Overshoot in Cerebral Perfusion Following Release of Simulated Obstructive Apnea




Liu, Xiaoli
White, David III
Akinbola, Ebunoluwa
Shi, Xiangrong


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Purpose: The purpose of this study was to examine and quantify the hypothesis that there is a surge in cerebral perfusion and arterial pressure, following the release of the modified Mueller maneuver. Methods: Nine healthy men (28 ±1 yr old) performed the Mueller maneuver (attempted inspiration against closed glottis after a forced expiration) and the modified Mueller maneuver (attempted inspiration against closed glottis after a normal expiration) for 15 seconds, respectively, in a random order. The study was approved by the IRB at UNTHSC (Project #2013-121). Heart rate (HR), mean arterial pressure (MAP), cerebral blood flow velocity of the middle cerebral artery (VMCA), arterial oxygen saturation (SaO2) and cerebral tissue oxygen saturation (ScO2) were continuously measured during the maneuvers. Cerebral vascular resistance index (CVRI) was estimated from the ratio of MAP/VMCA. Changes in the hemodynamic parameters were assessed during the first and last 5 seconds of simulated obstructive apnea, respectively, and the first 5 seconds after release of the apnea. Results: Variables were extrapolated to examine percent change from baseline for the first 5 seconds of the maneuver, last 5 seconds of the maneuver, and the release of the maneuver. Neither regular, nor modified, maneuvers elicited significant changes in cardiovascular variables. After the release of the maneuvers, however, both MAP and VMCA were significantly augmented. A significant decrease in CVRI was present after the Mueller maneuver. Conclusions: In conclusion, there is a surge in VMCA associated with an overshoot of MAP following release of simulated obstructive apnea. This sudden increase in cerebral perfusion seems to be driven by an augmented perfusion pressure in the modified Mueller maneuver. This study indicates that obstructive apnea simulated by either regular or modified Mueller maneuvers may lead to instability of cerebral perfusion during the initial phase of resuming breathing.