Abstract
Hypocapnia is known to affect patients with acute stroke and plays a key role in governing cerebral autoregulation. However, the impact of hypocapnia on brain tissue pulsations (BTPs) is relatively unexplored. As BTPs are hypothesised to result from cerebrovascular resistance to the inflow of pulsatile arterial blood, it has also been hypothesised that cerebral autoregulation changes mediated by hypocapnia will alter BTP amplitude. This healthy volunteer study reports measurements of BTPs obtained using transcranial tissue Doppler (TCTD). Thirty participants underwent hyperventilation to induce mild hypocapnia. BTP amplitude, EtCO2, blood pressure, and heart rate were then analysed to explore the impact of hypocapnia on BTP amplitude. Significant changes in BTP amplitude were noted during recovery from hypocapnia, but not during the hyperventilation manoeuvre itself. However, a significant increase in heart rate and pulse pressure and decrease in mean arterial pressure were also observed to accompany hypocapnia, which may have confounded our findings. Whilst further investigation is required, the results of this study provide a starting point for better understanding of the effects of carbon dioxide levels on BTPs. Further research in this area is needed to identify the major physiological drivers of BTPs and quantify their interactions with other aspects of cerebral haemodynamics.
Highlights
Carbon dioxide (CO2 ) levels affect vascular smooth muscle tone and play a pivotal role in cerebral autoregulation [1,2,3]
Changes in left and right brain tissue pulsations (BTPs) are reported as differences between median BTP amplitude values, with statistically significant changes identified using a Wilcoxon signed-rank test
Changes in left and right BTPs are reported as differences between median BTP amplitude values, with statistically significant changes identified a Wilcoxon signed-rank test
Summary
Carbon dioxide (CO2 ) levels affect vascular smooth muscle tone and play a pivotal role in cerebral autoregulation [1,2,3]. Cerebral autoregulation is a homeostatic mechanism, which maintains cerebral blood flow through regulation of various body systems, including the cardiovascular, respiratory, and nervous systems [4]. A prominent mechanism underlying cerebral autoregulation control is. Brain Sci. 2020, 10, 614 blood vessel vasoconstriction and vasodilation, which provide a mechanism for controlling cerebral blood flow (CBF). It is well documented that increased arterial pressure of carbon dioxide (PaCO2 ) is associated with vasodilation [2]. Studies measuring cerebral blood flow using transcranial Doppler (TCD) previously found a sigmoidal association between hypercapnia (high PaCO2 ) and increased cerebral blood flow velocity [2]
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