DOCSLIB.ORG

Adolescent Syncope

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Adolescent Syncope Adolescent Syncope Brett Goudie, M.D. Pediatric Cardiology Case 1 – Altar Boy • 14 yo boy presents to clinic following syncopal episode. Standing in church, felt hot and lightheaded before passing out. Witnessed event, parents described brief seizure like activity while he was down. No loss of bowel or bladder control, no CPR, no resp support. Brief LOC, woke up 5 sec later, was soon back to being alert and oriented. He noted visual changes and hearing became distant prior to the episode. • Cause? • Further testing? • Referral? • Recommendations? • From the Greek word synkoptein, which means “to cut short” • Syncope – “temporary loss of consciousness and postural tone resulting from an abrupt, transient, and diffuse cerebral dysfunction (hypoperfusion), and followed by spontaneous recovery” – cerebral blood flow ↓ 30-50% Syncope • Syncopized???? • Pre-syncopize? • Pre-syncope – prodromal dizziness and lightheadedness that precedes LOC – aka near-syncope • Sadly I have no financial disclosures related to this topic Case 2 – Track Star • 17 yo girl (no PMHx) presents after syncope with exercise. She was running the 100 m dash, and passed out suddenly while running. No preceding symptoms. Woke up 4-5 sec later, was confused, had trouble recognizing her track coach or track team. • Same questions • Cause? • Further testing? • Referral? • Recommendations? Syncope – why talk about it? • Common - 15-25% of children experience at least one episode (peak ages 15-19) (♀ > ♂) • Expensive clinical problem / testing / Up to 3 % of ER visits / treatable • Most pediatric syncopal episodes are totally benign • 80-90% is vasodepressor or cardioinhibitory → vasovagal • Only 1% of time due to arrhythmia or structural cardiac disease – hence there is a risk of sudden death • ANGST!!!!! Vasovagal Syncope Terminology • Vasodepressor (Vaso) • Cardioinhibitory (Vagal) • Neurocardiogenic • POTS – postural orthostatic tachycardia syndrome • Orthostatic Hypotension or Intolerance • Situational • Reflex • Neurally mediated • Dysautonomia Bryan Cannon, Philip Wackel Pediatrics in Review Apr 2016, 37 (4) 159-168 “Fainting Goat” Myotonia Congenita Presyncope • Lightheaded, dizziness • Visual changes - blurry vision, tunnel vision, spots, double vision • Altered hearing – distant voices • Altered mentation, confusion, panic, h/a • Weakness, poor balance • Warmth / rush, or cold and clammy • Sweating, nausea • Pallor or gray Syncope, at the Carotid Sinus • Upright posture, 25% of blood redistributed to lower extremities • Preload diminished, leads to diminished stroke volume by as much as 40%, CO = HR * SV • Baroreceptors activated (Carotid sinus) • Increased sympathetic activity increases HR, contractility, and SVR (systemic vascular resistance) • Failure of this response leads https://medicine.uiowa.edu/iowaprotocols/ca to vasodepressor syncope rotid-body-and-carotid-sinus-general- information Bezold-Jarisch Reflex Tilt Venous Return Vagal Efferent HR BP Vagal BP Reflex Afferent Brain Syncope Ventricles Stem Carotid Sinus Vasodilation Baroreceptors Sympathetic Withdrawal Catecholamines Increase HR, contractility, and BP Chang-Sing P. Cardiol Clinics. 1991;9(4):641-651. Albert von Bezold (1836-1868) • "Bezold-Jarisch reflex" is a triad of responses (bradycardia, hypotension, and apnea) from paradoxical stimulation of vagal mediated ventricular C fiber receptors. • Reflex is involved with the “Cardioinhibitory” or “Neurocardiogenic” Syncope • Bezold - intravenous injection of veratrum alkaloids, +/- vagal nerve ligation. Bezold – died from rheumatic Bezold - Munich, then in Univ of Berlin under disease, had both du Bois-Reymond (nerve action potential) arthritis and carditis (mitral • Adolf Jarisch Jr (1891–1965) replicated study stenosis), died at in cats with reversible cooling of vagal nerve. 32 Veratrum viride or album • Potent alkaloids, antagonism of adrenergic receptors • Highly toxic – nausea / vomiting, cold sweat and vertigo, slowing of respiration, bradycardia, hypotension, death • 1950-1960s extract known as alkavervir – antihypertensive • Some Native American nations – historical use for elections of new leader Bezold-Jarisch Reflex Tilt Venous Return Vagal Efferent HR BP Vagal BP Reflex Afferent Brain Syncope Ventricles Stem Carotid Sinus Vasodilation Baroreceptors Sympathetic Withdrawal Catecholamines Increase HR, contractility, and BP Chang-Sing P. Cardiol Clinics. 1991;9(4):641-651. History / Physical Exam / EKG • What are the circumstances leading to events? Sick with URI or other illness pre or post? Preceding mono or viral illness weeks or months prior? Growth spurt? • Abrupt onset or prodrome? Exercise? Post trauma? • Are there palpitations, visual changes, chest pain, shortness of breath, dizziness vs vertigo? • LOC details – duration? • Injury? Seizure? Loss of bowel/bladder control? CPR? • Eat or drink? Is there a history of caffeine use? Is his/her urine concentrated or clear? 2nd daily void Syncope after surprise, loud noises, anger No warning or while supine Prodrome of palpitations/tachycardia/severe chest pain Syncope Syncope with exercise *** History – Red Prolonged down time, pulseless, Flags CPR, residual neuro issue Other red flags Abnormal exam or EKG F Hx of sudden death / SIDS Hx of CHD Adult Syncope – more likely to be cardiac Benign Prodrome Brief Episode Single Episode Only while Upright Syncope Change of position History – Poor hydration Lots of dizziness with standing Green Flags OR Presyncope only – no flaccid LOC, full memory Family History / Physical Exam / EKG • Arrhythmias • Sudden death • SIDS • Cardiomyopathy • Pacemakers • Defibrillators / ICD • Deafness • Congenital Heart Disease • Fainters History / Physical Exam / EKG • Heart rate and blood pressure, both supine and standing, then standing again in a few minutes • Are the first and second heart sounds normal? • Is there a murmur? Does it get louder with standing? • Any ectopy noted? • Is there a click, gallop, rub, or filling rumble? • Leg plethora, edema, swelling Bryan Cannon, Philip Wackel Pediatrics in Review Apr 2016, 37 (4) 159-168 Bryan Cannon, Philip Wackel Pediatrics in Review Apr 2016, 37 (4) 159-168 Bryan Cannon, Philip Wackel Pediatrics in Review Apr 2016, 37 (4) 159-168 • Pseudoseizures or behavioral spells • no physiologic changes prior to syncope • Certain times, certain places, daily • > age 10. LOC > 10 min • Emotionally charged • Common after abuse (emotional or Psychogenic sexual) • 15 yo girl “passing out” many times Syncope per day. • Fluid, salt, cut caffeine • Florinef, mitodrine. • Put on the brakes BP high. • Episode during stress test, actually passed out with no BP change, no EKG change, nothing. No EKG change ????? Fainting Lark History / Physical Exam / EKG • Is the rhythm SINUS? • Is the rate appropriate? • Is there AV block? • Is there evidence of hypertrophy or strain? • Is there pre-excitation (short PR or delta)? • Is the QTc normal? • Any PVCs? EKG post syncope Diagnostic tests • Orthostatic HR and BP • ECG • Head Up Tilt Test - usually not necessary • Exercise stress test – syncope with exercise • 24 hour Holter / 30 day event/loop monitor / Reveal monitor • Echocardiogram with emphasis on chamber size, obstructive lesions, coronary arteries • Electrophysiology study • Labs – U/A (spec grav), CBC, glucose, Lytes, TSH, pregnancy, drugs • Brain imaging – only for focal neuro signs • EEG – can be abnormal after benign syncope The Tilt Lab Neurally-Mediated Syncope Tilt Table Response Sra JS. Ann Intern Med. 1991;114:1013-1019. Arrhythmias Causing Syncope • Bradycardia • Sinus Node Dysfunction • AV Block • Tachycardias • Wolff-Parkinson-White Syndrome • Long QT Syndrome • Brugada Syndrome • Arrhythmogenic RV Dysplasia (ARVD) • Catecholaminergic Polymorphic VT (CPVT) Sinus Node Dysfunction • Inappropriately slow (or fast) heart rate • SA node origin • Frequently seen in post-op hearts • <3 years old <100 • 3-9 years old <60 • 9-16 years old <50 • >16 years old <40 Complete AV Block Wolff-Parkinson-White Syndrome Not-so-subtle WPW Atrial Fibrillation in WPW The Long QT Syndrome • LQTS is present in 1:5,000 persons (over 50,000 people) in the USA • Estimated to cause as many as 3000 deaths (mostly in children and young adults) in the USA each year. • It is present in all races and ethnic groups • In as many as 30-40%, sudden death is the first event (8-40% of asymptomatic patients have SCD as first event) • 57% of patients who die will die by age 20 • Events rates are 5%/yr. for syncope and 0.9-2.5%/yr. for cardiac death Corrected QT Interval (QTc) • Include U wave if > 50% of T wave height • Upper limits of normal 450 PPV 100% Male >470 Female >480 PPV 93% >460 NPV 100% Male <400 Female <420 Torsades de Pointes ECG Phenotype of LQT3, 2, and 1 LQT3 LQT2 LQT1 Varieties of LQTS • LQT 1-Tend to have events at times of exertion or excitement. • LQT 2-Tend to have events when startled or with swimming. • LQT 3-Tend to have events when asleep. • LQT 1 and 2 account for 85% of total. LQT 3 accounts for about 10%. TdP following a sudden arousal (alarm clock) in a patient with a HERG defect. Wilde et al. JACC. 1999;33:327-32 Treatment of LQTS • Avoid all strenuous exercise, esp. swimming • Avoid startling (alarm clocks etc.) • Beta blocker therapy (Propranolol, Nadolol) w/ or w/o bradycardia pacing • ICD (QTc>550, noncompliant, FHx SCD) • Left Stellate ganglionectomy Drugs – QTDRUGS.ORG Brugada Syndrome • Leading cause of death in young Asian males • Arrhythmias tend to occur during febrile periods (exercise) and during sleep •
Load more

Recommended publications
  • Computational Diagnostic Techniques for Electrocardiogram Signal Analysis
    sensors Review Computational Diagnostic Techniques for Electrocardiogram Signal Analysis Liping Xie * , Zilong Li, Yihan Zhou, Yiliu He and Jiaxin Zhu College of Medicine and Biological Information Engineering, Northeastern University, Shenyang 110169, China; [email protected] (Z.L.); [email protected] (Y.Z.); [email protected] (Y.H.); [email protected] (J.Z.) * Correspondence: [email protected] Received: 8 September 2020; Accepted: 4 November 2020; Published: 5 November 2020 Abstract: Cardiovascular diseases (CVDs), including asymptomatic myocardial ischemia, angina, myocardial infarction, and ischemic heart failure, are the leading cause of death globally. Early detection and treatment of CVDs significantly contribute to the prevention or delay of cardiovascular death. Electrocardiogram (ECG) records the electrical impulses generated by heart muscles, which reflect regular or irregular beating activity. Computer-aided techniques provide fast and accurate tools to identify CVDs using a patient’s ECG signal, which have achieved great success in recent years. Latest computational diagnostic techniques based on ECG signals for estimating CVDs conditions are summarized here. The procedure of ECG signals analysis is discussed in several subsections, including data preprocessing, feature engineering, classification, and application. In particular, the End-to-End models integrate feature extraction and classification into learning algorithms, which not only greatly simplifies the process of data analysis, but also shows excellent accuracy and robustness. Portable devices enable users to monitor their cardiovascular status at any time, bringing new scenarios as well as challenges to the application of ECG algorithms. Computational diagnostic techniques for ECG signal analysis show great potential for helping health care professionals, and their application in daily life benefits both patients and sub-healthy people.
    [Show full text]
  • Ventricular Repolarization Components on the Electrocardiogram Cellular Basis and Clinical Significance Gan-Xin Yan, MD, PHD, Ramarao S
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE Journal of the American College of Cardiology providedVol. by Elsevier 42, No. - 3,Publisher 2003 Connector © 2003 by the American College of Cardiology Foundation ISSN 0735-1097/03/$30.00 Published by Elsevier Inc. doi:10.1016/S0735-1097(03)00713-7 STATE-OF-THE-ART PAPER Ventricular Repolarization Components on the Electrocardiogram Cellular Basis and Clinical Significance Gan-Xin Yan, MD, PHD, Ramarao S. Lankipalli, MD, James F. Burke, MD, FACC, Simone Musco, MD, Peter R. Kowey, MD, FACC Wynnewood, Pennsylvania Ventricular repolarization components on the surface electrocardiogram (ECG) include J (Osborn) waves, ST-segments, and T- and U-waves, which dynamically change in morphol- ogy under various pathophysiologic conditions and play an important role in the development of ventricular arrhythmias. Our primary objective in this review is to identify the ionic and cellular basis for ventricular repolarization components on the body surface ECG under normal and pathologic conditions, including a discussion of their clinical significance. A specific attempt to combine typical clinical ECG tracings with transmembrane electrical recordings is made to illustrate their logical linkage. A transmural voltage gradient during initial ventricular repolarization, which results from the presence of a prominent transient ϩ outward K current (Ito)-mediated action potential (AP) notch in the epicardium, but not endocardium, manifests as a J-wave on the ECG. The J-wave is associated with the early repolarization syndrome and Brugada syndrome. ST-segment elevation, as seen in Brugada syndrome and acute myocardial ischemia, cannot be fully explained by using the classic concept of an “injury current” that flows from injured to uninjured myocardium.
    [Show full text]
  • Determinants of Myocardial Lactate Production During Acetylcholine
    ORIGINAL RESEARCH Determinants of Myocardial Lactate Production During Acetylcholine Provocation Test in Patients With Coronary Spasm Koichi Kaikita, MD, PhD; Masanobu Ishii, MD; Koji Sato, MD, PhD; Masafumi Nakayama, MD, PhD; Yuichiro Arima, MD, PhD; Tomoko Tanaka, MD, PhD; Koichi Sugamura, MD, PhD; Kenji Sakamoto, MD, PhD; Yasuhiro Izumiya, MD, PhD; Eiichiro Yamamoto, MD, PhD; Kenichi Tsujita, MD, PhD; Megumi Yamamuro, MD, PhD; Sunao Kojima, MD, PhD; Hirofumi Soejima, MD, PhD; Seiji Hokimoto, MD, PhD; Kunihiko Matsui, MD, MPH; Hisao Ogawa, MD, PhD Background-—Myocardial lactate production in the coronary circulation during acetylcholine (ACh)-provocation test (abbreviated as lactate production) provides supporting evidence for coronary spasm–induced myocardial ischemia. The purpose of this study was to examine the clinical features, predictive factors, and prognosis of patients with coronary vasospastic angina (VSA) and lactate production. Methods and Results-—We examined all 712 patients who underwent both myocardial lactate measurement during ACh- provocation test in the left coronary artery and genetic screening test of a –786T/C polymorphism in the 50-flanking region of the endothelial nitric oxide synthase (eNOS) gene between January 1991 and December 2010. Lactate production was observed in 252 of the 712 patients and in 219 of 356 VSA patients diagnosed by ACh-provocation test. Compared with lactate production– negative VSA patients, the lactate production–positive counterparts were more likely to be nonsmoker female diabetics with – 786T/C eNOS polymorphism (61% vs 31%, P<0.001, 62% vs 34%, P<0.001, 24% vs 14%, P=0.016, and 25% vs 15%, P=0.018, respectively). Multivariable logistic regression analysis identified female sex, diabetes mellitus, and –786T/C eNOS polymorphism to correlate with lactate production (odds ratio 3.51, 95% CI 2.16 to 5.70, P<0.001; odds ratio 2.53, 95% CI 1.38 to 4.65, P=0.003; and odds ratio 1.85, 95% CI 1.02 to 3.35, P=0.044, respectively).
    [Show full text]
  • Tively Assess Myocardial Function: New Hypothesis and Validation Experiment Regarding the U Wave
    Journal of ISSN:2378-6914 Heart and Cardiology OPEN ACCESS Research Article DOI: 10.15436/2378-6914.20.2813 Changing Electrocardiogram Waveforms to Quantita- tively Assess Myocardial function: New Hypothesis and Validation Experiment regarding the U Wave Kenneth Tsan He1*, Helena Ai He2 1Princeton International School of Mathematics and Science, 11th grade student, 19 Lambert Drive, Princeton 2Princeton International School of Mathematics and Science, 10th grade student, 19 Lambert Drive, Princeton *Corresponding author: Kenneth Tsan He, Princeton International School of Mathematics and Science, 11th grade student, 19 Lambert Drive, Princeton, NJ, Tel: 08540; 1-732-705-0282; Email: [email protected] Abstract A hypothesis regarding the U wave is proposed, where the collision of the heart apex and chest wall causes delayed repolar- ization of some myocardial cells due to compression and deformation, leading to the presence of the U wave on ECG. Under normal conditions, the stronger the myocardial contractility, the greater the mass of the heart, the closer the distance to the chest wall, the more intense the apex beat, the more cells deformed and repolarization delayed, and the longer the delay time. To test the hypothesis, 41 high school student volunteers participated in a clinical trial. The results showed that when the position was changed from the supine position to the left lateral position, the U wave increased significantly (0.24±0.095×0.1 mv, a=99%), the T wave significantly decreased (-1.3±0.74×0.1 mv, a=99%), the time difference between the two peaks significantly increased (0.38±0.12×40 ms, a= 99%), indicating a strong co-rrelation between those three values ( r= 0.87 and 0.39).
    [Show full text]
  • Dysrhythmias
    CARDIOVASCULAR DISORDERS DYSRHYTHMIAS I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES A. Standard ECG and rhythm strips 1. Recordings are obtained at a paper speed of 25 mm/sec. 2. The vertical axis measures distance; the smallest divisions are 1 mm ×1 mm. 3. The horizontal axis measures time; each small division is 0.04 sec/mm. B. Normal morphology Courtesy of Dr. Michael McCrea 1. P wave = atrial depolarization a. Upright in leads I, II, III, aVL, and aVF; inverted in lead aVR b. Measures <0.10 seconds wide and <3 mm high c. Normal PR interval is 0.12–0.20 seconds. 2. QRS complex = ventricular depolarization a. Measures 0.06-0.10 seconds wide b. Q wave (1) <0.04 seconds wide and <3 mm deep (2) Abnormal if it is >3 mm deep or >1/3 of the QRS complex. c. R wave ≤7.5 mm high 3. QT interval varies with rate and sex but is usually 0.33–0.42 seconds; at normal heart rates, it is normally <1/2 the preceding RR interval. 4. T wave = ventricular repolarization a. Upright in leads I, II, V3–V6; inverted in aVR b. Slightly rounded and asymmetric in configuration c. Measures ≤5 mm high in limb leads and ≤10 mm high in the chest leads 5. U wave = a ventricular afterpotential a. Any deflection after the T wave (usually low voltage) b. Same polarity as the T wave c. Most easily detected in lead V3 d. Can be a normal component of the ECG e. Prominent U waves may indicate one of the following: (1) Hypokalemia (<3 mEq/L) (2) Hypercalcemia (3) Therapy with digitalis, phenothiazines, quinidine, epinephrine, inotropic agents, or amiodarone (4) Thyrotoxicosis f.
    [Show full text]
  • The Enigmatic Sixth Wave of the Electrocardiogram: the U Wave
    Cardiology Journal 2008, Vol. 15, No. 5, pp. 408–421 Copyright © 2008 Via Medica REVIEW ARTICLE ISSN 1897–5593 The enigmatic sixth wave of the electrocardiogram: The U wave Andrés Ricardo Pérez Riera1, Celso Ferreira1, Celso Ferreira Filho1, Marcelo Ferreira1, Adriano Meneghini1, Augusto Hiroshi Uchida2, Edgardo Schapachnik3, Sergio Dubner4, Li Zhang5 1For International VCG Investigators, ABC Faculty of Medicine (FMABC), Foundation of ABC (FUABC), Santo André, Brazil 2Heart Institute of the University of São Paulo Medical School, São Paulo, Brazil 3Dr. Cosme Argerich Hospital, Buenos Aires, Argentina 4Clínica and Maternidad Suizo Argentina, Buenos Aires, Argentina 5Main Line Health Heart Center, Jefferson Medical College, Philadelphia, PA, USA Electro-Vectorcardigraphic Section, ABC Medical School, ABC Foundation, Santo André, São Paulo, Brazil Abstract The U wave is the last, inconstant, smallest, rounded and upward deflection of the electrocar- diogram. Controversial in origin, it is sometimes seen following the T wave with the TU junction along the baseline or fused with it and before P of the following cycle on the TP segment. In this review we will study its temporal location related to monophasic action potential, cardiac cycle and heart sounds, polarity, voltage or amplitude, frequency and shape- contour. We will analyze the clinical significance of negative, alternant, prominent U wave, and the difference between T wave with two peaks (T1–T2) and true U wave. Finally we will analyze the four main hypotheses about the source of U wave: repolarization of the intraven- tricular conducting system or Purkinje fibers system, delayed repolarization of the papillary muscles, afterpotentials caused by mechanoelectrical hypothesis or mechanoelectrical feedback, and the prolonged repolarization in the cells of the mid-myocardium (“M-cells”).
    [Show full text]
  • "U" Wave Kenneth M Eyer* 369 Old Sawmill Road, Sagle, Idaho 83860, USA Letter to the Editor U Wave
    Journal of Integrative Cardiology Letter to the Editor ISSN: 2058-3702 The etiology of the ECG "U" wave Kenneth M Eyer* 369 Old Sawmill Road, Sagle, Idaho 83860, USA Letter to the Editor U wave. What followed were years of watching ECG's and the U waves to see if there was ever an exception to this rule. When I was a Cardiology Fellow in the 1950's at the University of Washington, I was curious why the U wave had been observed for 100 Post extra-systolic pulsus alternans is a well-known sign of impaired years but had never been explained. Because it looked like a miniature left ventricular function. I reasoned that the ECG should also show U T wave researchers had assumed it had to be late repolarization wave alternans and I watched for it. One night on the coronary care unit the resident showed me a rhythm strip on a patient and there it somewhere in the heart. But search as they may, they couldn't find it. was. I took members of the house staff to the patient's bedside and we I looked at the large book "The U Wave" by Katz and found the each put a finger on a pulse. A PVC came along and we each noticed most help on the first page. They are largest in the chest leads of transient pulsus alternans. young males and always follow the aortic second sound. I attached Later, six of my patients who had been in heart failure volunteered a phonocardiogram and ECG leads to myself and varied my stroke to be monitored in our Heart Center.
    [Show full text]
  • The U Wave in the Electrocardiogram. More Than an Academic Curiosity
    ARTÍCULO DE REVISIÓN The U wave in the electrocardiogram. More than an academic curiosity Raúl Carrillo-Esper,* Luis Daniel Carrillo-Córdova,** Dulce María Carrillo-Córdova,*** Carlos Alberto Carrillo-Córdova*** RESUMENS ABSTRACTTC La onda U fue descrita por Einthoven en 1903. A pesar del tiempo The electrocardiographic U wave was describe by Einthoven in transcurrido desde su descripción inicial las bases electrofisiológi- 1903. Despite the time elapsed since its description the electrophy- cas que expliquen su génesis no son claras, por lo que se han siological basis underlying the genesis of the U wave has not been propuesto varias teorías. La adecuada evaluación e interpretación precisely elucidated and several hypothesis have been proposed. de la onda U es importante en la práctica clínica, ya que su presen- Proper evaluation and interpretation of the U wave is useful to the cia puede ser marcador de enfermedad cardiaca. El objetivo de clinician because it is a marker of heart disease. The aim of this este artículo es revisar los conceptos actuales relacionados con la paper is to review current concepts related to U wave, its genesis, onda U, su génesis, significado y adecuada interpretación. significance and proper interpretation. Palabrasb s clave.v . Onda U. Electrocardiograma. Cardiopatía is- Keyy words.d dKey U wave. Electrocardiogram. Ischemic heart disease. quémica. THE U WAVE IN THE ELECTROCARDIGRAM. MORE THAN ACADEMIC CURIOSITY Willem Einthoven developed the first electrocardiogra- ph machine. It was a simple string galvanometer capable of mesuring small changes in the electrical potential as the heart contracted and relaxed (Figure 1). After having decribed the electrocardiogram (ECG) in 1895, Einthoven first recognized in 1903 the U wave and extended the notion of the ECG in a seminal paper publis- hed in the Lancet in 1912.
    [Show full text]
  • Clinical Relevance of Cardiac Arrhythmias Generated by Afterdepolarizations Role of M Cells in the Generation of U Waves, Triggered Activity an Torsade De Pointes
    JACC Vol . 23, No . I January 1994 : 25 9 -77 259 REVIEW ARTICLE Clinical Relevance of Cardiac Arrhythmias Generated by Afterdepolarizations Role of M Cells in the Generation of U Waves, Triggered Activity an Torsade de Pointes CHARLES ANTZELEVITCH, PHD, SERGE SICOURI, MD Utica, New York Recent findings point to an important heterogeneity in the etectri- review examines the implications of some of these new findings cal behavior of cells spanning the ventricular wall as well as within the scope of what is already known about early and delayed important differences 1rn the response of the various cell types to Mrdepolayistions and triggered activity and discusses the pos- cardioactive drugs and pathophysiologic states . These observa- sible relevance of these mechanisms to clinical arrhyllintias. tons have permitted a fine totting and, in some cases, a reevalu- (I A a Coll Cardiol 1994;23 .259-77) ation of basic concepts of arrhythmia mechanisms . This brief Despite important advances in cardiology in recent years, basic concepts of arrhythmia mechanisms . Our aim in this cardiac arrhythmias remain an important cause of mortality brief review is to examine the implications of some of these and morbidity . Pharmacologic control of cardiac arrhyth- new findings within the scope of what is already known mias is largely empiric, and the criteria that can be applied to about early and delayed afterdepolarizations and triggered the differential diagnosis of arrhythmia mechanisms are few activity and to discuss the possible relevance of these and far between . Differential diagnosis of cardiac arrhyth- mechanisms to clinical arrhythmias . inias requires an understanding of basic mechanisms and The number of excellent studies that form the foundation establishment of mechanism-specific electrophysiologic cri- of our present-day understanding of this field are far too teria.
    [Show full text]
  • ECG) Signal in the Magnetic Resonance Imaging (MRI
    University of Central Florida STARS Electronic Theses and Dissertations, 2004-2019 2007 Signal Processing Of An Ecg Signal In The Presence Of A Strong Static Magnetic Field Aditya Gupta University of Central Florida Part of the Electrical and Electronics Commons Find similar works at: https://stars.library.ucf.edu/etd University of Central Florida Libraries http://library.ucf.edu This Doctoral Dissertation (Open Access) is brought to you for free and open access by STARS. It has been accepted for inclusion in Electronic Theses and Dissertations, 2004-2019 by an authorized administrator of STARS. For more information, please contact [email protected]. STARS Citation Gupta, Aditya, "Signal Processing Of An Ecg Signal In The Presence Of A Strong Static Magnetic Field" (2007). Electronic Theses and Dissertations, 2004-2019. 3185. https://stars.library.ucf.edu/etd/3185 SIGNAL PROCESSING OF AN ECG SIGNAL IN THE PRESENCE OF A STRONG STATIC MAGNETIC FIELD by ADITYA GUPTA M.S. University of Central Florida, 2006 B. S. M S Ramaiah Institute of Technology, 2002 A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Electrical and Computer Engineering in the College of Engineering and Computer Science at the University of Central Florida Orlando, Florida Fall Term 2007 Major Professor: Arthur Weeks © 2007 Aditya Gupta ii ABSTRACT This dissertation addresses the problem of elevation of the T wave of an electrocardiogram (ECG) signal in the magnetic resonance imaging (MRI). In the MRI, due to the strong static magnetic field the interaction of the blood flow with this strong magnetic field induces a voltage in the body.
    [Show full text]
  • Handgrip-Induced Negative U-Wave in Electrocardiogram of Hypertensive Subjects
    Handgrip-Induced Negative U-Wave in Electrocardiogram of Hypertensive Subjects Long Tai Fu, M.D., Nobumitsu TAKAHASHI, M.D., Machiko YAMAMOTO, B.S., Masao KUBOKI, M.D., and Shintaro KOYAMA, M.D. SUMMARY To study clinical significance and possible mechanism of negative U- wave observed in hypertensive patients, we applied handgrip test (HG) to 35 patients with hypertension and 20 age-matched normal subjects. HG was sustained for 3min at 50% of maximum voluntary contraction. ECG recording and measurement of blood pressure were made before, during, and after HG. During HG, systolic blood pressure was 188.7•}3.4mmHg (mean•} SE) and diastolic blood pressure was 114.8•}2.1mmHg in hypertensives, while 145.3•}2.6mmHg and 93.8•}1.1mmHg in normals; the difference between hypertensives and normals was statistically significant (p<0.001). Incidence of HG-induced negative U-wave was 0% in normals, while 68.6% in hypertensives. In hypertensive subjects, HG-induced nega- tive U-wave appeared in 24 of the 28 patients (85.7%) with minimum to moderate left ventricular hypertrophy, while it was not seen in all 7 pa- tients (0%) with marked left ventricular hypertrophy shown by ECG and/or UCG findings (QRS-T angle>130•‹ with left high voltage: left ven- tricular wall thickness>12mm). Further we recorded UCG during HG in 14 subjects. In 4 patients, negative U waves appeared simultaneously with increase in left ventricular dimension during diastole. In the re- maining 10 cases that included both normals and hypertensives, however, neither increase in left ventricular end diastolic dimension nor negative U waves were observed.
    [Show full text]
  • Distinct U Wave Changes in Patients with Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
    Distinct U Wave Changes in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) Yoshiyasu AIZAWA,1 MD, Satoru KOMURA,1 MD, Shinsuke OKADA,1 MD, Masaomi CHINUSHI,1 MD, Yoshifusa AIZAWA,1 MD, Hiroshi MORITA,2 MD, and Tohru OHE,2 MD SUMMARY Although catecholaminergic polymorphic ventricular tachycardia (CPVT) is associ- ated with fatal ventricular arrhythmias and sudden death, the ECG findings are not fully understood. In this paper, we report on alterations in the U-wave. Seven patients from 6 families with CPVT in which bidirectional tachycardia and polymorphic VT were induced by exercise or isoproterenol infusion visited our hospitals. VT was not inducible by programmed electrical stimulation. A novel gene mutation of the ryanodine receptor 2 (RyR2) was confirmed in 2 families. In one of these patients, U-wave alternans was observed following ventricular pacing at 160 beats/min. In the other patient, U-wave alternans was observed during the recovery phase after the exercise stress test, which was terminated because of polymorphic VT. In both cases, leads V3-V5 were the leads showing alternans most clearly. In the third patient, a negative U-wave became positive following a pause from sinus arrest and a change in T-wave was also noted. Since such findings were not found in the other subjects who underwent electrophys- iologic study, isoproterenol infusion or exercise stress testing, the phenomenon seems to be relevant to the underlying pathogenesis of CPVT. The genesis and significance of U- wave alteration need to
    [Show full text]