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Background: Systemic hypothermia with bilateral antegrade selective cerebral perfusion (ASCP) is the preferred cerebral protective strategy for type A aortic dissection surgery. The optimal ASCP flow rate remains uncertain and the target flow cannot always be reached due to pressure limitations. The aim of this study was to assess the correlation between ASCP flow and regional cerebral oxygen saturation (rSO2)., Methods: A retrospective analysis was performed on 140 patients with acute type A aortic dissection who underwent surgery with moderate hypothermic circulatory arrest and bilateral ASCP between 2015 and 2021. Pearson correlation analysis was performed between ASCP flow and rSO2., Results: The median circulatory arrest duration was 46.5 (IQR:37.0-61.0) minutes. There was no significant correlation between ASCP flow and rSO2 for both the right (r = -.02, p = .851), and the left hemisphere (r = - .04, p = .618). The rSO2 values for ten patients who received > 10 mL/kg/min flow did not differ significantly from 130 patients who received 10 mL/kg/min or less for both the left hemisphere ( p = .135), and the right hemisphere ( p = .318). The ASCP flow was 5.1 (IQR:5.0- 6.5) mL/kg/min in five patients with, and 7.2 (IQR:5.8-8.3) mL/kg/min in 135 patients without a watershed infarction ( p = .098)., Conclusions: There was no correlation between ASCP flow rate and rSO2 in patients with acute type A aortic dissection. Furthermore, ASCP flow below 10 mL/kg/min was not associated with a reduction in rSO2. Definitive associations between ASCP flow and neurological outcome after type A aortic dissection surgery need further investigation., Competing Interests: Declaration of conflicting interestsThe authors received no financial support for the research, authorship and/or publication of this article.

Introduction: Histidine-tryptophan-ketoglutarate cardioplegia is used for prolonged myocardial protection in complex cardiac surgery. Administration leads to acute hyponatremia in a majority of patients, because of its low sodium concentration (15 mmol/L). However, histidine-tryptophan-ketoglutarate solution's osmolality is slightly hypertonic (310 mOsm/kg). Hypothesized was that acute isotonic hyponatremia will be induced, which does not need to be corrected with hypertonic saline., Methods: Cardiac surgery patients who received histidine-tryptophan-ketoglutarate cardioplegia were included in this prospective single center study. Serial blood samples were taken from each patient at five different time points: after induction of anesthesia (T1) and 10 minutes (T2), 6 hours (T3), 12 hours (T4), and 18 hours (T5) after administration of histidine-tryptophan-ketoglutarate cardioplegia, respectively. Blood samples were analyzed for sodium concentration, osmolality, and acid-base balance., Results: Twenty-five patients were included. Median blood sodium levels decreased from 140 [138-141] at T1 to 128 [125-130] mmol/L at T2 (p < 0.001). At T3, T4, and T5, median blood sodium concentrations were 136 [134-138], 139 [137-140], and 140 [137-142] mmol/L, respectively. Median osmolality was 289 [286-293] at T1 and increased to 296 [291-299] mOsm/kg (p < 0.001) at T2. At T3, T4, and T5, osmolality was 298 [292-302], 298 [294-304], and 300 [297-306] mOsm/kg, respectively. Median pH decreased from 7.38 [7.36-7.40] at T1 to 7.30 [7.27-7.32] at T2 (p < 0.001)., Conclusion: Administration of histidine-tryptophan-ketoglutarate cardioplegia during cardiac surgery leads to acute moderate to severe isotonic hyponatremia, which resolves spontaneously in the first 18 hours perioperatively. Correction with hypertonic saline is not necessary.