It has been suggested that Pulse oximeter be merged into this article or section. (Discuss)
A modern pulse oximeter that also provides pulse co-oximetry.

Pulse oximetry is a non-invasive method allowing the monitoring of the oxygenation of a patient's hemoglobin.

A sensor is placed on a thin part of the patient's anatomy, usually a fingertip or earlobe, or in the case of a neonate, across a foot, and a light containing both red and infrared wavelengths is passed from one side to the other. Changing absorbance of each of the two wavelengths is measured, allowing determination of the absorbances due to the pulsing arteria blood alone, excluding venous blood, skin, bone, muscle, fat, and (in most cases) fingernail polish. Based upon the ratio of changing absorbance of the red and infrared light caused by the difference in color between oxygen-bound (bright red) and oxygen unbound (dark red or blue, in severe cases) blood hemoglobin, a measure of oxygenation (the per cent of hemoglobin molecules bound with oxygen molecules) can be made.

Contents

Indication

Pulse oximetry data is necessary whenever a patient's oxygenation is unstable, including intensive care, critical care, and emergency department areas of a hospital. Data can also be obtained from pilots in unpressurized aircraft and for assessment of any patient's oxygenation in primary care.[citation needed] A patient's need for oxygen is the most essential element to life; no human life thrives in the absence of oxygen (cellular or gross). Although pulse oximetry is used to monitor oxygenation, it cannot determine the metabolism of oxygen, or the amount of oxygen being used by a patient. For this purpose, it is necessary to also measure carbon dioxide (CO2) levels. It is possible that it can also be used to detect abnormalities in ventilation. However, the use of pulse oximetry to detect hypoventilation is impaired with the use of supplemental oxygen, as it is only when patients breathe room air that abnormalities in respiratory function can be detected reliably with its use. Therefore, the routine administration of supplemental oxygen may be unwarranted if the patient is able to maintain adequate oxygenation in room air, since it can result in hypoventilation going undetected.[citation needed]

History

In 1935 Matthes developed the first 2-wavelength ear O2 saturation meter with red and green filters, later switched to red and infrared filters. This was the first device to measure O2 saturation.[citation needed]

In 1949 Wood added a pressure capsule to squeeze blood out of ear to obtain zero setting in an effort to obtain absolute O2 saturation value when blood was readmitted. The concept is similar to today's conventional pulse oximetry but suffered due to unstable photocells and light sources. This method is not used clinically. In 1964 Shaw assembled the first absolute reading ear oximeter by using eight wavelengths of light. Commercialized by Hewlett Packard, its use was limited to pulmonary functions and sleep laboratories due to cost and size.[citation needed]

Pulse oximetry was developed in 1972, by Aoyagi at Nihon Kohden using the ratio of red to infrared light absorption of pulsating components at the measuring site. It was commercialized by Biox in 1981 and Nellcor in 1983. Biox was founded in 1979, and introduced the first pulse oximeter to commercial distribution in 1981. Biox initially focused on respiratory care, but when the company discovered that their pulse oximeters were being used in operating rooms to monitor oxygen levels, Biox expanded its marketing resources to focus on operating rooms in late 1982. A competitor, Nellcor (now part of Covidien, Ltd.), Incorporated in 1982, and began to compete with Biox for the US operating room market in 1983. Prior to its introduction, a patient's oxygenation was determined by a painful arterial blood gas, a single point measure which typically took a minimum of 20-30 minutes processing by a laboratory. (In the absence of oxygenation, damage to the brain starts in 5 minutes with brain death in another 10-15 minutes). In the US alone, approximately $2 billion was spent annually on this measurement. With the introduction of pulse oximetry, a non-invasive, continuous measure of patient's oxygenation was possible, revolutionizing the practice of anesthesia and greatly improving patient safety. Prior to its introduction, studies in anesthesia journals estimated US patient mortality as a consequence of undetected hypoxemia at 2,000 to 10,000 deaths per year, with no known estimate of patient morbidity.[citation needed]

By 1987, the standard of care for the administration of a general anesthetic in the US included pulse oximetry. From the operating room, the use of pulse oximetry rapidly spread throughout the hospital, first in the recovery room, and then into the various intensive care units. Pulse oximetry was of particular value in the neonatal unit where the patients do not thrive with inadequate oxygenation, but also can be blinded with too much oxygen. Furthermore, obtaining an arterial blood gas from a neonatal patient is extremely difficult.[citation needed]

In 1996, Masimo, a California-based company, introduced the first pulse oximeter able to provide accurate measurements during periods of patient motion or low peripheral perfusion, long thought to be limitations of pulse oximetry technology that could not be overcome. [1] The ability to provide accurate measurements under these difficult clinical conditions meant pulse oximetry could be used outside the operating room, where patients were generally well perfused and not moving, allowing for adoption in neonatal intensive care units, ambulances, and other challenging settings.[2]

By 2008, the accuracy and capability of Pulse Oximetry had continued to increase, and had allowed for the adoption of the term High Resolution Pulse Oximetry (HRPO).[3][4][5] One area of particular interest in the area of Pulse Oximetry, is the use of Pulse Oximetry in conducting portable and in-home sleep apnea screening and testing.[6][3]

Limitations and Advancements

This is a measure solely of oxygenation, not of ventilation, and is not a substitute for blood gases checked in a laboratory as it gives no indication of carbon dioxide levels, blood pH, or sodium bicarbonate levels. The metabolism of oxygen can be readily measured by monitoring expired CO2. Saturation figures also give no information about blood oxygen content, as a patient can be severely anemic but still fully saturated.

Falsely low readings may be caused by hypoperfusion of the extremity being used for monitoring (often due to the part being cold or from vasoconstriction secondary to the use of vasopressor agents); incorrect sensor application; highly calloused skin; and movement (such as shivering), especially during hypoperfusion. To ensure accuracy, the sensor should return a steady pulse and/or pulse waveform. Falsely high or falsely low readings will occur when hemoglobin is bound to something other than oxygen. In cases of carbon monoxide poisoning, the falsely high reading may delay the recognition of hypoxemia (low blood oxygen level). Methemoglobinemia characteristically causes pulse oximetry readings in the mid-80s. Cyanide poisoning can also give a high reading because it reduces oxygen extraction from arterial blood (the reading is not false, as arterial blood oxygen is indeed high in early cyanide poisoning).

Pulse oximetry only reads the percentage of bound hemoglobin. It can be bound to other gasses such as carbon monoxide and still read high even though the patient is hypoxic. The only noninvasive methodology that allows for the continuous and noninvasive measurement of the dyshemoglobins is a pulse co-oximeter. Pulse CO-Oximetry was invented in 2005 by Masimo and currently allows clinicians to measure total hemoglobin levels in addition to carboxyhemoglobin, methemoglobin and PVI, which initial clinical studies have shown may provide clinicians with a new method for noninvasive and automatic assessment of patient fluid volume status.[7][8][9] Appropriate fluid levels are vital to reducing postoperative risks and improving patient outcomes as fluid volumes that are too low (under hydration) or too high (over hydration) have been shown to decrease wound healing, increase risk of infection and cardiac complications.[10]

See also

References

  1. ^ Barker SJ, Shah NK (October 1996). "Effects of motion on the performance of pulse oximeters in volunteers". Anesthesiology 85 (4): 774–81. doi:10.1097/00000542-199610000-00012. PMID 8873547. http://www.anesthesiology.org/pt/re/anes/fulltext.00000542-199610000-00012.htm;jsessionid=LgzLhCRl1xxQ2j5NJZsjccHQy1wGXpGSsSmWsGGDSMxDnfKYhShL!-1123973585!181195628!8091!-1. Retrieved on 11 August 2008. 
  2. ^ Giuliano KK, Higgins TL (January 2005). "New-generation pulse oximetry in the care of critically ill patients". Am. J. Crit. Care 14 (1): 26–37; quiz 38–9. PMID 15608106. http://ajcc.aacnjournals.org/cgi/content/full/14/1/26. Retrieved on 11 August 2008. 
  3. ^ a b http://www.sleepreviewmag.com/issues/articles/2008-04_10.asp
  4. ^ http://www.maxtecinc.com/assets/docs/pulsox/ml187.p300iDataSheet.pdf
  5. ^ http://www.anesthesiology.org/pt/re/anes/fulltext.00000542-200809000-00004.htm
  6. ^ http://www.post-gazette.com/pg/08009/847751-114.stm
  7. ^ Keller G, Cassar E, Desebbe O, Lehot JJ, Cannesson M (2008). "Ability of pleth variability index to detect hemodynamic changes induced by passive leg raising in spontaneously breathing volunteers". Crit Care 12 (2): R37. doi:10.1186/cc6822. PMID 18325089. 
  8. ^ Cannesson M, Delannoy B, Morand A, et al (April 2008). "Does the Pleth variability index indicate the respiratory-induced variation in the plethysmogram and arterial pressure waveforms?". Anesth. Analg. 106 (4): 1189–94, table of contents. doi:10.1213/ane.0b013e318167ab1f (inactive 27 September 2008). PMID 18349191. 
  9. ^ Cannesson M, Desebbe O, Rosamel P, et al (August 2008). "Pleth variability index to monitor the respiratory variations in the pulse oximeter plethysmographic waveform amplitude and predict fluid responsiveness in the operating theatre". Br J Anaesth 101 (2): 200–6. doi:10.1093/bja/aen133. PMID 18522935. 
  10. ^ Ishii M, Ohno K (March 1977). "Comparisons of body fluid volumes, plasma renin activity, hemodynamics and pressor responsiveness between juvenile and aged patients with essential hypertension". Jpn. Circ. J. 41 (3): 237–46. PMID 870721. 
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