Abstract
An increase in arterial PCO2 is the most common stressor used to increase cerebral blood flow for assessing cerebral vascular reactivity (CVR). That CO2 is readily obtained, inexpensive, easy to administer, and safe to inhale belies the difficulties in extracting scientifically and clinically relevant information from the resulting flow responses. Over the past two decades, we have studied more than 2,000 individuals, most with cervical and cerebral vascular pathology using CO2 as the vasoactive agent and blood oxygen-level-dependent magnetic resonance imaging signal as the flow surrogate. The ability to deliver different forms of precise hypercapnic stimuli enabled systematic exploration of the blood flow-related signal changes. We learned the effect on CVR of particular aspects of the stimulus such as the arterial partial pressure of oxygen, the baseline PCO2, and the magnitude, rate, and pattern of its change. Similarly, we learned to interpret aspects of the flow response such as its magnitude, and the speed and direction of change. Finally, we were able to test whether the response falls into a normal range. Here, we present a review of our accumulated insight as 16 “lessons learned.” We hope many of these insights are sufficiently general to apply to a range of types of CO2-based vasoactive stimuli and perfusion metrics used for CVR.
Highlights
For the last two decades, our laboratory has been engaged in interrogating cerebral vascular function
The overarching approach has been to observe changes in regional brain flow in response to a vasoactive stimulus. This is referred to as cerebrovascular reactivity, or cerebral vascular reactivity (CVR)
Our laboratory employs precise targeting of end-tidal PCO2 (PETCO2) and blood oxygen-level-dependent (BOLD) magnetic resonance imaging (MRI) as the surrogate measure of cerebral blood flow (CBF)
Summary
For the last two decades, our laboratory has been engaged in interrogating cerebral vascular function. Failing precise targeting of PaCO2, a reasonable fallback position is to assume that the ΔPETCO2 is close to ΔPaCO2 and can be used to index the change in flow for the stimulus by dividing it by ΔPETCO2 and defining the This view is the basic model we followed in studying CVR in the first 434 patients examined (Spano et al, 2013). In our early investigations of the way in which CBF responds to PaCO2, we applied a gradual “ramp” increase in PaCO2 from resting baseline to baseline + 15 mmHg over 4 min (Sobczyk et al, 2014) The results made it clear that, in the presence of cerebrovascular disease, many vascular beds, some as large as an entire hemisphere, have complex flow responses that are decidedly not sigmoidal, nor could they be accurately summarized by a linear regression. A ramp stimulus generates the data in a form that can be analyzed for intrinsic vascular resistance (Duffin et al, 2017, 2018; McKetton et al, 2019)
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