QRS Complex Detection and Analysis of Cardiovascular Abnormalities: a Review
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The ECG Made Very Easy Indeed: a Beginner’S Guide
Part 1 The ECG made very easy indeed: a beginner’s guide The ECG made very easy indeed 1 What is an ECG? 1 The heart is a pump driven by intrinsic electrical When do you need an ECG? 1 impulses which make the heart beat. An ECG is a paper recording of that electrical activity. The ECG records where How to record an ECG 2 electrical impulses start and how they flow through the How to interpret an ECG: the basics 2 heart. It does not measure how well the heart is pumping. The electrical activity of the heart starts in the ‘inter- The ECG waves and what they mean 2 nal pacemaker’, which is called the sinoatrial node. This Interpretation starts here! 4 is in the right atrium. The normal rhythm is called ‘sinus rhythm’ (properly it should be called sinoatrial rhythm, Rhythms you must be able to recognize 8 but it isn’t). The way electrical impulses flow through the Patterns you must be able to recognize 10 heart is called conduction. Abnormalities in the electrical activity of the heart can The normal ECG and its variants 13 result in abnormal conduction or rhythms where the heart ECG red flags 14 may go too quickly, too slowly, or beat irregularly. Changes to the normal flow of electricity through the heart can be shown on an ECG and may indicate damaged This guide has been written for those who are just starting heart muscle. Heart muscle can be damaged by many to use ECGs in their clinical practice. -
Acute Coronary Syndrome
Technology Assessment Systematic Review of ECG-based Signal Analysis Technologies for Evaluating Patients With Acute Coronary Syndrome Technology Assessment Program Prepared for: Agency for Healthcare Research and Quality October 2011 540 Gaither Road Rockville, Maryland 20850 Systematic Review of ECG-based Signal Analysis Technologies for Evaluating Patients With Acute Coronary Syndrome Technology Assessment Report Project ID: CRDD0311 October 2011 Duke Evidence-based Practice Center Remy R. Coeytaux, M.D., Ph.D. Philip J. Leisy, B.S. Galen S. Wagner, M.D. Amanda J. McBroom, Ph.D. Cynthia L. Green, Ph.D. Liz Wing, M.A. R. Julian Irvine, M.C.M. Gillian D. Sanders, Ph.D. DRAFT – Not for citation or dissemination This draft technology assessment is distributed solely for the purpose of peer review and/or discussion at the MedCAC meeting. It has not been otherwise disseminated by AHRQ. It does not represent and should not be construed to represent an AHRQ determination or policy. This report is based on research conducted by the Duke Evidence-based Practice Center under contract to the Agency for Healthcare Research and Quality (AHRQ), Rockville, MD (Contract No. HHSA 290-2007-10066 I). The findings and conclusions in this document are those of the authors, who are responsible for its contents. The findings and conclusions do not necessarily represent the views of AHRQ. Therefore, no statement in this report should be construed as an official position of the Agency for Healthcare Research and Quality or of the U.S. Department of Health and Human Services. None of the investigators has any affiliations or financial involvement related to the material presented in this report. -
Basic Rhythm Recognition
Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat. -
Prof. Jonathan S Steinberg
Revised June 2006 CURRICULUM VITAE PERSONAL DATA Name: Jonathan S. Steinberg, M.D. Business Address: St. Luke's/Roosevelt 1111 Amsterdam Avenue New York, NY 10025 Home Address: 268 Underhill Road South Orange, NJ 07079 Social Security No. 092-44-3548 Birthdate: March 28, 1956 Birthplace: New York Marital Status: Married, Two Children Citizenship: USA ACADEMIC TRAINING 9/72 – 6/76 AB - Queens College of the City University of New York 9/76 – 6/80 MD - Mt. Sinai School of Medicine, New York, NY TRAINEESHIP 7/80 – 6/81 Medical Intern New York University - New York VA Medical Center New York, NY 7/81 – 6/83 Medical Resident New York University - New York VA Medical Center New York 7/83 – 6/84 Chief Medical Resident New York University New York VA Medical Center New York, NY TRAINEESHIP (cont’d) 7/84 – 6/86 Clinical Cardiology Fellow George Washington University Medical Center, Washington, DC 7/86 – 6/88 Fellowship - Electrophysiology Columbia - Presbyterian Medical Center, New York, NY LICENSURE New York - 147162 New Jersey - MA57755 BOARD CERTIFICATION 1980 Diplomate, National Board of Medical Examiners 1983 Diplomate, American Board of Internal Medicine 1987 Diplomate, Subspecialty of Cardiovascular Diseases 1992 Diplomate, Clinical Electrophysiology PROFESSIONAL ORGANIZATIONS AND SOCIETIES Fellow - American College of Cardiology Fellow - American College of Physicians Fellow - Council on Clinical Cardiology, American Heart Association Member - North American Society of Pacing & Electrophysiology Member - International Society of Holter -
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. -
Cardiology- the ABC's of the PQRST
Cardiology- the ABC’s of the PQRST Heather Carter LVT, VTS (Anesthesia & Analgesia) Introduction Understanding cardiology can provide the anesthetist with the ability to trouble shoot and treat various problems. Knowing when and how to treat a bradycardia versus a tachycardia can ensure a smooth anesthetic event. Origin of the Heartbeat http://i.pinimg.com/736x/9b/70/59/9b7059c20a452fc655a26e9e3e4b40ad.jpg Understanding the origin of the heartbeat can help the anesthetist know when and how to identify a potential problem. An ECG complex consists of a PQRST complex. The sinoatrial node (SA) is the pacemaker of the heart and produces the P wave. The QRS wave is produced by the atrioventricular node (AV). The P wave in an ECG complex indicates atrial depolarization. The QRS is responsible for ventricular depolarization and the T wave is ventricular repolarization. If a P wave is absent there is a lack of atrial depolarization. This is also known as atrial standstill. P waves that are combined in the QRS complexes are indicative of ventricular tachycardia or a junctional tachycardia. Present P waves that are without a QRS are indicative of an atrial depolarization that has not been conducted through the AV node. A QRS complex without a P wave demonstrate premature or escape beats. Essentials Arrhythmias can be identified with ease if several essentials are in place. ECG leads should be placed correctly: White- Right forelimb Black- Left forelimb Green- Right hind limb Red- Left hind limb Determining the paper speed (25mm/sec vs 50mm/sec) will also help the anesthetist determine if a bradycardia or tachycardia is present. -
04. the Cardiac Cycle/Wiggers Diagram
Part I Anaesthesia Refresher Course – 2018 4 University of Cape Town The Cardiac Cycle The “Wiggers diagram” Prof. Justiaan Swanevelder Dept of Anaesthesia & Perioperative Medicine University of Cape Town Each cardiac cycle consists of a period of relaxation (diastole) followed by ventricular contraction (systole). During diastole the ventricles are relaxed to allow filling. In systole the right and left ventricles contract, ejecting blood into the pulmonary and systemic circulations respectively. Ventricles The left ventricle pumps blood into the systemic circulation via the aorta. The systemic vascular resistance (SVR) is 5–7 times greater than the pulmonary vascular resistance (PVR). This makes it a high-pressure system (compared with the pulmonary vascular system), which requires a greater mechanical power output from the left ventricle (LV). The free wall of the LV and the interventricular septum form the bulk of the muscle mass in the heart. A normal LV can develop intraventricular pressures up to 300 mmHg. Coronary perfusion to the LV occurs mainly in diastole, when the myocardium is relaxed. The right ventricle receives blood from the venae cavae and coronary circulation, and pumps it via the pulmonary vasculature into the LV. Since PVR is a fraction of SVR, pulmonary arterial pressures are relatively low and the wall thickness of the right ventricle (RV) is much less than that of the LV. The RV thus resembles a passive conduit rather than a pump. Coronary perfusion to the RV occurs continuously during systole and diastole because of the low intraventricular and intramural pressures. In spite of the anatomical differences, the mechanical behaviour of the RV and LV is very similar. -
AE Berezin, VA Vizir, OV Demidenko
MINISTRY OF HEALTH OF UKRAINE ZAPORIZHZHIA STATE MEDICAL UNIVERSITY Department Internal Medicine no2 A. E. Berezin, V. A. Vizir, O. V. Demidenko CARDIOVASCULAR DISEASE («INTERNAL MEDICINE» MODULE 2) PART 1 The executive task force for students of medical faculty of 5th cource Zaporizhzhia 2018 UDC 616.12(075.8) B45 Ratified on meeting of the Central methodical committee of Zaporizhzhia State Medical University and it is recommended for the use in educational process for foreign students. (Protocol no 5 from 24 may 2018 ) Reviewers: V. V. Syvolap - MD, PhD, professor, Head of Department of Propedeutics of In- ternal Diseases with the Course of Patients’ Care, Zaporizhzhia State Medical Uni- versity; O. V. Kraydashenko - MD, PhD, professor, Head of Department of Clinical Pharmacology, Pharmacy and Pharmacotherapy with the Course of Cosmetology, Zaporizhzhia State Medical University. Authors: A. E. Berezin - MD, PhD, professor, Department of Internal Diseases 2; V. A. Vizir - MD, PhD, professor, Department of Internal Diseases 2; O. V. Demidenko -MD, PhD, Head of Department of Internal Diseases 2. Berezin A. E. B45 Cardiovascular diseases («Internal Medicine». Modul 2). Part 1=Серцево-судинні захворювання («Внутрішня медицина». Модуль 2). Ч. 1 : The executive task force for students of 5th course of medical faculty / A. E. Berezin, V. A. Vizir, O. V. Demidenko. – Zaporizhzhia : ZSMU, 2018. – 220 p. The executive task force is provided for students of 5th courses of medical faculties for helping to study of some topics in the fields of cardiovascular diseases incorporated into the discipline «Internal Medicine». There is the information about the most impor- tant topics regarding diagnosis of cardiac diseases. -
High-Frequency Signature of the QRS Complex Across Ischemia Quantified by QRS Slopes
High-Frequency Signature of the QRS Complex across Ischemia Quantified by QRS Slopes E Pueyo, A Arciniega, P Laguna Comm Techn Group, Aragon Institute of Eng Research, University of Zaragoza, Spain Abstract specificity values. The reason for this could be in the hy- pothesis itself or in the way the high-frequency compo- In this study two new indexes that measure the upward nents are usually quantified by high-pass filtering of the and downward slopes of the QRS complex are proposed to narrow transient QRS signal. The filtering introduces leak- quantify variations in the depolarization period due to in- age in frequency and smearing in time that can mask the duced ischemia during Percutaneous Transluminal Coro- very nature of the localized HF-QRS features. To further nary Angioplasty. Our results show that QRS slopes turn investigate on this we hypothesize that if the decrease in out to be substantially less steep during artery occlusion, the HF-QRS components is due to a reduction of the con- being this effect more manifested for the downward slope duction velocity in the region of ischemia [4], such a phe- than for the upward one. Comparing the proposed indexes nomenon could be also quantified by measuring the up- with a previously reported index that quantifies the energy ward and downward slopes of the QRS complex. of the high-frequency QRS signal (150-250 Hz), it is shown To test our hypothesis, we analyze recordings of pa- that the ability of the slope indexes for ischemia detection tients before and during prolonged Percutaneous Translu- is clearly superior. -
Decrease in the High Frequency QRS Components Depending on the Local Conduction Delay
Jpn Circ J 1998; 62: 844–848 Decrease in the High Frequency QRS Components Depending on the Local Conduction Delay Tetsu Watanabe, MD; Michiyasu Yamaki, MD; Hidetada Tachibana, MD; Isao Kubota, MD; Hitonobu Tomoike, MD The high frequency components contained in the QRS complex (HF-QRS) are a powerful indicator for the risk of sudden cardiac death. However, it is controversial whether conduction delay increases or decreases the HF- QRS. In 21 anesthetized, open-chest dogs, the right atrium was constantly paced. A cannula was inserted into the left anterior descending artery and flecainide, lidocaine or disopyramide was infused to slow the local conduc- tion. Sixty unipolar electrograms were recorded from the entire ventricular surface and were signal-averaged. Data were filtered (30–250Hz) by using fast-Fourier transform. The HF-QRS was calculated by integrating the filtered QRS signal. Activation time (AT; dV/dt minimum) was delayed and the HF-QRS was reduced in the area perfused by flecainide, lidocaine or disopyramide. The percent increase in AT closely correlated the percentage decrease in the HF-QRS; the correlation coefficients were 0.75, 0.83 and 0.76 for flecainide, lido- caine and disopyramide infusion, respectively, (p<0.001). Decrease in the HF-QRS linearly correlated with the local conduction delay. This study proved that conduction delay decreases the HF-QRS, and that the HF-QRS is a potent indicator of disturbed local conduction. (Jpn Circ J 1998; 62: 844–848) Key Words: Disopyramide; Fast-Fourier transform; Flecainide; Lidocaine; Signal averaging ate potentials, or high-frequency low-amplitude anesthetized with sodium pentobarbital (30mg/kg, iv) and signals in the terminal portion of the QRS received supplemental doses as needed. -
Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives
Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives ▪ Describe the normal cardiac anatomy and physiology and normal electrical conduction through the heart. ▪ Identify and relate waveforms to the cardiac cycle. Cardiac Anatomy ▪ 2 upper chambers ▪ Right and left atria ▪ 2 lower chambers ▪ Right and left ventricle ▪ 2 Atrioventricular valves (Mitral & Tricuspid) ▪ Open with ventricular diastole ▪ Close with ventricular systole ▪ 2 Semilunar Valves (Aortic & Pulmonic) ▪ Open with ventricular systole ▪ Open with ventricular diastole The Cardiovascular System ▪ Pulmonary Circulation ▪ Unoxygenated – right side of the heart ▪ Systemic Circulation ▪ Oxygenated – left side of the heart Anatomy Coronary Arteries How The Heart Works Anatomy Coronary Arteries ▪ 2 major vessels of the coronary circulation ▪ Left main coronary artery ▪ Left anterior descending and circumflex branches ▪ Right main coronary artery ▪ The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia behind the aortic valve leaflets. Physiology Blood Flow Unoxygenated blood flows from inferior and superior vena cava Right Atrium Tricuspid Valve Right Ventricle Pulmonic Valve Lungs Through Pulmonary system Physiology Blood Flow Oxygenated blood flows from the pulmonary veins Left Atrium Mitral Valve Left Ventricle Aortic Valve Systemic Circulation ▪ Blood Flow Through The Heart ▪ Cardiology Rap Physiology ▪ Cardiac cycle ▪ Represents the actual time sequence between -
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.