BackgroundNeonates with hypoxic-ischemic encephalopathy (HIE) are at risk of cerebral blood flow dysregulation. Our objective was to describe the relationship between autoregulation and neurologic injury in HIE.MethodsNeonates with HIE had autoregulation monitoring with the hemoglobin volume index (HVx) during therapeutic hypothermia, rewarming, and the first 6 h of normothermia. The 5-mmHg range of mean arterial blood pressure (MAP) with best vasoreactivity (MAPOPT) was identified. The percentage of time spent with MAP below MAPOPT and deviation in MAP from MAPOPT were measured. Neonates received brain MRIs 3–7 days after treatment. MRIs were coded as no, mild, or moderate/severe injury in five regions.ResultsHVx identified MAPOPT in 79% (19/24), 77% (17/22), and 86% (18/21) of neonates during hypothermia, rewarming, and normothermia, respectively. Neonates with moderate/severe injury in paracentral gyri, white matter, basal ganglia, and thalamus spent a greater proportion of time with MAP below MAPOPT during rewarming than neonates with no or mild injury. Neonates with moderate/severe injury in paracentral gyri, basal ganglia, and thalamus had greater MAP deviation below MAPOPT during rewarming than neonates without injury.ConclusionMaintaining MAP within or above MAPOPT may reduce the risk of neurologic injuries in neonatal HIE.

Background Cerebrovascular autoregulation after resuscitation has not been well studied in an experimental model of pediatric cardiac arrest. Furthermore, developing noninvasive methods of monitoring autoregulation using near-infrared spectroscopy (NIRS) would be clinically useful in guiding neuroprotective hemodynamic management after pediatric cardiac arrest. We tested the hypotheses that the lower limit of autoregulation (LLA) would shift to a higher arterial blood pressure between 1 and 2 days of recovery after cardiac arrest and that the LLA would be detected by NIRS-derived indices of autoregulation in a swine model of pediatric cardiac arrest. We also tested the hypothesis that autoregulation with hypertension would be impaired after cardiac arrest. Methods Data on LLA were obtained from neonatal piglets that had undergone hypoxic-asphyxic cardiac arrest and recovery for 1 day (n=8) or 2 days (n=8), or that had undergone sham surgery with 2 days of recovery (n=8). Autoregulation with hypertension was examined in a separate cohort of piglets that underwent hypoxic-asphyxic cardiac arrest (n=5) or sham surgery (n=5) with 2 days of recovery. After the recovery period, piglets were reanesthetized, and autoregulation was monitored by standard laser-Doppler flowmetry and autoregulation indices derived from NIRS (the cerebral oximetry [COx] and hemoglobin volume [HVx] indices). The LLA was determined by decreasing blood pressure through inflation of a balloon catheter in the inferior vena cava. Autoregulation during hypertension was evaluated by inflation of an aortic balloon catheter. Results The LLAs were similar between sham-operated piglets and piglets that recovered for 1 or 2 days after arrest. The NIRS-derived indices accurately detected the LLA determined by laser-Doppler flowmetry. The area under the curve of the receiver operator characteristic curve for cerebral oximetry index was 0.91 at 1 day and 0.92 at 2 days after arrest. The area under the curve for hemoglobin volume index was 0.92 and 0.89 at the respective time points. During induced hypertension, the static rate of autoregulation, defined as the percent change in cerebrovascular resistance divided by the percent change in cerebral perfusion pressure, was not different between postarrest and sham-operated piglets. At 2 days recovery from arrest, piglets exhibited neurobehavioral deficits and histologic neuronal injury. Conclusions In a swine model of pediatric hypoxic-asphyxic cardiac arrest with confirmed brain damage, the LLA did not differ 1 and 2 days after resuscitation. The NIRS-derived indices accurately detected the LLA compared to laser-Doppler flow measurements at those time points. Autoregulation remained functional during hypertension.

After hypoxic brain injury, maintaining blood pressure within the limits of cerebral blood flow autoregulation is critical to preventing secondary brain injury. Little is known about the effects of prolonged hypothermia or rewarming on autoregulation after cardiac arrest. We hypothesized that rewarming would shift the lower limit of autoregulation (LLA), that this shift would be detected by indices derived from near-infrared spectroscopy (NIRS), and that rewarming would impair autoregulation during hypertension. Anesthetized neonatal swine underwent sham surgery or hypoxic-asphyxic cardiac arrest, followed by 2 h of normothermia and 20 h of hypothermia, with or without rewarming. Piglets were further divided into cohorts for cortical laser-Doppler flow (LDF) measurements during induced hypotension or hypertension. We also tested whether indices derived from NIRS could identify the LDF-derived LLA. The LLA did not differ significantly among groups with sham surgery and hypothermia (29 ± 8 mmHg), sham surgery and rewarming (34 ± 7 mmHg), arrest and hypothermia (29 ± 10 mmHg), and arrest and rewarming (38 ± 11 mmHg). The LLA was not affected by arrest (P = 0.60), temperature (P = 0.08), or interaction between arrest and temperature (P = 0.73). The NIRS-derived indices detected the LLA accurately, with the area under the receiver-operator characteristic curves of 0.81-0.96 among groups. In groups subjected to arrest and hypothermia, with or without rewarming, the slope of LDF relative to cerebral perfusion pressure during hypertension was not significantly different from zero (P > 0.10). In conclusion, rewarming did not shift the LLA during hypotension or affect autoregulation during hypertension after asphyxic cardiac arrest. The NIRS-derived autoregulation indices identified the LLA accurately.