Pulse oximetry is a great tool, however they are inherently inaccurate... their most important role is to detect TRENDS in the progression/deterioration of a person. To answer some of the questions (which on the most part, have been answered correctly), I've simply copied and pasted one of my learning packages (a collaborative learning package) that I put together for my students (My day job sees me lecturing in pre-hospital medicine). The document is long, but thought it useful for those interested in the subject.
The use of oximetry was first reported by German researchers in 1939 using an ear meter
with red and infra-red light, but it was not until the Second World War that interest in
oximetry was established due to the need to evaluate oxygenation of pilots at high altitude
(Treacher and Leach 1998).
It was the British researcher Glenn Allan Millikan who between 1940 and 1942 produced a
lightweight ear oxygen meter he called an ‘oximeter’. Over the years many modifications
were made and the oximeter was used in various studies in physiology and aviation,
however the expense of the machines and their bulky nature prevented widespread clinical
use. In the 1970s the Japanese bioengineer Takuo Aoyagi recognised the importance of
oximetry while looking for a non-invasive way to measure cardiac output. Following this a
period of corporate interest and development led to significant reductions in size and cost,
resulting in the hand-held machines encountered today (Treacher and Leach 1998).
How it works
The principle of pulse oximetry is based on the absorption of red and infrared light by
oxygenated and deoxygenated haemoglobin (Limon 2008). Oxygenated haemoglobin
absorbs more infrared light and allows more red light to pass through. Deoxygenated (or
reduced) hemoglobin absorbs more red light and allows more infrared light to pass through
(Bilan et al 2010).
Pulse oximetry uses a light emitter with red and infrared LEDs that shine through a
reasonably translucent location with good blood flow. Typical adult/paediatric locations are
the finger, toe and the pinna (top) or lobe of the ear. Infant sites are the foot or palm of the hand and the big toe or thumb. Opposite the emitter is a photo detector that receives the
light that passes through the measuring site (Sedaghat-Yazdi et al 2010; Vestbo et al 2009).
After the transmitted red (R) and infrared (IR) signals pass through the measuring site and
are received at the photo-detector, the R/IR ratio is calculated and a saturation reading given
(Kamaras et al 2010).
At the measuring site there are constant light absorbers which are always present: skin,
tissue, venous blood and the arterial blood (Bishop and Nolan 1991). However, with each
heart beat the heart contracts and there is a surge of arterial blood which momentarily
increases arterial blood volume across the measuring site. This results in more light
absorption during the surge. If light signals received at the photo detector are looked at as a waveform (Bishop and Nolan 1991), there should be peaks with each heartbeat and troughs
between heartbeats. Hence, pulse oximetry is the measurement of the saturation of
peripheral oxygen (SpO2) of haemoglobin in the arterial blood. It also serves as an indirect
indicator of cardiac output (Bishop and Nolan 1991).
What is Oxygen Saturation?
Oxygen saturation (SpO2) is a measure of how much oxygen the blood is carrying as a
percentage of the maximum it could carry. Oxygen is carried in the red blood cells attached
to haemoglobin molecules (Simmonds and Simmonds 2004).
One haemoglobin molecule can carry a maximum of four molecules of oxygen (Simmonds
and Simmonds 2004). If a haemoglobin molecule is carrying three molecules of oxygen then
it is carrying 3/4 or 75% of the maximum amount of oxygen it could carry.
One hundred haemoglobin molecules could together carry a maximum of 400 (100 x 4)
oxygen molecules. If these 100 haemoglobin molecules were carrying 380 oxygen
molecules, they would be carrying (380 / 400) x 100 = 95% of the maximum number of
oxygen molecules they could carry and combined would be 95% saturated.
Evaluation of SpO2 Measurements
SpO2 of greater than 95% is generally considered normal. A fit, healthy person should have
oxygen saturation on room air in excess of 95%. With deep or rapid breathing, this can be
increased to 98-99%. While breathing oxygen enriched air (40% - 100%), the oxygen
saturation can be pushed to 100% (Oh 2003).
· SpO2 of 92% or less (at sea level) suggests hypoxemia (Oh 2003)
· In a patient with acute respiratory illness (e.g. influenza) or breathing difficulty, a SpO2
of 92% or less indicates a need for oxygen supplementation (Oh 2003)
· In a patient with stable chronic disease (e.g. COPD) a SpO2 of 92% or less should
prompt referral for further investigation of the need for long term oxygen therapy (Oh
Oxygen saturation will fall if:
· Inspired oxygen levels are diminished, such as at increased altitudes
· Upper or middle airway obstruction exists (e.g. asthma)
· Significant alveolar lung disease exists, interfering with the free flow of oxygen across
the alveolar membrane e.g. COPD ( Limon 2008)
Oxygen saturation will rise if:
· Deep or rapid breathing occurs
· Inspired oxygen levels are increased, with supplementary oxygen, such as a Hudson
mask (Hampson, 1998)
What is Partial Pressure?
Partial pressure is the individual pressure exerted by a particular gas within a mixture of
gases. The air we breathe is a mixture of gases: primarily nitrogen, oxygen and carbon
dioxide (Hampson 1998). That part of the total pressure generated by oxygen is the 'partial
pressure' of oxygen, while that generated by carbon dioxide is the 'partial pressure' of
carbon dioxide (Limon 2008; Hampson 1998).
Given that total atmospheric pressure (at sea level) is about 760 mmHg and air is about 21%
oxygen, (Hampson 1998) then the partial pressure of oxygen in the air is 0.21 times 760 mm
Hg or 160 mmHg (Milton 2009).
With external respiration (exchange of oxygen and carbon dioxide between the atmosphere
and body cells) a pressure gradient exists, therefore partial pressure of oxygen in arterial
blood under normal resting circumstances is approximately 104 mmHg. This equates to a
fully saturated haemoglobin molecule.
PO2 (Partial Pressure of Oxygen) reflects the amount of oxygen gas dissolved in the
blood. It is determined by inspired oxygen concentration, barometric pressure, alveolar
ventilation, oxygen diffusion and distribution (Hampson 1998). It primarily measures the
effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere.
Elevated pO2 levels are associated with:
· Increased oxygen levels in the inhaled air
· Oxygen therapy and ventilation (Hampson 1998)
Decreased PO2 levels are associated with:
· Decreased oxygen levels in the inhaled air (such as at high altitude)
· Heart failure
· Chronic obstructive pulmonary disease
· Hypoventilation (Limon 2008; Hampson 1998)
Physiology of Oxygen Transport
Movement of air in and out of the lungs is referred to as ventilation. Air reaches the alveoli and gas exchange then occurs across the thinly walled capillaries. Once oxygen has
crossed into the cardiovascular system, it is transported in the blood in two forms,
approximately 97% is bound to haemoglobin and the remaining 3% is unbound in the
plasma. Arterial oxygen saturation is referred to as SaO2, or when measured non-invasively
as SpO2, with peripheral monitoring providing a high degree of accuracy for saturations
between 70%-100% (Bishop and Nolan 1991).
The cardiovascular system may deliver oxygen to the tissues, but as oxygen has an affinity
(attraction) to haemoglobin, it may not readily release the oxygen molecule. When the
percentage of saturation of arterial haemoglobin with oxygen is plotted against the partial
pressure of oxygen (PO2), which is a measure of the oxygen concentration in the
surrounding medium, the oxyhaemoglobin dissociation curve is created, as shown in the
Google the oxyhaemoglobin dissociation curve and pull up a picture.
As illustrated, the thick black line shows the usual relationship between oxygen saturation
and the affinity it has for haemoglobin.
SpO2 levels above 95%, or when haemoglobin is nearly fully saturated, correlates to a PO2
value in the normal range of 80 to 100 mmHg (Simmonds and Simmonds 2004).
Functionally, this corresponds to the physiological situation in the lungs, where we want the
haemoglobin to have a high affinity to O2, pick it up, hold onto it and carry it to the tissues.
An SpO2 of 90% or below correlates to a PO2 of 60 mmHg or below. It is important to note
the shape of the curve, and recognise that as PO2 falls there is a precipitous drop in SpO2.
This corresponds to the situation in the peripheral tissues and capillaries, where we want thehaemoglobin to release the bound O2 to the tissues. Therefore, the PO2 of the blood
determines the amount of O2 that binds to haemoglobin in the red blood cells (or the affinity
of haemoglobin for O2).
This relationship can change, dependent on the conditions within the body, such as
temperature, pH (as reflected by H+) and amount of 2-3 DPG (a by-product of metabolism
that helps release O2 from haemoglobin). If the curve shifts to the left, it means that oxygen is more tightly bound to the haemoglobin, and can be caused by increased pH, decreased
temperature or decreased PaCO2. If the curve shifts to the right, it means that oxygen is not
as tightly bound to haemoglobin, and can be caused by decreased pH, increased
temperature and increased PaCO2 (Simmonds and Simmonds 2004). This makes it harder
for haemoglobin to bind to oxygen (requiring a higher partial pressure to achieve the same
oxygen saturation), but it makes it easier for the haemoglobin to release bound oxygen to
the tissues. Conversely, a leftward shift increases the affinity of haemoglobin to oxygen
resulting in reduced tissue oxygenation (Limon 2008).
The key points of the oxyhaemoglobin dissociation curve include:
· Oxygen saturation indicates the amount of oxygen bound to haemoglobin
· Oxygen saturation does not reflect oxygen delivery to the tissues
· As PO2 drops, oxygen saturation falls off precipitously
· The relationship between oxygen and haemoglobin can be affected by a number of
physiological factors, which then impact oxygen delivery to the tissues
What is Oxygen Delivery?
Oxygen delivery is a result of the respiratory system working in conjunction with the
cardiovascular system to supply oxygen to all cells of the body and to eliminate waste,
primarily carbon dioxide (Davis, Hwang and Dunford 2008).
Effective oxygen delivery requires the following:
· Ventilation moving air into your lungs
· External respiration, moving the oxygen from alveoli into your blood (Davis et al
· Enough normal haemoglobin to carry the oxygen
· An efficiently working cardiovascular system to transport the blood around your body
However the oxygen has still not reached the body’s cells.
The last stage of the journey is for the oxygen to get from the haemoglobin in the red blood
cells to all the other cells within the body, a process known as internal respiration (Davis et al 2008). In the capillaries oxygen detaches from the haemoglobin and diffuses through the
capillary wall to the cells around the capillary (Simmonds and Simmonds 2004).
If any of these factors are compromised, patients may present short of breath due to
underlying hypoxia. Hypoxia is defined as a state of decreased oxygen content at the tissue
level, while hypoxaemia is a state of decreased oxygen content of arterial blood (Simmonds
and Simmonds 2004)
Types of Hypoxia:
Hypoxaemic hypoxia: the decreased oxygen level in the blood results in decreased oxygen
diffusion to the tissues. It may be caused by hypoventilation, high altitude, pulmonary
embolism, atelectasis or other pulmonary diffusion defects (Davis et al 2008).
Anaemic hypoxia: occurs when either the total amount of haemoglobin is too small to
supply the body's oxygen needs (as in anaemia or severe haemhorrage), or haemoglobin
that is present is rendered non-functional. A transient example of the latter case is carbon
monoxide poisoning, in which carbon monoxide preferentially binds to haemoglobin
(displacing oxygen) resulting in diminished oxygen carrying capacity (Oh 2003; Davis et al
Stagnant hypoxia: blood flow through the capillaries is insufficient to supply the tissues.It
may result from heart disease that impairs the circulation, impairment of venous return or low flow states such as shock or cardiac arrest. Local stagnant hypoxia may be due to any
condition that reduces or prevents the circulation of blood in any area of the body. Examples
include thrombosis, Reynaud’s disease and Buerger's disease (which restrict circulation in
the extremities) and the application of a tourniquet to control bleeding (Davis et al 2008).
Hystotoxic hypoxia: the cells of the body are unable to use the oxygen, although the
amount in the blood may be normal and under normal tension. Although characteristically
produced by cyanide, it may be caused by any agent that decreases cellular respiration.
Some of these agents are narcotics, alcohol, formaldehyde, acetone, and certain
anaesthetic agents (Davis et al 2008).
Signs of Hypoxia
Symptoms of hypoxia vary greatly depending on the severity and may include:
· Visual impairment
· Shortness of breath
· Altered conscious state
· Seizure activity
(Davis et al 2008)
• Lethargy • Restlessness
• Bradycardia • Tachypnoea
• Hypotension • Tachycardia (bradycardia late sign)
• Apnoea • Cyanosis
Limitations of Pulse Oximetry
Pulse oximetry has limitations in its ability to provide a useful clinical measurement, and it is important for paramedics to have an appreciation of these in order to use it as an effective tool:
Motion artefact: due to oximetry measuring the difference between pulsatile (arterial) and
non-pulsatile (veins, bone, muscle) tissue, motion of the patient can cause a false reading by inducing pulsations in usually non-pulsatile tissue. Patient movement may lead to disrupted signals and artefacts (Pruitt and Jacobs 2004; Bilan et al 2010).
Poor perfusion: it can be difficult to get a reading on a poorly perfused or vasoconstricted
patient, due to the lack of pulsatile tissue in the periphery where the SpO2 sensor is reading.
Pulse oximetery is not reliable in conditions of severe hypotension and in such conditions an
ear probe may be more reliable than a finger probe (Bishop and Nolan 1991).
Similarly, avoid compromising blood flow to the limb (e.g. by inflating a BP cuff) to which the probe is attached to prevent a false low reading.
Dyshaemoglobins: pulse oximeters only differentiate between two haemoglobin species.
The presence of alternative haemoglobin types, such as COHb and MetHb can influence the
oximeter readings and give false SpO2 readings.
Pigmentation/dyes: skin pigmentation, dyes or other colourings such as nail polish can
provide interference resulting in false readings (Bishop and Nolan 1991). Dark pigmentation
may have a small effect, usually overestimating SpO2. If nail polish is thought to be
interfering in readings the probe can be placed sideways on the finger, or an ear probe used.
Irregular Pulsations: arrhythmias may not provide uniform pulsations, which can interfere
with oximeter readings (Bishop and Nolan, 1991). Venous congestion/tricuspid
incompetence may also cause inaccurate readings due to substantial venous pulsations.
Improper fit: if the probe does not fit properly, the light can be shunted from the LEDs
directly to the photo-detector affecting the accuracy of the measurement (Bishop and Nolan
Oxygen saturation only: the pulse oximeter measures oxygenation, not ventilation, that is
not CO2 levels, and not work of breathing. This is particularly important to remember, given
that there can be a time lag from a change in patient condition to the reading on the oximeter
(Bishop and Nolan 1991).
Alarm fatigue: as with any machine that has an alarm, if it goes off too often, paramedics
will tend to ignore it, or fail to explore why it has alarmed (Limon 2008).
Low readings: oximeter readings can be inaccurate below 70%. This is because the
original trials to establish oximetry readings done on human subjects were deliberately
Advantages of Pulse Oximetry
· Indicates early hypoxia more effectively than vital signs
· Identifies hypoxia before the onset of cyanosis
· Measures effective treatment
· Useful in assessing trends
· Non-invasive method of continuous SpO2 monitoring
· No calibration required
· 2% accurate between SpO2 70%-100%
(Bishop and Nolan 1991; Mardirossian and Schneider 1992)
· Pulse oximetry is a noninvasive method that enables rapid measurement of the oxygen
saturation of hemoglobin in arterial blood, thereby providing an early warning of
dangerous hypoxemia, prior to symptoms being obvious
· Pulse oximetry can be a useful aid to clinical decision-making, but it is not a substitute
for clinical assessment. Understanding that patient presentations vary considerably and
that pulse oximetry has limitations, pulse oximetry readings may not truly reflect the
· Remember to treat the patient and not necessarily the numbers
· The PO2 of the blood determines the amount of O2 that binds to haemoglobin, as
represented by the oxyhaemoglobin dissociation curve
· Most of the oxygen in the blood is carried by haemoglobin so in severe anaemia the
blood will carry less total oxygen, despite the haemoglobin being 100% saturated
(Sedaghat-Yazdi et al 2008). As such, pulse oximetry must be used as an adjunct to
CPG A0103: Respiratory Status Assessment
· Pulse oximetry has limitations in its ability to provide a useful clinical measurement, and
it is important for paramedics to have an appreciation of these in order to use it as an
So there you have it. The smaller units produced today are as accurate, and should be treated with the same caution, speculation and respect as the larger ones.
Ps. Pulse oximeters may or may not reflect accurate oxygen saturation, depending on the type of anaemia that is present. A person may be anaemic yet have 100% oxygen saturation, and vice versa.