This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Tisdall, M. M. Articles by Smith, M. PubMed PubMed Citation Articles by Tisdall, M. M. Articles by Smith, M. Related Collections Neuroanesthesia Physiology Ventilation

---

NEUROSURGICAL ANESTHESIOLOGY AND NEUROSCIENCE

The Effect on Cerebral Tissue Oxygenation Index of Changes in the Concentrations of Inspired Oxygen and End-Tidal Carbon Dioxide in Healthy Adult Volunteers

Martin M. Tisdall, MD^*, Christopher Taylor, FRCA^*, Ilias Tachtsidis, PhD, Terence S. Leung, PhD, Clare E. Elwell, PhD, and Martin Smith, FRCA^*

From the *Department of Neuroanaesthesia and Neurocritical Care, The National Hospital for Neurology and Neurosurgery, University College London Hospitals; and Department of Medical Physics and Bioengineering, University College London, London, UK.

Address correspondence and reprint requests to Martin Smith, FRCA, Department of Neuroanaesthesia and Neurocritical Care, Box 30, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. Address e-mail to martin.smith{at}uclh.nhs.uk.

Abstract

BACKGROUND: A variety of near-infrared spectroscopy devices can be used to make noninvasive measurements of cerebral tissue oxygen saturation (ScO₂). The ScO₂ measured by the NIRO 300 spectrometer (Hamamatsu Photonics, Japan) is called the cerebral tissue oxygenation index (TOI) and is an assessment of the balance between cerebral oxygen delivery and utilization. We designed this study to investigate the effect of systemic and intracranial physiological changes on TOI.

METHODS: Fifteen healthy volunteers were studied during isocapneic hyperoxia and hypoxemia, and normoxic hypercapnea and hypocapnea. Absolute cerebral TOI and changes in oxy- and deoxyhemoglobin concentrations were measured using a NIRO 300 spectrometer. Changes in arterial oxygen saturation (Sao₂), ETco₂, heart rate, mean arterial blood pressure (MBP), and middle cerebral artery blood flow velocity (V_mca) were also measured during these physiological challenges. Changes in cerebral blood volume (CBV) were subsequently calculated from changes in total cerebral hemoglobin concentration.

RESULTS: Baseline TOI was 67.3% with an interquartile range (IQR) of 65.2%–71.9%. Hypoxemia was associated with a median decrease in TOI of 7.1% (IQR –9.1% to –5.4%) from baseline (P < 0.0001) and hyperoxia with a median increase of 2.3% (IQR 2.0%–2.5%) (P < 0.0001). Hypocapnea caused a reduction in TOI of 2.1% (IQR –3.3% to –1.3%) from baseline (P < 0.0001) and hypercapnea an increase of 2.6% (IQR 1.4%–3.7%) (P < 0.0001). Changes in Sao₂ (P < 0.0001), ETco₂ (P < 0.0001), CBV (P = 0.0003), and MBP (P = 0.03) were significant variables affecting TOI. Changes in V_mca (P = 0.7) and heart rate (P = 0.2) were not significant factors.

CONCLUSION: TOI is an easy-to-monitor variable that provides real-time, multisite, and noninvasive assessment of the balance between cerebral oxygen delivery and utilization. However, TOI is a complex variable that is affected by Sao₂ and ETco₂, and, to a lesser extent, by MBP and CBV. Clinicians need to be aware of the systemic and cerebral physiological changes that can affect TOI to interpret changes in this variable during clinical monitoring.