Bio

Richard J. Levy, MD, FAAP is Professor at Stanford University School of Medicine and Chief of Pediatric Cardiac Anesthesiology at Lucile Packard Children’s Hospital. He has been an NIH-funded clinician-scientist for over 20 years. His laboratory currently investigates the neurotoxic and cardiotoxic effects of anesthetics in the developing brain and developing heart, respectively. Dr. Levy specifically focuses on both the mechanisms of action of anesthetics within mitochondria. He is currently funded to study and develop a benzoquinone molecule as a novel anesthetic. He is an Associate Editor for Frontiers in Pediatrics, Frontiers in Cardiovascular Medicine, and Survey of Anesthesiology and serves as a regular reviewer for Anesthesiology, British Journal of Anaesthesiology, Critical Care Medicine, Anesthesia & Analgesia, Neurotoxicology and Teratology, PLOS One, The Journal of Thoracic and Cardiovascular Surgery, World Journal for Pediatric and Congenital Heart Surgery, and the American Journal of Physiology. In addition, Dr. Levy has served as an ad hoc reviewer for Science, Nature Medicine, Scientific Reports, and Nature Reviews Cardiology.

Clinical Focus

  • Pediatric Anesthesiology
  • Pediatric Cardiac Anesthesiology

Academic Appointments

Administrative Appointments

  • Chief of Pediatric Cardiac Anesthesiology, Stanford University, Lucile Packard Children's Hospital (2026 - Present)

Professional Education

  • Board Certification: American Board of Anesthesiology, Pediatric Anesthesiology (2013)
  • Fellowship: Childrens Hospital of Philadelphia Pediatric Critical Care Fellowship (2003) PA
  • Fellowship: Childrens Hospital of Philadelphia (2003) PA
  • Board Certification: American Board of Anesthesiology, Anesthesia (2002)
  • Residency: Hospital of Univ of Pennsylvania (2001) PA
  • Residency: Childrens Hospital of Philadelphia (1998) PA
  • Medical Education: New York Medical College (1995) NY

Contact

  • Academic
    levyri@stanford.edu
    University - Faculty Department: Anesthesia - Pediatric Position: Professor-Univ Med Line
  • Clinical (Primary)  Department of Anesthesiology, Perioperative and Pain Medicine Stanford University School of Medicine, Center for Academic Medicine 453 Quarry Road, 4th Floor Palo Alto, CA 94304 (650) 721-4264 (fax)

Additional Clinical Info

Additional Info

All Publications

  • Targetable Effects of the Anesthetic, Ubiquinone-5, on Murine Cardiac Rhythm FASEB JOURNAL Lim, H., Lu, R., Shi, C., Levy, R. J. 2026; 40 (4): e71598

    Abstract

    General anesthetics can adversely affect the heart, negatively impacting chronotropy, electrical conduction, and myocardial contractility. The intravenous sedative-hypnotic, propofol, for example, impairs ventricular contraction at clinically relevant doses and can cause dysrhythmias and atrioventricular block with acute administration. In addition, high cumulative propofol doses can induce bradyarrhythmias, cardiac conduction abnormalities, and myocardial failure. As with propofol, the recently identified intravenous anesthetic agent, ubiquinone-5 (Ub5), causes bradycardia and complete heart block at supratherapeutic doses. However, the cardiac effects of clinically relevant Ub5 doses are unknown. Thus, we aimed to determine how therapeutic doses of Ub5 impact cardiac rhythm, hypothesizing that Ub5 would interfere with dromotropy. We tested our hypothesis in vivo in the young adult mouse and ex vivo in the isolated-perfused murine heart. We then determined mechanistic contributors of Ub5-induced cardiotoxicity in isolated cardiomyocyte mitochondria. We found that Ub5 caused type 1 s-degree heart block and compromised the mitochondrial membrane potential in isolated cardiomyocyte mitochondria by inhibiting electron transport and inducing excessive proton leak. Pharmacological inhibition of the aspartate-glutamate carrier, Aralar, rescued Ub5-mediated disturbances in cardiac rhythm in the isolated-perfused heart. The findings suggest that Ub5 can impact cardiac conduction in a targetable manner, carrying importance for future drug development efforts.

    View details for DOI 10.1096/fj.202504065RR

    View details for Web of Science ID 001692326700001

    View details for PubMedID 41693609

    View details for PubMedCentralID PMC12908110

  • Multicenter Population Pharmacokinetics of Fentanyl in Neonatal Surgical Patients Using Dried Blood Spot Specimen Collection Demonstrates Maturation of Elimination Clearance. Anesthesia and analgesia Rzasa Lynn, R. S., Henthorn, T. K., Zuk, J., Hammer, G. B., Drover, D. R., Levy, R. J., Maxwell, L. G., Sadhasivam, S., Suresh, S., Galinkin, J. L. 2024; 138 (2): 447-455

    Abstract

    Fentanyl is widely used for analgesia and sedation in neonates, but pharmacokinetic (PK) analysis in this population has been limited by the relatively large sample volumes required for plasma-based assays.In this multicenter observational study of fentanyl kinetics in neonates up to 42 weeks of postmenstrual age (PMA) who received fentanyl boluses and continuous infusions, dried blood spots were used for small-volume sampling. A population PK analysis was used to describe fentanyl disposition in term and preterm neonates. Covariates for the model parameters, including body weight, PMA, birth status (preterm or term), and presence of congenital cardiac disease, were assessed in a stepwise manner.Clearance was estimated to be greater than adult clearance of fentanyl and varied with weight. Covariate selection did not yield a significant relationship for age as a continuous or dichotomous variable (term or preterm, the latter defined as birth with PMA of <37 weeks) and clearance.A supra-allometric effect on clearance was determined during covariate analyses (exponential scaling factor for body weight >0.75), as has been described in population PK models that account for maturation of intrinsic clearance (here, predominantly hepatic microsomal activity) in addition to scaling for weight, both of which impact clearance in this age group.

    View details for DOI 10.1213/ANE.0000000000006808

    View details for PubMedID 38215717

  • Anesthetic and Sedative Neurotoxicity in the Patient with Congenital Heart Disease ANESTHESIA FOR CONGENITAL HEART DISEASE, 3RD EDITION Levy, R. J., Wise-Faberowski, L., Andropoulos, D. B. edited by Andropoulos, D. B., Stayer, S., Mossad, E. B., MillerHance, W. C. 2015: 184–98

    View details for Web of Science ID 000385225800010

https://orcid.org/0000-0002-3406-5836