Abstract

Reductions in cerebral oxygen saturation (ScO2) measured by near infra-red spectroscopy have been found during compensated hypovolemia in the lower body negative pressure (LBNP)-model, which may reflect reduced cerebral blood flow. However, ScO2 may also be contaminated from extracranial (scalp) tissues, mainly supplied by the external carotid artery (ECA), and it is possible that a ScO2 reduction during hypovolemia is caused by reduced scalp, and not cerebral, blood flow. The aim of the present study was to explore the associations between blood flow in precerebral arteries and ScO2 during LBNP-induced hypovolemia. Twenty healthy volunteers were exposed to LBNP 20, 40, 60 and 80 mmHg. Blood flow in the internal carotid artery (ICA), ECA and vertebral artery (VA) was measured by Doppler ultrasound. Stroke volume for calculating cardiac output was measured by suprasternal Doppler. Associations of changes within subjects were examined using linear mixed-effects regression models. LBNP reduced cardiac output, ScO2 and ICA and ECA blood flow. Changes in flow in both ICA and ECA were associated with changes in ScO2 and cardiac output. Flow in the VA did not change during LBNP and changes in VA flow were not associated with changes in ScO2 or cardiac output. During experimental compensated hypovolemia in healthy, conscious subjects, a reduced ScO2 may thus reflect a reduction in both cerebral and extracranial blood flow.

Highlights

  • Cerebral blood flow (CBF) has generally been assumed to be autoregulated [1], meaning that CBF is maintained as long as mean arterial pressure (MAP) is kept between a lower and upper limit

  • The main findings of the present study were that changes in ScO2 were associated with changes in blood flow in both internal carotid artery (ICA) and external carotid artery (ECA) during lower body negative pressure (LBNP)

  • The association between ScO2 and cardiac output found in the present study (S2 Fig, left panel) could hold promise for the use of near infra-red spectroscopy (NIRS) as a non-invasive tool to detect hypovolemia in unanesthetised patiens, e.g. trauma patients, the estimated reduction in ScO2 was only 2.3% for a reduction in cardiac output of 1 l/min

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Summary

Introduction

Cerebral blood flow (CBF) has generally been assumed to be autoregulated [1], meaning that CBF is maintained as long as mean arterial pressure (MAP) is kept between a lower and upper limit. Cerebral blood flow regulation is complex, and studies have shown that cardiac output may affect CBF independently of MAP [2,3,4,5]. Precerebral blood flow and cerebral oximetry in experimental hypovolemia

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