• M Pöyhönen, S Syväoja, J Hartikainen, E Ruokonen, and J Takala.
• Department of Anesthesiology and Intensive Care, Kuopio University Hospital, 70211 Kuopio, Finland.
• Acta Anaesthesiol Scand. 2004 Jan 1; 48 (1): 93-101.

BackgroundHeart rate variability (HRV) has been used for assessment of depth of anesthesia. Alterations in respiratory rate and tidal volume modulate the sympatovagal neural drive to the heart. The changes in PaCO2 that accompany changes in breathing pattern may, through chemoreceptors in the brainstem, independently influence the autonomic control of the heart and modulate HRV.MethodsWe measured the effects of PaCO2, tidal volume and respiratory rate on HRV during spontaneous and mechanical ventilation in 22 healthy volunteers and in 25 mechanically ventilated anesthetized patients.ResultsAdding CO2 to the inspiratory gas increased high frequency (HF) and low frequency (LF) components of HRV in awake volunteers both during spontaneous and mechanical ventilation, while this effect of CO2 was abolished in patients during anesthesia. Increase of tidal volume increased HF component of HRV only in volunteers during spontaneous ventilation. On the other hand, when respiratory rate was reduced, the balance of HF and LF power moved toward LF power in all study groups. Breathing frequency altered HRV independent on PaCO2, tidal volume and the level of consciousness. In contrast, the effect of PaCO2 appeared to be related to normal level of consciousness, suggesting that a cortical modulation of the autonomic nervous activity contributes to the effects of PaCO2 on HRV.ConclusionsPaCO2, tidal volume and respiratory rate should be controlled when HRV power spectrum is measured in conscious patients or volunteers, while in anesthetized patients small changes in end-tidal CO2 or tidal volume do not modulate HRV if respiratory rate remains unchanged.

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