Abstract Title

Association of low-frequency oscillations in arterial pressure and cerebral blood flow on cerebral oxygenation during stimulated hemorrhage

Presenter Name

Tyler Petree

RAD Assignment Number

1501

Abstract

Background: Sustaining adequate cerebral perfusion and oxygenation are essential for maintaining consciousness. It has been shown that healthy individuals subjected to central hypovolemia show a continuum of tolerance to this stress, including simulated hemorrhage induced via application of lower body negative pressure (LBNP). Differences in tolerance to central hypovolemia have been associated with elevated release of vasoactive hormones, increased compensatory tachycardia and vasoconstriction, and higher endogenous low frequency (LF; ~0.1 Hz) arterial pressure and cerebral blood flow oscillations. We hypothesize that an increase in oscillations in middle cerebral artery velocity (MCAv) during maximal LBNP will result in an attenuated decrease in cerebral oxygenation, subsequently resulting in higher tolerance to this stress.

Methods: 25 healthy human subjects were subjected to pre-syncopal limited LBNP. Continuous waveform data was obtained for mean arterial pressure (MAP), MCAv, and cerebral oxygen saturation (ScO2). Spectral analysis was performed on MAP and MCAv to assess oscillations in the low frequency range (LF; 0.04-0.15 Hz). Subjects were divided into “Oscillators” and “Non-oscillators” based upon the increase or decrease in LF oscillations in MAP. The % change in ScO2 was assessed between “Oscillators” and “Non-oscillators” to determine if the presence of oscillations caused attenuated decrease in ScO2. Coefficients of determination (R2) were calculated between % changes in ScO2 and LF oscillations, and % changes in ScO2 and LBNP tolerance across all subjects.

Results: By design, MAP LF power was higher in the “Oscillators” vs. “Non-oscillators” (17.6 ± 3.6 vs. 6.5 vs. 1.3 mmHg2; P=0.01). This also resulted in higher MCAv LF power in the “Oscillators” (5.9 ± 1.2 vs. 2.9 ± 0.6 cm/s2; P=0.03). Contrary to our hypothesis, however, the “Oscillators” exhibited a greater reduction in ScO2 vs. the “Non-oscillators” (-7.1 ± 0.7 vs. -4.1 ± 1.6%; P=0.04), but there was no difference is LBNP tolerance time between groups (Oscillators: 1558 ± 81 s vs. Non-oscillators: 1661 ± 162 s; P=0.27). There were also poor associations between % changes in ScO2 vs. MAP LF power (R2=0.06), and % change in ScO2 vs. LBNP tolerance (R2=0.001).

Conclusions: These results suggest that increased oscillations in arterial pressure and cerebral blood flow do not result in an attenuated decrease in cerebral oxygen saturation.

Research Area

Integrative Physiology

Presentation Type

Poster

This document is currently not available here.

Share

COinS
 

Association of low-frequency oscillations in arterial pressure and cerebral blood flow on cerebral oxygenation during stimulated hemorrhage

Background: Sustaining adequate cerebral perfusion and oxygenation are essential for maintaining consciousness. It has been shown that healthy individuals subjected to central hypovolemia show a continuum of tolerance to this stress, including simulated hemorrhage induced via application of lower body negative pressure (LBNP). Differences in tolerance to central hypovolemia have been associated with elevated release of vasoactive hormones, increased compensatory tachycardia and vasoconstriction, and higher endogenous low frequency (LF; ~0.1 Hz) arterial pressure and cerebral blood flow oscillations. We hypothesize that an increase in oscillations in middle cerebral artery velocity (MCAv) during maximal LBNP will result in an attenuated decrease in cerebral oxygenation, subsequently resulting in higher tolerance to this stress.

Methods: 25 healthy human subjects were subjected to pre-syncopal limited LBNP. Continuous waveform data was obtained for mean arterial pressure (MAP), MCAv, and cerebral oxygen saturation (ScO2). Spectral analysis was performed on MAP and MCAv to assess oscillations in the low frequency range (LF; 0.04-0.15 Hz). Subjects were divided into “Oscillators” and “Non-oscillators” based upon the increase or decrease in LF oscillations in MAP. The % change in ScO2 was assessed between “Oscillators” and “Non-oscillators” to determine if the presence of oscillations caused attenuated decrease in ScO2. Coefficients of determination (R2) were calculated between % changes in ScO2 and LF oscillations, and % changes in ScO2 and LBNP tolerance across all subjects.

Results: By design, MAP LF power was higher in the “Oscillators” vs. “Non-oscillators” (17.6 ± 3.6 vs. 6.5 vs. 1.3 mmHg2; P=0.01). This also resulted in higher MCAv LF power in the “Oscillators” (5.9 ± 1.2 vs. 2.9 ± 0.6 cm/s2; P=0.03). Contrary to our hypothesis, however, the “Oscillators” exhibited a greater reduction in ScO2 vs. the “Non-oscillators” (-7.1 ± 0.7 vs. -4.1 ± 1.6%; P=0.04), but there was no difference is LBNP tolerance time between groups (Oscillators: 1558 ± 81 s vs. Non-oscillators: 1661 ± 162 s; P=0.27). There were also poor associations between % changes in ScO2 vs. MAP LF power (R2=0.06), and % change in ScO2 vs. LBNP tolerance (R2=0.001).

Conclusions: These results suggest that increased oscillations in arterial pressure and cerebral blood flow do not result in an attenuated decrease in cerebral oxygen saturation.