Exercise induced oxygen desaturation as a rule out tool for acute pulmonary embolism?
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Report By: Hyun Choi - ED Consultant
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Search checked by Nasser Ahmed - ED Consultant
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Institution: University Hospital Lewisham
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Date Submitted: 22nd March 2015
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Last Modified: 20th April 2015
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Status: Blue (submitted but not checked)
Three Part Question
In an [adult patient suspected of having an acute pulmonary embolism], what is the diagnostic utility of [exercise induced oxygen desaturation] in [stratifying the risk of pulmonary embolism]?Clinical Scenario
A 48 year old man presents to the Emergency Department with an exertional dyspnoea for a few days. He has no risk factors for PE and no signs of DVT, but his D-dimer comes back positive. Your respiratory physician colleagues suggest that an acute PE diagnosis is more likely if his oxygen saturation would drop on exertion. You wonder if there is any evidence to support the use of exercise induced hypoxia as a risk stratification tool for acute pulmonary embolism.
Search Strategy
MEDLINE 1946- 15/ 03 using the OVID interface
[exp pulmonary embolism/ OR pulmonary embol$.mp. OR PE.mp. OR exp thromboembolism/ OR pulmonary infarct$.mp. OR lung infarct$.mp] AND [hypoxia.mp. OR exp oxygen/ OR oxygen saturation.mp. OR oxygen desaturation.mp OR pO2.mp ORpartial pressure oxygen.mp] AND [exp exercise test/ OR exp exercise tolerance/ OR exp exercise/ OR exp physical exertion/ OR exp physiological stress] LIMIT to human AND English Language
Search Outcome
58 papers were identified from the literature search; none of them were relevant to the clinical question.
Comment(s)
Arterial PO2 gives valuable information about the adequacy of pulmonary gas exchange. Its concentration depends on variables such as the alveolar PO2, the ventilation to perfusion (V/Q) balance and the metabolic status of the patient. A number of gas exchange abnormalities occur in acute pulmonary embolism: ventilation and perfusion become mismatched, arterial PO2 decreases and the alveolar-arterial oxygen tension gradient increases.
During exercise, the PaO2 worsens as exercise intensity increases. This is caused by the combination of acid shifts in arterial blood and increases in core temperature.
Therefore, it could be suggested that in the presence of the existing lung architecture abnormalities as in acute PE, a drop of PaO2 would be accentuated and such measurement could be incorporated into the risk stratification strategy for acute PE. However, this BestBET exercise could not identify any relevant papers that directly addressed this question.
Clinical Bottom Line
There is no published evidence to support the use of post-exercise oxygen saturation measurement in the diagnostic work up of acute pulmonary embolism.