DOCSLIB.ORG

Equine Electrocardiography: Exploration of New Diagnostic Strategies

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Equine Electrocardiography: Exploration of New Diagnostic Strategies EQUINE ELECTROCARDIOGRAPHY: EXPLORATION OF NEW DIAGNOSTIC STRATEGIES Tinne Verheyen Dissertation submitted in fulfilment of the requirements for the degree of Doctor of Philosophy (PhD) in Veterinary Sciences 2012 Promotors: Prof. dr G. van Loon Prof. dr P. Deprez Prof. dr S.U. Sys Department of Large Animal Internal Medicine Faculty of Veterinary Medicine Ghent University Equine electrocardiography: exploration of new diagnostic strategies Tinne Verheyen Vakgroep Interne geneeskunde en Klinische Biologie van de Grote Huisdieren Faculteit Diergeneeskunde Universiteit Gent ISBN:978-90-5864-313-1 “He who maintains that new knowledge of electrocardiography is no longer possible, ignores history” Dr. Charles Fisch TABLE OF CONTENTS LIST OF ABBREVIATIONS PREFACE 1 GENERAL INTRODUCTION 1. Electrical properties of the heart 7 2. Electrocardiography in human and veterinary medicine 10 CHAPTER 1.1 An overview of electrocardiographic recording techniques in the horse 25 CHAPTER 1.2 An overview of electrocardiographic interpretation in the horse 39 CHAPTER 2 Scientific aims 59 SECTION 1 CHAPTER 3 Electrocardiography in horses with atrial fibrillation 65 CHAPTER 4 Electrocardiography in horses with atypical myopathy 87 SECTION 2 CHAPTER 5 Esophageal electrocardiography in horses 111 CHAPTER 6 Intra-atrial electrocardiography in horses 143 GENERAL DISCUSSION 163 SUMMARY 191 SAMENVATTING 197 CURRICULUM VITAE 205 BIBLIOGRAPHY 209 DANKWOORD 215 LIST OF ABBREVIATIONS 2DST two-dimensional speckle tracking AERP atrial effective refractory period AFCL atrial fibrillation cycle length Am peak radial wall motion velocity during late diastole AM atypical myopathy Ao aortic diameter APD atrial prelature depolarisation AV atrioventricular CD contraction duration by TDI CDSC time to peak circumferential strain CDSL time to peak longitudinal strain CDSR time to peak radial strain CK creatine kinase cTnI cardiac troponin I DHA docosahexaenoic acid E early diastolic filling EAD early afterdepolarisation ECG electrocardiogram E/E10/20/30 intra-esophageal recording with interelectrode distance of 10, 20 or 30 cm Em peak radial wall motion velocity during early diastole E/Shigh/mid/low combined esophageal-surface recording with surface electrode positioned high, mid or low FS fractional shortening HW height at the withers IVRT isovolumic relaxation time IVS interventricular septum MADD multiple acyl-CoA dehydrogenase deficiency mSR maintenance of sinus rhythm LLA left atrial diameter measured from a left parasternal view LAsa left atrial internal diameter measured from a short axis view LVFW left ventricular free wall LVPEP left ventricular pre-ejection period LVET left ventricular ejection time LQTS long QT syndrome MEA mean electrical axis p5 5th percentile P/QRSmagn ratio of P wave magnitude and QRS complex magnitude PSM postsystolic motion rAF recurrence of atrial fibrillation RLA left atrial diameter measured from a right parasternal view QTc QT interval with Fridericia’s correction method ROI region of interest SC peak circumferential strain SD standard deviation SL peak longitudinal strain Sm peak radial wall motion velocity during systole SR peak radial strain STI synchronicity time index TDI tissue Doppler imaging t-MVO time to mitral valve opening T-PMVT torsade-like polymorphic ventricular tachycardia TVEC transvenous electrical cardioversion Uhigh/mid/low unipolar surface recording with electrode positioned high, mid or low VLADD very long-chain acyl-CoA dehydrogenase deficiency VPD ventricular premature depolarization VT ventricular tachycardia PREFACE PREFACE Equine electrocardiography (ECG) is still poorly developed when compared to electrocardiography in human and small animal medicine. Until now, the clinical use of ECG in horses is restricted to surface ECG recordings for diagnosis of rate and rhythm disturbances. Limited attention is given to electrode position and different lead recordings. Apart from a series of studies on vectorcardiography and the clinical significance of changes in T waves fifty years ago, hardly any research was dedicated to the potential of electrocardiography in horses. Nowadays, with affordable wireless ECG units available to the equine clinician, dysrhythmias appear more common than expected. As a result, more questions emerge regarding normal values, diagnosis and mechanisms of cardiac dysrhythmias, driving research into the field of equine dysrhythmias and electrocardiography. In the introduction of this thesis, a brief overview is given of the extensive knowledge regarding cardiac electrograms in human and small animal medicine. In a second part, a summary is provided regarding standard ECG recording in horses with emphasis on the recording technique and the interpretation of the surface ECG. The research part of the thesis is divided in two sections. In the first section the clinical importance of surface ECG recordings was studied in two diseases that are known to affect the heart. The second section describes new recording techniques which have specific advantages to investigate the atrial electrical activity of the equine heart. 3 GENERAL INTRODUCTION GENERAL INTRODUCTION ELECTRICAL PROPERTIES OF THE HEART Throughout history, horses have been admired for their extraordinary athletic ability. Decades of selective breeding have further contributed to the extraordinary cardiovascular capacity of horses. The central and most important organ in maintaining this cardiovascular capacity is the heart. Essentially, the heart functions as a pump. With each contraction, deoxygenated blood transported from the body to the right side of the heart is pumped to the lungs for oxygenation; oxygenated blood returning to the left side of the heart is subsequently distributed throughout the body. In order for this pump function to be effective, the cardiac contraction needs to be completed in an orderly fashion, where first the two atria contract, followed by contraction of both ventricles. Contraction of cardiac myocytes occurs only in response to an action potential. The electrical impulse starts in the sino-atrial (SA) node, located in the right atrium, and spreads sequentially to the left atrium, through the atrioventricular (AV) node, over the Bundle of His, the left and right bundle branches and the terminal fibers of the widely spread Purkinje system to the equine ventricular myocardium.1,2 Upon appropriate stimulation, tiny pores and channels in the cardiac cells open and close in a predefined way to allow specific ions to move across the cell membrane. This movement of ions results in changes in the transmembrane potential and generation of an action potential.3 Each time an action potential is generated, myocardial cells go through a process of depolarization, followed by repolarization and a resting phase. In certain specialized conducting cells, called pacemaker cells, the transmembrane potential does not remain constant in the resting phase, but slowly depolarizes. When this spontaneous depolarization reaches the threshold potential, it generates an action potential by itself, a process called ‘automaticity’ (Fig. 1).3,4 7 GENERAL INTRODUCTION Figure 1: Phases of the cardiac action potential in ventricular myocardial cells (A) and pacemaker cells (B). Phase 0 is the upstroke of the action potential, which is faster in ventricular myocardial cells where it is due to an inward movement of both sodium and calcium. Phase 1 is the rapid repolarization, primarily due to an almost complete inactivation of the inward sodium and calcium current. Phase 2 is the plateau phase of the action potential, which is prominent in ventricular muscle but not in pacemaker cells. It depends on a continued entry of sodium and calcium ions through their major channels and a minor membrane current due to the Na+-Ca2+ exchanger. Phase 3 is the repolarization phase which is due to an outward current of potassium. Phase 4 is the electrical diastolic phase or resting phase of the action potential. In pacemaker cells, changes in the currents of potassium, calcium and the funny current (constituted by sodium and potassium) produce pacemaker activity.5 The rate of spontaneous depolarization is fastest in SA nodal cells, but the AV node and Purkinje fibers also have automaticity and will take over as a pacemaker if the SA node fails to depolarize.5 During the processes of depolarization and repolarization, the movement of ions causes a current to flow across the cell membrane at various points, and a difference in potential arises between one part of the cell and another. When the current is flowing, an electrical field is set up around the cell, which acts as a dipole. When the cell is depolarized or repolarized and hence in a stable state, no current is flowing across the cell, and no electrical field is formed around it. Each myocyte forms its own electrical field, but the individual fields summate to produce an electrical field around the whole heart, which can be regarded as a single dipole.3,6 If the changes in the electrical field are large enough, they can be detected on the body surface by electrocardiography (ECG). The electrical field changes associated with SA node depolarization are too small to be 8 GENERAL INTRODUCTION detected on the surface ECG. But when the electrical impulse spreads from the SA node over the atrial myocardium, the generated electrical potentials produce a P wave on the surface ECG. The impulse is then conducted slowly through the AV node and rapidly over the His bundle and bundle branches, producing electrical
Load more

Recommended publications
  • Aberrant Ventricular Conduction Types and Concealed Conduction
    ABERRANT VENTRICULAR CONDUCTION TYPES AND CONCEALED CONDUCTION Others denominations: Aberrancy, ventricular aberration. Aberrant ventricular conduction definition: It is a term applied to alterations in QRS contour of supraventricular beats resulting from impulse transmition during periods of physiologic refractoriness and/or depressed conductivity. The supraventricular electrical impulse is conducted abnormally through the ventricular conducting system. This results in a wide QRS complex that may be confused with a ventricular ectopic beat. RELATIVE FREQUENCY OF EXPERIMENTAL ABERRATION1 Aberrant ventricular conduction was induced in 44 subjects by introduction of atrial premature beats through a transvenous catheter-electrode. Multiple patterns of aberrant ventricular conduction were obtained in 32 patients and, in the whole group, 116 different configurations were recorded. Of these, 104 showed a classical pattern of mono- or biventricular conduction disturbance. Right Bundle Branch Block (RBBB) 24%, RBBB combined with Left Anterior Fascicular Block (LAFB) 18%, LAFB 15%, RBBB combined with Left Posterior Fascicular Block (LPFB) 10%, LPFB 9%, LBBB 5%, Incomplete LBBB (ILBBB) 6%, trivial changes of the QRS contour 6% and marked anterior displacement or Prominent Anterior Forces( LSFB) 4%. Totals: RBBB: 52, LAFB: 33, LPFB: 19, LBBB: 14, trivial modifications of the QRS contour in 7 of them. In the other 5 instances, aberrant conduction manifested itself by a conspicuous anterior displacement of the QRS loop (Prominent Anterior Forces = PAF), with increased duration of anterior forces. The latter observation is worthy of notice, as it indicates that, in the differential diagnosis of the VCG pattern characterized by, conduction disturbances should be considered a possible etiological factor in addition to right ventricular hypertrophy, and true posterior wall myocardial infarction (or lateral MI in the new Bayes de Luna nomenclature concept).
    [Show full text]
  • ECG Interpretations in Anesthesiology Topics Components of The
    ECG Interpretations for the ECG Interpretations in Anesthesia Professional Anesthesiology • ECG skills are valuable at every phase of Brian C. Weiford M.D., FACC the continuum of care Postgraduate Symposium on – Preoperative: PAT clinic, etc Anesthesiology – Intraoperative April 11, 2014 – Postoperative Topics Components of the ECG - Review P – Wave: Atrial Depolarization. • The normal ECG • Can be positive, biphasic, negative. QRS Complex: Ventricular Depolarization. • Arrhythmias • Q – Wave: 1st negative deflection wave before R-Wave. – Ectopy • R – Wave: The positive deflection wave. st – Supraventricular • S – Wave: 1 negative deflection wave after R – wave. T – Wave: Ventricular Repolarization. – Ventricular • Can be positive, biphasic, negative. • Coronary Ischemia, Injury, and Infarct • Pacemakers • Miscellaneous fun with ECGs Normal Sinus Rhythm with Normal ECG Normal variant Juvenile T wave pattern From Braunwald’s Heart Disease, 7th Ed. Sinus Arrhythmia/Dysrhythmia Sinus Bradycardia •Sinus rate < 60 bpm, but usually not clinically significant unless < 50 bpm •Sinus rate is usually > 40 bpm in normal subjects Two forms of Sinus Dysrhythmia: •HR < 40 bpm can be seen commonly in normal subjects during sleep 1) more commonly, due to respiratory variability and changes in and in well-trained athletes vagal tone •Sinus rate affected by numerous medications •Beta blockers, calcium channel blockers, digoxin, antiarrhythmics, clonidine, neostigmine, etc. 2) In elderly subjects with heart disease, and probably related to •For sinus rates
    [Show full text]
  • Understanding This Complex Condition Part 2 - Management, Miscellaneous Causes, and Pitfalls
    UC Irvine Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health Title Wide Complex Tachycardias: Understanding this Complex Condition Part 2 - Management, Miscellaneous Causes, and Pitfalls Permalink https://escholarship.org/uc/item/7n5688sq Journal Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health, 9(2) ISSN 1936-900X Author Garmel, Gus M Publication Date 2008 Peer reviewed eScholarship.org Powered by the California Digital Library University of California REVIEW Wide Complex Tachycardias: Understanding this Complex Condition Part 2 - Management, Miscellaneous Causes, and Pitfalls Gus M. Garmel, MD Stanford University School of Medicine / Kaiser Permanente, Santa Clara Supervising Section Editors: Sean O. Henderson, MD Submission history: Submitted August 18, 2007; Revision Received October 19, 2007; Accepted November 26, 2007. Reprints available through open access at www.westjem.org [WestJEM. 2008;9:97-103.] INTRODUCTION to “diagnose” the ECG as “wide complex tachycardia of Patients who present with electrocardiograms (ECGs) unknown (or uncertain) etiology.” This may allow the demonstrating wide complex tachycardias (WCTs) are often treating clinician to focus on the patient and his or her challenging to clinicians. Not only may the patient present hemodynamic status, rather than the academic exercise of with (or be at risk for) hemodynamic compromise, but their ECG interpretation. The most important aspect of treating treatment may result in hemodynamic collapse if the incorrect patients who present with WCTs is to select a therapeutic pharmacologic agent is selected. In Part 1 of this article,1 approach that does no harm. Several diagnostic algorithms the identification, epidemiology, and electrophysiology of were provided for the interpretation of WCTs, although none WCTs were discussed.
    [Show full text]
  • Day 9: Rhythms: Cardiac Arrhythmias
    1. 2. 1. 1. Sinus rhythm @ ~90 bpm (arrows) 2. Junctional escape rhythm (50 bpm) with LBBB 3. Complete AV dissociation (due to 3rd degree AV block) 2. 1. Sinus rhythm 80 bpm) 2. Type II (Mobitz) 2nd degree AV block with 3:2 and 2:1 conduction 3. RBBB V1 3. 4. II V1 * * 3. 1. Sinus rhythm @ 75 bpm (arrows); 2 sinus captures (*) with RBBB aberration 2. Accelerated junctional rhythm @ 80 bpm 3. Incomplete AV dissociation due to the faster junctional rhythm; note: there is no AV block; the sinus captures whenever there is an opportunity for conduction. * * * 4. II Sinus rhythm with nonconducted PAC’s (*) in a pattern of bigeminy 5. V1 6. * * * 5. V1 1. Normal sinus rhythm (PR=220ms, QRS=120 ms) 2. Late (i.e., end-diastolic) PVC’s (*) of LV origin rsR’ 6. 1. Atrial fibrillation with one aberrantly conducted (RBBB) beat (note long cycle-short cycle rule of aberrancy, aka Ashman phenomenon) 7. V1 8. V1 7. V1 * * 1. Sinus rhythm (~70 bpm) with 2 nonconducted PAC’s (arrows) 2. Aborted 2nd degree AV block (Type I); note the PAC’s are early and they reset the sinus timing) 3. Two junctional escapes (*) 8. V1 Atrial flutter (240 bpm) with variable conduction V1 9. 10. V1 V1 9. 2:1 3:1 1. Sinus tachycardia (105 bpm) 2. 2nd degree AV block (type II); note 2:1 and 3:1 conduction ratios 3. LBBB * * * * 10. 2:1 AVB V1 F 1. Sinus rhythm (75 bpm) 2. 2nd degree AV block (2:1 conduction) with RBBB (it’s Mobitz II because the last beat has same PR interval ) 3.
    [Show full text]
  • Ashman Phenomenon: an Often Unrecognized Entity in Daily Clinical Practice
    Acta Clin Croat 2010; 49:99-100 Letter to the Editor ASHMAN PHENOMENON: AN OFTEN UNRECOGNIZED ENTITY IN DAILY CLINICAL PRACTICE Nenad Lakušić1, Darija Mahović2and Valentina Slivnjak1 1Department of Cardiology, Hospital for Medical Rehabilitation, Krapinske Toplice; 2University Department of Neurology, Zagreb University Hospital Center, Zagreb, Croatia Dear Editor, riod when supraventricular impulse reaches the His- Purkinje system resulting in a complex with RBBB2,3. We decided to reply with this letter regarding Ashman phenomenon is principally diagnosed by a the entity that is often unrecognized in daily clinical 12-lead surface electrocardiogram (ECG). Rarely, in practice. diffi cult cases, invasive electrophysiological studies Ashman phenomenon is an aberrant ventricular will be required to establish the source of an arrhyth- conduction most frequently seen during atrial fi bril- mia whether supraventricular or ventricular4. lation. Th is phenomenon is an intraventricular con- For daily use, useful criteria to establish the diag- duction abnormality caused by a change in the heart nosis of Ashman phenomenon are those described by rate. Ashman beat is typically seen when a relatively Fisch5: 1) relatively long cycle immediately preceding long cycle is followed by a relatively short cycle1. Th e the cycle terminated by the aberrant QRS complex; 2) beat with a short cycle often has right bundle-branch RBBB-form aberrancy with normal orientation of the block (RBBB) morphology (Fig. 1a). Th is phenom- initial QRS vector, a series of wide QRS supraven- enon may cause diagnostic confusion with premature tricular beats is possible; 3) irregular coupling of aber- ventricular complexes (PVCs) (Fig. 1b), and a series rant QRS complexes; and 4) lack of fully compensa- of consecutive aberrantly conducted supraventricular tory pause.
    [Show full text]
  • Master Visual Diagnosis of ECG a Short Atlas
    Master Visual Diagnosis of ECG A Short Atlas Master Visual Diagnosis of ECG A Short Atlas (Learn ECG Through ECG) Shahzad Khan MD Ren Jiang Hua MBBS MD Cardiologist Interventional Cardiologist Wuhan University School of Medicine Wuhan University School of Medicine China China ® JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • London • Philadelphia • Panama ® Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd. 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: [email protected] Overseas Offices J.P. Medical Ltd. Jaypee-Highlights Medical Publishers Inc. 83, Victoria Street, London City of Knowledge, Bld. 237, Clayton SW1H 0HW (UK) Panama City, Panama Phone: +44-2031708910 Phone: +507-301-0496 Fax: +02-03-0086180 Fax: +507-301-0499 Email: [email protected] Email: [email protected] Jaypee Brothers Medical Publishers Ltd Jaypee Brothers Medical Publishers (P) Ltd The Bourse 17/1-B Babar Road, Block-B, Shaymali 111 South Independene Mall East Mohammadpur, Dhaka-1207 Suite 835, Philadelphia, PA 19106, USA Bangladesh Phone: +267-519-9789 Mobile: +08801912003485 Email: [email protected] Email: [email protected] Jaypee Brothers Medical Publishers (P) Ltd Shorakhute, Kathmandu Nepal Phone: +00977-9841528578 Email: [email protected] Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2013, Jaypee Brothers Medical Publishers All rights reserved. No part of this book may be reproduced in any form or by any means without the prior permission of the publisher. Inquiries for bulk sales may be solicited at: [email protected] This book has been published in good faith that the contents provided by the authors contained herein are original, and is intended for educational purposes only.
    [Show full text]
  • The Gouaux-Ashman Phenomenon: His Bundle Recordings*
    The Gouaux-Ashman Phenomenon: His Bundle Recordings* BENJAMIN J. SCHERLAG, Ph.D. From the Division of Cardiovascular Disease, Department of Internal Medicine, Mount Sinai Medical Center, Miami Beach, Florida, and the Department of Medicine, University of Miami School of Medicine, Coral Gables, Florida The differentiation of ventricular premature logical behavior of A-V nodal and His bundle con­ beats from supraventricular beats with aberrant duction under these two circumstances. ventricular conduction is often difficult on the basis Figure I, taken from a study by Damato et al. of the surface electrocardiogram. The diagnosis of (1), shows the response of the His-Purkinje system aberrant conduction has been based largely on the to atrial premat~re beats delivered at varying in­ presence of a right bundle branch block pattern ap­ tervals after the previous cardiac cycle. A slight pearing in a short cycle subsequent to a longer cycle degree of aberration can be seen even with no pro­ (2). Several other criteria for diagnosing aberrant longation of the H-V or H-Q time. However, more conduction of a supraventricular beat such as vari­ marked aberration occurs with the prolongation of able coupling time have been used to differentiate His-Purkinje conduction time from 45 to 65 msec. these abnormal ventricular complexes from ventric­ Finally, block is shown distal to the recorded His ular premature beats which are most commonly fol­ bundle deflection, and these properties of the His­ lowed by a full compensatory pause. This differenti­ Purkinje system during premature activation have ation is often inexact and under some critical clinical been confirmed in other clinical laboratories.
    [Show full text]
  • Original Article
    DOI: 10.14260/jemds/2014/3398 ORIGINAL ARTICLE CLINICAL AND EPIDEMIOLOGICAL STUDY ON ATRIAL FIBRILLATION: ORIGINAL REPORT 1 2 3 4 5 Hariom Gupta , Singh K. D , Prashanth Mathew M , Shaunak Valame , Sherin Ann George HOW TO CITE THIS ARTICLE: Hariom Gupta, Singh K. D, Prashanth Mathew M, Shaunak Valame, Sherin Ann George. “Clinical and Epidemiological Study on Atrial Fibrillation: Original Report”. Journal of Evolution of Medical and Dental Sciences 2014; Vol. 3, Issue 43, September 11; Page: 10733-10742, DOI: 10.14260/jemds/2014/3398 ABSTRACT: CONTEXT: Atrial fibrillation is the most common cardiac arrhythmia in clinical practice. In developing countries like India, the high morbidity and mortality associated with this condition, warrants detailed assessment. AIMS: To find the epidemiological and etiological factors associated with atrial fibrillation. SETTINGS & DESIGN: The study was conducted in Shyam Shah Medical College and associated Sanjay Gandhi Medical Hospital in Rewa (MP), during 2010 and 2011 on 125 patients. METHODS & MATERIAL: A complete general and systemic examination to be carried out on subjects presenting with Atrial Fibrillation on Electrocardiography followed by Echocardiographic analysis. RESULTS: Out of 125 patients, who presented with Atrial Fibrillation (AF), 56.8% were females and 43.2% were males. While 102(81.6%) patients were above 40 years, 23(18.4%) were below 40 years of age. 84% of cases were reported from rural area whereas 16% were from urban area. Most common aetiology associated with AF was rheumatic heart disease (RHD) (45.6%) followed by coronary artery disease (CAD) (18.4%) and hypertension (12%). Most common etiologic factor found among rural population was RHD (51.4%).
    [Show full text]
  • I. General Principles and Definitions II. ECG Electrodes
    I. General Principles and Definitions A. Depolarization: Electrical activation of the myocardium B. Repolarization: Restoration of the electrochemical gradient of the myocardial cell creating a potential difference (voltage) across the cell membrane. C. Sequence: Depolarization begins within the pacemaker cells of the sinoatrial (SA) node and travels through internodal tracts of to the left atrium and atrioventricular (AV) node. The signal then traverses the AVN to reach the Bundle of His, which divides into right and left bundle branches; left bundle branch divides into left anterior and posterior fascicles. The signal for depolarization is spread by this specialized conduction system to coordinate activation of contractile myocardium. 1. The spread of depolarization through the cardiac chambers creates the surface shifts in the electrical field that we record as a deflection on the ECG. D. ECG: A galvanometer whose poles are a series of electrodes with six limb leads and six chest leads that records the electrical forces generated by the heart during depolarization and repolarization. The electrocardiogram is recorded on graph paper with 1 mm divisions. Each mm on the horizontal axis represents 40 msec and on the vertical axis 0.1 mV. E. P wave: ECG deflection representing atrial depolarization. F. QRS: ECG deflection representing ventricular depolarization. G. T wave: ECG deflection representing ventricular repolarization. II. ECG Electrodes A. Two lead arrangements are used for standard electrocardiography. The important concept to understand about their arrangement is that their ability to detect a change in the electrical field is limited. A lead arrangement is a “dipole” and may only detect field shifts that occur in the direction that the electrodes are “looking”, ie., it can only see the component dipole vector of the total vector generated by the heart.
    [Show full text]
  • Lorenz Plot Analysis in Dogs with Sinus Rhythm and Tachyarrhythmias
    animals Article Lorenz Plot Analysis in Dogs with Sinus Rhythm and Tachyarrhythmias Giovanni Romito 1 , Carlo Guglielmini 2,* , Helen Poser 2 and Marco Baron Toaldo 1,† 1 Department of Veterinary Medical Sciences, Alma Mater Studiorum—University of Bologna, 40064 Bologna, Italy; [email protected] (G.R.); [email protected] (M.B.T.) 2 Department of Animal Medicine, Production and Health, University of Padova, 35020 Padua, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-04-9827-2505 † Current address: Department for Small Animals, Division of Cardiology, Clinic for Small Animal Internal Medicine, Vetsuisse Faculty, University of Zurich, CH-8057 Zurich, Switzerland. Simple Summary: The Lorenz plot (LP) is a geometrical method to assess the dynamics of heart rate variability. It consists of a two-dimensional Cartesian coordinate system derived from electrocar- diographic monitoring, in which each recorded R-R interval is plotted as a function of the previous R-R interval, and the values of each pair of successive R-R interval define a dot in the plot. The resultant clusters of dots can be evaluated quantitatively and qualitatively, and categorized into distinct geometrical patterns. In humans, several studies have demonstrated that the analysis of LP patterns (LPPs) has the potential to speed-up and improve the accuracy of arrhythmia detection and differentiation, especially in patients with tachyarrhythmias. As data on LP analysis are limited in dogs, this study describes the graphic features of LP derived from Holter recordings obtained in dogs with sinus rhythm and tachyarrhythmias, and analyzes the usefulness of LPP recognition in Citation: Romito, G.; Guglielmini, C.; this species.
    [Show full text]
  • Wide Complex Tachycardias & Aberrancies
    WIDE COMPLEX TACHYCARDIAS & Objectives ABERRANCIES Upon completion of this course, the learner will: PRESENTED BY: Describe the electrophysiology of the 3 KATHY J. NOYES, DNP, APRN, FNP, BC, ACNP, BC types of Wide Complex Tachycardias Describe the criteria for 3 algorithms used to HEALTHCARE EDUCATIONAL RESOURCES & differentiate Ventricular Tachycardia (VT) SEMINARS, LLC and Supraventricular Tachycardia (SVT)with an Aberrancy Demonstrate the utilization of the diagnostic criteria for differentiating VT and SVT with Aberrancy 1 2 Mechanisms of Arrhythmias: Disclosures Classifications No Affiliations or Conflicts of Interest Arrhythmias can be Rhythms due to classified as either: abnormal impulse conduction Bonus Slides Included in the Presentation Rhythms due to including Anti-Arrhythmic Medications abnormal impulse Ex: A-fib, A-flutter, generation AV nodal reentry, tachycardias with Ex: Sinus Brady, Sinus associated Tachycardia, accessory Escape Rhythms, pathways, VT, VF Acc. Junctional or Ventricular rhythms 3 4 Types of Wide Complex Wide Complex Tachycardia's Tachycardias Intraventricular Blocks: RBBB, LBBB, Hemiblocks, Non- Definition of WCT : heart rhythms >100 bpm with a specific IVCDs QRS duration of > 0.12 sec May be supraventricular (SVT) with an Aberrancy (i.e., with BBB/ Accessory Pathways) or ventricular Aberrant Ventricular Conduction: Ashman’s (VT, VF) in origin Phenomenon, Re-entry Tachycardias, WPW Aberrancy: refers to alteration of impulse conduction from a normal pathway characterized Ventricular Arrhythmias:
    [Show full text]
  • Usmle Step 2 Ck Review ~ Cardiovascular
    USMLE STEP 2 CK REVIEW ~ CARDIOVASCULAR ISCHEMIC HEART DISEASE . Coronary Artery Disease (CAD) o Accumulation of atheromatous plaques within walls of coronary arteries that supply O2 to myocardium . Blood flow causes ischemia of myocardial cells due to lack of oxygen Effects of ischemia reversible if blood flow to heart improved . Complete occlusion of artery causes irreversible cell death called myocardial infarction o Risk Factors: . DM, HTN, tobacco, age >45, hyperlipidemia, LDL, HDL, homocysteine . FHx of premature CAD or MI in 1st-degree relative – men <45yrs & women <55yrs o Clinical Presentation Asymptomatic, stable angina, unstable angina, MI, sudden cardiac death o Canadian Cardiovascular Society (CCS) Angina Classification: . Class I Angina w/strenuous or rapid activity – no angina from ordinary physical activity . Class II Slight limitation of ordinary activity – angina after >2 blocks or >1 flight of stairs . Class III Marked limitation of ordinary activity – angina after <2 blocks or <1 flight of stairs . Class IV Any physical activity causes discomfort – angina may be present at rest o Diagnosis: . Resting ECG: Prior MI Q waves UA ST segment or T-wave abnormalities seen during episode of chest pain . Stress ECG: Recording ECG before, during & after exercise on treadmill 75% sensitive only if able to exercise sufficiently to reach 85% of predicted maximum HR o Predicted maximum HR = 220 − Patient’s age Should undergo cardiac catheterization if results from stress test Positive findings for CAD: o ST elevation Transmural infarct o ST depression Subendocardial ischemia o Failure to exercise >2mins due to symptoms o Hypotension o Ventricular arrhythmia . Stress Echocardiography: Performed before & immediately after exercise – preferred over stress ECG More sensitive in detecting ischemia, can assess LV size, EF & diagnose valvular disease Ischemia evidenced by wall motion abnormalities not seen at rest – akinesis or dyskinesis Should undergo cardiac catheterization if test results .
    [Show full text]