Cardiopulmonary bypass (CPB) provides cerebral oxygenation and blood flow (CBF) during neonatal congenital heart surgery, but the impacts of CPB on brain oxygen supply and metabolic demands are generally unknown. To elucidate this physiology, we used diffuse correlation spectroscopy and frequency-domain diffuse optical spectroscopy to continuously measure CBF, oxygen extraction fraction (OEF), and oxygen metabolism (CMRO₂) in 27 neonatal swine before, during, and up to 24 h after CPB. Concurrently, we sampled cerebral microdialysis biomarkers of metabolic distress (lactate–pyruvate ratio) and injury (glycerol). We applied a novel theoretical approach to correct for hematocrit variation during optical quantification of CBF in vivo. Without correction, a mean (95% CI) +53% (42, 63) increase in hematocrit resulted in a physiologically improbable +58% (27, 90) increase in CMRO₂ relative to baseline at CPB initiation; following correction, CMRO₂ did not differ from baseline at this timepoint. After CPB initiation, OEF increased but CBF and CMRO₂ decreased with CPB time; these temporal trends persisted for 0–8 h following CPB and coincided with a 48% (7, 90) elevation of glycerol. The temporal trends and glycerol elevation resolved by 8–24 h. The hematocrit correction improved quantification of cerebral physiologic trends that precede and coincide with neurological injury following CPB.

Lidocaine in del Nido cardioplegia solution prolongs the refractory period of cardiomyocytes, yielding a longer arrest per dose. Serum lidocaine concentrations >8 mg/L are associated with seizure and cardiotoxicity. We evaluated serum lidocaine concentrations in patients receiving del Nido solution during cardiac surgery. Forty consecutive patients undergoing cardiac surgical procedures with del Nido cardioplegia were selected for serum lidocaine concentration measurements determined immediately after aortic cross-clamp removal. Variables included weight, body surface area, operation, cardiopulmonary bypass time, aortic cross-clamp time, and total volume of del Nido solution. The primary outcome was serum lidocaine concentration relative to total volume of del Nido solution. Descriptive statistics and Pearson correlations were computed. Median weight was 78.3 kg (range, 43-132.4 kg), and mean body surface area was 1.9 ± 0.2 m². Operations included coronary artery bypass grafting (n = 26 [65%]), a combination procedure (n = 5 [12.5%]), isolated mitral valve repair or replacement (n = 4 [10%]), isolated aortic valve replacement (n = 3 [7.5%]), and aortic repair or replacement (n = 2 [5%]). Median total volume of del Nido solution was 1870 mL (range, 800-5800 mL). Mean serum lidocaine concentration was 2.2 ± 0.6 mg/L. Serum lidocaine concentration was weakly correlated with del Nido solution volume (R² = 0.21). The highest total volume of del Nido solution (5800 mL) did not yield the highest serum lidocaine concentration of 3.5 mg/L. Serum lidocaine concentration during cardiac surgical procedures weakly correlates with the volume of del Nido solution used and does not reach toxic levels even at high doses of del Nido solution. The results of this study may help alleviate concerns for lidocaine toxicity with high doses of del Nido solution.

Objectives: We previously demonstrated cerebral mitochondrial dysfunction in neonatal swine immediately following a period of full-flow cardiopulmonary bypass (CPB). The extent to which this dysfunction persists in the postoperative period and its correlation with other markers of cerebral bioenergetic failure and injury is unknown. We utilized a neonatal swine model to investigate the early evolution of mitochondrial function and cerebral bioenergetic failure after CPB. Methods: Twenty piglets (mean weight 4.4 ± 0.5 kg) underwent 3 h of CPB at 34 °C via cervical cannulation and were followed for 8, 12, 18, or 24 h (n = 5 per group). Markers of brain tissue damage (glycerol) and bioenergetic dysfunction (lactate to pyruvate ratio) were continuously measured in cerebral microdialysate samples. Control animals (n = 3, mean weight 4.1 ± 1.2 kg) did not undergo cannulation or CPB. Brain tissue was extracted immediately after euthanasia to obtain ex-vivo cortical mitochondrial respiration and frequency of cortical microglial nodules (indicative of cerebral microinfarctions) via neuropathology. Results: Both the lactate to pyruvate ratio ( P < .0001) and glycerol levels ( P = .01) increased in cerebral microdialysate within 8 h after CPB. At 24 h post-CPB, cortical mitochondrial respiration was significantly decreased compared with controls ( P = .046). The presence of microglial nodules increased throughout the study period (24 h) ( P = .01, R²= 0.9). Conclusion: CPB results in impaired cerebral bioenergetics that persist for at least 24 h. During this period of bioenergetic impairment, there may be increased susceptibility to secondary injury related to alterations in metabolic delivery or demand, such as hypoglycemia, seizures, and decreased cerebral blood flow.