Patrick K Boyle
- Clinical Associate Professor
Dr. Patrick K. Boyle was born and raised in New Mexico, After pursuing a course of studies in biomedical engineering he graduated in 1982. He has served as the Vice Chairman of Clinical Affairs, Interim Department Chairman, Head Scheduler, Operating Room Medical Director and of most recent and significant established an Acute Pain/Regional Anesthesia Service at his former institution. Dr. Boyle joined the faculty at the University of Arizona College of Medicine in July 2007 as an Assistant Professor.
- Uniformed Services University of the Health Sciences, Bethesda, Maryland, United States
- Rank I Inductrial Hygine Toxicology
- University of Arizona College of Pharmacy, Tucson, Arizona, United States
- Completed work toward Masters not finished secondary to acceptance to medical school
- University of New Mexico College of Engineering, Albuquerque, New Mexico, United States
- Clinical Assistant Professor, Anesthesiology, University of Arizona College of Medicine, Tucson, Arizona (2014 - Ongoing)
- Assistant Professor, Anesthesiology, University of Arizona College of Medicine, Tucson, Arizona (2007 - 2014)
- Anesthesiology Faculty, Naval Medical Center San Diego (2000 - 2007)
Licensure & Certification
- License, Arizona State Medical Board (2007)
- License, California State Medical Board (1994)
- Certification, Amreican College of Surgeons Advanced Trauma Life Support Instructor (2007)
- Certification, American Board of Anesthesiology (2001)
Continued development and expansion of the role ultrasound in regional anesthesiaDevelopment and organization of Multi-discipline treatment of pain and pain syndromesOperating Room Efficiency
2004-pres. Naval Medical Center San Diego, Department of Anesthesia CIP #S-03-164, Associate Investigator, Utility of Acoustic Reflectometry in Various Clinical Situations. 2002-2005 Naval Medical Center San Diego, Department of Anesthesia CIP# S-03-001, Associate Investigator, Analysis of Intrathecal Lipophilic Narcotics in a Bupivicaine-Morphine Mixture for Cesarean Section. 2002-2004 Naval Medical Center San Diego, Department of Anesthesia CIP# S-01-110, Associate Investigator, A Comparison of Prophylactic Dolasetron Versus Ondansetron in Patients at High Risk for Post-operative Nausea and Vomiting. 2002-2003 Naval Medical Center San Diego, Department of Anesthesia CIP# S-03-015, Associate Investigator, Mechanisms of False Positive and False Negative Results When Using Various Esophageal Detection Devices. Use of the Esophageal Detection Device in Confirming Placement of Needle Cricothyroidotomy.
No activities entered.
- Nielsen, V., Redford, D., & Boyle, P. (2017). Effect of iron and carbon monoxide on fibrinogenase-like degradation of plasmatic coagulation by venoms of four Crotalus species. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis.More infoAnnually, thousands suffer poisonous snake bite, often from defibrinogenating species. Iron and carbon monoxide (CO) improve coagulation kinetics by modulation of fibrinogen as demonstrated in various Agkistrodon species and Crotalus atrox. Thus, we sought to determine whether pretreatment of plasma with iron and CO could attenuate venom-mediated catalysis of fibrinogen obtained from four common Crotalus species with known fibrinogenase activity. Human plasma was pretreated with ferric chloride (0-10 μmol/l) and CO-releasing molecule-2 (0-100 μmol/l) prior to exposure to venom from a Northern Pacific rattlesnake, Arizona black rattlesnake, prairie rattlesnake, or red diamond rattlesnake. The concentration of venom used decreased coagulation function of one or more kinetic parameters by at least 50% of normal values. Coagulation kinetics were determined with thrombelastography.Three snake venoms significantly degraded plasmatic coagulation kinetics, prolonging the onset to clot formation, diminishing velocity of clot growth and decreasing clot strength. However, red diamond rattlesnake venom exposure resulted in mixed coagulation kinetics, significantly decreasing the time to onset of coagulation without decreasing the velocity of clot growth. Iron and CO attenuated these coagulation kinetic changes in a species-specific manner. Further in vitro investigation of other fibrinogenolytic venoms is indicated to determine if iron and CO can attenuate venom compromised coagulation.
- Nielsen, V. G., Redford, D. T., & Boyle, P. K. (2016). Effect of Iron and Carbon Monoxide on Fibrinogenase-like Degradation of Plasmatic Coagulation by Venoms of Six Agkistrodon Species. Basic & clinical pharmacology & toxicology.More infoAnnually, thousands suffer poisonous snake bite, often from defibrinogenating species. It has been demonstrated that iron and carbon monoxide change the ultrastructure of plasma thrombi and improve coagulation kinetics. Thus, the present investigation sought to determine if pre-treatment of plasma with iron and carbon monoxide could attenuate venom-mediated catalysis of fibrinogen obtained from Agkistrodon species with fibrinogenase activity. Human plasma was pre-treated with ferric chloride (0-10 μM) and carbon monoxide releasing molecule-2 (CORM-2, 0-100 μM) prior to exposure to 0.5-11 μg/ml of six different Agkistrodon species' venom. The amount of venom used for experimentation needed to decrease coagulation function of one or more kinetic parameters by at least 50% of normal values for (e.g., half the normal speed of clot formation). Coagulation kinetics were determined with thrombelastography. All six snake venoms degraded plasmatic coagulation kinetics to a significant extent, especially prolonging the onset to clot formation and diminishing the speed of clot growth. Pre-treatment of plasma with iron and carbon monoxide attenuated these venom-mediated coagulation kinetic changes in a species-specific manner, with some venom effects markedly abrogated while others were only mildly decreased. Further in vitro investigation of other pit viper venoms that possess fibrinogenolytic activity is indicated to identify species amenable to or resistant to iron and carbon monoxide-mediated attenuation of venom-mediated catalysis of fibrinogen. Lastly, future preclinical investigation with animal models (e.g., rabbit ear bleed model) is planned to determine if iron and carbon monoxide can be used therapeutically after envenomation. This article is protected by copyright. All rights reserved.
- 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.
- Nielsen, V., Galvani, C., Boyle, P., Steinbrenner, E., & Matika, R. (2015). Bariatric patients have plasmatic hypercoagulability and systemic upregulation of heme oxygenase activity. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis, 26(2), 200-4.More infoMorbid obesity is associated with significant thrombophilia. Of interest, adipocytes obtained from obese patients have increased heme oxygenase (Hmox) activity, the endogenous enzyme responsible for carbon monoxide (CO) production. Given that CO enhances plasmatic coagulation, we determined whether morbidly obese patients undergoing bariatric surgery had an increase in endogenous CO and plasmatic hypercoagulability. CO was determined by noninvasive pulse oximetry measurement of carboxyhemoglobin (COHb). A thrombelastographic method to assess plasma coagulation kinetics and formation of carboxyhemefibrinogen (COHF) was utilized. Nonsmoking bariatric patients (n = 20, BMI 47 ± 8 kg/m, mean ± SD) had abnormally increased COHb concentrations of 2.7 ± 1.9%, indicative of Hmox upregulation. When coagulation kinetics of these bariatric patients were compared with values obtained from normal individuals' (n = 30) plasma, 70% (95% confidence interval 45.7-88.1%) had abnormally great velocity of clot formation, abnormally large clot strength, and COHF formation. Future investigation of Hmox-derived CO in the pathogenesis of obesity-related thrombophilia is warranted.
- Boyle, P. K. (2015, October). Peripheral Nerve Block Workshop: Ultrasound. American Society of Anesthesiologists Annual Meeting. San Diego, CA.
- Chen, A., & Boyle, P. (2015, May). Cleft Palate and Malocclusion Presenting as Potential Difficult Airway in a Two Year Old Patient. Western Anesthesia Residents Conference. Seattle, WA.
- Boyle, P. K. (2014, October). The Use of Ultrasound for Regional Anesthesia. University of Arizona Health Care Network Health Segment.More infoUniversity of Arizona Health Care Network Health Segment. Televised on local television channels 10/2014-1/2015.
- Nielsen, V. G., Galvani, C. A., Boyle, P. K., Nielsen, V. G., Galvani, C. A., & Boyle, P. K. (2013, December 3). Obesity-Mediated Hypercoagulability: Role of Hemeoxygenase-1. IRB 13-0745.