Hemodynamic Orthostatic Dizziness/Vertigo: Diagnostic Criteria
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Orthostatic Intolerance V1 4.2.11, F10 Overview V2 6036-7,7038,7040,7042 Orthostatic Intolerance
NASA-STD-3001 Technical Brief Orthostatic Intolerance V1 4.2.11, F10 Overview V2 6036-7,7038,7040,7042 Orthostatic Intolerance Executive Summary Orthostatic intolerance (OI) is an abnormal response to standing upright caused by an inability to maintain arterial blood pressure and perfuse cerebral tissue. It can result in presyncope and, ultimately, syncope (i.e. loss of consciousness). Specifically in the spaceflight community, OI is a major concern when crewmembers are re-introduced to gravity after landing due to decreased plasma volume and sympathetic nervous system dysfunction. OI must also be considered for standing crew experiencing acceleration loads. A variety of countermeasures can be implemented to reduce the symptoms of and/or completely mitigate OI. Standards Overview NASA-STD-3001 Vol. 1 4.2.11 Fitness-for-Duty Orthostatic Hypotension Standard (with Appendix F.10) All approved countermeasures (fluid loading and compression garments) shall be utilized to mitigate symptoms of orthostatic hypotension (presyncopal/syncopal symptoms) to prevent impacts to performance of critical mission tasks. NASA-STD-3001 Vol. 2 6.3.2.8 Fluid Loading Water Quantity for Earth Entry [V2 6036] 6.3.2.9 Crew recovery Water Quantity [V2 6037] 7.4.1 Physiological Countermeasures Capability [V2 7038] The system shall provide countermeasures to meet crew bone, muscle, sensory-motor, and cardiovascular requirements defined in NASA-STD-3001, Vol. 1. 7.4.3 Physiological Countermeasure Operations [V2 7040] The physiological countermeasure system design shall allow the crew to unstow supplies, perform operations, and stow items within the allotted countermeasure schedule. 7.4.5 Orthostatic Intolerance Countermeasures [V2 7042] The system shall provide countermeasures to mitigate the effects of orthostatic intolerance when transitioning from microgravity to gravity environments. -
Control Study of Pregnancy Complications and Birth Outcomes
Hypertension Research (2011) 34, 55–61 & 2011 The Japanese Society of Hypertension All rights reserved 0916-9636/11 $32.00 www.nature.com/hr ORIGINAL ARTICLE Hypotension in pregnant women: a population-based case–control study of pregnancy complications and birth outcomes Ferenc Ba´nhidy1,Na´ndor A´ cs1, Erzse´bet H Puho´ 2 and Andrew E Czeizel2 Hypotension is frequent in pregnant women; nevertheless, its association with pregnancy complications and birth outcomes has not been investigated. Thus, the aim of this study was to analyze the possible association of hypotension in pregnant women with pregnancy complications and with the risk for preterm birth, low birthweight and different congenital abnormalities (CAs) in the children of these mothers in the population-based data set of the Hungarian Case–Control Surveillance of CAs, 1980–1996. Prospectively and medically recorded hypotension was evaluated in 537 pregnant women who later had offspring with CAs (case group) and 1268 pregnant women with hypotension who later delivered newborn infants without CAs (control group); controls were matched to sex and birth week of cases (in the year when cases were born), in addition to residence of mothers. Over half of the pregnant women who had chronic hypotension were treated with pholedrine or ephedrine. Maternal hypotension is protective against preeclampsia; however, hypotensive pregnant women were at higher risk for severe nausea or vomiting, threatened abortion (hemorrhage in early pregnancy) and for anemia. There was no clinically important difference in the rate of preterm births and low birthweight newborns in pregnant women with or without hypotension. The comparison of the rate of maternal hypotension in cases with 23 different CAs and their matched controls did not show a higher risk for CAs (adjusted OR with 95% confidence intervals: 0.66, 0.49–0.84). -
Neurocardiogenic Syncope and Associated Conditions: Insight Into Autonomic Nervous System Dysfunction
Türk Kardiyol Dern Arş - Arch Turk Soc Cardiol 2013;41(1):75-83 doi: 10.5543/tkda.2013.44420 75 Neurocardiogenic syncope and associated conditions: insight into autonomic nervous system dysfunction Nörokardiyojenik senkop ve ilişkili durumlar: Otonomik sinir sistemi işlev bozukluğuna bir bakış Antoine Kossaify, M.D., Kamal Kallab, M.D. Department of Syncope and Electrophysiology, ND Secours/USEK University Hospital, Byblos, Lebanon Summary– Neurocardiogenic syncope is known to be asso- Özet– Nörokardiyojenik senkopun mekanizması hala tam ola- ciated with autonomic nervous system dysfunction, although rak aydınlatılamamasına ragmen otonom sinir sistemi işlev the mechanism has not been entirely elucidated. In this study, bozukluğu ile ilişkili olduğu bilinmektedir. Bu yazıda nörokardi- we sought to highlight the pathogenic role of the autonomic yojenik senkop patogenezinde otonom sinir sisteminin rolünü nervous system in neurocardiogenic syncope and to review destekleyen en göze çarpıcı konuları araştırırken, temelinde the associated co-morbidities known to have a dysautonomic otonom sinir sistemi bozukluğunun olduğu bilinen komorbid basis. Herein we discuss migraine, orthostatic hypotension, durumları da gözden geçidik. Bu amaçla otonom sinir siste- postural orthostatic tachycardia syndrome, endothelial dys- minin patogenezdeki rolü ve klinik çıkarımları üzerine odak- function, chronic fatigue syndrome, and carotid sinus hyper- lanarak migren, ortostatik hipotansiyon, postüral ortostatik sensitivity with a focus on the pathogenic role of the autonom- taşikardi sendromu, endotel işlev bozukluğu, kronik yorgunluk ic nervous system and any consecutive clinical implications. sendromu ve karotis sinüs hipersensitivitesi tartışıldı. Tilt testi Other conditions, such as pre-syncopal heart rate acceleration sırasında ortaya çıkabilen senkop öncesi kalp atımlarında hız- and/or instability and pre-syncopal breathing instability, which lanma ve/veya instabilite ve senkop öncesi instabil solunum occur during a tilt test, are discussed in the same perspective. -
Ehlers-Danlos Syndrome and the Overlap with Orthostatic Intolerance
10/9/2014 Ehlers‐Danlos Syndrome Ehlers‐Danlos Syndrome and the Overlap with Orthostatic Intolerance • Heterogeneous disorder of connective tissue • Characterized by varying degrees of: October 9, 2014 Skin hyperextensibility Joint hypermobility Cutaneous fragility Peter C. Rowe, MD •Most forms of EDS result from mutations in genes Sunshine Natural Wellbeing Foundation Professor of encoding fibrillar collagens or the collagen‐ Chronic Fatigue and Related Disorders modifying enzymes Johns Hopkins University School of Medicine 1. Royce PM, Steinmann B, Superti‐Furga A. The Ehlers‐Danlos syndrome. In: Connective Tissue and its Heritable Baltimore, USA Disorders. New York: Wiley‐Liss, 1993: 351‐407. 2. de Paepe A, Malfait F. The Ehlers‐Danlos syndrome, a disorder with many faces. Clin Genetics 2012;82:1‐11. Presenter Disclosure Information Ehlers‐Danlos Syndrome Peter C. Rowe, MD • Prevalence unknown, estimated at 1:5000 •Because fibrillar collagen provides strength and structure to essentially all tissues and organs, EDS •No relationships to disclose has widespread clinical manifestations •Early varicose veins, easy bruising •Easy fatigability and widespread pain common Royce PM, Steinmann B, Superti‐Furga A. The Ehlers‐Danlos syndrome. In: Connective Tissue and its Heritable Disorders. New York: Wiley‐Liss, 1993: 351‐407. EDS, JH, and Orthostatic Intolerance Classification of EDS Beighton P, et al. Am J Med Genetics 1998;77:31‐7. Overview of Ehlers‐Danlos Syndrome Classical Illustrative case (formerly EDS I and II) Orthostatic intolerance in EDS and JH Hypermobility (formerly EDS III) Challenges Vascular (formerly EDS IV) Kyphoscoliosis Arthrochalasia 3 generations with Classical EDS. Note hemosiderin deposition in knees and Dermatosparaxis shins, varicose vein stripping on R 1 10/9/2014 de Paepe A, Malfait F. -
GP GUIDE to Pots (Postural Tachycardia Syndrome)
GP GUIDE TO PoTS (Postural Tachycardia Syndrome) 1 WHAT IS PoTS? PoTS was characterised in 1993, but previously existed under various other names including irritable heart, soldier’s heart and idiopathic orthostatic intolerance. It is a heterogeneous group of disorders sharing similar characteristics. On assuming upright posture, there is an excessive increase in heart rate associated with symptoms of orthostatic intolerance and sympathetic over-activity. There is brain hypoperfusion, usually in the absence of hypotension. When humans adopt upright posture, approximately 500ml of blood drops into the abdominal cavity and limbs. A normal autonomic nervous system responds with immediate peripheral vasoconstriction and an increase in heart rate of up to 20bpm. In POTS, it is considered that vasoconstriction is inadequate, resulting in pooling of blood, relative hypovolaemia and reduced venous return to the heart. Heart rate, inotropic status and, in some patients, catecholamine levels increase further to compensate. Dizziness and syncope can occur in the presence of normal BP; in fact some patients with PoTS have a hypertensive response to standing. HOW COMMON IS PoTS? The incidence in the UK is unknown. However, it is probably under-diagnosed due to lack of awareness and non-specific symptomatology. It is five times more common in women and tends to affect people age 15 to 50. 2 SYMPTOMS OF PoTS Dizziness GI upset Syncope / pre-syncope Sweating Orthostatic headache Nausea Fatigue Insomnia Poor memory Weakness Poor concentration Visual greying or blurring Sense of anxiety Acrocyanosis (purplish hands/feet) Exercise intolerance Palpitations (tachycardia / ectopics) Tremulousness Neck/shoulder pain (muscle ischaemia) Patients may have some or all of the above symptoms. -
What Is the Autonomic Nervous System?
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.suppl_3.iii31 on 21 August 2003. Downloaded from AUTONOMIC DISEASES: CLINICAL FEATURES AND LABORATORY EVALUATION *iii31 Christopher J Mathias J Neurol Neurosurg Psychiatry 2003;74(Suppl III):iii31–iii41 he autonomic nervous system has a craniosacral parasympathetic and a thoracolumbar sym- pathetic pathway (fig 1) and supplies every organ in the body. It influences localised organ Tfunction and also integrated processes that control vital functions such as arterial blood pres- sure and body temperature. There are specific neurotransmitters in each system that influence ganglionic and post-ganglionic function (fig 2). The symptoms and signs of autonomic disease cover a wide spectrum (table 1) that vary depending upon the aetiology (tables 2 and 3). In some they are localised (table 4). Autonomic dis- ease can result in underactivity or overactivity. Sympathetic adrenergic failure causes orthostatic (postural) hypotension and in the male ejaculatory failure, while sympathetic cholinergic failure results in anhidrosis; parasympathetic failure causes dilated pupils, a fixed heart rate, a sluggish urinary bladder, an atonic large bowel and, in the male, erectile failure. With autonomic hyperac- tivity, the reverse occurs. In some disorders, particularly in neurally mediated syncope, there may be a combination of effects, with bradycardia caused by parasympathetic activity and hypotension resulting from withdrawal of sympathetic activity. The history is of particular importance in the consideration and recognition of autonomic disease, and in separating dysfunction that may result from non-autonomic disorders. CLINICAL FEATURES c copyright. General aspects Autonomic disease may present at any age group; at birth in familial dysautonomia (Riley-Day syndrome), in teenage years in vasovagal syncope, and between the ages of 30–50 years in familial amyloid polyneuropathy (FAP). -
Have Already Been Described to Occur with Some
804 Letters, Correspondence, Book reviews have already been described to occur with Correspondence to: Dr D Michel, Service de Neu- some mutations. rologie, Hôpital de Bellevue, 42055 Saint-Etienne, There are only two previous reports Cedex 2, France. relating to three pairs of identical twins with CMT and known genetic defects. In the two 1 Goldsmith P, Rowe D, Jäger R, et al. Focal ver- pairs with the 17p11.2 duplication there was tebral artery dissection causing Brown- remarkable clinical variability.6 We have also Séquard’s syndrome. J Neurol Neurosurg Psy- seen a pair of identical twins with a P0 muta- chiatry 1998;64:415–16. 2 Gutowski NJ, Murphy RP, Beale DJ. Unilateral tion in whom there was marked variability in upper cervical posterior spinal artery syndrome early ages (unpublished data). Apart from the following sneezing. J Neurol Neurosurg Psychia- asymmetry of toe responses in one of the try 1992;55:841–3. probands, the genetically identical twins 3 Bergqvist CAG, Goldberg HI, Thorarensen O, et al. Posterior cervical spinal cord infarction described here are phenotypically very simi- following vertebral artery dissection. Neurology lar, suggesting that the expression of this 1997;48:1112–5. mutation was not influenced by other non- 4 Hundsberger T, Thömke F, Hopf HC, et al. genetic factors. Symmetrical infarction of the cervical spinal cord due to spontaneous bilateral vertebral Codon 39 seems to be of particular Sagittal T2 weighted MRI of the cervicodorsal artery dissection. Stroke 1998;29:1742. importance to Cx32 protein function as cord : high linear signal extending from C4 to 5 Masson C. -
Spinal Cord Injury Manual
Spinal Cord Injury Manual A publication of the Regional Spinal Cord Injury Center of the Delaware Valley The Regional Spinal Cord Injury Center of the Delaware Valley provides a comprehensive program of patient care, community education, and research. It is a federally designated program of Thomas Jefferson University and its affiliated institutions of Thomas Jefferson University Hospital and Magee Rehabilitation Hospital. JG 10-1325 Spinal Cord Injury Patient-Family Teaching Manual A Publication of the Regional Spinal Cord Injury Center of the Delaware Valley Researched and prepared by the clinical personnel of Thomas Jefferson University Hospital and Magee Rehabilitation Hospital Available online at: www.spinalcordcenter.org © 1993, 2001, 2009 Thomas Jefferson University. This publication is the property of Thomas Jefferson University. All rights reserved. This Manual is intended for use in a total system of care that meets all applicable CARF standards for SCI Centers. Neither Thomas Jefferson University Hospital, nor Magee Rehabilitation Hospital is responsible for any liability, claims, demands or damages asserted to be the result, either directly or indirectly, of the information contained herein. The use or reprinting of any part of this manual requires the express permission of Thomas Jefferson University. 3.11.10 3.11.10 Dedication The Handbook Committee of the RSCICDV gratefully acknowledges the assistance and dedication of all who contributed to this manual, and all the others who worked so hard to make this Handbook a reality. -
Orthostatic Hypotension in a Cohort of Hypertensive Patients Referring to a Hypertension Clinic
Journal of Human Hypertension (2015) 29, 599–603 © 2015 Macmillan Publishers Limited All rights reserved 0950-9240/15 www.nature.com/jhh ORIGINAL ARTICLE Orthostatic hypotension in a cohort of hypertensive patients referring to a hypertension clinic C Di Stefano, V Milazzo, S Totaro, G Sobrero, A Ravera, A Milan, S Maule and F Veglio The prevalence of orthostatic hypotension (OH) in hypertensive patients ranges from 3 to 26%. Drugs are a common cause of non-neurogenic OH. In the present study, we retrospectively evaluated the medical records of 9242 patients with essential hypertension referred to our Hypertension Unit. We analysed data on supine and standing blood pressure values, age, sex, severity of hypertension and therapeutic associations of drugs, commonly used in the treatment of hypertension. OH was present in 957 patients (10.4%). Drug combinations including α-blockers, centrally acting drugs, non-dihydropyridine calcium-channel blockers and diuretics were associated with OH. These pharmacological associations must be administered with caution, especially in hypertensive patients at high risk of OH (elderly or with severe and uncontrolled hypertension). Angiotensin-receptor blocker (ARB) seems to be not related with OH and may have a potential protective effect on the development of OH. Journal of Human Hypertension (2015) 29, 599–603; doi:10.1038/jhh.2014.130; published online 29 January 2015 INTRODUCTION stabilization, and then at 1 and 3 min after standing. The average of the Orthostatic hypotension (OH) is defined as the reduction in blood last two SBP and DBP values measured in the supine position and the pressure (BP) of at least 20 mmHg systolic and/or 10 mm Hg lowest value during standing were considered. -
Blood Pressure Management
Blood Pressure Management By Karen J. McConnell, Pharm.D., FCCP, BCPS-AQ Cardiology; and William L. Baker, Pharm.D., FCCP, FACC, BCPS, AQ-Cardiology Reviewed by Tyan F. Thomas, Pharm.D., BCPS; and Stacy L. Elder, Pharm.D., BCPS LEARNING OBJECTIVES 1. Distinguish key differences between various national and international hypertension (HTN) guidelines. 2. Demonstrate appropriate drug selection and blood pressure goals for the treatment of HTN according to the presence of concomitant conditions. 3. Devise an evidence-based treatment strategy for resistant HTN to achieve blood pressure goals. 4. Justify the use of ambulatory blood pressure monitoring. 5. Develop treatment strategies for hypertensive urgency and emergency. 6. Construct appropriate drug therapy plans for the treatment of hypotension. 7. Assess the potential effect of pharmacogenomics on blood pressure. EPIDEMIOLOGY ABBREVIATIONS IN THIS CHAPTER Hypertension (HTN) is a persistent, nonphysiologic elevation in blood ABPM Ambulatory blood pressure monitoring pressure; it is defined as (1) having a systolic blood pressure (SBP) ACE Angiotensin-converting enzyme of 140 mm Hg or greater; (2) having a diastolic blood pressure (DBP) AGT Angiotensinogen of 90 mm Hg or greater; (3) taking antihypertensive medication; or ARB Angiotensin receptor blocker (4) having been told at least twice by a physician or other health ASCVD Atherosclerotic cardiovascular professional that one has HTN. According to WHO, almost 1 billion disease people had uncontrolled HTN worldwide in 2008. The American Heart CAD Coronary artery disease Association (AHA) estimates that 41% of the U.S. population will have CCB Calcium channel blocker a diagnosis of HTN by 2030, an increase of 8.4% from 2012 estimates. -
Venous Thromboembolism: Lifetime Risk and Novel Risk Factors A
Venous Thromboembolism: Lifetime risk and novel risk factors A DISSERTATION SUBMITTED TO THE FACULTY OF THE GRADUATE SCHOOL OF THE UNIVERSITY OF MINNESOTA BY Elizabeth Jean Bell, M.P.H. IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY Adviser: Aaron R. Folsom, M.D., M.P.H. March 2015 © Elizabeth Jean Bell 2015 ACKNOWLEDGEMENTS This research was supported by a training grant in cardiovascular disease epidemiology and prevention, funded by the National Institutes of Health. This fellowship has significantly enhanced my doctoral training experience. I could not have completed this research without the support of a great many people. I would first like to thank my advisor, Aaron Folsom. Thank you for taking me on as a mentee, not only at the doctorate level, but also at the master’s level. Undoubtedly you were an influence in my choice to continue my education with a doctorate in the first place. I recognize and appreciate the countless hours you have spent teaching and guiding; thank you for your thorough comments, quick turnaround times, and for always challenging me to achieve. I have learned much from you, including a passion for research. A huge thank you to Pam Lutsey, who has served as an informal mentor to me throughout my master’s and doctorate programs. Thank you for a countless number of things, including guiding my data analyses back before I knew how to do data analyses, sharing your expertise on every paper I have led, and being a role model to aspire to. Thank you to Alvaro Alonso and Saonli Basu, who have each offered their expertise through serving on my doctoral committee. -
Summary of Pure Autonomic Failure
Downloaded from www.dysautonomiainternational.org Summary of Pure Autonomic Failure Pure Autonomic Failure (PAF) is a peripheral degenerative disorder of the autonomic nervous system (ANS).1 PAF was formerly known as Bradbury-Eggleston Syndrome, after the two researchers who first described it in 1925. PAF is also referred to as idiopathic orthostatic hypotension by some physicians.4,6 PAF is one of three diseases classified as a primary autonomic disorder, the other two being Multiple System Atrophy and Parkinson's Disease. Symptoms PAF usually affects more men than women, in middle to later life. However, it is occasionally seen in younger patients.1,2,6 PAF is characterized by orthostatic hypotension (low blood pressure upon standing), a low resting supine plasma noradrenaline concentration that does not increase significantly upon standing,2,3,4 a decreased ability to sweat, persistent neck pain that is often relieved when lying down, raised blood pressure while laying down, changes in urinary habits, and poor tolerance of high altitude. In men with PAF, impotence often occurs.1-6 What Causes PAF? Researchers are not certain of the underlying pathology of PAF yet, but at least in some cases, a loss of nerve cells in the spinal cord has been documented.1,2 Treatment Treatment often focuses on counteracting the effects of orthostatic hypotension, and supine hypertension, which can be difficult.5,6 Patients are often advised to increase fluid and salt intake, wear compression stockings, sleep with the head of their bed at an upright angle, and to use pharmacological options as directed by their physician.1,2,3 Prognosis The prognosis is good for PAF compared to other similar disorders, such as Multiple System Atrophy, with a slower progression and more lifestyle and pharmacological treatment options.1,2,3,4 Most PAF patients survive 20 years or more after diagnosis, many into their 80's.1 The cause of death is often recurrent infection or a pulmonary embolism.