Question of the Week: October 29, 1999



My patient's oxygen saturation is being measured continuously by pulse oximetry.  When should I measure blood gases?

Answer:

Pulse oximetry provides an indirect measurement of the arterial oxygen saturation (SaO2).  Oxygen saturation measured by pulse oximetry is referred to as the "SpO2".  If the pulse oximeter generates a crisp waveform with a pulse rate that is consistent with the individuals heart rate, the pulse oximeter reading provides a good indication of blood oxygen levels.  Patient response to increases or decreases in oxygen therapy can be evaluated without repeated blood gas analysis.

While pulse oximetry can reduce the need to measure arterial blood gases to evaluate oxygen status, it is important to recognize its limitations.  Most importantly, pulse oximetry only provides an indication of an individuals arterial oxygenation; pulse oximetry does not provide information regarding acid base balance or the adequacy of ventilation.

When Should Blood Gases be Drawn?
If an individual has an arterial blood gas drawn which demonstrates adequate oxygenation with normal acid - base balance, and the individual is breathing comfortably at a rate < 25 breaths per minute, it is not necessary to repeat blood gases if the following criteria are met:

  • the SpO2 remains stable
  • the respiratory rate and effort remains unchanged
  • the minute volume/ventilation remains stable
In a ventilated patient, it is important to identify the Total Minute Volume (minute ventilation) at the time that blood gases were drawn.  The blood gases tell us whether this minute volume is meeting the patient's needs.  A respiratory acidosis indicates that the minute volume is too low; a respiratory alkalosis indicates that the minute volume is higher than needed.  Blood gas measurements are generally not indicated if a patient appears comfortable, and their minute volume remains unchanged.

Minute volume will rise with any increase in metabolic rate or activity, therefore, it should be evaluated with the patient at rest.  An upward trend in the "at rest" minute volume indicates an increased rate of metabolism (for example, with fever, sepsis, decreased sedation or discontinuation of neuromuscular blockade).  A decrease in the minute volume may be an appropriate response to a decrease in the metabolic rate (e.g. decreased fever, increased sedation or sleeping).  Alternatively, an inappropriate fall in the minute volume can occur from depression of the respiratory centre, decreased lung compliance or increased airway resistance.

The only way to know whether the minute volume/ventilation is meeting the patients needs is to evaluate a blood gas.

Blood gases are required to evaluate ventilation (or to detect metabolic acid - base disturbances) in any of the following scenarios, regardless of the pulse oximetry reading:
 

  • a significant change in the "at rest" respiratory rate (not related to changes in level of sedation, temperature, wakefulness etc.)

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  • respiratory distress, diaphoresis or increased work of breathing

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  • a sudden and unexplained change in the "at rest" minute volume associated with cardiorespiratory distress, decreased SpO2 or altered neurological status.

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    An acute decrease in minute volume with distress, could indicate pulmonary complications such as pneumothorax, airway obstruction or an ETT in right mainstem bronchus.
     

  • blood gases should be repeated intermittently (e.g. q 12 h and prn) for an upward trend or rapidly changing minute ventilation/volume (SpO2 monitoring alone is insufficient)

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  • for any patient at risk for metabolic acidosis such as:
    • low cardiac output states (e.g. lactic acidosis)
    • cardiovascular instability, need for sympathomimetic drugs
    • active bleeding or large blood/volume replacement therapy
    • renal failure
    • liver failure
    • poisonings
    • ketoacidosis

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  • following administration of bicarbonate (potential for alkalosis) or acetazolamide (increases bicarbonate loss and blocks bicarbonate production with potential for acidosis)

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  • patients requiring > 50% oxygen therapy

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  • when pulse oximetry may over-estimate the oxygen saturation (nitric oxide, nitroprusside, nitroglycerine, smoke inhalation/carbon monoxide poisoning)

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Clinical decisions regarding the frequency for measuring blood gases should be based on the severity of the patient's clinical condition, and the number of interventions being introduced.  For patients with any of the indications listed above, blood gases should be evaluated at least once per 12 hour shift and prn following changes in the clinical status, or to reassess the effects of interventions aimed at correcting acid - base disturbances.

Assessment of Oxygenation
Pulse oximetry can be useful for identifying low oxygen saturations or changes in the blood oxygen concentration.  One limitation of pulse oximetry is the inability to distinguish between normal PaO2's and excessively high PaO2's.  Once the oxygen saturation reaches the maximum level of 100%, additional increases in the PaO2 will not be detected by changes in SpO2.  For example, an individual could be on 100% oxygen therapy, with a PaO2 of 95 mmHg and an oxygen saturation of 100%.  As the patient improves, the PaO2 could rise for example to 300 mmHg, however, the SpO2 would remain 100%.  Only an arterial blood gas measurement would identify the hyperoxygenation.

One way to avoid excessive oxygen concentrations in the blood is to wean high FiO2s until the SpO2 drops below 100% (e.g. 97-99%) (this indicates that the PaO2 is low enough to produce changes in the SpO2).

There is another important reason to occasionally evaluate blood gases in a patient requiring high FiO2s (> 50% oxygen therapy)......anyone with an oxygenation problem severe enough to require 100% oxygen may also have problems with ventilation (breathing enough to clear carbon dioxide from the blood)!

Assessment of Ventilation
The only way to identify whether an individual is breathing enough (or ventilating adequately), is to evaluate an arterial blood gas!  It is important to recognize that with supplemental oxygen therapy, an individual can have an SpO2 that is normal, despite a significant acid - base disturbance.  Acid - base disturbance can only be determined by blood gas analysis.

Respiratory acidosis indicates respiratory failure, or, inadequate ventilation (or a minute volume that is not as high as the individual needs).  This requires an increase in the Total Minute Volume = (Mechanical RR X Mechanical Tidal Volume) + (Spontaneous RR X Spontaneous Tidal Volume).   Total minute volume can be increased by increasing the rate of the mechanical ventilator (AC/CMV or SIMV), or by increasing the mechanical tidal volumes (rarely done).  The spontaneous minute volumes can be increased by enhancing the spontaneous tidal volumes with increased Pressure Support (Pressure Support will only help the spontaneous breaths).

Respiratory alkalosis indicates hyperventilation, or, too much ventilation.  If an individual is on a mechanical ventilator, the minute volume needs to be decreased (alkalosis can constrict cerebral and coronary vessels and decrease the ability of hemoglobin to release oxygen to the cells).

If an individual who is spontaneously breathing has a respiratory alkalosis, it is important to assess the adequacy of their oxygenation.   Hyperventilation (overbreathing)  that is psychological in origin should be associated with a higher than normal PaO2 (if I am overbreathing to the point that I make myself hypocarbic, I should have a generous intake of oxygen).  An important clinical finding is hyperventilation in the presence of a low, or low normal PaO2 (or high oxygen concentration).  This indicates that the individual is overbreathing in response to a low oxygen level instead of hypercarbia.  If the oxygen problem is not corrected, the individual is at risk of fatiguing the muscles of respiration.   This will then lead to respiratory failure.

Important Limitations of Pulse Oximetry Technology:
All molecules reflect unique wavelengths of light.  The wavelength of hemoglobin that is saturated with oxygen is different than the wavelength reflected from hemoglobin that is desaturated.  The variation in the wavelength is used to determine oxygen saturation.

Ear oximetry can be less accurate than digit monitoring, because the earlobe thickness and pigmentation can alter the wavelength transmission.  Additionally, the probe may have difficulty differentiating arterial and venous blood.

Pulse oximeters, most frequently applied to digits, must be able to detect pulsatile blood flow.  The photodectors are designed to detect light of alternating intensity, minimizing the risk of measuring blood from veins or nonpulsating tissue.  The accuracy of the pulse oximetry reading can be impaired by reduced blood flow to the site of measurement (i.e. hypothermia, shock or vasoconstriction) or extremely low hemoglobin counts.

Pulse oximetry technology assumes that no more than 5% of the hemoglobin present in the blood is "other" hemoglobin, such as methemoglobin (metHb) or carboxyhemoglobin (COHb).  Because other hemoglobins have wavelengths similar to oxyhemoglobin, they will reflect the same wavelength.  Therefore, if > 5% of the total hemoglobin is methemoglobins (e.g. nitroglycerine, nitric oxide, nitroprusside) or carboxyhemoglobins (e.g. smoke inhalation or other sources of carbon monoxide inhalation), the pulse oximeter will "see" them as oxyhemoglobin, displaying a falsely elevated oxygen saturation.  Pulse oximetry should not be relied upon as an accurate reflection of blood oxygen concentration in carbon monoxide poisoning.  Caution should be used to monitor arterial blood gases intermittently when nitroglycerine, nitroprusside or nitric oxide therapy is prolonged.

Certain nail polishes, very darkly pigmented skin, or thick nails can interfere with pulse oximtry.
 

References:

Simonson, S.,  Piantadosi, C.  (1999).  Management of specific poisons: in Webb, A., Shapiro, M., Singer, M., and Suter, P. (1999). Oxford Textbook of Critical Care.  Oxford: Oxford. pp 654-653.
 

Marino, P. (1998). The ICU Book.  Philadelphia: Lea & Febiger.
 
 


 
 
 
 
 
 

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Last Updated March 24, 2009 | © 2007, LHSC, London Ontario Canada