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`»AT=
`Fetal presenting - ~ pk
`part
`
`Figure 13.5 Placement of fetal probe within the uterus (Chung and MeNamara 1993). The
`sensor rests on the infant' s temple when the physician's fingers reach the saggital suture of the
`fetus's head.
`
`Handle
`
`Plastic tube
`-"'&:41-~ ~~
`Base assembly L
`
`Spiral probe
`
`Photodiode »51/
`lw-
`
`External monitor
`
`Optical fiber LEDs
`
`Power control
`
`Figure 13.6 Fetal pulse oximetry apparatus with the LEDs located outside of the uterus and
`transmitted via optical fiber (Jogeph and Guzman 1995).
`
`13.5 NEONATAL AND PEDIATRIC CARE
`
`A fetus generally has an Sa02 of about 50%. Within the first 15 min after birth,
`it normally rises to 90% (Oliver et al 1961). It is important to monitor the
`progress of this process and provide ventilatory aid if needed. Infants who
`experience problematic births are especially vulnerable. For example, infants
`delivered by cesarean section may be desaturated due to complications which
`made this type of delivery necessary. Premature infants sometimes develop
`retinoparhy due to hyperoxia . High levels of retinal oxygen cause spam of the
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`developing vasculature, leading to ischemia and blindness (Moyle 1994). Pulse
`oximeters are often used by new parents in the home as a precaution to prevent
`sudden infant death syndrome.
`
`Optical fiber
`
`Ey- z~*14-Reference electrode
`
`Electrical
`wires which
`connect to
`photodiode
`- Photodiode
`- Rubber collar
`
`Electrical
`wires which
`connect to
`spiral probe
`
`41
`
`Spiral probe
`
`Aperture
`
`Figure 13.7 Close up cross sectional view of the sensor, showing the helical termination of the
`optical fiber which is inserted in the fetus's scalp (adapted from Joseph and Guzman 1995),
`
`Determining alarm limits for pulse oximetry in neonatal care can be
`difficult. Figure 13.8 shows that during the weeks following birth, fetal
`hemoglobin is replaced by adult hemoglobin. Since the oxyhemoglobin
`dissociation curve of a fetus is to the left of that of the mother, the curve moves
`towards the right as the transition to adult hemoglobin takes place. This means
`that oxygen saturation levels considered safe may correspond to unsafe PA
`levels and cause hypoxia. Paky and Koeck (1995) detennined limits for detecting
`hypoxemia and hyperoxemia in neonates and found that limits to maintain an
`oxygen tension of 40 to 90 mmHg could only be established with less than 90%
`reliability. Attempting to obtain better reliability resulted in a SpO2 alarm limit
`for hypoxemia which was greater than that for hyperoxemia. This is obviously
`clinically unacceptable. However, with 85% reliability the range was only 92.5%
`to 95%. Deckardt and Steward (1984) determined that infant Sa02 levels between
`80% and 95% are acceptable. Fanconi (1988) found detecting hypoxia in infants
`problematic due to inaccuracies in pulse oximeters at arterial oxygen saturations
`less than 65%.
`Morozoff et al (1993) developed a system which uses a pulse oximeter as a
`controller to automatically adjust the air-oxygen mixture received by a neonate.
`The analog signal (plethysmographic waveform) measured by the pulse oximeter
`is input into a controller for a motorized gas blender. The blender adjusts the
`infant's inspired air-oxygen mixture, replacing the need for constant manual
`adjustment by an attending nurse. The benefits of this system are that it increases
`the amount of time the infant spends at normal Sa02 levels, reduces the need for
`human intervention, and reduces hospital costs by promoting early removal of
`oxygen therapy.
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`
`II
`
`Norm:,l loim inlarls
`
`7
`6-23
`3-\
`1~.
`
`(1) Day 1
`12) Day 5
`13) 3 weeks
`14) 6-9 weeks
`(51 3-4 months
`16) 6 nionlhs
`(7) 8-11 months
`
`1
`10
`
`1
`20
`
`1
`30
`40
`PO, (mm Hg: pH 7 4)
`
`1
`50
`
`60
`
`90 -
`
`80 -
`
`70
`
`60 -
`
`50 -
`
`40 -
`
`30 -
`
`20 -
`
`10 -
`
`0
`
`HbO: saturation (%1
`
`Figure 13.8 Mean oxyhemoglobin dissociation curves of infants ranging from i day old to 11
`months, From Delivoria-Papadopoulous ct /1 (1971).
`
`The Sa02 controller operates according to the following algorithm. A
`patient's oxygen saturation is measured with a pulse oximeter. The signal is
`converted to a digital representation and low-pass filtered. The corner frequency
`of the filter is determined by the user and sets the sensitivity of the controller.
`The observed SpO2 minus the desired Sa02 is denoted as the error. The signs of
`the error's magnitude, velocity, and acceleration are input into a state machine.
`The state machine determines the trend of the Sa02 error. It analyzes the signs of
`the three inputs and determines if the neonate's Sa02 is on target, above the
`target, or be]ow the target. If it is off target, the state machine goes on to
`determine if it is accelerating, decelerating, moving at a constant velocity, or not
`changing. If it is moving, it determines if the movement is toward or away from
`the target. Once the trend is identified by the state machine, it adjusts the 602
`mixture relative to the current mixture. There is also a delay so that the system
`can react to the adjustment made. Alarms were added for mechanical or electrical
`failure as well as for Sa02 and FjO2 limits. Manual intervention can override the
`controller at all times.
`Smaller probes are needed for both neonatal and pediatric care. Infants and
`children are much less willing to accept the application of a probe and remain
`still. Probe displacement and motion artifacts due to ill fitting probes can be a big
`problem. Ear probes made for adults can squeeze the softer newborn tissue too
`tightly. After a short time they can occlude the artery and have to be moved to
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`regain a signal. Howell et al (1993) developed a modified probe design for
`children which uses a 5 ml syringe barrel cut in half to house the sensor. The
`probe is secured to the syringe and can be slipped onto the child's finger.
`Disposable probes with adhesive bandages are often the best for neonatal and
`pediatric application. The LEDs and photodiode are attached to the bandage with
`the proper spacing so that they are positioned correctly when the adhesive is
`wrapped around the infant or child's finger or toe. Meier-Stauss et al (1990)
`studied the use of pulse oximetry during the first 17 min of life and determined
`that signal detection occurs faster when a probe is applied to an infant's hand as
`opposed to its foot. They also found that saturation values from the hand were
`always higher than those from the foot. This observation suggests that pulse
`oximetry can be used to document right-to-left shunting in newboms during the
`first few minutes of life (Meier-Stauss er al 1990). This is the passage of blood
`from the right to the left side of the heart or from pulmonary circulation to
`systemic circulation.
`
`1
`
`Target
`Sa02
`
`I
`
`d/dt
`
`1-
`- State -. Blender -. Patient
`E-1 machine
`
`LP filter -•---~ ADC ~ 1
`
`Pulse
`oximeter
`
`Figure 13.9 Block diagram of SA controller. Adapted from Morozoff et al (1993)
`
`13.6 SLEEP STUDIES AND PHYSICAL STRESS TESTING
`
`Many people are able to maintain normal oxygen saturation levels while pursuing
`normal daily activities, but become desaturated during sleep or heavy exercise.
`The most common cause of desaturation during sleep is due to a disorder known
`as sleep apnea. Desaturation can occur duririg heavy exercise due to such things as
`poor ventilation or chronic obstructive pulmonary disease (COPD). The use of
`pulse oxiinetry during sleep and exercise aids in the diagnosis of these respiratory
`problems.
`
`13.6.1 Sleep
`
`Pulse oximetry monitoring is used during sleep to diagnose sleep disorders which
`cause desaturation. Sleep is composed of several stages with different
`characteristics. The first stage is when the person is still awake, but is drowsy and
`less in tune to stimuli. Two other stages which alternate throughout the night are
`REM (rapid eye movement) sleep and non-REM or quiet sleep. During REM
`sleep, rapid changes in metabolic rate do not seem to affect respiration. Sleep
`apnea is the most common sleep disorder which causes desaturation. It is defined
`as the cessation in breathing due to the relaxation of upper airway musculature.
`There are three types of sleep apnea: obstructive, central, and mixed. Obstructive
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`sleep apnea is the most common type and is (,ften caused by anati,mical
`abnormalities such as a nasal obstruction, enlarged tonsils or adenoids, or an
`abnormal bone structure (Hauri 1992). Patients with obstructive sleep apnea often
`snore and are obese. They often experience bradycardia and cardiac arrhythmias
`and are at risk of sudden death during sleep. Central apneas are characterized by
`the absence „f respiratory effort due to a neurological or cardiac problem. As
`described in chapter 1, respiratory muscles are controlled by neurons in the
`brainstem as well as chemoreceptors and mechanoreceptors. In patients with
`central sleep apnea, these neurons cease to provide control during sleep. As the
`muscles relax, the airway shrinks. The pressures associated with inhalation cause
`the airway to collapse and become completely closed off. Once breathing has
`stopped. the patient's oxygen saturation begins to fall. The lack of oxygen is soon
`detected by chemoreceptors which cause the patient to wake up, renewing control
`by neurons in the brainstem. The airway muscles become firm again and allow
`breathing to resume. However, once the patient falls asleep, the airway muscles
`will relax again. This cycle affects heniod.vnumics, autonomic tone, and arterial
`blood gas tensions (Davies and Stradling 1993).
`Poly.vom,fography is the standard for diagnosing sleep apnea. It measures and
`records the EEG, EMG, ECG, che,1 wall plethysmogram, airway flow, and
`arterial oxygen saturation. However, it is both expensive and of limited
`availability. Pulse oximetry is easy to use and widely available. Not all
`desaturation during sleep is indicative of sleep apnea. It could be due to hypopnea
`labnormal. shallow breathing), artifact, hypoventilation, or ventilation/perfusion
`imbalance.
`Siem et at ( 1995) used a pulse oximeter in conjunction with a
`polysomnograph and determined particular patterns of desaturation to be
`associated with sleep apnea, They divided desaturation patterns into three
`categories: periodic, cluster, and isolated. Periodic consisted of a minimum of
`four events with a fall in Sp02 of 2% or more with less than 2 min between
`events. A cluster consisted ot 3 or more events with a fall in SpO2 of 3% or more
`and 2 to 10 min between events. Isolated events were separated from any other
`event by more than 10 min. They found that all periodic patterns were associated
`with sleep apnea, 65% of clusters were associated with sleep apnea, and none of
`the isolated events were associated with sleep apnea. Therefore, identifying
`patterns of desaturation with a pulse oximeter can help to identify sleep apnea.
`Lynn (1995) patented a method and apparatus for specifically diagnosing
`moderate to severe sleep apnea using only a pulse oximeter (no polysomnograph).
`His method involved analyzing the slopes of the desaturation and resaturation
`events throughout the night, where an event was defined if the oxygen saturation
`fell below a specified level for a specified period of time. During an apneic event,
`the initial fall in arterial oxygen saturation is a function of the oxygen saturation
`of mixed venous blood and oxygen uptake from residual in the lungs. Then it
`continues to fall as a function of oxygen consumption and global oxygen stores.
`Oxygen stores exist first in the lungs, then arleries, tissue, and veins in that order.
`During apnea. oxygen depletion occurs first in the tissue, then the veins, lungs,
`and arteries. Therefore, desaturation of arterial blood occurs only after
`desaturation in other areas. The slope of the desaturation of an event must be
`within a certain range to be characteristic of sleep apnea. If the slope is too big
`(rapid desaturation) it is considered an artifact, and if the slope is to small (slow
`desaturation) it is considered to be due to either hypoventilation,
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`ventilation/perfusion imbalance, or an artifact. Lynn 0995) performed a study
`and found that specifically the descending slope as shown in figure 13.10 is a fall
`in SpO2 within the range of 1.1% per second and 0.3% per second. The mean was
`0.8% per second. Once the desaturation is detected by the chemoreceptors.
`resulting in arousal, oxygen rushes into the lungs. The resaturalion slope is much
`larger than the desaturation slope. Specifically, Lynn (1995) found tiial R is a ilse
`in ~02 in the range of 2.5% per second and 8.3% per second, the mean being
`7.690. The duration of an apneic event is 3 to 3.5 min.
`Other parameters are considered in Lynn's diagnosis of sleep apnea.
`Consecutive events have similar desaturation slopes. Also, an event can increase
`the initial desaturation slope of a following event. This occurs because oxygen
`stores do not have enough time to replenish between events. The depletion of
`oxygen stores is not always detected by the pulse oximeter because arteries
`replenish their oxygen supply before tissue and veins. Desaturation slope
`increases occur when cyclic apneic events occur with less than 10 s between and
`when the depth of desaturation of the first event is larger than 15%. Thus the
`initial desaturation slope depends on the mixed venous saturation at the onset of
`sleep apnea and the amount of oxygen left in the lungs after the onset of sleep
`apnea. The continuing desaturation slope is a function of oxygen consumption
`versus stores.
`
`OXYGEN SATURATION(%1
`
`OA10-1 If0001
`
`~-A l-~ C~TR
`
`90 £-ASD
`
`100
`
`80
`
`70
`
`60
`
`TIME
`
`Mdl ... AW/6 TR
`
`ISR
`
`1
`
`lip. Asoj76-0
`
`1
`
`1
`
`Figure 13.10 A typical apneic event. Thc vertical lines are 30 s apart. Air, is tlic fall in
`saturation. ASR is the rise in saturation, ATD is the duration of the fall in saturation, 67* is tile
`duration of Ilic risc in saturation, MD is the slope of the desaturation. MR is the slope of
`resaturacton, Al is the apneic interval, OA[ is the occult apneic interval (apnea 128 begun. but the
`arterial oxygen saturation is maintaincd via oxygen stores), and OOD[ ts the occult apnea interval
`111 is is tile period following the return to baseline after a desaturation. If another apneic event
`occurs within this interval it will have an increased desaturation slope (Lynn 1995).
`
`The operation of Lynn' s method begins with measuring the patient's oxygen
`saturation with a pulse oximeter for a period of 10 min. A mean baseline
`measurement of arterial oxygen saturation is made during this interval. During
`subsequent recording, a desaturation event is defined and the duration and slope
`of the event is determined. The resaturation slope is then determined. Events in
`which the duration of the desaturation and resaturation is less than a particular
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`Design of pulse oximeters
`
`value and the desaturation slope falls within a finite range are defined as phasic
`desaturations. The ratio of desaturation slope to resaturation slope of the phasic
`desaturation events is measured. From the above data, the number of apneic
`events which have occurred can be determined and marked. The apnea can then
`be treated and the diagnosis process can be repeated to confirm the success of the
`treatment. Figure 13.11 shows that the measurement of the slopes, computation of
`the ratios, and comparison of the parameters with known characteristics of sleep
`apnea is all done within a microprocessor. The microprocessor can be connected
`to a printer to obtain a hard copy of apneic event data for further analysis by a
`physician. A variation on the above method is to use the area under the
`desaturation slope and the area under the resaturation slope. A ratio of these areas
`can be used instead of the ratio of the slopes. When the microprocessor identifies
`a phasic desaturation event, it can trigger the collection and/or storage of another
`parameter such as sound or video. For example a microphone. either separate or
`as part of the probe can be used to record such things as snoring, which is
`characteristic of obstructive sleep apnea. Sound could be recorded throughout the
`night, but only stored during a suspected apneic event. In Lynn's design, sound
`would be stored for the duration of the event and 1 min prior to and following
`the event. Short, low-frequency sounds often occur prior to apnea, and high-
`frequency sounds due to hyperventilation often precede the recovery period.
`
`Probe
`
`Finger
`
`Microphone
`
`~ Pulse oximeter
`
`Microprocessor
`
`Printer
`
`'-- Aud,oprocessor
`
`Positive pressure
`
`controller1
`
`Nasal continuous positive
`pressure system
`
`Figure 13.11 A block diagram of the apparatus used along with a pulse oximeter for sleep apnea
`diagnosis (adapted from Lynn 1995)
`
`Many pulse oximeters such as the portable Protocol Propaq 1 06EL contain
`apnea delay alarms. The alarms go off when they detect more than one event of
`desaturation below a specified level within a specified amount of time. When
`patients experience recurring apnea events of 15 to 20 per hour, they are in
`danger and must undergo some kind of treatment. There are several methods of
`treating sleep apnea. A simple solution can sometimes be sleeping in a more
`upright position. Another way is by applying contintious positive airway pressure
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`
`(CPAP) via the nasal passages to support the airway and prevent the collapse of
`pharyngeal tissue when the muscles relax. This type of treatment requires
`wearing a mask while sleeping and the air flow can be uncomfortable for
`patients. Finally, in extreme cases uvulopalatopharyngoplasty (UPPP) or
`tracheostomy may be necessary. UPPP is a surgical procedure in which excess
`tissue or a bony abnormality is removed. A tracheostomy involves removing part
`of the trachea to make a new airway opening.
`Other conditions which can cause desaturation during sleep although the
`patient maintains normal saturation levels while awake are bronchopulmonary
`dysplasia (BPD), chronic obstructive lung disease (COLD), cystic fibrosis, central
`alveolar hypoventilation syndrome (CAHS), hypopnea, airway resistance
`syndrome, and neuromuscular disease.
`
`t
`
`13.6.2 Exercise
`
`Pulse oximetry can be used to evaluate pulmonary or circulatory dysfunction and
`performance limitations during exercise. During heavy exercise, a reduction in
`the partial pressure of oxygen can cause hypoxemia (Dempsey 1986). Miyachi
`and Tabata (1992) found that ventilation is also a major factor. Athletes tend not
`to desaturate as quickly as those who do not exercise as often. This is because
`trained athletes breathe less per unit of metabolic rate than the untrained.
`Monitoring the oxygen saturation of an athlete can thus determine his physical
`condition. Also, patients with COPD experience limited ventilation during
`exercise (Vas Fragoso et al 1993). If the condition is severe, ventilation is limited
`and thus the patient desaturates more quickly during exercise. Pulse oximeters
`tend to underestimate S~02 readings during extreme exercise, possibly due to
`high levels of catecholamines and neural activity which restrict cutaneous blood
`flow (Norton et al 1992). Catecholamines are chemical compounds derived from
`catechol (C6H602) which can affect nervous transmission and muscle tone.
`
`13.7 MANAGEMENT OF CARDIOPULMONARY RESUSCITATION
`
`Pulse oximeters were added as part of the emergency equipment carried by a
`British anesthetic resuscitation registrar to determine the effectiveness of pulse
`oximetry to aid in the management of CPR (Spittal 1993). The oximeters used
`were standard Nonin 8500 with Flex Sensor ear probes. The team found the pulse
`oximeter to be helpful in primary respiratory arrest, but not too useful in cardiac
`arrest. Its use during the cases with primary respiratory arrest helped determine
`if a tracheal tube was needed or if a tracheal tube already in use was not
`positioned properly. For example, in one patient the tube had been inadvertently
`placed in the esophagus. External cardiac massage often produces a distorted
`ECG and it is difficult to obtain reliable oxygen saturation readings. Seventeen
`patients the team worked on suffered from cardiac arrest and required chest
`compressions. During compressions, saturation readings were detected for only
`seven of the patients, and of the seven only three readings were thought to be
`reliable. The team felt that better fitting ear probes would have been useful
`because chest compressions cause the body to move and create motion artifacts.
`Also audible tones to indicate a satisfactory pulse signal and SpO2 level would
`have been useful because it is difficult to watch a display while administering
`CPR.
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`13.8 COMPUTER-CONTROLLED OXYGEN WEANING
`
`Pulse oximetry can be used to monitor the weaning process of ventilated patients.
`During this process, the air/oxygen mixture is gradually adjusted, reducing the
`amount of oxygen until it matches that of room air. Often the amount of oxygen
`in the mixture has to be raised and lowered several times if the patient is not able
`to adiust. Strickland and Hasson ( 1993) developed a computer-controlled weaning
`system for patients with complex medical problems. The system was tested on
`elderly patients recovering from respiratory failure requiring ventilation. An
`external computer monitored the patient's oxygen saturation as measured with a
`pulse oximeler as well as the ventilator data. If the respiration rate, tidal volume,
`and oxygen saturation of the patient were normal, the computer decreased the
`rate of oxygen inhalation by 2 mUkg every 2 h until a rate of 2 mL/kg was
`reached. If the measuird values were not normal, it raised the ventilator support
`to the previous setting. Five minutes were allowed between measurements for the
`patients to stabilize. They found that the computer-controlled weaning reduced
`the need for blood gas sampling, shortened the weaning time, and reduced the
`time the patient spent with an unacceptable respiration rate and tidal volume, as
`compared with physician-controlled weaning.
`
`13.9 SYSTOLIC BLOOD PRESSURE MEASUREMENT
`
`A pulse oximeter will only obtain an oxygen saturation measurement and a
`plethysmographic waveforin if pulsatile blood Ilow is detected. This
`characteristic was exploited by Chawla et al ( 1992) to develop a method to
`measure blood pressure using a pulse oximeter. An occlusive cuff and a
`sphyginomanometer are used along with a pulse oximeter. The cuff is occluded
`until the plethysmographic waveform disappears and the pressure is recorded.
`The disappearance of the waveform indicates that the artery has been occluded
`such that blood flow is too weak to be detected by the pulse oximeter. The cuff is
`then inflated rapidly to 200 mmHg and gradually denated until the waveform
`reappears. This indicates that blood flow has increased to a detectable level in the
`artery. The pressure is again recorded. Specifically, the two pressure values
`correspond to 8.6% and 4% of the original blood flow respectively. Taking the
`average of the two pressure values results in a systolic blood pressure
`measurement which is at most 14 mmHg in error. This is within the clinically
`acceptable error range. This measurement technique is useful for patients with
`Takayasu's syndrome (pulseless disease) and critically ill patients with a weak
`pulse.
`
`13.10 CEREBRAL OXYGEN SATURATION
`Pulse oximetry on the retinal fundus allows measurement of cerebral oxygen
`saturation because blood supply to the retinal arteries comes from the ophthalmic
`artery which supplies cerebral
`tissue. Cerebral
`tissue is more vulnerable to
`permanent damage during hypoxemia. Also retinal circulation, unlike peripheral
`circulation is not affected during shock, hypothermia, and hemorrhage. Retinal
`oximetry is extremely useful in the critically ill who have weak peripheral
`circulation. Problems with retinal circulation and oxygen saturation are
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`associated with diseases such as diabetic retinopathy, hypertension, sickle cell
`disease, and vascular occlusive diseases and can result in severe damage to retinal
`tissue (Delori 1988). De Kock et al (1993) designed special apparatus for retinal
`pulse oximetry monitoring. Figure 13.12 shows that a black Plexiglas cone was
`glued to a haptic contact lens. Holes were drilled to allow a vacuum environment
`and create suction. The suction kept the lens in place. Slight displacement from
`the center of the pupil would result in loss of a signal as the light would no longer
`hit the retinal arteries. An aluminum tube (8 mm in diameter and 1 mm thick)
`fitted inside the cone and was divided into two sections by a metallic screen. One
`section contained the LEDs and the other the photodiode. The LEDs and
`photodiode had been removed from a Nellcor finger probe. When the apparatus
`was tested on patients, the eye was put under local anesthesia and the pupil dilated
`to 6 mm. A pulsatile signal was obtained, but blinking and eye movement
`hindered the pulse oximeter readings.
`
`Ophthalmic
`
`Haptic contact lens
`
`UDS
`
`Retinal 1
`artery
`
`2; Optic disc L
`
`) area\4 / A
`
`1 61 Al-
`
`U
`
`Lens
`
`Iris Cornea
`
`Photodiode
`
`Fenestration
`
`Sclera
`
`Ciliary body
`
`Figure 13.12. Cross section of an adapted haptic contact lens and pulse oximeter probe for use
`in cerebral oxygen saturation measurement. Adapted from de Kock er al (19931
`
`1
`1
`
`13.11 VETERINARY CARE
`
`Pulse oximetry is often used in veterinary care. Pulse oximeters need to be able
`to monitor a wide range of heart rates to accommodate the metabolisms of
`different animals. Also, specialized probes are used. Common sites for probe
`placement include the tongue and ear for large animals, Achilles tendon, across
`the paw pads of dogs and cats, esophagus, nasal septum, rectum, and caudal tail.
`Limitations associated with the application of pulse oximetry to animals are low
`perfusion, motion artifacts, darkly pigmented skin, thick skin, and excessive hair
`(Allen 1990). Whitehair et al (1990) noted that oxygen saturation measurements
`were not obtained when a human ear probe was used on horses' nostrils, lips, and
`vulva. This could have been because the LEDs were not strong enough to allow
`sufficient light to be transmitted through the thick skin to the photodiode. Pulse
`oximeters are often used during anesthesia because the position of ruminant
`
`250
`
`MASIMO 2053
`Apple v. Masimo
`IPR2022-01299
`
`

`

`RX-0035.0251
`
`APL_MAS_ITC_00015868
`
`234
`
`Design of pulse oximeters
`
`animals can cause bloating, which in turn can lead to compromised respiration,
`regurgitation, and death (Allen 1992). Detection of hypoxemia early can prevent
`the unnecessary demise of the animal. Sensor Devices Inc. and Palco both make
`pulse oximeters specially designed for veterinary use, The SDI Vet/Ox Plus and
`4402 Pulse Oximeter can both measure pulse rates between 20 and 350 bpm with
`an accuracy of 2%. They also have widely variable gains to accommodate small
`or large pulse amplitudes.
`
`13.12 FUTURE IMPROVEMENTS FOR PULSE OXIMETRY
`
`Although pulse oximetry seems to be at the peak of its development, there are
`still improvements to be made. Many of these improvements relate to specific
`applications. Improvements which will increase the performance of pulse
`oximetry during transport are to lengthen the battery life in portable units, create
`even better algorithms for motion artifact reduction, and further miniaturize
`units. Reducing the occurrence of faIse alarms would be beneficial in all
`applications, but especially during long term monitoring when staff cannot always
`be in the room. In hospital environments for monitoring during surgery,
`recovery, and intensive care, all-in-one monitors seem to be the goal. HORNET
`(Hospitai Operating Room Network) is a prototype for this type of monitoring
`(Lecky er al 1988). It is designed to monitor respiratory and circulatory variables
`such as ECG, blood pressure, oxygen saturation. and inspiratory and expiratory
`gas. It is also designed to handle physiological, demographic, and administrative
`data. It is to be used for scheduling, intraoperative monitoring, preparation of
`reports, permanent storage of perioperative information, and research. In
`addition to all-in-one monitors, the aim is to eventually equip hospitals to
`transmit information via radio waves to central stations.
`
`REFERENCES
`Allen JL 1990 Proc. /990 Am. Assoc Zoo Veterinarians 163
`Allen JL 1992 Pulse oximetry: everyday uses in a zoological practice Ves. Record 130 354-5
`Bone ME, Galler D and Flynn P ]1987 Arterial oxygen desaturation during general anae<thesia
`for pacdiatric dental extractions Anaesthesia 42 879-82
`Buchanan D C 1991 Endotraclical tube with oximetry means US patent 5,005, 573
`Campbell M B, Lightstone A D, Smith J M. Kirpalani H and Perlman M 1984 Mechanical
`vibration sound levels experienced in neonatal transport Am. 1 Dis. Child. 138 967-JO
`Calley DM, Thorton C. Jordon C, Tech B, Lchanc JR. Royston D and Jones JGI 985
`Pronounced episodic oxygen desaturation in the post-operative period: its association with
`venti latory pattern And analgesic regimen Anesthesiology 63 20-8
`Chawla R, Kumarvel V, Girdhar K K, Sethi A K, Indrayan A and Bhattacharya A 1992 Can pulse
`oximetry be used to measure systolic blood pressure? Anesth. Analg. 14 196-200
`Chung C and MeNumaraHM 1993 Fetal pulse oximetry apparatus and method of use US patenf
`5.228,440
`Clark SL, Pavlov Z, Greenspoon J, Horenstein J and Phelan JP1986 Squamous cells in the
`maternal pulmonary circulation Am. 1. Obst.'f. Gynecol. 154 1~4-6
`
`Clay NR and Dent CM 1991 Limitations of pulse ox imetry to assess limb vascularity Br. 1 Bone
`Join/ Surg. 71-8 141
`Committee on Hospital Care-American Academy of Pediatrics 1986 Guidelines for air and
`ground transportation of pediatric patients Pediatrics 1& 943-50
`Cooper J B et al 1984 An analysis of anestlietic mishaps from medical liability claims /m.
`Anesthesia Clinics 60: 39
`Cottrell J J, Lebovitz B L, Fenne] RG and Kohn G M 1995 Inflight arterial saturation: continuous
`monitoring by pulse oximetry Aviation, Space, Environ. Med 66 126-30
`
`t
`1
`
`251
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`MASIMO 2053
`Apple v. Masimo
`IPR2022-01299
`
`

`

`RX-0035.0252
`
`APL_MAS_ITC_00015869
`
`Applications of pulse oximetry
`
`235
`
`Cunningham F G, MacDonald P C and Gant N F 1989 WiNiams Obstetrics 18th edn (Norwalk,
`CT: Appleton-Century-Crofts) pp 95,96,805
`David H G 1991 Pulse oximetry in closed limb fractures Ann. R. Cdt. Surg. England13 283-4
`Davies RJ O and Stradling J R 1993 Acute effects of obstructive sleep apnoea Br. J. Anaesth. 71
`725-9
`de Kock J P, Tarassenko L, Glynn C J and Hill A R 1993 Reflectance pulse oximetry
`measurements from the retinal fundus IEEE Trans. Biomed Eng. 40 817-22
`Deckardt R and Steward D J 1984 Non-invasive arterial hemoglobin oxygen saturation versus
`transcutaneous oxygen tension monitoring in the preterm infant Crit. Care Med 12 935-9
`Delivoria-Papadopoulous M, Roncevic N and Oski F A 1971 Postnatal changes in oxygen
`transport of term, preterm, and sick infants: the role of red cell 2,3-diphosphoglycerate and
`adult haemoglobin Pediatric Res. 5 235-45
`Delori F C 1988 Noninvasive technique for oximetry of blood in retinal vessels Appl. Opt. 27
`1113-25
`Dempsey J A 1986 Is the lung built for exercise? Med. Sci. Sports Exercise 18 143-55
`Dildy G A, Clark S L and Louks C A 1993 Preliminary experience with intrapartum fetal pulse
`oximetry in humans Obstet. Gynecol. 81 630-4
`Dildy G A, Clark S L and Louks C A 1994 Intrapartum fetal pulse oximetry: the effects of maternal
`hyperoxia on fetal arterial saturation Ant J. Obstet. Gynecol. 171 1120-4
`Ernest J T and Krill A E 1971 The effect of hypoxia on visual function Invest. Ophthalmol. 10
`323-8
`Fanconi S 1988 Reliability of pulse oximetry in hypoxic infants J. Pedi

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