ECG) Signal in the Magnetic Resonance Imaging (MRI
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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. -
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. -
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). -
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). -
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 -
Pulse Wave Analysis to Estimate Cardiac Output
CLINICAL FOCUS REVIEW Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M., Editor Pulse Wave Analysis to Estimate Cardiac Output Karim Kouz, M.D., Thomas W. L. Scheeren, M.D., Daniel de Backer, M.D., Bernd Saugel, M.D. ardiac output (CO)–guided therapy is a promising reference CO value measured using an indicator dilution Capproach to hemodynamic management in high-risk method (transpulmonary thermodilution or lithium dilu- patients having major surgery1 and in critically ill patients tion).5,9 CO measurement using indicator dilution methods with circulatory shock.2 Pulmonary artery thermodilu- requires a (central) venous catheter for indicator injection tion remains the clinical reference method for CO mea- upstream in the circulation and a dedicated arterial catheter Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/134/1/119/513741/20210100.0-00023.pdf by guest on 29 September 2021 surement,3 but the use of the pulmonary artery catheter and measurement system to detect downstream indicator decreased over the past two decades.4 Today, various CO temperature or concentration changes.5,9–11 monitoring methods with different degrees of invasiveness The VolumeView system (Edwards Lifesciences, are available, including pulse wave analysis.5 Pulse wave USA) and the PiCCO system (Pulsion Medical Systems, analysis is the mathematical analysis of the arterial blood Germany) calibrate pulse wave analysis–derived CO to pressure waveform and enables CO to be estimated con- transpulmonary thermodilution–derived CO. To measure tinuously and in real time.6 In this article, we review pulse CO using transpulmonary thermodilution, a bolus of cold wave analysis methods for CO estimation, including their crystalloid solution is injected in the central venous circu- underlying measurement principles and their clinical appli- lation.10 The cold indicator bolus injection causes changes cation in perioperative and intensive care medicine. -
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 -
Chapter 9 Monitoring of the Heart and Vascular System
Chapter 9 Monitoring of the Heart and Vascular System David L. Reich, MD • Alexander J. Mittnacht, MD • Martin J. London, MD • Joel A. Kaplan, MD Hemodynamic Monitoring Cardiac Output Monitoring Arterial Pressure Monitoring Indicator Dilution Arterial Cannulation Sites Analysis and Interpretation Indications of Hemodynamic Data Insertion Techniques Systemic and Pulmonary Vascular Resistances Central Venous Pressure Monitoring Frank-Starling Relationships Indications Monitoring Coronary Perfusion Complications Electrocardiography Pulmonary Arterial Pressure Monitoring Lead Systems Placement of the Pulmonary Artery Catheter Detection of Myocardial Ischemia Indications Intraoperative Lead Systems Complications Arrhythmia and Pacemaker Detection Pacing Catheters Mixed Venous Oxygen Saturation Catheters Summary References HEMODYNAMIC MONITORING For patients with severe cardiovascular disease and those undergoing surgery associ- ated with rapid hemodynamic changes, adequate hemodynamic monitoring should be available at all times. With the ability to measure and record almost all vital physi- ologic parameters, the development of acute hemodynamic changes may be observed and corrective action may be taken in an attempt to correct adverse hemodynamics and improve outcome. Although outcome changes are difficult to prove, it is a rea- sonable assumption that appropriate hemodynamic monitoring should reduce the incidence of major cardiovascular complications. This is based on the presumption that the data obtained from these monitors are interpreted correctly and that thera- peutic decisions are implemented in a timely fashion. Many devices are available to monitor the cardiovascular system. These devices range from those that are completely noninvasive, such as the blood pressure (BP) cuff and ECG, to those that are extremely invasive, such as the pulmonary artery (PA) catheter. To make the best use of invasive monitors, the potential benefits to be gained from the information must outweigh the potential complications. -
The Relation Between Cardiac Output and Body Size*
Br Heart J: first published as 10.1136/hrt.25.4.425 on 1 July 1963. Downloaded from Brit. Heart J., 1963, 25, 425. THE RELATION BETWEEN CARDIAC OUTPUT AND BODY SIZE* BY W. JEGIER, PAUL SEKELJ, P. A. M. AULD, R. SIMPSON, AND M. McGREGOR From the Joint Cardio-Respiratory Service of the Montreal Children's Hospital and the Royal Victoria Hospital, The Department of Anesthesia, The Montreal Children's Hospital, and the Department ofPhysiology, McGill University, Montreal, Quebec, Canada Received December 10, 1962 A prerequisite in the study of abnormal body function is the ability to establish the limits of normal. In the case of parameters such as cardiac output that vary with the size of the subject, it has become an accepted practice to standardize values in relation to the body surface area. Thus the cardiac index describes the cardiac output per square metre of body surface area, and the stroke index describes the volume of blood per heart beat per square metre of body surface area. The validity of these expressions depends on the premise that there is a constant or straight line relation between body surface area on the one hand, and cardiac output and stroke volume on the other, over the whole range of body size to be studied, and that the relation can be described by a simple regression equation cutting the intercept at zero. Only where this is so is it meaningful to refer to "the normal" cardiac index or stroke index. Though this premise is backed by observations in the case of adult or adolescent subjects, it was until recently entirely unsupported in the case of children and is still unsupported by any data for infants. -
Cardiac Output
Overview of Human Anatomy and Physiology: Cardiac Output Introduction Welcome to the Overview of Human Anatomy and Physiology course on the Cardiac System. This module, Cardiac Output, discusses measurement of heart activity and factors that affect activity. After completing this module, you should be able to: 1. Define stroke volume and cardiac output. 2. Discuss the relationship between heart rate, stroke volume, and cardiac output. 3. Identify the factors that control cardiac output. Measurement Cardiac Output The activity of the heart can be quantified to provide information on its health and efficiency. One important measurement is cardiac output (CO), which is the volume of blood ejected by the left ventricle each minute. Heart rate and stroke volume determine cardiac output. Heart rate (HR) is the number of heartbeats in one minute. The volume of blood ejected by the left ventricle during a heartbeat is the stroke volume (SV), which is measured in milliliters. Equation Cardiac output is calculated by multiplying the heart rate and the stroke volume. Average Values Cardiac output is the amount of blood pumped by the left ventricle--not the total amount pumped by both ventricles. However, the amount of blood within the left and right ventricles is almost equal, approximately 70 to 75 mL. Given this stroke volume and a normal heart rate of 70 beats per minute, cardiac output is 5.25 L/min. Relationships When heart rate or stroke volume increases, cardiac output is likely to increase also. Conversely, a decrease in heart rate or stroke volume can decrease cardiac output. What factors regulate increases and decreases in cardiac output? Regulation Factors Regulating Cardiac Output Factors affect cardiac output by changing heart rate and stroke volume. -
Role of ACE Inhibitors in Hypertension Complicated by Vascular Disease S 37
Br Heart Jf (Supplement) 1994; 72: 33-37 S 33 Role of ACE inhibitors in hypertension Br Heart J: first published as 10.1136/hrt.72.3_Suppl.S33 on 1 September 1994. Downloaded from complicated by vascular disease Gordon T McInnes Hypertension is an important risk factor for Locally produced angiotensin II may exert a vascular disease. Therefore, it is not surprising significant effect on vascular tone directly by that many patients with hypertension have contracting smooth muscle and indirectly by widespread atherosclerotic disease. Treatment releasing catecholamines from surrounding with conventional antihypertensive drugs can nerve endings. Direct clinical evidence be problematic in such patients. In this article suggests that tissue actions may influence I consider the use of angiotensin converting regional blood flow. Thus, enalapril, at a dose enzyme (ACE) inhibitors in managing hyper- which did not induce significant humoral or tension complicated by vascular disease, pay- systemic haemodynamic effects, reduced left ing particular attention to cerebrovascular ventricular inotropic state and increased disease and peripheral vascular disease affect- coronary blood flow when infused into the ing the legs. Coronary artery disease and coronary bed and increased forearm blood atherosclerotic renovascular disease are flow when infused into the forearm.' considered only briefly. Vascular angiotensin II may be a major ACE inhibitors reduce blood pressure in pathological factor in the development of hypertensive patients by decreasing peripheral atherosclerosis (figure), mediating the pro- resistance with little effect on cardiac output liferation of arterial smooth muscle cells by or heart rate. The lack of reflex tachycardia is many mechanisms, including a direct effect on likely to be due to downward resetting of growth factor production and reciprocal sup- baroceptor reflexes, though ACE inhibitor pression of arterial bradykinin concentrations. -
The Heart and Cardiovascular Function
18 The Heart and Cardiovascular Function Lecture Presentation by Lori Garrett © 2018 Pearson Education, Inc. Section 1: Structure of the Heart Learning Outcomes 18.1 Describe the heart’s location, shape, its four chambers, and the pulmonary and systemic circuits. 18.2 Describe the location and general features of the heart. 18.3 Describe the structure of the pericardium and explain its functions, identify the layers of the heart wall, and describe the structures and functions of cardiac muscle. 18.4 Describe the cardiac chambers and the heart’s external anatomy. © 2018 Pearson Education, Inc. Section 1: Structure of the Heart Learning Outcomes (continued) 18.5 Describe the major vessels supplying the heart, and cite their locations. 18.6 Trace blood flow through the heart, identifying the major blood vessels, chambers, and heart valves. 18.7 Describe the relationship between the AV and semilunar valves during a heartbeat. 18.8 Define arteriosclerosis, and explain its significance to health. © 2018 Pearson Education, Inc. Module 18.1: The heart has four chambers that pump and circulate blood through the pulmonary and systemic circuits Cardiovascular system = heart and blood vessels transporting blood Heart—directly behind sternum . Base—superior • where major vessels are • ~1.2 cm (0.5 in.) to left • 3rd costal cartilage . Apex—inferior, pointed tip • ~12.5 cm (5 in.) from base • ~7.5 cm (3 in.) to left • 5th intercostal space © 2018 Pearson Education, Inc. Borders of the heart © 2018 Pearson Education, Inc. Module 18.1: Heart location and chambers Heart = 2-sided pump with 4 chambers . Right atrium receives blood from systemic circuit .