Delays in the detection of hypoxemia due to site of pulse oximetry probe placement

Hamber, Elizabeth A.; Bailey, Peter L.; James, Scott W; Wells, David T.; Lu, Jeff Zhiqiang; Pace, Nathan L.

doi:10.1016/s0952-8180(99)00010-0

Cited by 42 publications

(10 citation statements)

References 22 publications

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“…Another limitation of this study is due to the use of finger pulse oximetry rather than the direct assessment of SaO 2 , which is less accurate at SaO 2 below 75–85% (Trivedi et al, 1997 ; Kolb et al, 2004 ). Another drawback of finger pulse oximetry is related to the slow response time of all pulse oximeters (Trivedi et al, 1997 ), with the delay being higher for finger than earlobe placements (Trivedi et al, 1997 ; Hamber et al, 1999 ). Consequently, the SpO 2 values recorded during the first 10 s of the transitions from hypoxia to higher P I O 2 underestimated the actual SaO 2 values.…”

Section: Discussionmentioning

confidence: 99%

Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect?

et al. 2016

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To determine the level of hypoxia from which muscle activation (MA) is reduced during incremental exercise to exhaustion (IE), and the role played by PIO2 in this process, ten volunteers (21 ± 2 years) performed four IE in severe acute hypoxia (SAH) (PIO2 = 73 mmHg). Upon exhaustion, subjects were asked to continue exercising while the breathing gas mixture was swiftly changed to a placebo (73 mmHg) or to a higher PIO2 (82, 92, 99, and 142 mmHg), and the IE continued until a new exhaustion. At the second exhaustion, the breathing gas was changed to room air (normoxia) and the IE continued until the final exhaustion. MA, as reflected by the vastus medialis (VM) and lateralis (VL) EMG raw and normalized root mean square (RMSraw, and RMSNz, respectively), normalized total activation index (TAINz), and burst duration were 8–20% lower at exhaustion in SAH than in normoxia (P < 0.05). The switch to a placebo or higher PIO2 allowed for the continuation of exercise in all instances. RMSraw, RMSNz, and TAINz were increased by 5–11% when the PIO2 was raised from 73 to 92, or 99 mmHg, and VL and VM averaged RMSraw by 7% when the PIO2 was elevated from 73 to 142 mmHg (P < 0.05). The increase of VM-VL average RMSraw was linearly related to the increase in PIO2, during the transition from SAH to higher PIO2 (R2 = 0.915, P < 0.05). In conclusion, increased PIO2 at exhaustion reduces fatigue and allows for the continuation of exercise in moderate and SAH, regardless of the effects of PIO2 on MA. At task failure, MA is increased during the first 10 s of increased PIO2 when the IE is performed at a PIO2 close to 73 mmHg and the PIO2 is increased to 92 mmHg or higher. Overall, these findings indicate that one of the central mechanisms by which severe hypoxia may cause central fatigue and task failure is by reducing the capacity for reaching the appropriate level of MA to sustain the task. The fact that at exhaustion in severe hypoxia the exercise was continued with the placebo-gas mixture demonstrates that this central mechanism has a cognitive component.

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Section: Discussionmentioning

confidence: 99%

Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect?

et al. 2016

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“…In adults, ear probes have been shown to respond more rapidly to transient changes in SpO 2 than peripheral (finger/toe) sensors . It is recommended that consideration and documentation of sensor site should be made in settings where transient changes in saturation may be expected (such as in sleep and exercise laboratories or in hyperbaric/hypobaric settings).…”

Section: Factors Affecting Pulse Oximetry Measurementsmentioning

confidence: 99%

Clinical use of pulse oximetry: Official guidelines from the Thoracic Society of Australia and New Zealand

et al. 2013

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Pulse oximetry provides a simple, non-invasive approximation of arterial oxygenation in a wide variety of clinical settings including emergency and critical-care medicine, hospital-based and ambulatory care, perioperative monitoring, inpatient and outpatient settings, and for specific diagnostic applications. Pulse oximetry is of utility in perinatal, paediatric, adult and geriatric populations but may require use of age-specific sensors in these groups. It plays a role in the monitoring and treatment of respiratory dysfunction by detecting hypoxaemia and is effective in guiding oxygen therapy in both adult and paediatric populations. Pulse oximetry does not provide information about the adequacy of ventilation or about precise arterial oxygenation, particularly when arterial oxygen levels are very high or very low. Arterial blood gas analysis is the gold standard in these settings. Pulse oximetry may be inaccurate as a marker of oxygenation in the presence of dyshaemoglobinaemias such as carbon monoxide poisoning or methaemoglobinaemia where arterial oxygen saturation values will be overestimated. Technical considerations such as sensor position, signal averaging time and data sampling rates may influence clinical interpretation of pulse oximetry readings.

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“…The PPG from the ear canal has also been shown to be far more sensitive than earlobe and finger PPG to amplitude variations that arise from respiration, thus allowing for a better measurement of respiration rate [ 18 ]. Furthermore, a significant delay has been observed between earlobe/behind-the-ear pulse oximetry, and pulse oximetry on the hand or the foot for detection of hypoxemia (low levels of blood oxygen) [ 12 , 19 ], which is primarily caused by the distance from the core blood supply. Although never previously shown, a similar fast response time was hypothesised from the ear canal given that its vasculature is supplied by the carotid artery, as is the brain.…”

Section: Introductionmentioning

confidence: 99%

In-Ear SpO2: A Tool for Wearable, Unobtrusive Monitoring of Core Blood Oxygen Saturation

Davies

Williams

Peters

et al. 2020

Sensors

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The non-invasive estimation of blood oxygen saturation (SpO2) by pulse oximetry is of vital importance clinically, from the detection of sleep apnea to the recent ambulatory monitoring of hypoxemia in the delayed post-infective phase of COVID-19. In this proof of concept study, we set out to establish the feasibility of SpO2 measurement from the ear canal as a convenient site for long term monitoring, and perform a comprehensive comparison with the right index finger—the conventional clinical measurement site. During resting blood oxygen saturation estimation, we found a root mean square difference of 1.47% between the two measurement sites, with a mean difference of 0.23% higher SpO2 in the right ear canal. Using breath holds, we observe the known phenomena of time delay between central circulation and peripheral circulation with a mean delay between the ear and finger of 12.4 s across all subjects. Furthermore, we document the lower photoplethysmogram amplitude from the ear canal and suggest ways to mitigate this issue. In conjunction with the well-known robustness to temperature induced vasoconstriction, this makes conclusive evidence for in-ear SpO2 monitoring being both convenient and superior to conventional finger measurement for continuous non-intrusive monitoring in both clinical and everyday-life settings.

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Delays in the detection of hypoxemia due to site of pulse oximetry probe placement

Cited by 42 publications

References 22 publications

Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect?

Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect?

Clinical use of pulse oximetry: Official guidelines from the Thoracic Society of Australia and New Zealand

In-Ear SpO2: A Tool for Wearable, Unobtrusive Monitoring of Core Blood Oxygen Saturation

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