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1 Center for Biomedical Engineering, University of Kentucky, Lexington, KY, USA
2 Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, USA
3 Center for Biomedical Engineering, University of Kentucky, Lexington, KY, USA; Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: abhijit{at}uky.edu.
In twenty eight healthy adults, we compared dynamic interaction between respiration and cerebral autoregulation in two groups of subjects; those who did and did not develop presyncopal symptoms during 70o passive head up tilt (HUT); i.e. Non-Presyncopal (23) and Presyncopal groups (5). Airflow, CO2, cerebral blood flow velocity (CBF), ECG, and blood pressure (BP) were recorded. To determine whether influences of mean blood pressure (MBP) and systolic blood pressure (SBP) on CBF were altered in presyncopal subjects, coherencies and transfer functions between these variables and mean and peak cerebral blood flow velocities (CBFm and CBFp) were estimated. To determine the influence of end-tidal CO2 (ETCO2) on CBF, relative CO2 reactivity (% change in CBFm per mmHg change in ETCO2) was calculated. We found that in Presyncopal subjects prior to symptoms during HUT, coherence between SBP and CBFp was higher (p=0.02) and gains of transfer functions between BP (MBP and SBP) and CBFm were larger (MBP, p=0.01, SBP, p=0.01) in the respiratory frequency region. In the last 3 minutes prior to presyncope, Presyncopals had a reduced relative CO2 reactivity (p=0.005), likely a consequence of larger decrease in ETCO2. We hypothesize that CO2 mediated increase in resistance attenuates autoregulation such that the relationship between systemic and cerebral hemodynamics is enhanced. Our results suggest that altered cardio-respiratory interaction involving cerebral hemodynamics may contribute in the cascade of events during tilt that culminate in unexplained syncope.
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