Our multimodal platform using optical imaging of the brain alongside peripheral blood pressure monitoring allowed us to simultaneously and continuously monitor CBF, brain metabolism, and peripheral blood pressure throughout the cardiac arrest experiment. Using the measured CBF and MAP, we estimated a surrogate measure of rCVR [
43‐
46]. We suspected that rCVR may be particularly sensitive to changes in CBF and blood pressure during anoxic SD given that SD is known to affect CBF and our data in this study support blood pressure changing after anoxic SD onset. Interestingly, we observed a significant increase in rCVR starting with the onset of SD-associated changes in optical scattering. During SD, there were morphological changes in tissue that increased scattering of light, which could be detected by spatial frequency domain imaging and used to determine the onset of SD [
9]. Under normoxic conditions, SD is known to induce vasodilation to increase CBF [
2], but in pathological conditions (e.g., ischemic or hypoxic), it has been shown to reduce vessel diameter [
18], thus increasing CVR. However, to our knowledge, the changes that occur in peripheral and cerebral hemodynamics as well as cerebral metabolism 30 s before, during, and 30 s after anoxic SD have not been analyzed with high temporal resolution. High temporal resolution was needed because it allowed us to separate the dynamics between these 30- and 60-s periods to provide insights into the physiology of cerebral and peripheral hemodynamics before, during, and after anoxic SD. In addition to the rise of CVR with anoxic SD onset, we also found that the peak of CVR coincided with the end of optical scattering changes (end of anoxic SD). After anoxic SD, CVR interestingly began to decrease. The time at which CVR peaked was also strongly correlated with the AUC (a measure of total magnitude) of optical scattering change during anoxic SD (
p < 0.0005,
r = 0.92). Additionally, peak CVR was also strongly correlated with the magnitude of optical scattering change during SD (
p < 0.05,
r = 0.75). Greater observed optical scattering changes may be related to anoxic SD-induced extracellular ion changes (i.e., increase K
+ ions) and thus greater vasoconstriction. This aligns with findings from another study in which extracellular K
+ was the predominant vasoconstrictor in SD [
2,
53]. This may explain how CVR peaks at the end of anoxic SD and how the magnitude of anoxic SD or extracellular K
+ ion change is correlated with the magnitude of CVR. Moreover, whereas immediately before, during, and after anoxic SD, CBF and CMRO
2 continuously drop, the ratio of rCBF/rCMRO
2, a metric of cerebral flow–metabolism coupling, showed a different trend. Specifically, during anoxic SD, rCBF/rCMRO
2 dramatically dropped but then returned to its previous state after anoxic SD. We speculate that the rise in CVR was caused by CBF decreasing more than CMRO
2, thus producing the flow–metabolism imbalance during anoxic SD.