How to Tell Heart Rate from an ECG?
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Some Observations on the Atrial Sound*
15 Oktober 1960 S.A. TYDSKRIF VIR GENEESKUNDE 887 SOME OBSERVATIONS ON THE ATRIAL SOUND* JOHN R BARLOW, M.R, RCH., M.R.C.P., Department of Medicine, University of The WiTwaTersralld. Johallllesburg The atrial sound, also known as the fourth heart sound Emotional factors probably play a large part in this; the or. presystolic gallop, has been defined' as an audible P-G interval may quickly horten again on the introduction ibration occurring more than 0·07 second after the of an intravenous needle or imilar procedure. beginning of the P wave of the simultaneous electrocardio 3. EffeCT of respiration. Whereas re piration produce gram (ECG) but preceding the onset of the QRS complex. no effect on the P-G interval in patients with hyperten ion It has been shown' that, unrelated to any alteration in the or ischaemia. the atrial sound of cor pulmonale both in P-R interval, the position of the atrial sound varies in creases in intensity and occurs earlier in the cardiac cycle relation to the first heart sound and to the simultaneous during inspiration as compared with expiration (Fig. 4). ECG. 4. EffeCT of various procedures. Jt has already been Jt is the purpose of this paper to demonstrate this mentioned that the intravenous administration of hypo variation in the timing of the atrial sound and to discuss tensive drugs will increase the P-G interval in hypertensive some of the clinical implications resulting from this varia patients. The inhalation of amyl nitrite has a similar effect bility. in hypertension (Fig. 5), though a change in the P-G METHODS AND OBSERVATIO S interval is seldom seen in cases with ischaemic heart disease following inhalation of this drug. -
Chronotropic and Dromotropic Responses to Localized Glutamate Microinjections in the Rat $ Nucleus Ambiguus
brain research 1542 (2014) 93–103 Available online at www.sciencedirect.com www.elsevier.com/locate/brainres Research Report Chronotropic and dromotropic responses to localized glutamate microinjections in the rat $ nucleus ambiguus Karla N. Sampaio1,He´lder Mauad2, K. Michael Spyer, Timothy W. Fordn Division of Biosciences, Faculty of Life Sciences, University College London, Gower Street, London WC1E 6BT, UK article info abstract Article history: The cardioinhibitory effects of cardiac vagal motoneurons (CVMs) are mediated by Accepted 18 October 2013 activation of postganglionic neurons in the epicardial ganglia which have been shown to Available online 24 October 2013 exert functionally selective effects on heart rate and atrioventricular conduction in the rat. Here we investigate whether CVMs producing these responses may occupy different Keywords: rostrocaudal positions within the nucleus ambiguus. Excitation of CVMs was attempted Autonomic nervous system by microinjections of glutamate into the nucleus ambiguus of an arterially perfused Vagus nerve preparation in a grid extending over 2 mm in the rostrocaudal plane using the obex as a Nucleus ambiguus reference point. Microinjections were paired, one made during pacing to measure changes Heart rate in atrioventricular conduction (P-R interval) independent of changes in heart rate and the Glutamate other looking for changes in heart period (P-P interval) un-paced. Although evidence of a differential distribution was found in 7 cases, in the majority (13/20), sites producing maximal effects on both variables coincided. Maximal changes in atrioventricular conduc- tion resulted from more rostral sites in 6 cases and from a more caudal site in only one. Overall, the ratio of the change in atrioventricular conduction to the change in heart rate for a given site was significantly greater 1 mm rostral to the obex than at either end of the test grid. -
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. -
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. -
Electrocardiography: a Technologist's Guide to Interpretation
CONTINUING EDUCATION Electrocardiography: A Technologist’s Guide to Interpretation Colin Tso, MBBS, PhD, FRACP, FCSANZ1,2, Geoffrey M. Currie, BPharm, MMedRadSc(NucMed), MAppMngt(Hlth), MBA, PhD, CNMT1,3, David Gilmore, ABD, CNMT, RT(R)(N)3,4, and Hosen Kiat, MBBS, FRACP, FACP, FACC, FCCP, FCSANZ, FASNC, DDU1,2,3,5 1Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales, Australia; 2Cardiac Health Institute, Sydney, New South Wales, Australia; 3Faculty of Science, Charles Sturt University, Wagga Wagga, New South Wales, Australia; 4Faculty of Medical Imaging, Regis College, Boston, Massachusetts; and 5Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia CE credit: For CE credit, you can access the test for this article, as well as additional JNMT CE tests, online at https://www.snmmilearningcenter.org. Complete the test online no later than December 2018. Your online test will be scored immediately. You may make 3 attempts to pass the test and must answer 80% of the questions correctly to receive 1.0 CEH (Continuing Education Hour) credit. SNMMI members will have their CEH credit added to their VOICE transcript automatically; nonmembers will be able to print out a CE certificate upon successfully completing the test. The online test is free to SNMMI members; nonmembers must pay $15.00 by credit card when logging onto the website to take the test. foundation for understanding the science of electrocardiog- The nuclear medicine technologist works with electrocardio- raphy and its interpretation. graphy when performing cardiac stress testing and gated cardiac imaging and when monitoring critical patients. -
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. -
Short PR Intervals and Tachyarrhythmias in Fabry's Disease
Postgraduate Medical Journal (1986) 62, 285-287 Postgrad Med J: first published as 10.1136/pgmj.62.726.285 on 1 April 1986. Downloaded from Clinical Reports Short PR intervals and tachyarrhythmias in Fabry's disease J. Efthimiou, J. McLelland and D.J. Betteridge Department ofMedicine, University College Hospital, London WCJE6JJ, UK. Summary: Two brothers with Fabry's disease presenting with palpitations were found to have intermittent supraventricular tachycardias. Their electrocardiograms, when symptom-free, revealed short PR intervals consistent with ventricular pre-excitation. Treatment of one of the brothers with verapamil resulted in improvement of the palpitations and reduction in frequency of the tachycardia. Recurrent supraventricular tachycardia associated with ventricular pre-excitation has not previously been described in Fabry's disease. Evidence suggests that this complication may be due to glycolipid deposition in the conducting system around the atrioventricular node. Introduction Fabry's disease (angiokeratoma corporis diffusum) is evidence of heart failure. an X-linked disorder of glycolipid metabolism result The full blood count, erythrocyte sedimentation ing in deposition ofceramide trihexoside, particularly rate, plasma electrolytes, cardiac enzymes, thyroid in the skin, kidneys and cardiovascular system. Car- function tests and chest radiograph were normal. The copyright. diac manifestations are numerous and include rhythm creatinine clearance was reduced at 51 ml/min, but disturbances, myocardial infarction, and congestive or urine analysis was normal with no proteinuria. The rarely hypertrophic cardiomyopathy (Colucci et al., electrocardiogram revealed a short PR interval (0.10 s) 1982). with no delta wave (Figure 1). Electrocardiograms We report on two brothers known to have Fabry's recorded 12 and 5 years earlier revealed normal PR disease who had intermittent tachyarrhythmias with intervals of0.16 s and 0.12 s respectively. -
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. -
JUGULAR VENOUS PRESSURE Maddury Jyotsna
INDIAN JOURNAL OF CARDIOVASCULAR DISEASES JOURNAL in women (IJCD) 2017 VOL 2 ISSUE 2 CLINICAL ROUNDS 1 WINCARS JVP- JUGULAR VENOUS PRESSURE Maddury Jyotsna DEFINITION OF JUGULAR VENOUS PULSE AND The external jugular vein descends from the angle of the PRESSURE mandible to the middle of the clavicle at the posterior Jugular venous pulse is defined as the oscillating top of border of the sternocleidomastoid muscle. The external vertical column of blood in the right Internal Jugular jugular vein possesses valves that are occasionally Vein (IJV) that reflects the pressure changes in the right visible. Blood flow within the external jugular vein is atrium in cardiac cycle. In other words, Jugular venous nonpulsatile and thus cannot be used to assess the pressure (JVP) is the vertical height of oscillating column contour of the jugular venous pulse. of blood (Fig 1). Reasons for Internal Jugular Vein (IJV) preferred over Fig 1: Schematic diagram of JVP other neck veins are IJV is anatomically closer to and has a direct course to right atrium while EJV does not directly drain into Superior vena cava. It is valve less and pulsations can be seen. Due to presence of valves in External Jugular vein, pulsations cannot be seen. Vasoconstriction secondary to hypotension (as in congestive heart failure) can make EJV small and barely visible. EJV is superficial and prone to kinking. Partial compression of the left in nominate vein is usually relieved during modest inspiration as the diaphragm and the aorta descend and the pressure in the two internal