Wayne K Jacobsen
- Chair, Department of Anesthesiology
- Professor, Anesthesiology - (Clinical Scholar Track)
- Professor, Anesthesiology
Wayne K. Jacobsen, MD, FCCM
Professor and Chair
Department of Anesthesiology
Dr. Jacobsen is the Chair and Professor of Anesthesiology at The University of Arizona College of Medicine. He was also the Anesthesiology Residency Program Director and Associate Head of Education for the Department of Anesthesiology.
He received his M.D. degree from Loma Linda University, where he also completed his Anesthesiology Residency and Critical Care Fellowship. He also completed a Pediatric Critical Care Fellowship at the Hospital for Sick Children in Toronto, Ontario, Canada. Returning to Loma Linda University, he became Director of the Pediatric Intensive Care Unit and subsequently Director of the Surgical Trauma Intensive Care Unit.
From 1995-2002 he was the Chair of the Anesthesiology Department at Loma Linda University School of Medicine. After resigning as Department Chair, he was Chief of Anesthesiology at the Loma Linda Veterans Administration Hospital. In 2004, Dr. Jacobsen moved to Tucson and joined the anesthesiology faculty at The University of Arizona.
Dr. Jacobsen has served on the Society of Critical Care Medicine, the Association of University Anesthesiologists, and the Anesthesiology Residency Review Committee of the Accreditation Council for Graduate Medical Education. His research interests have included ischemic organ reperfusion and residency education.
- M.D. Anesthesiology
- Loma Linda University Medical Center, Loma Linda, California, United States
- Chair, University of Arizona, Tucson, Arizona (2015 - Ongoing)
- Chief of Anesthesia, Jerry L. Pettis Memorial Veteran's Hospital (2002 - 2003)
- Chair, Loma Linda University School of Medicine (1995 - 2002)
Licensure & Certification
- California Medical License (1974)
- Arizona Medical License (2004)
- American Board of Anesthesiology, Certificate of Competence in Critical Care Medicine (1986)
- American Board of Anesthesiology (1979)
- Fellow, American College of Critical Care (1989)
- National Bard of Medical Examiners (1975)
No activities entered.
No activities entered.
- Nielsen, V. G., & Jacobsen, W. K. (2016). Iron modulates the alpha chain of fibrinogen. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine.More infoIron-bound fibrinogen has been noted to accelerate plasmatic coagulation in patients with divergent conditions involving upregulation of heme oxygenase activity, including hemodialysis, Alzheimer's disease, sickle cell anemia, and chronic migraine. Our goal was to determine if a site of iron-fibrinogen interaction was on the alpha chain. Using thrombelastography, we compared the coagulation kinetic profiles of plasma exposed to 0-10 µM ferric chloride after activation of coagulation with thrombin generated by contact activation of plasma with the plastic sample cup or by exposure to 1 µg/ml of Calloselasma rhodostoma venom (rich in ancrod activity), which causes coagulation via polymerization of alpha chain monomers. Venom mediated coagulation always occurred before thrombin activated thrombus formation, and ferric chloride always diminished the time of onset of coagulation and increased the velocity of clot growth. Iron enhances plasmatic coagulation kinetics by modulating the alpha chain of fibrinogen.
- Nielsen, V. G., Pretorius, E., Bester, J., Jacobsen, W. K., Boyle, P. K., & Reinhard, J. P. (2015). Carbon monoxide and iron modulate plasmatic coagulation in Alzheimer's disease. Current neurovascular research, 12(1), 31-9.More infoAlzheimer's disease (AD) is a significant source of morbidity and mortality for millions of people worldwide, and multiple potential etiologies have been postulated to contribute to AD. Among these, spontaneous cerebral emboli and increased cerebral and circulating heme oxygenase (Hmox) activity in AD patients are of particular interest, as two of the products of Hmox activity, carbon monoxide (CO) and iron enhance plasmatic coagulation and modify the ultrastructure of thrombi. We hypothesized that patients afflicted with AD would have coagulation kinetics modulated by CO and iron. Using viscoelastic assessments of coagulation, it was determined with a small cohort (n=11) of AD patients that all had enhancement of coagulation by CO, iron, or both. In a complementary fashion, it was determined that a separate cohort (n=12) of AD patients had thrombi with ultrastructural features consistent with iron and CO exposure as assessed with scanning electron microscopy. Further, when stratified by normal or abnormally increased serum ferritin concentrations (which can be increased by Hmox), the AD patients with abnormal ferritin concentrations had significantly thinner fibrin fiber diameters, not unlike that noted when normal plasma is mixed with iron or CO. In sum, AD patients were noted to have plasmatic coagulation kinetic and thrombus ultrastructural changes consistent with exposure to CO and iron. Future investigation of CO and iron in the pathogenesis of Alzheimer's disease is warranted.
- Shah, N., Welsby, I. J., Fielder, M. A., Jacobsen, W. K., & Nielsen, V. G. (2015). Sickle cell disease is associated with iron mediated hypercoagulability. Journal of thrombosis and thrombolysis, 40(2), 182-5.More infoSickle cell disease (SCD) is associated with a significant hypercoagulable state and several hemostatic anomalies have been identified in this disease state. Of interest, SCD patients can become iron overloaded after transfusion, and iron can enhance fibrinogen as a substrate for thrombin, resulting in thrombi that commence coagulation quickly and form rapidly. We hypothesized that SCD patients would display hypercoagulable plasma coagulation kinetics and an iron enhancement of coagulation. After obtaining IRB approval, we assessed coagulation kinetics and iron enhancement with viscoelastic methods in archived, citrated plasma obtained from ambulatory or hospitalized SCD patients (n = 20). All SCD patients had plasmatic hypercoagulability, and 65 % were positive for iron enhancement of coagulation. In conclusion, continuing investigation correlating such viscoelastic data with clinical symptoms may provide insight into the role played by iron in the setting of SCD, including complications such as vaso-occlusive crisis.
- Jacobsen, W. K. (2011). The correlation between evaluations of anesthesiology residents and the overuse of the first-person pronoun "I" in personal statements. Journal of Graduate Medical Education, 3(2), 151-154.