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Pulse oximetry
AUTHORS: C Crawford Mechem, MD, FACEP, Amal Jubran, MD
SECTION EDITOR: Polly E Parsons, MD
DEPUTY EDITOR: Geraldine Finlay, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: May 2025.

This topic last updated: May 24, 2024.

INTRODUCTION

Pulse oximetry measures peripheral arterial oxygen saturation as a surrogate marker for tissue
oxygenation. It has become the standard for continuous, noninvasive assessment of
oxygenation and is often considered the "fifth vital sign" [1-3]. Theoretical and clinical aspects of
pulse oximetry will be reviewed here. Other measures of oxygenation, mechanisms of
hypoxemia, and use of pulse oximetry in newborns for the detection of congenital heart disease
are discussed separately. (See "Measures of oxygenation and mechanisms of hypoxemia" and
"Newborn screening for critical congenital heart disease using pulse oximetry".)

PRINCIPLES AND EQUIPMENT

Pulse oximetry uses spectrophotometry to determine the proportion of hemoglobin that is

saturated with oxygen (ie, oxygenated hemoglobin; oxyhemoglobin) in peripheral arterial
blood. Light at two separate wavelengths illuminates oxygenated and deoxygenated
hemoglobin in blood. The ratio of light absorbance between oxyhemoglobin and the sum of
oxyhemoglobin plus deoxyhemoglobin is calculated and compared with previously calibrated
direct measurements of arterial oxygen saturation (SaO2) to establish an estimated measure of
peripheral arterial oxygen saturation (SpO2) [4].

The Beer-Lambert law — Pulse oximetry estimates peripheral SpO2 using a variation of the
Beer-Lambert law. This law states that the absorption of light of a given wavelength passing
through a non-absorbing solvent, which contains an absorbing solute, is proportional to the
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product of the solute concentration, the light path length, and an extinction coefficient. The
Beer-Lambert law can readily be applied to co-oximeters in a laboratory setting because the
light path length is known and hemoglobin is in solution. However, it must be modified for
pulse oximetry to overcome the obstacles associated with interference from tissue and pulsatile
flow. This modification involves measuring absorbance at two different wavelengths, one to
detect oxyhemoglobin and the other to detect deoxyhemoglobin [1,5].

Probes — Pulse oximeter probes consist of two light-emitting diodes and a photodetector.

● Emitters – Deoxyhemoglobin absorbs light maximally in the red band of the spectrum (600 to
750 nm), and oxyhemoglobin absorbs maximally in the infrared band (850 to 1000 nm) [1].
Thus, the emitters emit light at 660 nm and 940 nm for optimal detection of these two
substances.

● Detector – The detector (also known as sensor) detects the absorbance of light from exposed
tissue. The values are processed and a saturation determined. (See 'Calibration and
calculation' below.)

In general, detectors and emitters are positioned facing each other through interposed tissue
( picture 1) [6]. Probes are most frequently placed on the anterior and posterior aspect of
fingers, toes, or ear lobes [7]. The nasal ala is another option [8]. In infants, probes may also
be placed on the palms, feet, arms, cheeks, tongue, penis, nose, or nasal septum [9].
Forehead probes have the emitter and detector adjacent to each other so that saturation is
measured from light that is reflected back from (not through) exposed tissue. These sites are
preferentially used since they contain a high density of vascular tissue.

Although various types of probes are available, none has shown clear superiority over
another [10-13]. When clinicians cannot get a clear reading with one probe, another is often
tried. (See 'Troubleshooting sources of error' below.)

The response time to changes in oxygenation varies but is generally delayed for most available
probes. As an example, some studies have shown that ear probes and forehead probes respond
more quickly to a change than conventional finger probes (eg, 94 versus 100 seconds for
desaturation, and 23 versus 29 seconds for increases in saturation) [14,15].

Calibration and calculation — The saturation value is calculated using microprocessors that
utilize absorbance readings from light-exposed oxyhemoglobin and deoxyhemoglobin. The
emitters are switched on and off several hundred times per second [16]. Absorption during
pulsatile flow relates to the characteristics of arterial blood plus background tissue and venous
blood, whereas absorption during nonpulsatile flow is due only to the background tissue and

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venous blood ( figure 1) [17]. Absorption at the two wavelengths during pulsatile flow is
divided by absorption during nonpulsatile flow, and these ratios are fed into an algorithm in the
microprocessor to yield a saturation value. The displayed value is an average based on the
previous three to six seconds [6,16]. In addition to peripheral SpO2 many pulse oximeters also
display pulse rate and relative pulse amplitude [1,18].

The microprocessors of pulse oximeters are calibrated using reference tables of actual SaO2
measurements performed using co-oximetry and compiled using data from exposing healthy
volunteers exposed to decreasing fraction of inspired oxygen (FiO2) to yield SaO2 ranging from
100 to 75 percent. Because it would be unethical to intentionally generate lower saturations in
volunteers, values for an SaO2 less than 75 percent are obtained by extrapolation from these
volunteer data. Pulse oximeter manufacturers claim that reported values between 70 and 100
percent are accurate to within 2 to 3 percent of the true value, corresponding with FDA
standards [19,20]. In practice, the cut-off for acceptable accuracy is felt by many clinicians to be
80 percent (which usually reflects an arterial oxygen tension [PaO2] of approximately 50 mmHg
at a pH of 7.4), and varies depending on the model of pulse oximeter used [21].

ADVANTAGES AND DISADVANTAGES

There are many advantages of pulse oximetry over physical examination and arterial blood gas
(ABG) measurement:

● Rapid – Pulse oximetry is a rapid tool that accurately assesses oxygenation, particularly in
emergency situations. Oxygenation is difficult to assess on the basis of physical examination
alone. Frank cyanosis does not develop until the level of deoxyhemoglobin reaches 5 g/dL,
which corresponds to an arterial oxygen saturation (SaO2) of around 67 percent [4]. In
addition, the threshold at which cyanosis becomes apparent is affected by multiple variables
including peripheral perfusion, skin pigmentation, and hemoglobin concentration [6].
Similarly, compared with ABG analysis, pulse oximetry also provides immediate results both
before and after oxygen therapy.

● Noninvasive – Blood gas analysis by arterial puncture or arterial line sampling was for many
years the only available method of detecting hypoxemia, but this technique is painful and has
potential complications [22]. In contrast, pulse oximetry allows noninvasive measurement of
arterial hemoglobin saturation without the risks associated with arterial puncture. (See
"Arterial blood gases" and "Intra-arterial catheterization for invasive monitoring: Indications,
insertion techniques, and interpretation".)

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● Provides continuous data – Pulse oximetry, unlike clinical examination and an indwelling
arterial catheter, provides continuous data such that oxygen therapy can be easily adjusted to
a target level.

Limitations include the following:

● Inability to detect hyperoxemia – Pulse oximetry is unable to detect significant

hyperoxemia. This is due to the shape of the oxygen-hemoglobin dissociation curve, where
large changes in the partial pressure in arterial oxygen (PaO2) may result in no change in
oxygen saturation if the saturation is already near 100 percent (eg, patient with normal lung
function on mechanical ventilation receiving a fraction of inspired oxygen of 1). Therefore, in
patients at risk for profound hyperoxemia, SaO2 by pulse oximeter should be verified by ABG
[23]. (See "Measures of oxygenation and mechanisms of hypoxemia" and "Adverse effects of
supplemental oxygen".)

● Inability to measure arterial oxygen tension – Since pulse oximetry does not measure
PaO2, overreliance on pulse oximetry can miss detection of clinically significant hypoxemia in
adults but particularly in children [24]. A large decrease in PaO2 will not produce a significant
fall in SaO2 until the steeper portion of the oxygen hemoglobin dissociation curve is
encountered at a PaO2 of approximately 60 to 70 mmHg. This is particularly important in
patients receiving supplemental oxygen. As an example, a fall in PaO2 in such a patient from
140 to 65 mmHg would be required before a significant decrease in oxygen saturation is
detected. Furthermore, pulse oximetry results are signal-averaged over several seconds.
Therefore, the pulse oximeter may not detect a hypoxemic event for close to a minute after it
has occurred [25,26]. This delay may be of particular significance when the device is being
used for monitoring during intubation.

● Inability to measure ventilation – While pulse oximetry is a convenient way of measuring

arterial oxygenation, it does not measure the arterial carbon dioxide tension (PaCO2), which is
a measure of ventilation. In addition, supplemental oxygen administered on the basis of
oximetry alone in patients with hypercapnia may be harmful by worsening hypercapnia (ie,
oxygen-induced hypercapnia). Therefore, when hypercapnia or hypoventilation is suspected,
an ABG should be obtained or, alternatively, ventilation can be assessed with end tidal CO2
monitoring [27-30]. As an example, one inadvertently hypoventilated patient who was
administered 100 percent oxygen during hip arthroplasty and monitored with pulse oximetry
alone developed a PaCO2 of 265 mmHg and an arterial pH of 6.65, despite maintenance of
oxygen saturations of 94 to 96 percent [29]. (See "The evaluation and management of the
nonventilated adult with acute hypercapnic respiratory failure" and "Carbon dioxide
monitoring (capnography)".)
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COMPLICATIONS

Because of the noninvasive aspect of pulse oximetry, local complications are extremely rare,
especially when compared with arterial blood gas monitoring.

Digital injury has been reported on rare occasions in critically ill patients, although it is more
likely that the injury is due to the underlying poor digital perfusion and/or use of vasopressors
[31].

Burns have also been reported in patients undergoing magnetic resonance imaging (MRI),
although this complication can be avoided by temporarily removing the probe during MRI
[9,32]. This complication is believed to result from the generation of electrical skin currents
beneath the pulse oximeter cables, which act as an antenna. Notably, no permanent adverse
effects have been reported. (See "Patient evaluation for metallic or electrical implants, devices,
or foreign bodies before magnetic resonance imaging", section on 'Assessing implants, devices,
or foreign bodies for MRI'.)

Limitations are discussed above (See 'Advantages and disadvantages' above.)

APPLICATIONS

Pulse oximetry is indicated in any clinical setting where hypoxemia may occur. These settings
include patient monitoring in emergency departments, operating rooms, emergency medical
services (EMS) systems, postoperative recovery areas, endoscopy suites, sleep and exercise
laboratories, oral surgery suites, cardiac catheterization suites, facilities that perform conscious
sedation, labor and delivery wards, inter-facility patient transfer units, altitude facilities,
aerospace medicine facilities, and patients' homes [6,27,33-41]:

Despite its widespread use, the value of oximetry has been poorly studied with no trials
showing a convincing benefit on clinically meaningful outcome (eg, mortality, myocardial
infarction, resource allocation [26]). Nonetheless, examples where routine use of pulse oximetry
has some value include the following:

● In a pediatric intensive care unit (ICU), using pulse oximetry decreases the number of blood
gases obtained, prevents hyperoxia, and limits the duration of oxygen therapy without
jeopardizing patient outcome [35,42]. (See "Acute severe asthma exacerbations in children
younger than 12 years: Intensive care unit management" and "Overview of neonatal
respiratory distress and disorders of transition".)

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● In emergency departments, initial pulse oximetry readings in children with asthma

exacerbations are predictive of the need for hospitalization [43]. Several studies have shown
that use of pulse oximetry also reduces the number of arterial blood gases obtained in the
intensive care unit and emergency department [44,45].

● In postoperative patients, routine pulse oximetry has been shown to decrease the need for
rapid response team activation and transfer to the ICU [46]. In a randomized trial of 20,000
perioperative patients pulse oximetry use was associated with lower rates of hypoxemia when
compared with patients in whom oximetry was not used (0.4 versus 8 percent) [39]. (See
"Overview of post-anesthetic care for adult patients".)

● In newborns, pulse oximetry has value as a routine outpatient screen for congenital heart
disease. (See "Newborn screening for critical congenital heart disease using pulse oximetry".)

● The medical response to the coronavirus disease 2019 (COVID-19) pandemic has included
new applications for pulse oximetry. Because of increasingly limited healthcare resources,
including hospital beds, many COVID positive patients are being managed at home. Patients
can remain relatively asymptomatic despite disease progression with hypoxemia, placing
them at risk for rapid deterioration. Pulse oximetry is being used both to assist in deciding
which infected patients can be safely discharged from the emergency department and which
patients being managed at home should present to the emergency department for further
assessment and possible admission. A pulse oximetry reading in the 92 to 96 percent range is
often used as an indication of adequate oxygenation in these patients. However, given the
rapidly evolving understanding of the infection’s complex pathophysiology, pulse oximetry
results should be considered in the broader context of the patient’s overall clinical condition
[47]. Novel use of home pulse oximetry monitoring in COVID-19 patients discharged from the
emergency department identifies need for hospitalization [48,49].

INTERPRETING THE RESULTS

In most patients, peripheral oxygen saturation as measured by pulse oximetry (SpO2) provides
accurate information on tissue oxygenation, allowing the clinician to assess and treat patients
who are potentially hypoxemic. As a general principle, clinicians should pay attention to trends
in oxygenation. When treating patients with supplemental oxygen for hypoxemia, they should
target levels that are desirable for the specific etiology while simultaneously avoiding oxygen
toxicity. The clinician should be aware of the limitations and errors associated with pulse
oximetry and have a low threshold to obtain arterial blood for analysis. (See "Arterial blood
gases" and "Venous blood gases and alternatives to arterial carbon dioxide measurement in

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adults" and 'Advantages and disadvantages' above and 'Calibration and calculation' above and
'Troubleshooting sources of error' below.)

Waveform analysis — Peripheral oxygen saturation can only be interpreted when the
waveform is normal. A normal pulse oximeter waveform has a dicrotic notched appearance
typical of an arterial waveform ( figure 2) that synchronizes with a palpable or observed heart
rate. Inadequate waveforms are discussed below. (See 'Inadequate waveform' below.)

Correlation with arterial oxygen saturation — Pulse oximetry provides an estimate of the
proportion of hemoglobin that is saturated with oxygen (ie, SpO2), rather than partial pressure
of oxygen (PaO2). In most patients with SpO2 values of 90 percent or higher, the value lies
within 2 to 3 percent above or below the true arterial saturation (SaO2) reference standard [50-
52]. However, the accuracy worsens when the SaO2 is <90 percent, and especially below 80
percent [53]. Thus, SpO2 is less reliable in critically ill patients where oxygenation can rapidly
fluctuate and desaturation is common [50,54].

Important differences between arterial saturation and arterial oxygen tension should be noted:

● SpO2 and SaO2 reflect the main mechanism by which oxygen is carried to peripheral tissue (ie,
98 percent of arterial oxygen content is normally carried by hemoglobin).

● The PaO2 only measures the proportion that is dissolved in plasma (ie, the remaining 2
percent), representing the minor mechanism for oxygen transport. Although arterial blood
gas analysis can measure arterial saturation, the PaO2 is commonly used to estimate arterial
oxyhemoglobin saturation and oxygen content because the dissolved and hemoglobin-bound
oxygen pools are in equilibrium. However, changes in pH, temperature, and the concentration
of 2,3-diphosphoglycerate alter the PO2-SaO2 relationship, and may result in misleading
calculations of oxyhemoglobin saturation ( figure 3). (See "Structure and function of normal
hemoglobins" and "Measures of oxygenation and mechanisms of hypoxemia".)

Optimal oxygen saturation — There is no optimal level of oxygen saturation below which
tissue hypoxia occurs because of the large number of variables that contribute to hypoxia at the
tissue and cellular level (temperature, pH, tissue blood flow). As a result, there is no consensus
about what constitutes normal and abnormal oximetry. Nonetheless, at sea level, we and other
experts consider resting oxygen saturation ≤95 percent or exercise desaturation of ≥5 percent
as abnormal [55]. However, these values should not be considered in isolation. Trends in oxygen
saturation and the underlying disease process are important for interpretation. For example:

● A resting oxygen saturation of 96 percent could be abnormal if a patient previously had a

resting oxygen saturation of 99 percent.

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● A target level of 88 to 92 percent may be sufficient in a patient with an acute exacerbation of

chronic obstructive pulmonary disease (COPD) who is chronically hypercapnic. In contrast, a
target saturation of >95 percent may be considered optimal in a pregnant woman with acute
respiratory distress syndrome. (See "Critical illness during pregnancy and the peripartum
period", section on 'Mechanical ventilation'.)

Similarly, there is no optimal level of oxygen saturation above which tissue hyperoxia occurs
since hyperoxia cannot be assessed with oximetry or arterial blood gas analysis. Thus, clinicians
should titrate oxygen according to the specific etiology, while attempting to avoid any
theoretical potential for tissue hypoxia. As examples:

● In patients with an exacerbation of chronic obstructive pulmonary disease (COPD) with

chronic hypercapnia, targeting levels ≥92 percent may worsen hypercapnia, while patients
with carbon monoxide (CO) poisoning or air embolism should be treated with 100 percent
oxygen or hyperbaric oxygen to eliminate CO or air, respectively. (See "Air embolism", section
on 'Treatment' and "Carbon monoxide poisoning", section on 'Management' and "COPD
exacerbations: Management", section on 'Oxygen therapy'.)

● Oxygen toxicity, particularly in premature neonates can be limited by titrating oxygen to an

SpO2 of 90 percent, which usually reflects a PaO2 of approximately 60 mmHg at a pH of 7.4
[9,25]. (See "Adverse effects of supplemental oxygen".)

TROUBLESHOOTING SOURCES OF ERROR

Pulse oximetry is subject to artifactual and patient-related sources of error. The best defense
against error is a high index of suspicion. If a saturation reading is in doubt, a health care
worker can perform a quick quality assurance test by putting the probe on his or her own finger
as near as possible to the original patient site [17]. This ensures that abnormal readings are not
due to equipment error. The clinician should then investigate other potential sources of error,
most of which are easily resolved ( table 1).

Inadequate waveform — A normal pulse oximeter waveform has a dicrotic notched

appearance similar to an arterial waveform. Waveforms are considered inadequate when the
dicrotic notched appearance is lost (eg, low in amplitude or erratic). Because the signal is poor,
many of the reasons for an inadequate waveform (eg, hypoperfusion) will also give erroneously
low readings. (See 'Waveform analysis' above and 'Falsely low readings' below.)

Improper probe placement — Improper probe placement can occur in many scenarios and
is often associated with loss of amplitude of the waveform (ie, decreased or flattened pulse
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oximetry amplitude):

● Malposition or poor attachment to the skin can result in either a falsely elevated or
depressed reading (light from only one of the two light-emitting diodes passes through the
tissue) [56].

A similar problem can occur in infants and small children because the small size of fingers
or other tissues may result in differences in the path length of one light source compared
to the other.

Many of these problems can be resolved by ensuring the probe is properly attached with
the light sources and detectors opposite each other in a nontangential path (eg, switch to a
separate digit or use a different probe such as an ear or forehead probe) [57].

● Placement of the sensor on the same extremity as a blood pressure cuff or arterial line can
cause erroneous readings and should be avoided [58].

Motion or noise artifact — A poor signal-to-noise ratio will cause signal artifact and falsely
lower oximetry readings [4,18,59]. This most commonly results from motion due to shivering,
seizure activity, pressure on the sensor, or transport of the patient by ambulance or
helicopter. The waveform will typically appear erratic and lose its normal shape. Newer pulse
oximeters appear to be less influenced by motion artifact [60,61].

Hypoperfusion — Pulse oximetry readings can be falsely low due to signal failure in the
setting of hemodynamic instability or poor limb perfusion from extremity elevation,
vasoconstriction, or peripheral vascular disease [50,54,62].

In adults, the accuracy of standard pulse oximeters decreases dramatically when systolic
blood pressure falls below 80 mmHg, generally resulting in underestimation of the actual
arterial oxygen saturation [63]. Both falsely low and falsely elevated levels have been reported
in septic patients [64,65]. Repositioning the probe or using an alternate site may help.

There are conflicting data regarding superiority of forehead versus finger probes in
hypoperfused states such that switching from one to another type of probe is appropriate
when an inadequate tracing due to hypoperfusion is suspected [10,11,13]. When in doubt an
arterial blood gas (ABG) should be drawn.

Hypothermia — Hypothermia may interfere with pulse oximetry because of the associated
peripheral vasoconstriction and shivering. This can contribute to a delay in the recognition of
acute hypoxemia, particularly if finger probes are used [66]. Hypothermic patients should be
monitored using an ear or forehead probe, which are less likely to delay recognition of acute
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desaturation. Warming should correct the issue. (See "Accidental hypothermia in adults:
Clinical manifestations and evaluation".)

Falsely normal or high reading

Carboxyhemoglobin — Carboxyhemoglobin absorbs approximately the same amount of 660

nm light as oxyhemoglobin. Thus, the pulse oximetry reading represents an inexact
summation of oxyhemoglobin and carboxyhemoglobin ( figure 4) [4,7,67-69]. Due to the
interference of high levels of carboxyhemoglobin carbon monoxide (CO) poisoning, or in
chronic, heavy smokers, a falsely reassuring normal pulse oximetry reading may mask life-
threatening arterial desaturation. Arterial oxygen tension (PaO2) measurements tend to be
normal because PaO2 reflects O2 dissolved in blood, and this process is not affected by CO. In
contrast, hemoglobin-bound O2 (which normally comprises 98 percent of arterial O2 content)
is profoundly reduced in the presence of carboxyhemoglobin. (See 'Correlation with arterial
oxygen saturation' above.)

In such cases, whenever carboxyhemoglobinemia is suspected, co-oximetry (not pulse

oximetry) is recommended for the measurement of carboxyhemoglobin levels. While some
newer pulse oximeters may be able to detect carboxyhemoglobin, they are expensive, poorly
studied, and not universally available. (See 'Co-oximetry' below and "Carbon monoxide
poisoning".)

Glycohemoglobin A1c — Glycohemoglobin A1c levels greater than 7 percent in type 2

diabetics with poor glucose control have been shown to result in overestimation of arterial
oxygen saturation (SaO2) by pulse oximetry. This may be due to an increased hemoglobin
oxygen affinity. However, in our experience most patients with diabetes can be monitored
using pulse oximetry, but if doubt exists, ABG analysis may be warranted [70].

Skin pigmentation — Several studies suggest that skin pigmentation can falsely increase
pulse oximetry readings, resulting in "hidden hypoxemia" [9,17,71-79]. Given the importance
placed on the use of pulse oximetry to risk-stratify critically ill patients, the US Food and Drug
Administration has highlighted the need to address it through the development of more
accurate devices [80,81]. Thus, if there is a concern that skin pigmentation is impacting pulse
oximetry readings, an ABG should be obtained.

Several studies illustrate the impact of skin pigmentation [75,82-85]:

● In a review of 44 studies totaling over 222,000 patients, most studies consistently reported
overestimation of oxygenation by pulse oximetry in those with darker skin tones compared
with those who have lighter skin tones [85].

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● One multicenter study that compared pulse oximetry with ABG analysis in over 10,000 adult
inpatients [75]. Values in Black individuals were compared with light-skinned individuals. In
two separate cohorts, pulse oximetry ranging between 92 and 96 percent overestimated
oxygen saturation as measured by ABG in 12 to 17 percent of Black individuals compared
with 4 to 6 percent of White individuals. Pulse oximetry, in another study, was similarly
found to overestimate arterial oxygen saturation in Black, Hispanic, and other patients
compared with White patients with COVID-19, resulting in a delay in treatment [82].

● Similarly, in another study there was greater variability in oxygen saturation levels in
patients who self-identified as Black, followed by Hispanic, Asian, and White [84]. Moreover,
patients with "hidden" hypoxemia subsequently experienced higher organ dysfunction
scores and in-hospital mortality.

Pulse oximeters with narrow spectral bandwidths for light emission may improve
performance in patients with darker skin tones, but additional data are needed [86].

Falsely low readings

Methemoglobin — Methemoglobin absorbs at both 660 and 940 nm [7].

Methemoglobinemia should be suspected in those with cyanosis and normal PaO2. Up to a
methemoglobin level of 20 percent, SaO2 drops by about one-half of the methemoglobin
percentage. At higher methemoglobin levels, SaO2 trends toward 85 percent regardless of the
true percentage of oxyhemoglobin, thus leading to over- or underestimation of the true SaO2
[4,9,87,88]. When methemoglobinemia is suspected, co-oximetry should be used to
accurately determine the methemoglobin level. (See "Methemoglobinemia" and 'Co-oximetry'
below.)

Sulfhemoglobin — Sulfhemoglobin absorbs at 660 nm, similar to oxyhemoglobin. Its

absorbance at 940 nm is unknown. Sulfhemoglobinemia is most commonly caused by the
ingestion of oxidizing drugs (eg, dapsone, sulfonamides, metoclopramide, nitrates). Patients
present in a similar fashion to those with methemoglobinemia (cyanosis and normal PaO2)
[89-91]. Unlike methemoglobin however, sulfhemoglobin shifts the hemoglobin-oxygen
dissociation curve to the right, thereby "unloading" oxygen in the periphery such that the
adverse effects are not as clinically significant as with methemoglobinemia. High levels can
falsely reduce the SpO2, trending towards 85 percent, similar to methemoglobin. However,
multiwavelength co-oximetry does not accurately distinguish it from methemoglobin. If
suspected, specialized biochemical testing available in a limited number of centers is
required. While testing is ongoing the offending agent should be stopped, if feasible. Patients
do not respond to methylene blue therapy (ie, therapy for methemoglobinemia) which may

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also be a diagnostic clue. There is no known antidote, however, severe cases may respond to
exchange transfusion [91].

Sickle hemoglobin — Patients with sickle cell disease are at risk of hypoxemia caused by a
number of pulmonary complications, which are discussed separately. (See "Overview of the
pulmonary complications of sickle cell disease".)

Sickle hemoglobin generally produces pulse oximeter readings similar to normal hemoglobin.
Rare cases of falsely elevated and falsely low readings have been reported, especially during
vaso-occlusive crises (perhaps due to hypoperfusion). However, in general, the difference
between SaO2 and SpO2 measurements is not clinically significant [27,92-95]. When
hypoxemia is suspected or doubt exists, an ABG should be drawn.

Inherited forms of abnormal hemoglobin — Inherited forms of abnormal hemoglobin (Hb)

are rare but have been reported to result in falsely low SpO2 readings (eg, Hb Lansing, Hb
Bonn, Hb, Koln, Hb Hammersmith, and Hb Cheverly) [96-101].

Severe anemia — In vitro and animal studies suggest that pulse oximetry readings may be
affected by profoundly decreased hemoglobin concentration [27]. In vivo, low hemoglobin
concentrations appear to cause falsely low readings when the SaO2 is below 80 percent [9].
However, this effect is not clinically significant until the hemoglobin level is less than 5 g/dL
[54,102].

Venous congestion — Venous congestion due to tricuspid valve incompetence or

cardiomyopathy may yield falsely low SaO2 readings due to the generation of venous
pulsations. This results from the instrument detecting less oxygenated, pulsatile venous
blood as part of the arterial sample, thereby underestimating the actual SaO2 [9,103,104].
(See 'Calibration and calculation' above.)

Venous pulsations may occur when an adhesive probe is too tight around the finger resulting
in falsely low readings. Similarly, pulsations can also occur when the probe is in a dependent
position (eg, forehead probe in a patient in the Trendelenburg position) and rarely in patients
with arteriovenous shunting.

When venous pulsations are suspected, loosening the probe, repositioning the probe or the
patient, and/or drawing an ABG should be attempted.

Nail polish — The use of nail polish can potentially affect pulse oximeter readings if the
polish absorbs light at 660 nm and/or 940 nm [4,105-107]. An early study of volunteers
wearing black, green, and blue nail polish revealed a drop in SaO2 of 3, 5, and 6 percent,

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respectively [17]. Newer devices appear to be less affected, with the greatest reductions in
SpO2 found in those with black, blue, brown, or purple polish. Most likely these reductions are
not clinically significant [108,109].

The problem may be avoided by mounting the probe on the finger sideways, rather than in a
dorsal-ventral orientation (eg, single measurements in an outpatient facility) or removing the
nail polish (eg, patients in a critical care unit) [9]. An alternate site can also be used (eg,
earlobe, forehead, or toe provided similar nail polish is not on the toe).

Artificial acrylic nails may also affect the accuracy of pulse oximetry readings, depending on
the device used. This problem can be solved by mounting the probe sideways, using an
alternative site, or removing one of the acrylic nails by soaking in acetone [110].

Vital dyes — Vital dyes, such as methylene blue (used to treat methemoglobinemia, or during
endoscopic polypectomy), indocyanine green (used for measuring cardiac output, for
ophthalmic angiography, or for measuring liver blood flow), fluorescein (ophthalmic
angiography) and isosulfan blue (used intraoperatively to mark breast and melanoma
tumors), can cause erroneously low pulse oximetry readings due to absorption of light at 660
nm or 940 nm [17,111-116]. Methylene blue has the greatest impact as it absorbs significantly
at 670 nm. However, these effects tend to be transient and resolve rapidly as the dyes are
diluted and metabolized [17,18].

Others — All the causes of an inadequate signal such as motion artifact, poor probe
positioning, hypoperfusion, and hypothermia may result in low readings. (See 'Inadequate
waveform' above.)

Fetal hemoglobin gives pulse oximetry readings clinically indistinguishable from those of
adult hemoglobin such that pulse oximetry is as reliable in newborns as in adult SpO2 [18].

CO-OXIMETRY

Abnormal hemoglobins or hemoglobin variants may interfere with pulse oximetry if their
absorption properties are similar to those of oxyhemoglobin or deoxyhemoglobin.
Conventional pulse oximeters which use two light emitting diodes can only detect these two
substances and cannot detect abnormal forms of hemoglobins. Multiwavelength co-oximeters
use several, rather than two, wavelengths of light (eg, four to eight) to detect oxyhemoglobin,
deoxyhemoglobin, carboxyhemoglobin, and methemoglobin. They require a sample of arterial
whole blood and a specific laboratory request for its measurement [25,35]. (See
'Carboxyhemoglobin' above and 'Glycohemoglobin A1c' above and 'Methemoglobin' above and
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'Sulfhemoglobin' above and 'Sickle hemoglobin' above and 'Inherited forms of abnormal
hemoglobin' above.)

SUMMARY AND RECOMMENDATIONS

● Principles – Pulse oximetry measures peripheral arterial oxygen saturation (SpO2) as a

surrogate marker for tissue arterial oxygenation (SaO2). Pulse oximetry uses
spectrophotometry to determine the proportion of hemoglobin that is saturated with oxygen
(ie, oxyhemoglobin) in peripheral arterial blood. A variety of probes are available, none of
which have clear superiority over another ( picture 1). (See 'Principles and equipment'
above.)

● Advantages and disadvantages – Pulse oximetry is a rapid, noninvasive tool that can
provide continuous assessment of oxygenation and is associated with few complications
( figure 2). However, it cannot detect hyperoxemia or arterial oxygen or carbon dioxide
tension. (See 'Advantages and disadvantages' above and 'Complications' above.)

● Indications and use – Pulse oximetry is indicated in any setting where hypoxemia may occur.
It provides accurate assessment of tissue oxygenation in most patients. Importantly, clinicians
should pay attention to trends on oximetry, and when treating patients with supplemental
oxygen for hypoxemia, clinicians should target levels that are desirable for the specific
etiology while simultaneously avoiding oxygen toxicity. The clinician should be aware of the
limitations and errors associated with pulse oximetry and have a low threshold to obtain
arterial blood for analysis. (See 'Applications' above and 'Interpreting the results' above.)

● Troubleshooting sources of error – Pulse oximetry is subject to artifactual and patient-

related sources of error. The best defense against error is a high index of suspicion. If a
saturation reading is in doubt, equipment error can be quickly ruled out by putting the probe
on the healthcare worker's own finger. Once assured that equipment is functioning, the
clinician should investigate for other potential sources of error, most of which are readily
identified and resolvable ( table 1). (See 'Troubleshooting sources of error' above.)

Use of UpToDate is subject to the Terms of Use.

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GRAPHICS

Types of pulse oximetry probes

Graphic showing several types of oximetry probes; shown from left to right are a (A) finger, (B) ear lobe,
and (C) forehead probe.

Courtesy of Nonin Medical, Inc. Reproduced with permission. Copyright © 2016.

Graphic 107545 Version 1.0

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Principles of pulse oximetry: light absorption

This schematic diagram illustrates light absorption through living tissue. Note that the AC signal is due to
the pulsatile component of arterial blood, while the DC signal is comprised of all the nonpulsatile
absorbers in the tissue: nonpulsatile arterial blood, venous and capillary blood, and all other tissues.

Redrawn from Ohmeda Pulse Oximeter Model 3700 Service Manual, 1986, p. 22.

Graphic 80895 Version 2.0

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Pulse oximeter waveform

Common pulsatile signals on a pulse oximeter.

(A) Normal signal showing the sharp waveform with a clear dicrotic notch.
(B) Pulsatile signal during low perfusion showing a typical sine wave.
(C) Pulsatile signal with superimposed noise artifact giving a jagged appearance.
(D) Pulsatile signal during motion artifact showing an erratic waveform.

From: Jubran A. Pulse oximetry. Crit Care 2015; 19:272. Copyright © Jubran 2015. Reproduced under the terms of the Creative
Commons Attribution License (CC BY 4.0). Available at: http://ccforum.biomedcentral.com/articles/10.1186/s13054-015-0984-8
(Accessed on May 17, 2016).

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Oxyhemoglobin dissociation curve

The oxygen-hemoglobin dissociation curve correlates the oxygen saturation of hemoglobin across a
range of oxygen pressures. The solid black line shows the curve for normal adult hemoglobin (Hb A).
Notable points on the curve include:
p50 — The p50 is the pressure at which hemoglobin is 50% saturated (27 mmHg on the X-axis).
Arterial blood — Hemoglobin is approximately 100% saturated at an oxygen pressure of 100
mmHg.
Venous blood — Hemoglobin is approximately 75% saturated.

Conditions that shift the curve may affect oxygen delivery to the tissues; these effects are most
pronounced at low partial pressures of oxygen:
Left shift — Conditions that shift the curve to the left (dashed red line) increase the oxygen affinity;
hemoglobin holds more tightly onto oxygen and delivers less oxygen to the tissues at a given
arterial oxygen pressure. The left-shifted curve for Hb F is what allows transfer of oxygen from the
maternal to the fetal circulation.
Right shift — Conditions that shift the curve to the right (dashed blue line) decrease oxygen
affinity; hemoglobin holds less tightly onto oxygen and delivers more oxygen to the tissues at a
given arterial oxygen pressure.

Hb: hemoglobin; O2: oxygen gas; Hb F: fetal hemoglobin; R state: relaxed state of hemoglobin; T state:
tense state of hemoglobin.
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* The ferric hemes of methemoglobin do not bind oxygen, but they increase the oxygen affinity of the
normal ferrous heme in the hemoglobin tetramer, shifting the curve left. With high methemoglobin
levels, oxygen saturation will be low for a physiologic PaO2 due to inability of ferric heme to bind oxygen,
shifting the curve right.

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Causes and troubleshooting erroneous pulse oximetry readings

Problem and potential errors Solution

Inadequate waveform

Malposition of probe Reposition probe, alternate site

Motion artifact Reposition probe, alternate site

Hypoperfusion Reposition probe, alternate site, warming

Hypothermia Use ear or forehead probe, warming

Skin pigment Measure ABG

Falsely normal or elevated oximetry reading

Carboxyhemoglobin (eg, carbon monoxide Co-oximetry

poisoning)

High levels of glycohemoglobin A1c Measure ABG

metHb, sulfHb* Multiwavelength co-oximetry (metHb), biochemical

analysis (sulfHb)

Ambient light Remove ambient light source

Skin pigment Measure ABG

Falsely low oximetry reading

Inadequate waveform Reposition probe, alternate site

metHb* Multiwavelength co-oximetry

sulfHb* Biochemical analysis

HbS and inherited forms of abnormal Hb Measure HbS and abnormal Hb levels

Severe anemia Measure ABG

Venous pulsations or congestion Loosen probe, reposition patient or probe, measure

ABG

Ambient light Remove ambient light source

Nail polish Remove polish or change site

Vital dyes Usually transient, measure ABG

ABG: arterial blood gas; metHb: methemoglobin; sulfHb: sulfhemoglobin; HbS: sickle hemoglobin; Hb:
hemoglobin; SpO2: peripheral arterial oxygen saturation; SaO2: true arterial oxygen saturation.

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* In these conditions, SpO2 is low; when levels of metHb or sulfHb are mildly elevated, SpO2
underestimates the SaO2, but when levels are high, the SpO2 automatically trends towards 85% such that
pulse oximetry can overestimate SaO2.

Adapted from: Chan ED, Chan MM, Chan MM. Pulse oximetry: understanding its basic principles facilitates appreciation of its
limitations. Respir Med 2013; 107:789.

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Effect of carboxyhemoglobin on measured oxygen saturation by pulse oximetry

SpO2 and cooximetry versus carboxyhemoglobin (COHb) at FiO2 = 1.0. SpO2 consistently overestimates
O2 saturation in the presence of COHb. At COHb = 70 percent, SpO2 is still roughly 90 percent, while
oxyhemoglobin has fallen to 30 percent.

FiO2: fraction of inspired oxygen; O2: oxygen; SpO2: standard pulse oximetry.

Redrawn from: Barker SJ, Tremper KK, Anesthesiology 1987; 66:677.

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