Newly Published
Correspondence  |   November 2019
Intravenous Lidocaine and Postoperative Cognition: Reply
Author Notes
  • Duke University Medical Center, Durham, North Carolina (R.Y.K.). kling004@mc.duke.edu
  • Accepted for publication October 4, 2019.
    Accepted for publication October 4, 2019.×
Article Information
Correspondence
Correspondence   |   November 2019
Intravenous Lidocaine and Postoperative Cognition: Reply
Anesthesiology Newly Published on November 13, 2019. doi:https://doi.org/10.1097/ALN.0000000000003040
Anesthesiology Newly Published on November 13, 2019. doi:https://doi.org/10.1097/ALN.0000000000003040
We thank Drs. Cao and Zhu for their correspondence regarding our study on the effect of intravenous lidocaine on postoperative cognitive dysfunction after cardiac surgery.1 
Postoperative cognitive dysfunction has a complex pathophysiologic basis without a clear singular etiology in current understanding. As Drs. Cao and Zhu point out, intraoperative hypotension has been associated with an increased risk of postoperative delirium and cognitive dysfunction, although the evidence is conflicting. Chronic hypertension, along with other comorbidities, has long been thought to produce a rightward shift in the cerebral autoregulation curve, suggesting a higher risk of cerebral hypoperfusion in these patients. However, some studies have failed to find a difference in mean arterial pressure (MAP) at the lower limit of cerebral autoregulation in patients with these comorbidities and have generally found predicting the MAP to target during cardiopulmonary bypass (CPB) difficult based on clinical history and preoperative blood pressure.2  While it is generally believed that intraoperative MAP goals should be individualized to the patient’s physiology, how to monitor and target cerebral perfusion remains difficult without specialized equipment for real-time cerebral autoregulation monitoring. Near-infrared spectroscopy-based methods may provide an acceptable alternative for monitoring cerebral autoregulation during cardiac surgery, yet studies demonstrating the ability of this and similar monitoring techniques to improve neurocognitive outcomes after cardiac surgery remain limited by small cohort size, short duration of follow-up, and mixed results.2,3  Furthermore, cardiac surgical patients are at risk of hemodynamic instability beyond the intraoperative period; thus, cerebral hypoperfusion may occur outside of the monitored intraoperative environment and remains difficult to detect and preempt postoperatively. Given that blood pressure was not the focus of our current study, we did not employ specialized monitoring of cerebral autoregulation.