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Pulse Oximetry: Uses and Limitations

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A pulse oximeter is a non-invasive device used to measure oxygen saturation in the blood. This article will cover pulse oximetry, including its limitations and clinical application.

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How does pulse oximetry work?

The fundamental principle behind pulse oximetry is that oxygenated and deoxygenated haemoglobin (Hb) absorb light of different wavelengths, so if you shine lights of these 2 wavelengths at Hb that is moving in a pulsatile manner, you can measure the proportion of oxygenated and deoxygenated Hb travelling within the arterial circulation.

Therefore, you can determine how much Hb is saturated with oxygen (O2), which is presented as a percentage (SpO2).

However, it is important to understand that this measurement only tells you how much O2 has been ‘uploaded’ to Hb in the lungs and is now travelling bound to Hb in the arterial circulation.

It does not tell you what is happening downstream of the sensor in the vital organs, where O2 is ‘downloaded’ from Hb and taken up and utilised by the cells.

An arterial blood gas (ABG) measurement does give you this information and, therefore, provides a more accurate assessment of what is happening at a cellular level. This is why a SpO2 reading should be considered as only being an estimate of the gold standard ABG measurement.

Limitations of pulse oximetry

It is important to be aware of the concerns that have emerged during the COVID-19 pandemic about the potential for pulse oximeters to produce inaccurate readings.

The potential for inaccurate readings to occur in patients with darker skin pigmentation has been highlighted in several patient safety alerts and now features in some NICE guidelines.

However, there is a wide range of factors that can result in readings being either inaccurate or misinterpreted, and you must be aware of these for safe practice. In most cases, a SpO2 reading of 90% will represent an ABG measurement of between 86-94%, but other confounding factors may compound the inaccuracy.

Many clinical guidelines refer to specific or narrow ranges of SpO2 readings for making critical decisions regarding the care of patients, including referral to hospital, admission to hospital and initiating or changing treatment, including the administration of O2.

It is important to interpret SpO2 readings within the context of the patient, their symptoms, the other clinical assessment findings, their co-morbidities and an evaluation of the accuracy of the reading.

The use of pulse oximetry in patient assessment is currently being re-evaluated. You will need to monitor developments to ensure that you interpret SpO2 correctly and avoid making errors based on inaccurate readings.

At readings close to 100%, most readings will be accurate enough to exclude the presence of hypoxemia. However, as readings approach 90%, the risk of pulse oximetry not detecting or quantifying the degree of hypoxaemia increases. This is clinically significant as readings close to this threshold are used for making critical clinical decisions.

Light contamination/interference

Pulse oximeters measure how much light is absorbed as it passes through the tissue where the sensor is located, usually the finger or earlobe.

Anything which interferes with the absorption of light can affect the accuracy of readings, including false nails, nail varnish/gel, dirt on or under the nails, and henna finger tattoos.

Ambient light entering the sensor can also affect readings, so it is important to position and align the sensor correctly. A finger clip sensor which is too long for the finger will mean that light shines through bone, and one that is too short will mean that light shines through the tip of the finger where arterial and venous blood mix together in the capillaries.

It is particularly important to select the correct sized sensor in children and not to apply the sensor to a thumb or big toe if it increases the distance and angle between the two arms of the sensor.

Pulsatile haemoglobin

Pulse oximeters are designed to detect haemoglobin molecules that are moving in a pulsatile manner.

In situations where there is peripheral shutdown, this may result in the pulse oximeter not being able to find a signal. Conversely, excessive finger movement can result in signal interference.

Modern pulse oximeters now have sophisticated software designed to detect movement artefacts and low output states within the tissue being sampled, as well as visual and audible methods of assessing the quality of the signal being received (bar graph and plethysmographic representations of signal strength and quality).

It is important to use these systems to assess the quantity and quality of the signal being received. It is also good practice to assess the patient’s pulse at the wrist and compare it to the pulse rate reading produced by the pulse oximeter, as well as to check the capillary refill time before applying the sensor to the finger.

Clinical application of pulse oximetry

There are several factors that can adversely affect the ‘uploading’ of oxygen at the alveolar interface between the respiratory and circulatory systems.

It is helpful to think of the alveolar membrane as having a respiratory surface and a circulatory surface. Follow the oxygen molecule from the atmosphere to the bloodstream and then consider the factors which may prevent oxygen from coming into contact with Hb.

The first factor to be considered is the amount of O2 present in the atmosphere available to be inhaled, which varies with altitude and the presence of other gases in the atmosphere, such as carbon monoxide.

The volume of O2 inhaled is a function of the respiratory rate and depth, so anything that causes respiratory depression (head injuries, spinal injuries, respiratory depressant drugs) can cause hypoxaemia. Several other conditions can also reduce respiratory depth, such as restricted chest expansion from splinting of the chest wall due to pain from rib fractures.

Any condition which interferes with the ability to create negative intrathoracic pressure within the chest, which is required to draw air down the trachea, can result in hypoxaemia. This is the mechanism by which patients with a flail chest or tension pneumothorax; with muscular or neurological conditions affecting the ability of the chest to expand; or with conditions affecting the expansion of the diaphragm, become hypoxaemic.

Upper airway obstruction caused by the tongue, food or a foreign body, as well as from laryngeal spasm or infection; lower airway obstruction due to bronchospasm, musical wall oedema, or secretions will reduce the delivery of O2 to the alveoli.

Within the alveoli, the respiratory side of the interface can be obstructed by fluid (e.g. pulmonary oedema, pus and airway secretions). On the circulatory side of the interface, anything that decreases the delivery of Hb to the alveoli will prevent the uploading of O2, as is the case with a pulmonary embolus or with decreased blood flow due to profound shock.

It is important to consider all the potential causes for a low SpO2, especially if a clear cause is not immediately obvious or if the patient does not respond to treatment.

Causes of a low SpO2

Causes of a low SpO2 include:

  • Reduced atmospheric oxygen (e.g. high altitude, carbon monoxide-rich environment)
  • Respiratory depression (e.g. head injury, drug overdose)
  • Upper airway obstruction (e.g. epiglottitis, croup, inhaled foreign body)
  • Lower airway obstruction (e.g. bronchospasm, lung collapse/consolidation)
  • Restriction to chest/diaphragmatic expansion (e.g. pain from rib fractures, neurological conditions)
  • Restriction to lung expansion (e.g. haemothorax, large pleural effusion)
  • Inability to create negative intrathoracic pressure (e.g. flail chest, tension pneumothorax)
  • Obstruction to oxygen transfer across the alveolar wall (e.g. pulmonary oedema)

Pulse oximetry as an assessment tool

Pulse oximetry has been used to assess and monitor acutely unwell patients for many years. Measuring the SpO2 is routine in many clinical settings as part of taking basic observations (vital signs).

Many clinical guidelines use SpO2 readings to help decide whether or not action needs to be taken, such as administering O2.

It is important to recognise that the oxyhaemoglobin dissociation curve is steep, such that small drops in the SpO2 may have great physiological and clinical significance. This simply reflects the importance of O2 in aerobic cellular metabolism and how the body’s compensatory mechanisms function to try and maintain a 100% oxygen saturation level.

In previously fit patients with normal respiratory and circulatory systems, a fall in SpO2 of around ≥4% from normal should indicate the need for a careful assessment of the patient’s other physiological parameters, such as the heart and respiratory rate, to establish how well they are compensating for the low SpO2.

A fall in the SpO2 of 8-10% represents a significant degree of hypoxaemia and should trigger an immediate and thorough clinical assessment to establish the cause.

Guidelines recommend that patients with a SpO2 ≤94% should receive O2 to maintain a SpO2 of 94-98%. It is essential for patient safety that a careful evaluation of the patient and the accuracy of the reading are performed to ensure that an inaccurate reading does not lead to an underestimation of the degree of hypoxaemia present and O2 being withheld inappropriately.

The potential for sudden and unexpected decompensation in hypoxaemic patients is significant. They are likely to be symptomatic with shortness of breath and apprehension, progressing to agitation, confusion, restlessness and then a rapidly increasing level of unresponsiveness.

However, it is also important to be aware that some patients may have “silent hypoxaemia”, with relatively few symptoms or signs to alert the clinician. As hypoxia progresses, the patient may become bradycardia, and the respiratory rate may fall as hypoxia-induced respiratory depression ensues.

Patients with COPD

Patients with COPD develop compensatory mechanisms for coping with a chronically low SpO2, such as increasing the number of Hb molecules available and switching to the hypoxic drive mechanism.

SpO2 readings in these patients need to be assessed within the context of other physiological parameters, such as the mental state, pulse and respiratory rates and blood gases, to identify those in respiratory failure. This is why arterial blood gas is required to assess the O2 and CO2 levels.

Pulse oximetry as a screening tool

Whilst pulse oximetry can be useful in assessing patients with either known respiratory conditions or symptoms suggestive of respiratory conditions (e.g. breathlessness, cough),  it can also be of value as a screening tool to detect serious medical conditions that adversely affect O2 uploading at the alveolar interface.

Two such conditions are atypical pneumonia and pulmonary embolus (PE), where respiratory symptoms may not be the predominant ones or may be absent. A low SpO2 may be the only indicator of these two potentially life-threatening conditions.

There is one caveat to this, however, which is that the SpO2 may need to be assessed after exertion and not just at rest to expose the ventilation/perfusion deficit, especially if the patient is complaining of shortness of breath on exertion rather than breathlessness at rest.

Pulse oximetry cases

Case 1

Mr Jones is a 54-year-old male who reports that he has had a “flu-like” illness for 2 days with symptoms of “feeling hot and aching all over”. Symptom-based questioning provided no clues as to the focus of the infection, although a risk assessment revealed that he had been to a spa hotel the previous week. He was normally fit and well and had no previous medical history of note. His observations showed a regular pulse of 110, BP of 130/90, respiratory rate of 20, SpO2 was 92% and a temperature of 38.6°c. Clinical examination of his chest was unremarkable. He denied having any respiratory symptoms, such as cough, chest pain, or dyspnoea.

A fever with a low SpO2 should always raise the possibility that a patient has pneumonia, regardless of the absence of respiratory symptoms and positive findings on chest examination. The history of a spa holiday raises the question of hot tub usage, which is associated with the potential for Legionnaire’s disease. He was referred to the Emergency Assessment Unit, and a CXR revealed an area of consolidation, with Legionnaire’s antigen testing positive in his urine. His liver function tests were also noted to be grossly deranged. Within hours of arriving in hospital, the patient became increasingly unwell from multi-organ failure, requiring transfer to the intensive care unit.

With intravenous antibiotics and supportive care, the patient made a full recovery.

Case 2

Jenny is a 24-year-old woman with a 3-week history of increasing shortness of breath on exertion. Today she was forced to stop and rest several times whilst walking the dog. On examination, Jenny was sitting comfortably and talking easily, without interruption to draw breath. At rest, her observations revealed a regular pulse rate of 100 bpm, BP of 120/80, respiratory rate of 22,  SpO2 96% and a normal temperature.

Examination of her chest was unremarkable. As her symptom was shortness of breath on exertion, she was asked to walk around the room a few times and was then re-assessed. Her heart rate increased to 132 bpm, whilst her respiratory rate increased to 38. The SpO2 fell to 84%, and Jenny became breathless and uncomfortable, although her symptoms eased rapidly with rest and 100% O2. Her SpO2 remained stubbornly low at 95%, despite O2 therapy.

Jenny’s presentation is consistent with a diagnosis of pulmonary embolism (PE).

It is important to recognise both the typical and atypical presentations of this serious illness. A recent European study into the symptoms and signs of PE’s highlighted the need for clinicians to review our knowledge of how patients with a PE. The study found that only 50% of patients with a PE present with dyspnoea; 39% with pleuritic chest pain; 15% with substernal chest pain; and only 24% had clinical signs of a lower limb venous thromboembolism (VTE). In particular, patients with large, or centrally located PE often present with non-specific symptoms and signs, such as unexplained syncope or hypotension, sweating, central chest pain, or persistent dyspnoea. Of greater concern though, was the finding that over 40% of patients who died from a PE were undiagnosed pre-mortem and that only 7% of the patients who died early were correctly diagnosed as having had a PE before death.

The reason that pulse oximetry is of value is that over 60% of patients with a PE will have a low SpO2, although it may be necessary to exert the patient to expose the ventilation/perfusion deficit. As cyanosis may not become clinically apparent until the SpO2 is <85%, pulse oximetry can be an important tool for detecting hypoxaemia.

Key points

  • Pulse oximetry measures the amount of oxygenated haemoglobin circulating in the peripheral arterial circulation, presenting this as a percentage of the total haemoglobin.
  • A low SpO2 indicates that either oxygen is not reaching the alveoli or it is not being uploaded onto haemoglobin molecules and transported through the peripheral arterial circulation.
  • Pulse oximetry is not a perfect tool, and its readings can be adversely affected by several technical, physiological, clinical and environmental factors. It is essential to evaluate the accuracy of SpO2 readings when assessing a patient.
  • Pulse oximetry can be used to assess and monitor patients with known respiratory conditions or with respiratory symptoms to determine the severity of the illness and also as a screening tool in acutely unwell patients to detect conditions that can give rise to hypoxemia.
  • Pulse oximetry can be used to decide how to manage a patient in terms of whether or not oxygen therapy is required and whether the patient should be admitted to hospital. SpO2 levels feature in many of the risk assessment and clinical decision-making tools.


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