Summary of Syncopal Disorders
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IAEM Syncope
IAEM Clinical Guideline Management of syncope in the emergency department Version 1 April, 2019 Authors: Dr Áine Mitchell, in collaboration with Dr Rosa McNamara, Professor Rose Anne Kenny and the IAEM Guideline Development Committee. DISCLAIMER IAEM recognises that patients, their situations, Emergency Departments and staff all vary. These guidelines cannot cover all clinical scenarios. The ultimate responsibility for the interpretation and application of these guidelines, the use of current information and a patient's overall care and wellbeing resides with the treating clinician. GLOSSARY OF TERMS AAA: Abdominal aortic aneurysm AFib: Atrial fibrillation ARVC: Arrythmogenic right ventricular cardiomyopathy AV: Atrioventricular βHCG: Beta human chorionic gonadotropin BP: Blood pressure BSL: Blood sugar level CCF: Congestive cardiac failure CM: Cardiomyopathy ECG: Electrocardiogram ED: Emergency Department EF: Ejection fraction ESC: European Society of Cardiology FHx: Family history GI: Gastrointestinal GP: General practitioner HCT: Haematocrit HOCM: Hypertrophic obstructive cardiomyopathy Hx: History IAEM: Irish Association for Emergency Medicine ICD: Implanted cardioverter defibrillator IHD: Ischaemic heart disease MI: Myocardial Infarction OPD: Out-patient department PCM: Physical counter-pressure manoeuvres PE: Pulmonary embolus PMHx: Past Medical History PPM: Permanent pacemaker RSA: Road safety authority SAH: Sub-arachnoid haemorrhage SBP: Systolic blood pressure SCD: Sudden cardiac death SVT: Supra-ventricular tachycardia TIA: Transient ischaemic attack T-LOC: Transient loss of consciousness VT: Ventricular tachycardia WPW: Wolff-Parkinson-White 2 IAEM CG: Management of syncope in the emergency department Version 1 April 2019 INTRODUCTION Syncope is defined as a transient loss of consciousness (T-LOC) due to cerebral hypoperfusion. It is characterised by a rapid onset, short duration and spontaneous complete recovery. -
Stroke Mimics and Chameleons: Quandaries in the Field
Stroke Mimics and Chameleons: Quandaries in the Field Madeleine Geraghty, MD Rockwood Multicare What’s the difference Stroke mimic: Looks like a stroke, is something else Stroke chameleon: Looks like something else, is really a stroke! Scope of the Mimic Recent eval by Briard, et al: ◦ 960 patients transported by EMS during an 18 month period ◦ 42% mimics 55% other neurologic diagnoses 20% seizures, 19% migraines, 11% peripheral neuropathies 45% non-neurologic diagnoses Cardiac 16%, psychiatric 12%, infectious 9% ◦ Neurologic mimics were younger (~64 years) than non-neurologic mimics (~70 years) Entering a new era Large vessel occlusions Now a 24 hour time window for mechanical thrombectomy ◦ Most centers will likely activate the > 6 hour patients from within the ED, still working out those details Volume of stroke mimics/chameleons in the new time window? Effects on resource management? ◦ At the hospital level? ◦ At the regional level with distance transports? Need Emergency Responder Impressions now more than ever in order to learn for the future!! General Principles Positive symptoms Indicate an excess of central nervous system neuron electrical discharges Visual: flashing lights, zig zag shapes, lines, shapes, objects sensory: paresthesia, pain motor: jerking limb movements Migraine, Seizure are characterized with having “positive” symptoms Negative symptoms Indicate a loss or reduction of central nervous system neuron function – loss of vision, hearing, sensation, limb power. TIA/Stroke present with “negative” symptoms. -
Syncope Fainting, Or Syncope, Is the Sudden Loss of Consciousness and Ability to Stand
Northwestern Memorial Hospital Patient Education CONDITIONS AND DISEASES Syncope Fainting, or syncope, is the sudden loss of consciousness and ability to stand. It is also called “passing out.” This common If you have any problem is the cause of many falls and injuries. One third of people faint at least once during their life. Syncope may occur questions, ask without warning or can be signaled by: ■ Feelings of weakness your physician ■ Feeling hot or sweating ■ Dizziness or nurse. ■ Visual changes ■ Nausea ■ Palpitations Causes of syncope Fainting is due to a sudden decrease in blood flow and oxygen to the brain. There are many causes of syncope, but most fall into 1 of 3 major types. Abnormal nerve reflex Nerves that control heart rate, blood pressure and other body functions may respond in an abnormal way and cause syncope. This can be triggered by: ■ Standing ■ Pain ■ Unpleasant sight or smell ■ Stress, anxiety or emotional distress ■ Coughing, sneezing or swallowing ■ Urinating or having a bowel movement Fainting due to an abnormal nerve reflex is more likely to occur under certain conditions, such as dehydration, viral infection, after prolonged bed rest or a lack of sleep or regular food intake. Types of syncope that involve an abnormal nerve reflex include: ■ Vasovagal (neurocardiac) syncope is the most common type and can occur at any age. It often occurs when blood pools in the leg veins. This triggers a reflex where the heart rate, blood pressure or both may suddenly fall. It generally is not a dangerous condition and can be prevented by avoiding situations that can trigger syncope. -
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. -
Syncope in Adults: Systematic Review and Proposal of a Diagnostic and Therapeutic Algorithm
International Journal of Cardiology 162 (2013) 149–157 Contents lists available at SciVerse ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard Review Syncope in adults: Systematic review and proposal of a diagnostic and therapeutic algorithm Salvatore Rosanio a,⁎, Ernst R. Schwarz b, David L. Ware c, Antonio Vitarelli d a University of North Texas Health Science Center (UNTHSC) Department of Internal Medicine, Division of Cardiology 855 Montgomery Street 76107 Fort Worth, TX, United States b Cardiology Division, Cedars Sinai Medical Center, Los Angeles, CA, United States c Cardiology Division, University of Texas Medical Branch, Galveston, TX, United States d Cardio-Respiratory Department, La Sapienza University, Rome, Italy article info abstract Article history: This review aims to provide a practical and up-to-date description on the relevance and classification of syncope Received 19 June 2011 in adults as well as a guidance on the optimal evaluation, management and treatment of this very common clin- Received in revised form 28 October 2011 ical and socioeconomic medical problem. We have summarized recent active research and emphasized the value Accepted 24 November 2011 for physicians to adhere current guidelines. A modern management of syncope should take into account 1) use of Available online 20 December 2011 risk stratification algorithms and implementation of syncope management units to increase the diagnostic yield and reduce costs; 2) early implantable loop recorders rather than late in the evaluation of unexplained syncope; Keywords: fi Syncope and 3) isometric physical counter-pressure maneuvers as rst-line treatment for patients with neurally- Pacing mediated reflex syncope and prodromal symptoms. -
Latest Diagnostic and Treatment Strategies for the Congenital Long QT Syndromes
Latest Diagnostic and Treatment Strategies for the Congenital Long QT Syndromes Michael J. Ackerman, MD, PhD Windland Smith Rice Cardiovascular Genomics Research Professor Professor of Medicine, Pediatrics, and Pharmacology Director, Long QT Syndrome Clinic and the Mayo Clinic Windland Smith Rice Sudden Death Genomics Laboratory President, Sudden Arrhythmia Death Syndromes (SADS) Foundation Learning Objectives to Disclose: • To RECOGNIZE the “faces” (phenotypes) of the congenital long QT syndromes (LQTS) • To CRITIQUE the various diagnostic modalities used in the evaluation of LQTS and UNDERSTAND their limitations • To ASSESS the currently available treatment options for the various LQT syndromes and EVALUATE their efficacy WINDLAND Smith Rice Sudden Death Genomics Laboratory Conflicts of Interest to Disclose: • Consultant – Boston Scientific, Gilead Sciences, Medtronic, St. Jude Medical, and Transgenomic/FAMILION • Royalties – Transgenomic/FAMILION Congenital Long QT Syndrome Normal QT interval QT QT Prolonged QT 1. Syncope 2. Seizures 3. Sudden death Torsades de pointes Congenital Long QT Syndrome Normal QT interval QT QT ♥ 1957 – first clinical description – JLNS ♥ 1960s – RomanoProlonged-Ward QT syndrome ♥ 1983 – “Schwartz/Moss score”1. Syncope ♥ 1991 – first LQTS chromosome locus 2. Seizures ♥ March 10, 1995 – birth of cardiac 3. Sudden channelopathies death Torsades de pointes Congenital Long QT Syndrome Normal QT interval QT QT Prolonged QT 1. Syncope 2. Seizures 3. Sudden death Torsades de pointes Congenital Long QT Syndrome Normal -
STARS Reflex Syncope (VVS) Booklet.Indd
Reflex Syncope (Vasovagal Syncope) Working together with individuals, families and medical professionals to off er support and information on syncope and refl ex anoxic seizures www.stars.org.ukRegistered Charity No. 1084898 Registered Charity No. 1084898 Glossary of terms Refl ex syncope Refl ex syncope is a transient condition resulting from intermittent dysfunction of the autonomic nervous Contents system, which regulates blood pressure and heart rate. 12-lead ECG What is refl ex 12-lead electrocardiogram (ECG) is used to record heart syncope? rhythms whilst in hospital. Heart rhythm monitor What are the Heart rhythm monitors are used to record heart rhythms symptoms? for up to a week whilst away from hospital. ILR How do I obtain a Implantable loop recorder (ILR) is a small thin device diagnosis? inserted under the skin to record heart rhythms. The device can remain in place for up to three years. What should I do if I Tilt table test feel dizzy or faint? A tilt table test is an autonomic test used to induce an attack whilst connected to heart and blood pressure What should my monitors. friends/family do Collapse if I faint? Abrupt loss of postural control Blackout/T-LoC What can I do to Transient loss of consciousness without neurological prevent syncope defi cit attacks? Syncope T-LoC due to transient global impairment of cerebral Are there any other perfusion treatments? Epilepsy Repeated episodes of excessive asynchronous discharge Driving and refl ex of cortical neurones leading to a clinical event syncope Psychogenic blackouts A cause of apparent blackouts without evidence of Flying and refl ex syncope or epilepsy syncope Fall Patient goes down freely under the infl uence of gravity Misdiagnosis TIA TIA (transient ischaemic attack) is caused by a temporary disruption in the blood supply to part of the brain (also known as a mini stroke) 2 What is reflex syncope? SYNCOPE (sin-co-pee) is a medical term for a This booklet is blackout caused by a sudden lack of blood supply designed for to the brain. -
Reflex Syncope in Children and Adolescents, Its Tclinical Characteristics and Syndromes, the Approach to Diagnosis, and Finally Treatment
Congenital heart disease REFLEX SYNCOPE IN CHILDREN AND Heart: first published as 10.1136/hrt.2003.022996 on 13 August 2004. Downloaded from ADOLESCENTS 1094 Wouter Wieling, Karin S Ganzeboom, J Philip Saul Heart 2004;90:1094–1100. doi: 10.1136/hrt.2003.022996 his article will address the epidemiology of reflex syncope in children and adolescents, its Tclinical characteristics and syndromes, the approach to diagnosis, and finally treatment. c EPIDEMIOLOGY Syncope can be defined as a temporary loss of consciousness and postural tone secondary to a lack of adequate cerebral blood perfusion. The incidence of syncope coming to medical attention appears to be clearly increased in two age groups—that is, in the young and in the old (fig 1).1 An incidence peak occurs around the age of 15 years, with females having more than twice the incidence of males.12 Syncope is an infrequent occurrence in adults. The incidence of syncope progressively increases over the age of about 40 years to become high in the older age groups. A lower peak occurs in older infants and toddlers, most commonly referred to as ‘‘breath-holding spells’’.3 The incidence of syncope in young subjects coming to medical attention varies from approximately 0.5 to 3 cases per 1000 (0.05–0.3%).2 Syncopal events which do not reach medical attention occur much more frequently. In fact, the recently published results of a survey of students averaging 20 years of age demonstrated that about 20% of males and 50% of females report to have experienced at least one syncopal episode.4 By comparison, the prevalence of seizures in a similar age group is about 5 per 1000 (0.5%)5 and cardiac syncope (that is, cardiac arrhythmias or structural heart disease) is even far less common. -
Syncope (Fainting) Information Sheet
Sunshine Coast Hospital and Health Service Syncope (fainting) information sheet • Orthostatic: These episodes are often caused by a sudden drop in blood pressure upon standing. These episodes can be caused by a number of factors including dehydration, some medications or even standing up too quickly. • Reflex/Vasovagal: These episodes are often caused by a disturbance in either the heart rate or blood pressure that is controlled by nerves in the brain. Often patients may have warning signs (feeling dizzy, unsteady on feet) prior to these events occurring. • Other: Even after extensive investigations we are What is Syncope? unable to determine a cause for these events in up Syncope is a broad medical term used for to 20 per cent of people. fainting or loss of consciousness due to a Treatment temporary decline in blood flow to the brain. In the emergency department, the person will be closely monitored and any injuries they may have Blood vessels continually adjust their width sustained will be treated. The person may have to ensure a constant blood pressure. For blood tests taken to assess a number of factors and these may assist the doctors in determining why this instance, the vessels constrict (tighten) when person has experienced this episode. we stand up to counteract the effects of gravity. Some people will need to stay in hospital for observation, particularly if they have more than Temporary, low blood pressure can be caused one episode or if the episode occurs without any by various events that prompt blood vessels warning signs. The person may be required to have to dilate (expand), including extreme heat, any number of the following tests: emotional distress or pain. -
Dictionary of Epilepsy
DICTIONARY OF EPILEPSY PART I: DEFINITIONS .· DICTIONARY OF EPILEPSY PART I: DEFINITIONS PROFESSOR H. GASTAUT President, University of Aix-Marseilles, France in collaboration with an international group of experts ~ WORLD HEALTH- ORGANIZATION GENEVA 1973 ©World Health Organization 1973 Publications of the World Health Organization enjoy copyright protection in accord ance with the provisions of Protocol 2 of the Universal Copyright Convention. For rights of reproduction or translation of WHO publications, in part or in toto, application should be made to the Office of Publications and Translation, World Health Organization, Geneva, Switzerland. The World Health Organization welcomes such applications. PRINTED IN SWITZERLAND WHO WORKING GROUP ON THE DICTIONARY OF EPILEPSY1 Professor R. J. Broughton, Montreal Neurological Institute, Canada Professor H. Collomb, Neuropsychiatric Clinic, University of Dakar, Senegal Professor H. Gastaut, Dean, Joint Faculty of Medicine and Pharmacy, University of Aix-Marseilles, France Professor G. Glaser, Yale University School of Medicine, New Haven, Conn., USA Professor M. Gozzano, Director, Neuropsychiatric Clinic, Rome, Italy Dr A. M. Lorentz de Haas, Epilepsy Centre "Meer en Bosch", Heemstede, Netherlands Professor P. Juhasz, Rector, University of Medical Science, Debrecen, Hungary Professor A. Jus, Chairman, Psychiatric Department, Academy of Medicine, Warsaw, Poland Professor A. Kreindler, Institute of Neurology, Academy of the People's Republic of Romania, Bucharest, Romania Dr J. Kugler, Department of Psychiatry, University of Munich, Federal Republic of Germany Dr H. Landolt, Medical Director, Swiss Institute for Epileptics, Zurich, Switzerland Dr B. A. Lebedev, Chief, Mental Health, WHO, Geneva, Switzerland Dr R. L. Masland, Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, USA Professor F. -
TREATMENT of VASOVAGAL SYNCOPE Where to Go for Help Syncope: HRS Definition
June 8, 2018, London UK TREATMENT OF VASOVAGAL SYNCOPE Where to go for help Syncope: HRS Definition ▪ Syncope is defined as: —a transient loss of consciousness, —associated with an inability to maintain postural tone, —rapid and spontaneous recovery, —and the absence of clinical features specific for another form of transient loss of consciousness such as epileptic seizure. 3 Syncope Cardiac Vasovagal Orthostatic Carotid sinus 4 Vasovagal Syncope: HRS Definition ▪ Vasovagal syncope is defined as a syncope syndrome that usually: 1. occurs with upright posture held for more than 30 seconds or with exposure to emotional stress, pain, or medical settings; 2. features diaphoresis, warmth, nausea, and pallor; 3. is associated with hypotension and relative bradycardia, when known; and 4. is followed by fatigue. 5 Physiology of Symptoms and Signs Decreased cardiac output Hypotension • Weakness • Lightheadness Retinal hypoperfusion • Blurred vision, grey vision, coning down Physiology of Symptoms and Signs Decreased cardiac output Reflex cutaneous vasoconstriction • Maintains core blood volume • Pallor, looks grey or very white Physiology of Symptoms and Signs Vasovagal reflex Worsened hypotension • More weakness • More lightheadness Vagal • Nausea and vomiting • Diarrhea • Abdominal discomfort Physiology of Symptoms and Signs Increase arterial conductance Rapid transit of core blood to skin • Hot flash • Warmth and discomfort • Lasts seconds • Pink skin SYNCOPE 9 Physiology of Symptoms and Signs Collapse • Preload restored • Reflexes end • Skin -
Update on the Diagnosis and Management of Familial Long QT Syndrome
Heart, Lung and Circulation (2016) 25, 769–776 POSITION STATEMENT 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2016.01.020 Update on the Diagnosis and Management of Familial Long QT Syndrome Kathryn E Waddell-Smith, FRACP a,b, Jonathan R Skinner, FRACP, FCSANZ, FHRS, MD a,b*, members of the CSANZ Genetics Council Writing Group aGreen Lane Paediatric and Congenital Cardiac Services, Starship Children’s Hospital, Auckland New Zealand bDepartment[5_TD$IF] of Paediatrics,[6_TD$IF] Child[7_TD$IF] and[8_TD$IF] Youth[9_TD$IF] Health,[10_TD$IF] University of Auckland, Auckland, New Zealand Received 17 December 2015; accepted 20 January 2016; online published-ahead-of-print 5 March 2016 This update was reviewed by the CSANZ Continuing Education and Recertification Committee and ratified by the CSANZ board in August 2015. Since the CSANZ 2011 guidelines, adjunctive clinical tests have proven useful in the diagnosis of LQTS and are discussed in this update. Understanding of the diagnostic and risk stratifying role of LQTS genetics is also discussed. At least 14 LQTS genes are now thought to be responsible for the disease. High-risk individuals may have multiple mutations, large gene rearrangements, C-loop mutations in KCNQ1, transmembrane mutations in KCNH2, or have certain gene modifiers present, particularly NOS1AP polymorphisms. In regards to treatment, nadolol is preferred, particularly for long QT type 2, and short acting metoprolol should not be used. Thoracoscopic left cardiac sympathectomy is valuable in those who cannot adhere to beta blocker therapy, particularly in long QT type 1. Indications for ICD therapies have been refined; and a primary indication for ICD in post-pubertal females with long QT type 2 and a very long QT interval is emerging.