Comparison of desaturation and resaturation response times between transmission and reflectance pulse oximeters

Background: In general, there is a response time between actual arterial hypoxemia and its detection by pulse oximeters. We compared the desaturation and resaturation response times between two types of pulse oximeters, transmission and reflectance pulse oximeters, to find out which oximeter has a more rapid response time. Methods: Thirty‐three ASA 1 or 2 patients were enrolled in this study. A transmission pulse oximeter was placed on the index finger and a reflectance pulse oximeter was placed on the forehead and monitored simultaneously. After the induction of general anesthesia without pre‐oxygenation, we waited until the oxygen saturation value of any of two pulse oximeters declined to 90%, and then mask ventilation was started with 100% oxygen. Oxygen saturation was recorded at an interval of 2 s during this time. Results: The desaturation response time of SpO₂ to 95% after apnea was 82.0 s (interquartile range: 67.0–98.5 s) vs. 94.0 s (interquartile range: 84.0–106.5 s) (P<0.001) and SpO₂ to 90% was 94.0 s (interquartile range: 75.5–109.5 s) vs. 100.0 s (interquartile range: 84.5–114.5 s) (P<0.001) in the reflectance and transmission oximeters, respectively. The resaturation response time from mask ventilation to 100% SpO₂ was 23.2±5.6 vs. 28.9±7.6 s (P<0.001) in the reflectance and transmission oximeters, respectively. Conclusion: In clinical situations in which rapid changes in oxygen saturation are expected, we recommend the forehead reflectance pulse oximeter because it responds more quickly in detecting oxygen desaturation and resaturation compared with the transmission pulse oximeter.     

The response times during anaesthesia of pulse oximeters measuring oxygen saturations during hypoxaemic events

Episodes of desaturation were recorded simultaneously by computer from two Ohmeda Biox 3700 pulse oximeters, one with an ear and one with a finger probe, on patients undergoing anaesthesia. Over a period of 6 months, 28 episodes of desaturation were detected. Analysis of the recordings showed the mean minimum saturations recorded for ear and finger probes were 86.3% and 83.5% respectively (p less than 0.01). The mean delay for finger compared to ear pulse oximetry was 4.4 s (p less than 0.01). Analysis at different saturation levels showed finger probe responses to be significantly slower than ear probe responses at saturations equal to and above 91% (p less than 0.05). At saturation levels of 90% or less no significant difference in probe response times were found.     

The accuracy of pulse oximeters

The accuracy of five commercially available pulse oximeters was compared against arterial blood oxygen saturation, under similar clinical conditions. The oximeters had very similar performance in the clinically useful range of 80-100%, with a tendency slightly to underestimate the true saturation.     

Accuracy of response of six pulse oximeters to profound hypoxia

Oxygen saturation, SpO2%, was recorded during rapidly induced 42.5 +/- 7.2-s plateaus of profound hypoxia at 40-70% saturation by 1 or 2 pulse oximeters from each of six manufacturers (NE = Nellcor N100, OH = Ohmeda 3700, NO = Novametrix 500 versions 2.2 and 3.3 (revised instrumentation), CR = Criticare CSI 501 + version .27 and version .28 in 501 & 502 (revised instrumentation), PC = PhysioControl Lifestat 1600, and MQ = Marquest/Minolta PulseOx 7). Usually, one probe of each pair was mounted on the ear, the other on a finger. Semi-recumbent, healthy, normotensive, non-smoking caucasian or asian volunteers (age range 18-64 yr) performed the test six to seven times each. After insertion of a radial artery catheter, subjects hyperventilated 3% CO2, 0-5% O2, balance N2. Saturation ScO2, computed on-line from mass spectrometer end-tidal PO2 and PCO2, was used to manually adjust FIO2 breath by breath to obtain a rapid fall to a hypoxic plateau lasting 30-45s, followed by rapid resaturation. Arterial HbO2% (Radiometer OSM-3) sampled near the end of the plateau averaged 55.5 +/- 7.5%. ScO2% (from the mass spectrometer) and SaO2% (from pH and PO2, by Corning 178) differed from HbO2% by + 0.2 +/- 3.6% and 0.4 +/- 2.8%, respectively. The mean and SD errors of pulse oximeters (vs. HbO2%) were: (table; see text) The plateaus were always long enough to permit instruments to demonstrate a plateau with ear probes, but finger probes sometimes failed to provide plateaus in subjects with peripheral vasoconstriction. Nonetheless, SpO2 read significantly too low with finger probes at 55% mean SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Response time of pulse oximeters assessed using acute decompression.

In human volunteers, the response times of 11 pulse oximeters to a 10% step reduction in arterial oxygen saturation were measured using an acute decompression technique. When finger probes were used, nine oximeters had similar response times and two were significantly slower (P less than 0.05). The ear probe response time was similar on six oximeters assessed, and faster than the finger probes. The response times of the oximeters to an acute increase in arterial saturation were tested by suddenly changing the inspired gas from air to 100% oxygen at an ambient pressure of 380 mm Hg. For ear probes, the response times were similar for all oximeters; for finger probes, three fast-responding and three slow-responding oximeters were identified (P less than 0.05). A faster response could be elicited by placing the probes on the thumb (P less than 0.05). We conclude that if a rapid indication of changes in arterial saturation is required, pulse oximeters with ear probes should be used. If finger probes are used, they should be placed on the thumb. The oximeter used will influence the response time if finger probes are used, but it will have little effect if ear probes are used.     

Pulse oximeters demonstrate different responses during hypothermia and changes in perfusion

PURPOSE: Several new pulse oximeters using updated algorithms are marketed as being resistant to motion and hypoperfusion. The purpose of this study was to compare the performance of three pulse oximeters under conditions of hypothermia and altered perfusion. METHODS: Ten male volunteers were enrolled in this study after Institutional approval and obtaining informed consent. The probe of the Dolphin 2100, Nellcor N-595, or Masimo SET radical version 4.2 was attached to the left index finger. Time from 'power on' to acquire the pulse wave and oxygen saturation (SpO2), time from the application of air tourniquet with 250 mmHg on the upper arm to loss of pulse wave and SpO2, and time from the release of the tourniquet to acquire the pulse wave and SpO2 were measured. Then, the patient's left hand and arm were cooled gradually to 27 degrees C dermal temperature in a room at 19 degrees C. The temperatures at loss of the pulse wave and SpO2 were recorded. RESULTS: The Nellcor N-595 was the slowest to detect SpO2 and pulse wave at 'power on'. The Masimo SET showed pulse wave and SpO2 longer than the other two monitors after 'tourniquet on'. The Nellcor N-595 was the fastest to show pulse wave and SpO2 following tourniquet release. CONCLUSION: The Masimo SET was the slowest to respond to the changes in perfusion, and the Nellcor N-595 responded the fastest. However, the Nellcor N-595 was the slowest to show SpO2 and pulse wave at 'power on'.     

Decreased circulation time in the upper limb reduces the lag time of the finger pulse oximeter response

To observe the influence of circulatory changes on the lag time of the pulse oximeter response, eight healthy patients scheduled for hand surgery were studied. After breath holding, the patients took a breath of oxygen and the time to an increase in SpO2 was measured before and after axillary brachial plexus block. It was found that the lag time with finger probe decreased from 28.6 +/- 7.1 sec to 15.8 +/- 1.1 sec (mean +/- SD) following brachial block (P less than 0.01). There was no change in arterial blood pressure. The results suggest that the lag time of the finger pulse oximeter response is primarily determined by blood flow.     

A comparison of two pulse oximeters

The accuracy of the Ohmeda Biox 3700 and the Nellcor N100E was assessed in 25 cyanosed children. The readings obtained from the two pulse oximeters were compared with arterial blood measurements using a Radiometer OSM-2 co-oximeter. Both pulse oximeters differed significantly from the co-oximeter measurements and in these patients the error of both machines exceeded the manufacturers' claims. However, the machines appeared to reflect changes in saturation accurately in the same patient.     

Performance of three new-generation pulse oximeters during motion and low perfusion in volunteers

Study ObjectiveTo evaluate pulse oximeter performance during motion and induced low perfusion in volunteers.DesignProspective volunteer study.SettingDirect Observation unit.Subjects10 healthy adult volunteers.InterventionsTen volunteers were monitored with three different pulse oximeters while they underwent desaturation to about 75% oxygen saturation (SpO₂) and performed machine-generated (MG) and volunteer-generated (VG) hand movements with the test hand, keeping the control hand stationary.MeasurementsSpO₂ and pulse rate readings from the motion (test) and stationary (control) hands were recorded as well as the number of times and the duration that the oximeters connected to the test hands did not report a reading. Sensitivity, specificity, performance index for SpO₂, and pulse rate (PR) were calculated for each pulse oximeter by comparing performance of the test hand with the control hand.Main ResultsDuring both MG and VG motion, the Masimo Radical had higher SpO₂ specificity (93% and 97%) than the Nellcor N-600 (67% and 77%) or the Datex-Ohmeda TruSat (83% and 82%). The Masimo Radical also had higher SpO₂ sensitivity (100% and 95%) than the Nellcor N-600 (65% and 50%) or the Datex-Ohmeda TruSat (20% and 15%) during both MG and VG motion. During MG motion, the Masimo Radical had the lowest PR failure rate (0%) compared with the Nellcor N-600 (22.2%) and Datex-Ohmeda TruSat (1.3%). However, during VG motion, the Masimo Radical had the lowest SpO₂ failure rate (0%) of the three devices (Nellcor N-600 16.4% and Datex-Ohmeda TruSat 1.7%). Both the Masimo Radical and the Datex-Ohmeda TruSat had lower PR failure rates (0% and 4.4%) than the Nellcor N-600 (33.9%). There were no significant differences in SpO₂ or PR performance index between the three devices.ConclusionsThe Masimo Radical had higher SpO₂ sensitivity and specificity than the Nellcor N-600 and Datex-Ohmeda TruSat during conditions of motion and induced low perfusion in this volunteer study.     

An assessment of the accuracy of pulse oximeters

Peripheral pulse oximetry has become a core monitoring modality in most fields of medicine. Pulse oximeters are used ubiquitously in operating theatres, hospital wards, outpatient clinics and general practice surgeries. This study used a portable spectrometer (Lightman^®, The Electrode Co. Ltd., Monmouthshire, UK) to measure the emission spectra of the two light emitting diodes within the pulse oximeter sensor and to determine the accuracy of 847 pulse oximeters currently in use in 29 NHS hospitals in the UK. The standard manufacturing claim of accuracy for pulse oximeters is ± 2–3% over the range of 70–100% S_pO₂. Eighty‐nine sensors (10.5%) were found to have a functional error of their electrical circuitry that could cause inaccuracy of measurement. Of the remaining 758 sensors, 169 (22.3%) were found to have emission spectra different from the manufacturers’ specification that would cause an inaccuracy in saturation estimation of > 4% in the range of 70–100% saturation. This study has demonstrated that a significant proportion of pulse oximeter sensors may be inaccurate.     

Effect of induction rate for mild hypothermia on survival time during uncontrolled hemorrhagic shock in rats

BACKGROUND: Rapid induction of hypothermia has been shown to improve survival in uncontrolled hemorrhagic shock (UHS) rat studies. We hypothesized that prolonged induction of hypothermia would be equally beneficial for survival during UHS. METHODS: Light anesthesia was induced with halothane in 30 rats, and spontaneous breathing was maintained. Rectal temperature (Tr) was monitored and maintained at 38 degrees C. UHS was induced by blood withdrawal of 2.5 mL/100 g during a 15-minute period, followed by 75% tail amputation. Immediately after cutting the tail, rats were randomized into three groups of 10 rats each: Group 1, maintained at Tr 38 degrees C; group 2, passively cooled to 34 degrees C by exposure to room temperature (23 degrees C); and group 3, actively cooled to 34 degrees C by applying alcohol to the skin and under an electric fan. Next, rats were controlled at each target Tr and observed without fluid resuscitation until either death or a maximum of 240 minutes. RESULTS: Cooling rate was -0.09 +/- 0.01 degrees C/min in group 2 and -0.36 +/- 0.9 degrees C/min in group 3 (p < 0.01). Mean survival time was 72 +/- 21 minutes in group 1 (38 degrees C), and was nearly doubled by hypothermia to 132 +/- 62 minutes for group 2 (p < 0.01 vs. group 1) and 150 +/- 69 minutes for group 3 (p < 0.01 vs. group 1). No significant difference in survival was noted between groups 2 and 3. Additional blood loss from the tail stump did not differ significantly between groups. CONCLUSION: Therapeutic mild hypothermia, induced either slowly (approximately -0.1 degrees C/min) or rapidly (approximately -0.4 degrees C/min) prolongs survival during lethal UHS in rats.     

Comparison of the Nellcor N-200 and N-3000 pulse oximeters during simulated postoperative activities

Twenty-six healthy volunteers were monitored simultaneously with the Nellcor N-200 and N-3000 pulse oximeters during nonhypoxaemic simulated postoperative activity. The overall number of registered events (hypoxaemic episodes or loss of signal) was fewer with the N-3000 than with the N-200 (8 vs. 32, p < 0.00005). Episodes of 'desaturation' of ≥5% from baseline were significantly fewer with the N-3000 than with the N-200 (5 vs. 19, p =0.0001), and lowest values below 90% occurred nine times on the N-200, but were not seen with the N-3000 (p <0.00005). Furthermore, episodes owing to loss of signal were significantly rarer with the N-3000 than with the N-200 (3 vs. 13, p =0.001). The Nellcor N-3000 oximeter may offer an advantage over the N-200 model when monitoring patients in the postoperative period.     

Thermogenetic response to mild hypothermia in anaesthetized infants and children

Metabolic correlates were related to room, core body and skin temperatures in 66 anaesthetized infants and children. Forty-one who had normal cardiorespiratory function were undergoing minor lower abdominal surgical procedures and were spontaneously breathing O₂/air mixture and halothane (body weight, 3.4–25.3 kg). Twenty-five had congenital heart malformations; 14 were cyanotic (weight, 3.4–24.3 kg) and 11 were acyanotic (weight, 3.7–20 kg). These 25 had balanced anaesthesia with halothane and their lungs were mechanically ventilated. Oxygen consumption (V?o₂), i. e. heat production, and CO₂ elimination (V?co₂) were measured by mass spectrometry. Indirect calorimetry was used for calculation of energy consumption. Temperatures were recorded in the lower third of the oesophagus (core temperature), at the mammillary level along the anterior axillary line (skin temperature), and in room air. Oesophageal temperatures ranged from 34.0°C to 38.1°C and skin temperatures from 32.1°C to 37.4°C (mean ± SD, 34.5°C ± 1.2°C). Heat production (V?o₂) was not related to body, skin or room temperatures. In concordance V?co₂ and energy expenditure were unrelated to the measured temperatures. Thermogenesis is thus eliminated in infants as well as in children, by the anaesthetic techniques used in the current study. This emphasizes the importance of prevention of heat loss in paediatric anaesthesia. Since the reduced skin and body temperatures in this study did not increase oxygen consumption, temperature regulation via an enhanced V?o₂ does not appear as a factor that aggravates hypoxaemia in cyanotic infants and children with congenital heart malformations.     

Brain protection with mild hypothermia during carotid artery clamping

A 71-year-old man was scheduled for removal of a Kirchner wire malpositioned in the mediastinum, which had been placed for fixing the fractured right clavicle five months before. Anesthesia was induced and maintained with propofol, fentanyl and vecuronium. The wire was found to be penetrating the brachiocephalic artery after sternotomy. An emergency angiography performed in the operating room showed that Willis arterial circle was sufficiently developed for clamping the brachiocephalic artery. The wire was removed under clamping the brachiocephalic artery for 9 minutes, but massive bleeding from the left common carotid artery continued, then the left common carotid artery was clamped and injured region was resected and reconstructed for 68 minutes. The body temperature was reduced to 32.5-33 degree with a cooling water mattress for brain protection and prostaglandin E1 was infused for vasodilation during hypothermia. Monitoring with somatosensory evoked potential was added during anesthesia. The surgery was performed uneventfully and the patient showed no neurological sequelae postoperatively.     

The antiinflammatory effects of propofol in endotoxemic rats during moderate and mild hypothermia

Purpose We previously found that propofol attenuated the mortality rate and inflammatory responses during endotoxemia in rats; however, whether propofol retains its antiinflammatory effects during hypothermia has not been determined. We investigated the effects of propofol on endotoxemic rats subjected to moderate or mild hypothermia. Methods Male Wistar rats (n = 88) were anesthetized intraperitoneally with pentobarbital sodium and assigned to one of two protocols: one representing moderate hypothermia (30°–32°C) and the other representing mild hypothermia (33°–35°C). Each protocol included four equal-sized groups: group A, Escherichia coli endotoxin (15 mg·kg⁻¹, i.v.) and normothermia; group B, propofol (10 mg·kg⁻¹·h⁻¹, i.v.) and normothermia after endotoxin injection; group C, endotoxin (15 mg·kg⁻¹, i.v.) and hypothermia; and group D, propofol (10 mg·kg⁻¹·h⁻¹, i.v.) and hypothermia after endotoxin injection. Rats then were warmed or cooled to maintain rectal temperatures as above for 6 h. The mortality rate was assessed up to 6 h after endotoxin injection. In addition, we assessed hemodynamics, acid–base status, and plasma cytokine concentrations. Results Endotoxemic rats developed hypotension and metabolic acidosis as well as increased plasma cytokine concentrations. Mortality rates 6 h after endotoxin injection were 70%, 40%, 10%, and 0% for groups A–D, respectively, at moderate hypothermia. Propofol administration to endotoxemic rats with hypothermia, whether moderate or mild, also attenuated the high mortality rate, metabolic acidosis, and elevation of cytokines, but these effects were not superior to those of hypothermia alone. Conclusion During hypothermia, propofol administration does not have additive beneficial antiinflammatory effects.     

The antiinflammatory effects of ketamine in endotoxemic rats during moderate and mild hypothermia

Endotoxemia is a common problem among critically-ill patients. We previously found that ketamine inhibited hypotension, metabolic acidosis, and increase of plasma cytokines during endotoxemia in rats. Although endotoxic patients often develop hypothermia, it has not been determined whether ketamine retains its antiinflammatory effects during hypothermia. We investigated the effects of ketamine on endotoxemic rats subjected to moderate and mild hypothermia. Male Wistar rats (n = 100) were anesthetized intraperitoneally with pentobarbital sodium and assigned to one of two protocols: one representing moderate hypothermia (30 degrees C-32 degrees C) and the other, mild hypothermia (33 degrees C-35 degrees C). Each protocol included 5 equal groups: 1). Escherichia coli endotoxin (15 mg/kg IV) in normothermia, 2). ketamine (10 mg x kg(-1) x h(-1) IV) during and after endotoxin injection in normothermia, 3). saline in hypothermia, 4). endotoxin (15 mg/kg IV) in hypothermia, and 5) ketamine (10 mg x kg(-1) x h(-1) IV) in hypothermia after endotoxin injection. Rats were then warmed or cooled to maintain rectal temperatures as above for 6 h. We assessed hemodynamics, acid-base status, and plasma concentrations of tumor necrosis factor-alpha, and interleukin-6. Endotoxemic rats developed hypotension and metabolic acidosis as well as increased plasma cytokine concentrations. At 6 h after endotoxin injection, the mean systolic arterial blood pressure decreased by 71% in the saline/normothermia/endotoxin group, whereas it decreased by only 6%, 41%, and 29% in the ketamine/normothermia/endotoxin, saline/moderate hypothermia/endotoxin, and ketamine/moderate hypothermia/endotoxin groups, respectively. Ketamine administration to endotoxemic rats with hypothermia, whether moderate or mild, also attenuated hypotension, metabolic acidosis, and cytokine increase, but these effects were not superior to those of hypothermia alone. Our findings suggest that, during hypothermia, ketamine administration may not have additive beneficial antiinflammatory effects. IMPLICATIONS: Although ketamine administration decreased the severity of hypotension and acidosis in endotoxemic rats, ketamine administration may not have additive beneficial antiinflammatory effects during hypothermia.     

A comparison of the failure times of pulse oximeters during blood pressure cuff-induced hypoperfusion in volunteers

Important information may not be obtained if the pulse oximetry signal is lost during inflation of a cuff for blood pressure measurement, particularly in patients with hemodynamic instability. In the present study, we compared the failure times of pulse oximeters during cuff-induced hypoperfusion in volunteers. A pulse oximeter sensor was attached to the index finger, and a blood pressure cuff was attached to the same arm of each volunteer. MasimoSET Radical (Masimo), Nellcor N-395 (N-395), Nellcor N-20PA, and Nellcor D-25 were tested. To evaluate the failure time of each pulse oximeter, time to peak of cuff pressure, time to loss of signal, time to recovery of signal, and failure interval were measured. All measurements were performed three times for each pulse oximeter and were averaged. There were no differences in hemodynamic measurements among the groups. Time to loss of signal was longer in Masimo than the other pulse oximeters. Masimo and N-395 showed significantly shorter times to recovery of signal than those of the other two pulse oximeters. Failure interval was in the order of Masimo < N-395 < Nellcor D-25 = Nellcor N-20PA. Masimo did not lose a signal as rapidly as the other oximeters studied. Masimo was similar in performance to the N-395 at providing useful data sooner than conventional technology after a loss of the signal. These observations suggest that data will be more available with fewer false-positive alarms when using the Masimo oximeter followed by the N-395 when compared with conventional oximeters.