. 1.

Fig. 1. Oxyhemoglobin dissociation curves. *

 Oxygen uptake in the lungs is represented by the upper, essentially flat, part of the curve. Changes in pO₂ cause only small changes in oxygen saturation, and the inspired pO₂ is normally adequate to almost fully saturate the hemoglobin.

 Release of oxygen to the tissues is represented by the lower part of the curve. Here small changes in pO₂ produce large alterations in the oxygen saturation. This is advantageous to the tissue because large amounts of oxygen can be extracted from the blood with relatively small decreases in pO₂.

The pO₂ value at which hemoglobin is 50 % saturated with oxygen (p₅₀) is an indication of the strength of the bond between hemoglobin and oxygen, referred to as hemoglobin oxygen affinity.

Four main factors affect the hemoglobin oxygen affinity: CH⁺, temperature, pCO₂, and 2,3-DPG (2,3-diphosphoglycerate concentration). Increase values of these factors will decrease hemoglobin oxygen affinity (Fig. 2). This results in a higher p₅₀ value.
An increase in the hemoglobin oxygen affinity can be caused by reduced cH⁺, temperature, pco₂, or 2,3-DPG. This results in a lower p₅₀ values, indicating that the oxygen unloading is impaired at normal tissue po₂ levels. 
It will be more difficult for oxyhemoglobin to dissociate at the tissue level, thus oxygen delivery is generally reduce. 

Fig. 2. Factors affecting the hemoglobin oxygen affinity. *

Other factors that affect the oxygen dissociation curve are abnormal hemoglobins, fetal hemoglobin, and dysfunctional hemoglobins such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin.

For most patients an oxygen saturation level in arterial blood of 92 – 97 % is considered adequate.

¬      Fig. 1 and 2 show entire oxyhemoglobin dissociation curves, even though the expected range for oxygen saturation for arterial blood is from a SaO₂ value of approximately 50 % and up.

Principle of operation

The Pulse OXImeter is a noninvasive arterial oxygen saturation monitor. Continuous pulse and oxygen saturation readings are obtained by ear, finger, or soft probes. The oximeter determines a patient’s arterial oxygen saturation and pulse rate by measuring the absorption of selected wavelengths of light passed through a living tissue sample. The Pulse OXImeter SaO₂ calculation is based on the assumption that hemoglobin exists as oxyhemoglobin (HbO₂) and reduced hemoglobin (Hb).

Oxyhemglobin and deoxyhemoglobin absorb light as known functions of wavelengths. It is possible to determine the relative percentage of each constituent and thereby the arterial oxygen saturation.

Two wavelengths of light, red and infrared, are utilized to gauge the presence of HbO₂ and Hb, fig. 3.

Fig. 3. Extinction versus wavelength.

To obtain true arterial SaO₂ values and to filter out absorption due to venous blood and other tissue constituents, signals from the pulsatile arterial blood only are used in the measurements.

Two Light Emitting Diodes (LEDs) transmit light through the tissue, and the probe’s photodetector transforms and modulates the received light into an electronic signals, Fig. 4.

Fig. 4 Principle of light transmission through a finger.

Since oxyhemoglobin and reduced hemoglobin allow different amounts of light to reach the photodetector at the selected wavelengths, the electronic signal varies, depending on the relative amounts of these constituents.

The Pulse OXImeter amplifies the received electronic signal. Analog and digital signal processing convert the light intensity information into SaO₂ and pulse rate values, and display them on the OXImeter front panel.

For a given site the absorption is constant, except for the absorption from the added blood volume due to arterial pulsations, Fig. 5.

Fig. 5 Absorption through a part of the body versus time.

Analog processing

This pulsation signal composite is extracted, amplified, and filtered simultaneously for both red and infrared light. Filtering the signals reduces the “noise” present due to motion of the probe, ambient lighting, electrical interference, etc. The constant signal levels (non-pulsating), e.g. from bone, fat, tissue, venous and non-pulsatile arterial blood are collected as well and used to normalize the pulsatile signals.

An analog to digital (A/D) converter receives the four signals from the filters and converts them to digital signals. A microprocessor performs complex calculations determining the oxygen saturation of measured arterial blood, Fig. 6.

Fig. 6. Electrical block diagram.

The probe consists of a light source and a photodetector. Two LEDs compose the light source: one red and one infrared, Fig. 7.

Fig.7. Soft probe showing emitter and detector.

The photodetector is a photo diode, i.e. an electronic device that produces an electrical current proportional to incident light intensity.

The photodector senses both the red and the infrared light and cannot distinguish between light wavelengths. Therefore a timing circuitry sequences the red and infrared light sources on and off, as follow:

·         red LED on

·         red LED off – infrared LED on

·         both LEDS off.

This sequence repeats itself in cycles of 480/400 times per second (60/50 Hz) to augment ambient light rejection.

The off point or “dark” portion in the light sequence is measured and utilized to eventually cancel the effects of the ambient light. The photodetector quantifies the light energy at the appropriate wavelengths by producing a current at appropriate points in the cycle, and an operational amplifier in the OXImeter converts each to a voltage for further processing.

Digital processing and display

The microprocessor performs mathematical processes comparing the data from the red and infrared channels. A ratio of the change in voltage of the red channel (rRED/RED) to the change in voltage of the infrared channel (rIR/IR) over a small interval of time is used to calculate SaO₂. This “instantaneous” arterial oxygen saturation is calculated 30/25 (60/50 Hz) times per second.

Theoretically, arterial oxygen saturation is calculated as:

                                                SaO₂ = K₁R² + K₂R + K₃

At any point in time arterial oxygen saturation is a function of the change in the red channel divided by the change in the infrared channel.

The physical optical characteristics of hemoglobin are the basis of the calibration coefficients: K₁, K₂ and K₃. The OXImeter processes the instantaneous arterial oxygen saturation values to produce the ”average saturation value.” The value appears on the OXImeter’s digital display.

One key digital processing function is to properly average the instantaneous oxygen saturation values. A running average gives a reasonable, but not excellent, result. A weighted average of instantaneous values provides for a much more acceptable result. The basis for the weight assigned to each instantaneous calculation is perfusion at the test site and the current average saturation. For example, movement at the probe site can cause signal distortion, thus creating some erroneous, instantaneous oxygen saturation values.

Since there are many saturation measurements per second, bad values can be discarded, and the displayed saturation remains stable. The weighting function gives a stable reading with low sensitivity to motion, while retaining quick response capability to saturation changes. At 60 Hz operation, this running, weighted average uses data over a 6 or 3 seconds of data collection (slow mode or fast mode), and is updated every 0.67 or 0.33 seconds (slow mode or fast mode). The corresponding values for 50 Hz operation are 20 % higher. However, the displays are updated only every 2 seconds in all modes.

Limitations

The arterial oxygen saturation value measured by the Pulse OXImeter (sometimes labeled functional saturation) is defined as:

It differs from the oxyhemoglobin fraction, xHbO₂, (sometimes called fractional oxygen saturation) defined as a percentage:

The difference is that total hemoglobin includes all forms of hemoglobin in blood, e.g. carboxyhemoglobin, methemoglobin, sulfhemoglobin. For example, an oxygen saturation value of 100 % would correspond to an oxyhemoglobin fraction of 90 % if the cardoxyhemoglobin fraction is 10 %. The SaO₂ measured by the Pulse OXImeter in the presence of carboxyhemoglobin will be slightly too low, due to a small interference from the carboxyhemoglobin.

Caution should be exercised when measuring on jaundiced patients and on patients where dye dilution measurement procedures are involved, since the Pulse OXImeter may display too low value.

Phototherapy and disturbing light paths can interfere with oxygen saturation accuracy. However, this problem is easily corrected by covering the skin probe with opaque material.

The technique is also sensitive to movement artifacts (only at the time of movement). Muscle activity sets the venous blood in motion, which can be falsely detected as pulsating arterial blood, causing false low SaO₂ readings and false high pulse readings.

Whenever oxygen management involves higher levels of inspired oxygen, caution should be exercised, because a SaO₂ display reading of 97 ± 3 % can correspond to oxygen partial pressure ranging from 70 mmHg and up, due to the sigmoid shape of the oxygen dissociation curve.

Generally, pO₂ cannot be estimated directly for SaO₂ due to the shifting of the oxygen dissociation curve caused by changes in cH⁺, temperature, pCO₂, 2,3-DPG, and type of hemoglobin present. Pulse oxygen saturation monitoring must be considered and accepted as a parameter in its own right for oxygenation management.

In vivo adjustment

Interfering substances in blood (e.g. cardiogreen) will cause false readings on the Pulse OXImeter (as well as some invasive oximeters), but the Pulse OXImeter may be adjusted using invasive blood oximetry measurement as a reference. This procedure should ensure that the used invasive and noninvasive values are truly corresponding.

The in vivo adjustment of the Pulse OXImeter should include memory retention of the pulse oximeter measurement (stable readings only) at the time of blood oximetry sampling.

When the blood oximetry results are obtained, the stored (memory) value can be recalled and adjusted according to the invasive SaO₂ result, obtained from an arterial blood sample (e.g. OSM3 HEMOXIMETER^®).

There are, however, some limitations to this procedure. In the Pulse OXImeter the adjustment is done with an offset value; whereas in fact the relationship between oxygen saturation and oxyhemoglobin fraction is more complex.

In view of the stated limitations of pulse oximetry monitoring, an arterial blood sample should be used as a reference at the onset of monitoring and at intervals throughout long-term use of Pulse OXImeter patient monitoring.

Major applications of pulse oximeters

The major use of the simple noninvasive Pulse OXImeter ranges from emergency applications to home care. The most common areas where pulse oximetry is used today are: operating rooms, intensive care units, recovery rooms, neonatal intensive care units, cardiac rehabilitation, stress testing, dental surgery, plastic/reconstructive surgery, and home care.

In addition to general hypoxemia screening, special application areas and the benefits of oximetry are briefly explained below.

Aerosol and Humidity Therapy: Continuous monitoring prior to, and concluding with, the discontinuance of therapy; demonstrates the possible gas exchange effects of such therapy.

Airway Suctioning: Monitoring incorporates individual assurance of adequate oxygen saturation during airway secretion removal.

Bronchial Provocation Testing: Possible adverse gas exchange effects of testing can be measured quickly and noninvasively.

Bronchoscopy: Immediate notification of hemoglobin desaturation is vital during this procedure, which includes partial occlusion of the airway.

Chest Physiotherapy: Monitoring ensures adequate oxygen saturation levels during therapeutic procedures, and helps evaluation of therapy effectiveness.

Exercise Testing: Oxygen saturation levels can be documented for cardiopulmonary testing, as well as for establishing exercise programs and goals for rehabilitation patients.

Incentive Spirometry: Oxygen saturation monitoring can provide possible gas exchange effects relative to this therapy.

Mechanical Ventilation: Monitoring provides arterial oxygen saturation information from patients requiring maximum mechanical ventilation and patients being weaned from mechanical ventilation.

Oxygen Administration: Monitoring ensures adequate oxygen administration for acute or chronic care situations.

Pharmacologic Intervention: Bronchodilatory therapy effects can be reviewed by continuous monitoring.

Endotracheal Intubation: Continuous monitoring can assure adequate supplemental oxygen during the intubation process.

Sleep Studies: Monitoring of nocturnal hypoxemia associated with neuromuscular disease or chronic obstructive pulmonary disease can be documented for appropriate oxygen therapy.