DOCSLIB.ORG

Cerebral Autoregulation-Based Blood Pressure Management

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cerebral Autoregulation-Based Blood Pressure Management Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine January 2020 Cerebral Autoregulation-Based Blood Pressure Management In The Neuroscience Intensive Care Unit: Towards Individualizing Care In Ischemic Stroke And Subarachnoid Hemorrhage Andrew Silverman Follow this and additional works at: https://elischolar.library.yale.edu/ymtdl Recommended Citation Silverman, Andrew, "Cerebral Autoregulation-Based Blood Pressure Management In The Neuroscience Intensive Care Unit: Towards Individualizing Care In Ischemic Stroke And Subarachnoid Hemorrhage" (2020). Yale Medicine Thesis Digital Library. 3951. https://elischolar.library.yale.edu/ymtdl/3951 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. Cerebral autoregulation-based blood pressure management in the neuroscience intensive care unit Towards individualizing care in ischemic stroke and subarachnoid hemorrhage A Thesis Submitted to the Yale University School of Medicine in Partial Fulfillment of the Requirements for the Degree of Doctor of Medicine by Andrew Silverman Class of 2020 ABSTRACT The purpose of this thesis is to review the concept of cerebral autoregulation, to establish the feasibility of continuous bedside monitoring of autoregulation, and to examine the impact of impaired autoregulation on functional and clinical outcomes following subarachnoid hemorrhage and ischemic stroke. Autoregulation plays a key role in the regulation of brain blood flow and has been shown to fail in acute brain injury. Disturbed autoregulation may lead to secondary brain injury as well as worse outcomes. Furthermore, there exist several methodologies, both invasive and non-invasive, for the continuous assessment of autoregulation in individual patients. Resultant autoregulatory parameters of brain blood flow can be harnessed to derive optimal cerebral perfusion pressures, which may be targeted to achieve better outcomes. Multiple studies in adults and several in children have highlighted the feasibility of individualizing mean arterial pressure in this fashion. The thesis herein argues for the high degree of translatability of this personalized approach within the neuroscience intensive care unit, while underscoring the clinical import of autoregulation monitoring in critical care patients. In particular, this document recapitulates findings from two separate, prospectively enrolled patient groups with subarachnoid hemorrhage and ischemic stroke, elucidating how deviation from dynamic and personalized blood pressure targets associates with worse outcome in each cohort. While definitive clinical benefits remain elusive (pending randomized controlled trials), autoregulation-guided blood pressure parameters wield great potential for constructing an ideal physiologic environment for the injured brain. The first portion of this thesis discusses basic autoregulatory physiology as well as various tools to interrogate the brain’s pressure reactivity at the bedside. It then reviews the development of the optimal cerebral perfusion pressure as a biological hemodynamic construct. The second chapter pertains to the clinical applications of bedside neuromonitoring in patients with aneurysmal subarachnoid hemorrhage. In this section, the personalized approach to blood pressure monitoring is discussed in greater detail. Finally, in the third chapter, a similar autoregulation-oriented blood pressure algorithm is applied to a larger cohort of patients with ischemic stroke. This section contends that our novel, individualized strategy to hemodynamic management in stroke patients represents a better alternative to the currently endorsed practice of maintaining systolic blood pressures below fixed and static thresholds. ACKNOWLEDGMENTS This work would not have been possible without the leadership and encouragement of Dr. Nils Petersen. I could not have asked for a more insightful, creative, and patient mentor. It has been an extraordinary opportunity learn about physiology, critical care, and balancing research and clinical work from such a dedicated and kind role model. Many thanks also to our larger research team, which includes Sumita Strander, Sreeja Kodali, Alex Kimmel, Cindy Nguyen, Krithika Peshwe, and Anson Wang. Sumita and Sreeja, now first-year medial students at Harvard and Yale, respectively, were incredible teammates throughout my research year. They helped enroll patients, problem solve, and run new scripts. Their energy and friendship sustained me during some of the longer days (and nights) of neuromonitoring and abstract construction before midnight deadlines. More gratitude to my thesis committee and mentors in the Neurology Department, including Dr. Emily Gilmore, Dr. Kevin Sheth, Dr. Charles Wira, and Dr. Charles Matouk. In particular, Dr. Gilmore volunteered her time to adjudicate clinical and radiologic scores for over 30 patients with subarachnoid hemorrhage. Many thanks overall to the Divisions of Vascular Neurology and Neurocritical Care for hosting me and providing me with a suitable workspace for an entire year. Thank you to Yale’s amazing Office of Student Research: Donna Carranzo, Kelly Jo Carlson, Reagin Carney, and Dr. John Forrest. Without their coordination efforts and sponsorship, I would not have been able to obtain funding from the American Heart Association, practice presenting my work at research in progress meetings, or learn about my peers’ awesome project developments – not to mention all the coffee and snacks they provided. Much gratitude, as always, to my grandma, my mom, my older brother, and to Lauren. Although they are not in the medical field and will probably never read this thesis, they have continually been enthusiastic and unconditionally supportive. Finally, I would like to thank the patients and families who volunteered to participate in our studies. Research reported in this publication was supported by the American Heart Association (AHA) Founders Affiliate training award for medical students as well as the Richard A. Moggio Student Research Fellowship from Yale. TABLE OF CONTENTS PART I ................................................................................................................................1 A. Introduction: a brief history of autoregulation research ...........................................1 B. Cerebral blood flow regulation and physiology........................................................8 C. Methods to measure cerebral autoregulation ..........................................................17 D. Autoregulation indices and signal processing.........................................................22 E. Comparisons between autoregulatory indices ........................................................28 F. Optimal cerebral perfusion pressure .......................................................................29 PART II.............................................................................................................................37 A. Subarachnoid hemorrhage ......................................................................................37 B. Clinical relevance of autoregulation following subarachnoid hemorrhage ............45 C. Pilot study on autoregulation monitoring in subarachnoid hemorrhage .................51 D. Results of the subarachnoid hemorrhage pilot study ..............................................65 E. Discussion ...............................................................................................................89 PART III ...........................................................................................................................95 A. Large-vessel occlusion (LVO) ischemic stroke ......................................................95 B. Clinical relevance of autoregulation following ischemic stroke .............................99 C. Pilot study on autoregulation monitoring in ischemic stroke ...............................103 D. Results of the ischemic stroke pilot study.............................................................111 E. Discussion .............................................................................................................122 PART IV .........................................................................................................................131 A. Concluding remarks and future studies.................................................................131 References .......................................................................................................................138 LIST OF PUBLICATIONS AND ABSTRACTS Peer-reviewed original investigations 1. Silverman A , Kodali S, Strander S, Gilmore E, Kimmel A, Wang A, Cord B, Falcone G, Hebert R, Matouk C, Sheth KN, Petersen NH. Deviation from personalized blood pressure targets is associated with worse outcome after subarachnoid hemorrhage . Stroke 2019 Oct;50(10):2729-37. 2. Silverman A* , Petersen NH*, Wang A, Strander S, Kodali S, Matouk C, Sheth KN. Exceeding Association of Personalized Blood Pressure Targets With Hemorrhagic Transformation and Functional Outcome After Endovascular Stroke Therapy . JAMA Neurology. 2019 Jul 29. doi:
Load more

Recommended publications
  • Baroreflex and Cerebral Autoregulation Are Inversely
    2460 NASR N et al. Circulation Journal ORIGINAL ARTICLE Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Hypertension and Circulatory Control Baroreflex and Cerebral Autoregulation Are Inversely Correlated Nathalie Nasr, MD, PhD; Marek Czosnyka, PhD; Anne Pavy-Le Traon, MD, PhD; Marc-Antoine Custaud, MD, PhD; Xiuyun Liu, BSc; Georgios V. Varsos, BSc; Vincent Larrue, MD Background: The relative stability of cerebral blood flow is maintained by the baroreflex and cerebral autoregulation (CA). We assessed the relationship between baroreflex sensitivity (BRS) and CA in patients with atherosclerotic carotid stenosis or occlusion. Methods and Results: Patients referred for assessment of atherosclerotic unilateral >50% carotid stenosis or oc- clusion were included. Ten healthy volunteers served as a reference group. BRS was measured using the sequence method. CA was quantified by the correlation coefficient (Mx) between slow oscillations in mean arterial blood pres- sure and mean cerebral blood flow velocities from transcranial Doppler. Forty-five patients (M/F: 36/9), with a me- dian age of 68 years (IQR:17) were included. Thirty-four patients had carotid stenosis, and 11 patients had carotid occlusion (asymptomatic: 31 patients; symptomatic: 14 patients). The median degree of carotid steno-occlusive disease was 90% (IQR:18). Both CA (P=0.02) and BRS (P<0.001) were impaired in patients as compared with healthy volunteers. CA and BRS were inversely and strongly correlated with each other in patients (rho=0.58, P<0.001) and in healthy volunteers (rho=0.939; P<0.001). Increasing BRS remained strongly associated with im- paired CA on multivariate analysis (P=0.004).
    [Show full text]
  • Njit-Etd1997-108
    Copyright Warning & Restrictions The copyright law of the United States (Title 17, United States Code) governs the making of photocopies or other reproductions of copyrighted material. Under certain conditions specified in the law, libraries and archives are authorized to furnish a photocopy or other reproduction. One of these specified conditions is that the photocopy or reproduction is not to be “used for any purpose other than private study, scholarship, or research.” If a, user makes a request for, or later uses, a photocopy or reproduction for purposes in excess of “fair use” that user may be liable for copyright infringement, This institution reserves the right to refuse to accept a copying order if, in its judgment, fulfillment of the order would involve violation of copyright law. Please Note: The author retains the copyright while the New Jersey Institute of Technology reserves the right to distribute this thesis or dissertation Printing note: If you do not wish to print this page, then select “Pages from: first page # to: last page #” on the print dialog screen The Van Houten library has removed some of the personal information and all signatures from the approval page and biographical sketches of theses and dissertations in order to protect the identity of NJIT graduates and faculty. ABSTRACT COMPUTER SIMULATION OF CEREBROVASCULAR CIRCULATION. ASSESSMENT OF INTRACRANIAL HEMODYNAMICS DURING INDUCTION OF ANESTHESIA. by Steven D. Wolk The purpose of this project was to develop a computer model of cerebrovascular hemodynamics interacting with a pharmacokinetic drug model to examine the effects of various stimuli during anesthesia on cerebral blood flow and intracranial pressure.
    [Show full text]
  • Cerebral Pressure Autoregulation in Traumatic Brain Injury
    Neurosurg Focus 25 (4):E7, 2008 Cerebral pressure autoregulation in traumatic brain injury LEONARDO RANGE L -CASTIL L A , M.D.,1 JAI M E GAS C O , M.D. 1 HARING J. W. NAUTA , M.D., PH.D.,1 DAVID O. OKONK W O , M.D., PH.D.,2 AND CLUDIAA S. ROBERTSON , M.D.3 1Division of Neurosurgery, University of Texas Medical Branch, Galveston; 3Department of Neurosurgery, Baylor College of Medicine, Houston, Texas; and 2Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregula- tion is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperven- tilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.
    [Show full text]
  • Regulation of the Cerebral Circulation: Bedside Assessment and Clinical Implications Joseph Donnelly1, Karol P
    Donnelly et al. Critical Care 2016, 18: http://ccforum.com/content/18/6/ REVIEW Open Access Regulation of the cerebral circulation: bedside assessment and clinical implications Joseph Donnelly1, Karol P. Budohoski1, Peter Smielewski1 and Marek Czosnyka1,2* Abstract Regulation of the cerebral circulation relies on the complex interplay between cardiovascular, respiratory, and neural physiology. In health, these physiologic systems act to maintain an adequate cerebral blood flow (CBF) through modulation of hydrodynamic parameters; the resistance of cerebral vessels, and the arterial, intracranial, and venous pressures. In critical illness, however, one or more of these parameters can be compromised, raising the possibility of disturbed CBF regulation and its pathophysiologic sequelae. Rigorous assessment of the cerebral circulation requires not only measuring CBF and its hydrodynamic determinants but also assessing the stability of CBF in response to changes in arterial pressure (cerebral autoregulation), the reactivity of CBF to a vasodilator (carbon dioxide reactivity, for example), and the dynamic regulation of arterial pressure (baroreceptor sensitivity). Ideally, cerebral circulation monitors in critical care should be continuous, physically robust, allow for both regional and global CBF assessment, and be conducive to application at the bedside. Regulation of the cerebral circulation is impaired not only in primary neurologic conditions that affect the vasculature such as subarachnoid haemorrhage and stroke, but also in conditions that affect the regulation of intracranial pressure (such as traumatic brain injury and hydrocephalus) or arterial blood pressure (sepsis or cardiac dysfunction). Importantly, this impairment is often associated with poor patient outcome. At present, assessment of the cerebral circulation is primarily used as a research tool to elucidate pathophysiology or prognosis.
    [Show full text]
  • Arterial Baroreflex Regulation of Cerebral Blood Flow in Humans
    J Phys Fitness Sports Med, 1(4): 631-636 (2012) JPFSM: Review Article Arterial baroreflex regulation of cerebral blood flow in humans Shigehiko Ogoh1*, Ai Hirasawa1 and James P. Fisher2 1 Department of Biomedical Engineering, Toyo University, 2100 Kujirai, Kawagoe-shi, Saitama 350-8585, Japan 2 School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, West Midlands B15 2TT UK Received: October 12, 2012 / Accepted: November 19, 2012 Abstract The arterial baroreflex plays an essential role in the short-term regulation of arterial blood pressure, and thus helps ensure that the vital organs are adequately perfused. For stand- ing humans, appropriate arterial baroreflex control of cardiac output and vasomotor tone are particularly important for cerebral blood flow regulation. However, the numerous mechanisms implicated in the regulation of the cerebral vasculature (e.g. cerebral autoregulation, carbon dioxide reactivity) mean that the precise nature of the direct and indirect effects of the arterial baroreflex on cerebral blood flow regulation are highly complex and remain incompletely un- derstood. This review paper provides an update on recent insights into the influence of the arte- rial baroreflex on cerebral circulation. Keywords : arterial blood pressure, cardiac output, cerebral autoregulation, cerebral CO2 reactiv- ity, autonomic nervous system control cerebral vascular resistance3). Introduction The concept that CA is a powerful mechanism of blood Adequate oxygen delivery is essential for the mainte- flow regulation in the brain has become well established. nance of cerebral function, and a loss of consciousness However, in the early studies of Lassen (1959), the CA rapidly results from inadequate cerebral perfusion and curve relating CBF to MAP was derived from eleven oxygen delivery.
    [Show full text]
  • Cardiovascular Physiology
    Dr Matthew Ho BSc(Med) MBBS(Hons) FANZCA Cardiovascular Physiology Electrical Properties of the Heart Physiol-02A2/95B4 Draw a labelled diagram of a cardiac action potential highlighting the sequence of changes in ionic conductance. Explain the terms 'threshold', 'excitability', and 'irritability' with the aid of a diagram. 1. Cardiac muscle contraction is electrically activated by an action potential, which is a wave of electrical discharge that travels along the cell membrane. Under normal circumstances, it is created by the SA node, and propagated to the cardiac myocytes through gap junctions (intercalated discs). 2. Cardiac action potential: a. Phase 4 – resting membrane potential: i. Usually -90mV ii. Dependent mostly on potassium permeability, and gradient formed from Na-K ATPase pump b. Phase 0 - -90mV-+20mV i. Generated by the opening of fast Na channels Na into cell potential inside rises > 65mV (threshold potential) positive feedback further Na channel opening action potential ii. Threshold potential also triggers opening Ca channels (L type) at -10mV iii. Reduced K permeability c. Phase 1 – starts + 20mV i. The positive AP causes rapid closure of fast Na channels transient drop in potential d. Phase 2 – plateau i. Maximum permeability of Ca through L type channels ii. Rising K permeability iii. Maintenance of depolarisation e. Phase 3 – repolarisation i. Na, Ca and K conductance returns to normal ii. Ca. Na channels close, K channels open 3. Threshold: the membrane potential at which an AP occurs a. Usually-65mV in the cardiac cell b. AP generated via positive feedback Na channel opening 4. Excitability: the ease with which a myocardial cell can respond to a stimulus by depolarising.
    [Show full text]
  • Assessment of Cerebral Autoregulation Indices
    www.nature.com/scientificreports OPEN Assessment of cerebral autoregulation indices – a modelling perspective Xiuyun Liu1,2 ✉ , Marek Czosnyka1,3, Joseph Donnelly 1,4, Danilo Cardim1,5, Manuel Cabeleira1, Despina Aphroditi Lalou 1, Xiao Hu6, Peter J. Hutchinson1 & Peter Smielewski 1 Various methodologies to assess cerebral autoregulation (CA) have been developed, including model - based methods (e.g. autoregulation index, ARI), correlation coefcient - based methods (e.g. mean fow index, Mx), and frequency domain - based methods (e.g. transfer function analysis, TF). Our understanding of relationships among CA indices remains limited, partly due to disagreement of diferent studies by using real physiological signals, which introduce confounding factors. The infuence of exogenous noise on CA parameters needs further investigation. Using a set of artifcial cerebral blood fow velocities (CBFV) generated from a well-known CA model, this study aims to cross-validate the relationship among CA indices in a more controlled environment. Real arterial blood pressure (ABP) measurements from 34 traumatic brain injury patients were applied to create artifcial CBFVs. Each ABP recording was used to create 10 CBFVs corresponding to 10 CA levels (ARI from 0 to 9). Mx, TF phase, gain and coherence in low frequency (LF) and very low frequency (VLF) were calculated. The infuence of exogenous noise was investigated by adding three levels of colored noise to the artifcial CBFVs. The result showed a signifcant negative relationship between Mx and ARI (r = −0.95, p < 0.001), and it became almost purely linear when ARI is between 3 to 6. For transfer function parameters, ARI positively related with phase (r = 0.99 at VLF and 0.93 at LF, p < 0.001) and negatively related with gain_VLF(r = −0.98, p < 0.001).
    [Show full text]
  • Effect of Cerebral Flow Autoregulation Function on Cerebral Flow Rate Under Continuous Flow Left Ventricular Assist Device Support
    Artificial Organs Effect of Cerebral Flow Autoregulation Function on Cerebral Flow Rate under Continuous Flow Left Ventricular Assist Device Support Journal: Artificial Organs Manuscript ID AO-00391-2017.R1 Manuscript Type: Main Text left ventricular assist device, CF-LVAD, cerebral flow, cerebral Keywords: autoregulatory function LVAD, IABP < Total Artificial Heart/Cardiac & Circulatory Assistance , Specialty/Area of Expertise: Biomedical Engineering, Engineering (Chem/Elec/Mech), Physics, Physiology Page 1 of 38 Artificial Organs 1 2 3 1 Effect of Cerebral Flow Autoregulation Function on Cerebral Flow Rate under 4 5 6 2 Continuous Flow Left Ventricular Assist Device Support 7 8 3 Abstract 9 10 11 4 Neurological complications in Continuous Flow Left Ventricular Assist Device (CF-LVAD) 12 13 5 patients are the second-leading risk of death after multi-organ failure. They are 14 15 16 6 associated with altered blood flow in the cardiovascular system because of CF-LVAD 17 18 7 support. Moreover, an impaired cerebral autoregulation function may also contribute to 19 20 8 complications such as hyperperfusion in the cerebral circulation under mechanical 21 22 9 23 circulatory support. The aim of this study is to evaluate the effect of cerebral 24 25 10 autoregulatory function on cerebral blood flow rate under CF-LVAD support. A lumped 26 27 11 parameter model was used to simulate the cardiovascular system including the heart 28 29 12 chambers, heart valves, systemic and pulmonary circulations and cerebral circulation 30 31 32 13 which includes entire Circle of Willis. A baroreflex model was used to regulate the 33 34 14 systemic arteriolar and cerebral vascular resistances and a model of the Micromed CF- 35 36 15 LVAD was used to simulate the pump dynamics at different operating speeds.
    [Show full text]
  • Review Course Lectures
    Review Course Lectures International Anesthesia Research Society IARS 2011 REVIEW COURSE LECTURES The material included in the publication has not undergone peer review or review by the Editorial Board of Anesthesia and Analgesia for this publication. Any of the material in this publication may have been transmitted by the author to IARS in various forms of electronic medium. IARS has used its best efforts to receive and format electronic submissions for this publication but has not reviewed each abstract for the purpose of textual error correction and is not liable in any way for any formatting, textual, or grammatical error or inaccuracy. 2 ©2011 International Anesthesia Research Society. Unauthorized Use Prohibited IARS 2011 REVIEW COURSE LECTURES Table of Contents Perioperative Implications of Emerging Concepts In Management of the Malignant Hyperthermia Vascular Aging, Health And Disease Patient In Ambulatory Surgery Charles W. Hogue, MD ..............................1 Denise J. Wedel, MD ...............................38 Professor of Anesthesiology and Professor of Anesthesiology, Mayo Clinic Critical Care Medicine Rochester, Minnesota Chief, Division of Adult Anesthesia The Johns Hopkins University School of Medicine, Central Venous Access Guideline The Johns Hopkins Hospital Development and Recommendations Baltimore, Maryland Stephen M. Rupp, MD ..............................41 Anesthesiologist Perioperative Management of Pain and PONV in Medical Director, Perioperative Services Ambulatory Surgery Virginia Mason Medical Center, Seattle, Washington Spencer S. Liu, MD .................................5 Clinical Professor of Anesthesiology Pediatric Anesthesia and Analgesia Outside the OR: Director of Acute Pain Service What You Need To Know Hospital for Special Surgery Pierre Fiset, MD, FRCPC............................47 New York, New York Department Head, Anesthesiology Montreal Children’s Hospital Colloid or Crystalloid: Any Differences In Outcomes? Montreal, Quebec, Canada Tong J.
    [Show full text]
  • Medical Physiology of the Cardiovascular System October 10
    Medical Physiology of the Cardiovascular System HAPS Institute Graduate Credit Course offered in conjunction with Alverno College October 7 to December 7, 2020 Instructor: Patrick Eggena, M.D. Novateur Medmedia, LLC 39 Terry Hill Road Carmel, NY 10512 [email protected] Class size: 3-7 Graduate Credits: 3 Prerequisite: Human Physiology Description of the course: This course in Medical Physiology of the Cardiovascular System is primarily for HAPS professors who teach pre-medical, medical, or nurse practitioner students. It is a self- study course where participants attend 13 hours of live video-lectures by Dr. Eggena in cardiovascular physiology and read pertinent information related to the lectures. After the lecture series students follow Dr. Eggena on his 16-hour night tour at a hospital where they apply the physiology learned in class to patient care in the emergency room and at the patient’s bedside. Participants taking the course for graduate credits are given a 2-hour proctored examination with 60 true/false and 4 graphic essay questions. The following iBooks are required for this course: 1. Lectures in Cardiovascular Physiology by Patrick Eggena, M.D. Apple iBooks ($10) 2. Physiology Correlates of a Physician’s Diary by Patrick Eggena, M.D. Apple iBooks ($9). 3. Medical Physiology of the Heart-Lung-Kidney by Patrick Eggena, M.D. Apple iBooks ($15). Syllabus A. From: ‘Lectures in Cardiovascular Physiology’ by Patrick Eggena M.D. Apple iBooks. Instructions 1. (1) Watch: Cardiac Electrophysiology: In this 1-hour video-lecture Dr. Eggena gives an overview of the cardiovascular system and considers cardiac action potentials.
    [Show full text]
  • Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's
    Journal of Alzheimer’s Disease 46 (2015) 35–53 35 DOI 10.3233/JAD-142976 IOS Press Review CORE Metadata, citation and similar papers at core.ac.uk Provided by SZTE Publicatio Repozitórium - SZTE - Repository of Publications Is Vasomotion in Cerebral Arteries Impaired in Alzheimer’s Disease? Luigi Yuri Di Marcoa,∗, Eszter Farkasb, Chris Martinc, Annalena Vennerid,e and Alejandro F. Frangia aCentre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK bDepartment of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Szeged, Hungary cDepartment of Psychology, University of Sheffield, Sheffield, UK dDepartment of Neuroscience, University of Sheffield, Sheffield, UK eIRCCS, Fondazione Ospedale S. Camillo, Venice, Italy Handling Associate Editor: Mauro Silvestrini Accepted 11 February 2015 Abstract. A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer’s disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this path- way. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-␤ (A␤) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter dam- age. Vasomotion—the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brain—is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia.
    [Show full text]
  • Different Effects of Various Vasodilators on Autoregulation of Renal Blood Flow in Anesthetized Dogs
    Different Effects of Various Vasodilators on Autoregulation of Renal Blood Flow in Anesthetized Dogs Nobuyuki OGAWA and Hiroshi ONO Department of Pharmacology and Toxicology, Hatano Research Institute, Food and Drug Safety Center, 729-5 Ochiai, Hadano, Kanagawa 257, Japan Accepted March 24, 1986 Abstract-In order to examine whether the autoregulation of renal blood flow is equally influenced by all kinds of vasodilators, kidney perfusion experiments were performed in anesthetized dogs. The perfused kidney usually showed excellent autoregulation of blood flow over the perfusion pressure between 120 and 200 mmHg. Renal blood flow was increased by the renal arterial infusion of diltiazem (100 /cg/min), papaverine (10 mg/min) or nicorandil (300 ig/min) (at the basal perfusion pressure of 100 mmHg) and was maintained at an increased level while the infusion was continued. On the other hand, renal blood flow was increased only transiently by the infusion of nitroglycerin (50 ,ug/min), and the blood flow gradually decreased to the basal level in spite of the continuous infusion. Infusions of diltiazem and papaverine abolished the autoregulation of renal blood flow besides the vasodilator effect, but infusions of nitroglycerin and nicorandil have no effect on the autoregulation. Furthermore, sodium nitroprusside (30 /~g/min) and sodium nitrite (5 mg/min), which are assumed to produce vasodilation through cyclic GMP, also have no effect on the autoregulation of renal blood flow. In conclusion, all the vasodilators do not influence the renal blood flow autoregulation , and vasodilation caused by cyclic GMP is unconnected with the myogenic mechanism regulating the renal blood flow. The autoregulation of renal blood flow is renal blood flow.
    [Show full text]