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Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans

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The objective of the study was to evaluate the effects of moderate hypoxia and hypocapnia on the latency and amplitude of cortical somatosensory evoked potentials (SSEPs) in conscious human subjects.


In ten volunteers the amplitude and latency of the cortical somatosensory evoked potentials were recorded during stimulation of the left posterior tibial nerve. Measurements of SSEPs and respiratory variables were made breathing ambient air, air containing a reduced oxygen percentage (17% O2, 14% O2(n = 6) or 11% O2 (n = 10)), and again during voluntary hyperventilation breathing ambient air (PEtCO2 = 20 mmHg, n = 10).


Hypoxia (11% O2) caused mild stimulation of ventilation (P < 0.05) but had no effects on the latency or amplitude of the SSEP. Lesser degrees of hypoxia had no effects. Hyperventilation caused a small (2–4%) decrease) in the latency of the SSEP and an increase in the amplitude of the SSEP (P< 0.05).


These findings in conscious subjects were consistent with previous observations in anaesthetized humans and anaesthetized dogs and show that the decrease in latency of the SSEP associated with hypocapnia is not due to changes in the depth of anaesthesia. These effects of hypocapnia may contribute to small variations in the latency of the SSEP when monitoring is performed during surgery, but are unlikely to be large enough to be of clinical concern.



Évaluer les effets de l’hypoxie et de l’hypocapnie modérées sur la latence et l’amplitude des potentiels somatosensoriels corticaux évoqués (PSSE) chez des humains conscients.


Chez dix volontaires, l’amplitude et la latence des potentiels somatosensoriels corticaux évoqués ont été enregistré pendant la stimulation du nerf tibial postérieur gauche. La mesure des PSSE et des variables respiratoires a été réalisée en air ambiant, en air avec un pourcentage réduit d’oxygène (17% O2, 14% O2 (n = 6) ou 11% O2 (n = 10)) et par la suite en air ambiant pendant l’hyperventilation volontaire (PEtCO2 = 20 mmHg, n = 10).


L’hypoxie (11% O2) a provoqué une légère stimulation de la ventilation (P < 0,05) mais n’a pas eu d’effet sur la latence et l’amplitude des PSSE. Les degrés moindres d’hypoxie n’ont pas eu d’effet. L’hyperventilation a provoqué une petite diminution (2–4%) de latence et une augmentation de l’amplitude des PSSE (P < 0,05).


Ces constatations chez des sujets conscients sont cohérentes avec les observations antérieures notées chez des sujets conscients et chez des chiens anesthésiés et montrent que la baisse de latence des PSSE n’est pas causée par des changements de profondeur d’anesthésie. Ces effets de l’hypocapnie peuvent contribuer à de petites variations de la latence des PSSE décelées par le monitorage en chirurgie, mais ils est peu probable qu’elles soient assez importantes pour inquiéter.


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Correspondence to John R. Ledsome.

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This work was supported by the Canadian Space Agency

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Ledsome, J.R., Cole, C. & Sharp-Kehl, J.M. Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans. Can J Anaesth 43, 1025 (1996). https://doi.org/10.1007/BF03011904

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Key words

  • Hypocapnia
  • Hypoxia
  • Monitoring: evoked potentials