Abstract 4136290: Toward Quantitative Assessment of Cerebrovascular Autoregulation in Neonates using Ultrafast Ultrasound Power Doppler

Introduction: Newborns with congenital heart diseases requiring cardiopulmonary bypass are at risk of neurodevelopmental impairment. The impact of deep hypothermia during cardiopulmonary bypass (DH-CPB) on cerebrovascular autoregulation (CAR) that controls brain perfusion in the presence of variable blood pressure is not well understood. Recently, Ultrafast Power Doppler (UPD) showed potential to study CAR in neonates based on the measurement of cerebral blood volume (CBV). However, since CAR relies mainly on the arterial vasoconstriction/vasodilation, the interpretation of brain perfusion based on CBV requires further separation of arterial CBV from total CBV. This study aims to use UPD to monitor CAR during DH-CPB in neonates. Methods: An ultrasonic probe (5.7 MHz) was placed on the anterior fontanel of 6 newborns before, during and after DH-CPB. Using ultrafast sequences generated by a Verasonic Vantage research system, mid-coronal plane images were acquired (PRF of 9 kHz, 5 compounded diverging waves). An adaptive spatiotemporal singular value decomposition was used to separate the blood signal from tissue signal and obtain UPD. CBV was computed in the deep gray matter (DGM). This region was chosen due to its higher susceptibility to hypoxic-ischemic injury. Arterial CBV was isolated from total CBV based on the upward arterial flow obtained using signed-power Doppler (See Fig A). Pearson correlation ® was computed between mean arterial blood pressure (MAP) and arterial CBV to study CAR. Results: Before and after DH-CPB, negative correlations were found between arterial CBV and MAP: -0.30 and -0.43 respectively. This indicates that an increase in MAP is associated with a decrease in cerebral arterial blood volume. This decrease in arterial CBV likely arises from arterial vasoconstriction, suggesting an active CAR response. Conversely, during DH-CPB, no correlation was found (r = -0.02). This means that despite the increase in MAP, arterial CBV remains unchanged. This lack of variation of arterial CBV is likely due to absent arterial vasoconstriction, suggesting an impaired CAR response. Conclusion: Our findings highlight the potential of UPD for continuous monitoring of CAR, paving the way for improving neurovascular management strategies during DH- CPB.