2018 Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay
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Guidelines on the Diagnosis and Management of Pericardial
European Heart Journal (2004) Ã, 1–28 ESC Guidelines Guidelines on the Diagnosis and Management of Pericardial Diseases Full Text The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology Task Force members, Bernhard Maisch, Chairperson* (Germany), Petar M. Seferovic (Serbia and Montenegro), Arsen D. Ristic (Serbia and Montenegro), Raimund Erbel (Germany), Reiner Rienmuller€ (Austria), Yehuda Adler (Israel), Witold Z. Tomkowski (Poland), Gaetano Thiene (Italy), Magdi H. Yacoub (UK) ESC Committee for Practice Guidelines (CPG), Silvia G. Priori (Chairperson) (Italy), Maria Angeles Alonso Garcia (Spain), Jean-Jacques Blanc (France), Andrzej Budaj (Poland), Martin Cowie (UK), Veronica Dean (France), Jaap Deckers (The Netherlands), Enrique Fernandez Burgos (Spain), John Lekakis (Greece), Bertil Lindahl (Sweden), Gianfranco Mazzotta (Italy), Joa~o Morais (Portugal), Ali Oto (Turkey), Otto A. Smiseth (Norway) Document Reviewers, Gianfranco Mazzotta, CPG Review Coordinator (Italy), Jean Acar (France), Eloisa Arbustini (Italy), Anton E. Becker (The Netherlands), Giacomo Chiaranda (Italy), Yonathan Hasin (Israel), Rolf Jenni (Switzerland), Werner Klein (Austria), Irene Lang (Austria), Thomas F. Luscher€ (Switzerland), Fausto J. Pinto (Portugal), Ralph Shabetai (USA), Maarten L. Simoons (The Netherlands), Jordi Soler Soler (Spain), David H. Spodick (USA) Table of contents Constrictive pericarditis . 9 Pericardial cysts . 13 Preamble . 2 Specific forms of pericarditis . 13 Introduction. 2 Viral pericarditis . 13 Aetiology and classification of pericardial disease. 2 Bacterial pericarditis . 14 Pericardial syndromes . ..................... 2 Tuberculous pericarditis . 14 Congenital defects of the pericardium . 2 Pericarditis in renal failure . 16 Acute pericarditis . 2 Autoreactive pericarditis and pericardial Chronic pericarditis . 6 involvement in systemic autoimmune Recurrent pericarditis . 6 diseases . 16 Pericardial effusion and cardiac tamponade . -
Cardiac Involvement in COVID-19 Patients: a Contemporary Review
Review Cardiac Involvement in COVID-19 Patients: A Contemporary Review Domenico Maria Carretta 1, Aline Maria Silva 2, Donato D’Agostino 2, Skender Topi 3, Roberto Lovero 4, Ioannis Alexandros Charitos 5,*, Angelika Elzbieta Wegierska 6, Monica Montagnani 7,† and Luigi Santacroce 6,*,† 1 AOU Policlinico Consorziale di Bari-Ospedale Giovanni XXIII, Coronary Unit and Electrophysiology/Pacing Unit, Cardio-Thoracic Department, Policlinico University Hospital of Bari, 70124 Bari, Italy; [email protected] 2 AOU Policlinico Consorziale di Bari-Ospedale Giovanni XXIII, Cardiac Surgery, Policlinico University Hospital of Bari, 70124 Bari, Italy; [email protected] (A.M.S.); [email protected] (D.D.) 3 Department of Clinical Disciplines, School of Technical Medical Sciences, University of Elbasan “A. Xhuvani”, 3001 Elbasan, Albania; [email protected] 4 AOU Policlinico Consorziale di Bari-Ospedale Giovanni XXIII, Clinical Pathology Unit, Policlinico University Hospital of Bari, 70124 Bari, Italy; [email protected] 5 Emergency/Urgent Department, National Poisoning Center, Riuniti University Hospital of Foggia, 71122 Foggia, Italy 6 Department of Interdisciplinary Medicine, Microbiology and Virology Unit, University of Bari “Aldo Moro”, Piazza G. Cesare, 11, 70124 Bari, Italy; [email protected] 7 Department of Biomedical Sciences and Human Oncology—Section of Pharmacology, School of Medicine, University of Bari “Aldo Moro”, Policlinico University Hospital of Bari, p.zza G. Cesare 11, 70124 Bari, Italy; [email protected] * Correspondence: [email protected] (I.A.C.); [email protected] (L.S.) † These authors equally contributed as co-last authors. Citation: Carretta, D.M.; Silva, A.M.; D’Agostino, D.; Topi, S.; Lovero, R.; Charitos, I.A.; Wegierska, A.E.; Abstract: Background: The widely variable clinical manifestations of SARS-CoV2 disease (COVID-19) Montagnani, M.; Santacroce, L. -
Clinical Significance of Exit Block*
Clinical Significance of Exit Block* IRANY M. DE AZEVEDO, M.D. YOSHIO WATANABE, M.D. LEONARD S. DREIFUS, M.D. From the Departments of Medicine, Physiology, and Biophysics, Hahnemann Medical College, Philadelphia, Pennsylvania The confinement of an ectopic discharge to its ily reserved for ectopic pacemakers, rather than the focus, and its consequent inability to invade the ad sinus node. jacent myocardium when falling outside of the re High Grade Atrioventricular Block. In vi rtu fractory period of the heart, is a well established ally all instances, exit block occurs in the presence phenomenon called "exit block." This cardiac ar of higher degrees of A-V block. Failure of the rhythmia was originally described by Kaufmann impulse to propagate from the subsidiary ectopic and Rothberger ( 8) to explain the failure of a para focus to either the ventricles, atria, or both is char systolic focus to activate the heart. All pacemakers acteristic of this form of exit block. Several exam are subject to exit block (9, 13, 15, 14, 11 , 16, 12, ples are illustrated. In figure 2, there is high grade 3, 10, 7, 1), however, by convention, conduction A-V block causing A-V dissociation. The atria are disturbances involving the sinus node (S-A block) under the control of the sinus node at a rate of 71 are usually excluded from this concept, and the term per minute, and the ventricles are controlled by a is reserved for ectopic pacemakers. Recent electro subsidiary ectopic pacemaker, probably originating physiological and clinical studies have shown that in the right bundle branch at a rate of approximately exit block may complicate reentrant arrhythmias and 40 per minute. -
Wide Flbs & QRS Tachycardias
Wide FLB’s and QRS Tachycardias Reading Assignment (p30-41 and 42-44) Welcome to the “5-Step Method” ECG #: Mearurements: Rhythm (s): Conduction: Waveform: Interpretation: A= V= PR= QRS= QT= Axis= 1. Compute the 5 basic measurements: HR, PR interval, QRS duration, QT interval, Axis 2. What’s the basic rhythm and other rhythm statements (e.g., PACs and PVC’s) 3. Any conduction abnormalities (SA blocks, AV blocks (Types I or II), and IV blocks 4. Waveform abnormalities beginning with P waves, QRS complexes, ST-T, and U waves 5. Final interpretations: Normal ECG or Borderline or Abnormal ECG (list final conclusions) 44 Year old man in the ER with palpitations and lightheadedness 7-1 rsR’ Mearurements: Rhythm (s): Conduction: Waveform: Interpretation: A= V=210 Wide QRS tachycardia • IVCD • rsR‘ in V1 Abnormal ECG: • Late S (rightward forces) in 1. High probability SVT with RBBB PR= I, aVL, V6 Clues: classic triphasic (rsR‘) RBBB QRS=1120 morphology in V1 is very unlikely to be VT. The most likely SVT mechanism in this QT=240 ECG is AVNRT with RBBB. 7-1 Axis= indeterminate 65 Year old man in the ICU with hypotension 7-2 qR in V1 rS in V6 Mearurements: Rhythm (s): Conduction: Waveform: Interpretation: A= V=140 Wide QRS tachycardia • IVCD • Northwest quadrant axis Abnormal ECG: (lead I and II both negative) • Left ventricular tachycardia PR= • qR pattern in V1 • rS pattern in V6 ECG Clues for VT in this case: 1) NW QRS=150 quadrant axis; 2) qR in V1; rS in V6. QT=340 Clinical clues: hypotension 7-2 Axis= -120 (NW Quadrant) I II III 7-3 75 Year old man in the ICU with recent acute coronary syndrome Mearurements: Rhythm (s): Conduction: Waveform: Interpretation: A= V= 135 Wide QRS tachycardia • IVCD • fat R in V1 (red arrows) Abnormal ECG: • Notch on downstroke of S 1. -
J Wave Syndromes
Review Article http://dx.doi.org/10.4070/kcj.2016.46.5.601 Print ISSN 1738-5520 • On-line ISSN 1738-5555 Korean Circulation Journal J Wave Syndromes: History and Current Controversies Tong Liu, MD1, Jifeng Zheng, MD2, and Gan-Xin Yan, MD3,4 1Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, 2Department of cardiology, The Second Hospital of Jiaxing, Jiaxing, China, 3Lankenau Institute for Medical Research and Lankenau Medical Center, Wynnewood, Pennsylvania, USA, 4The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China The concept of J wave syndromes was first proposed in 2004 by Yan et al for a spectrum of electrocardiographic (ECG) manifestations of prominent J waves that are associated with a potential to predispose affected individuals to ventricular fibrillation (VF). Although the concept of J wave syndromes is widely used and accepted, there has been tremendous debate over the definition of J wave, its ionic and cellular basis and arrhythmogenic mechanism. In this review article, we attempted to discuss the history from which the concept of J wave syndromes (JWS) is evolved and current controversies in JWS. (Korean Circ J 2016;46(5):601-609) KEY WORDS: Brugada syndrome; Sudden cardiac death; Ventricular fibrillation. Introduction History of J wave and J wave syndromes The concept of J wave syndromes was first proposed in 2004 The J wave is a positive deflection seen at the end of the QRS by Yan et al.1) for a spectrum of electrocardiographic (ECG) complex; it may stand as a distinct “delta” wave following the QRS, manifestations of prominent J waves that are associated with a or be partially buried inside the QRS as QRS notching or slurring. -
Abnormalities Caused by Left Bundle Branch Block - Print Article - JAAPA
Marquette University e-Publications@Marquette Physician Assistant Studies Faculty Research and Physician Assistant Studies, Department Publications 12-17-2010 Abnormalities Caused by Left undB le Branch Block James F. Ginter Aurora Cardiovascular Services Patrick Loftis Marquette University, [email protected] Published version. Journal of the American Academy of Physician Assistants, Vol. 23, No. 12 (December 2010). Permalink. © 2010, American Academy of Physician Assistants and Haymarket Media Inc. Useded with permission. Abnormalities caused by left bundle branch block - Print Article - JAAPA http://www.jaapa.com/abnormalities-caused-by-left-bundle-branch-block/... << Return to Abnormalities caused by left bundle branch block James F. Ginter, MPAS, PA-C, Patrick Loftis, PA-C, MPAS, RN December 17 2010 One of the keys to achieving maximal cardiac output is simultaneous contraction of the atria followed by simultaneous contraction of the ventricles. The cardiac conduction system (Figure 1) coordinates the polarization and contraction of the heart chambers. As reviewed in the earlier segment of this department on right bundle branch block (RBBB), the process begins with a stimulus from the sinoatrial (SA) node. The stimulus is then slowed in the atrioventricular (AV) node, allowing complete contraction of the atria. From there, the stimulus proceeds to the His bundle and then to the left and right bundle branches. The bundle branches are responsible for delivering the stimulus to the Purkinje fibers of the left and right ventricles at the same speed, which allows simultaneous contraction of the ventricles. Bundle branch blocks are common disorders of the cardiac conduction system. They can affect the right bundle, the left bundle, or one of its branches (fascicular block), or they may occur in combination. -
The Syndrome of Alternating Bradycardia and Tachycardia by D
Br Heart J: first published as 10.1136/hrt.16.2.208 on 1 April 1954. Downloaded from THE SYNDROME OF ALTERNATING BRADYCARDIA AND TACHYCARDIA BY D. S. SHORT From the National Heart Hospita. Received September 15, 1953 Among the large number of patients suffering from syncopal attacks who attended the National Heart Hospital during a four-year period, there were four in whom examination revealed sinus bradycardia alternating with prolonged phases of auricular tachycardia. These patients presented a difficult problem in treatment. Each required at least one admission to hospital and in one case the symptoms were so intractable as to necessitate six admissions in five years. Two patients had mitral valve disease, one of them with left bundle branch block. One had aortic valve sclerosis while the fourth had no evidence of heart disease. THE HEART RATE The sinus rate usually lay between 30 and 50 a minute, a rate as slow as 22 a minute being observed in one patient (Table I). Sinus arrhythmia was noted in all four patients, wandering of TABLE I http://heart.bmj.com/ RATE IN SINus RHYTHM AND IN AURICULAR TACHYCARDIA Rate in Case Age Sex Associated Rate in auricular tachycardia heart disease sinus rhythm Auricular Venliicular 1 65 M Aortic valve sclerosis 28-48 220-250 60-120 2 47 F Mitral valve disease 35-75 180-130 90-180 on September 26, 2021 by guest. Protected copyright. 3 38 F Mitral valve disease 22-43 260 50-65 4 41 F None 35-45 270 110 the pacemaker in three, and periods of sinus standstill in two (Fig. -
Pacemaker Syndrome Pacemaker Therapy Has Become an Important Therapeutic Option for Patients with Heart Rhythm Conditions Worldwide
360 Cardiology Pacemaker syndrome Pacemaker therapy has become an important therapeutic option for patients with heart rhythm conditions worldwide. Te number of elderly patients needing pacemakers is on the increase due to an ageing population worldwide. Pacemaker syndrome consists of the cardiovascular signs and symptoms of heart failure and hypotension induced by right ventricular (RV) pacing. Dr Satnam Singh Research Registrar, University of Aberdeen, Level 3, Polwarth building, Aberdeen email [email protected] Pacemaker syndrome is a term syndrome occurring in dual trial was a single blinded study proposed in 1979 by Erbel and chamber modes.5,6 It can even enrolling around 2000 patients refers to symptoms and signs in occur with AAI pacing with long with sick sinus syndrome. the pacemaker patient caused by PR intervals. All patients were implanted inadequate timing of atrial and dual chamber pacemakers ventricular contractions.1 It was first programmed to VVIR or DDDR described in 1969 by Mitsui et al2 as Incidence before implantation. Pacemaker an iatrogenic disease characterised syndrome was a secondary by the disappearance of symptoms Te overall incidence of pacemaker endpoint studied. Severe with restoration of atrioventricular syndrome is very difficult to pacemaker syndrome developed synchrony (AV synchrony). estimate but is about 20% in a in nearly 20% of VVIR-paced It means if atria and ventricles landmark trial called the Mode patients and improved with contract at appropriate timings (as Selection Trial (MOST).7 It occurs reprogramming to the dual- close to physiological), pacemaker with equal frequency in both sexes chamber pacing mode. syndrome can be prevented. -
LBBB Cardiomyopathy and His- Bundle Pacing
LBBB Cardiomyopathy and His- Bundle Pacing Rajeev Singh General Cardiology Fellow October 2018 Disclosures • No relevant disclosures Goals of this Presentaon • I. Background: Introduce the audience to the concept of LBBB Cardiomyopathy • II. IU Experience with His Bundle Pacing and LeQ Bundle Branch Cardiomyopathy • III. Novel Concepts and Future Work Background: His Bundle Pacing Carlson, Joe. “Making pacemakers easier on the heart may come down to connections.” Star Tribune. May 27, 2017. Background: LBBB Cardiomyopathy • First proposed in 2013; based on JACC arIcle which retrospecIvely analyzed 375 paents form 2007-2010 • Six Paents were idenIfied that fit pre-exisIng criteria which included 1) History of typical LBBB > 5 years 2) LVEF > 50% 3) Decrease LVEF < 40% and development of HF to NYHA II-IV 4) Major mechanical dyssychrony 4) Idiopathic eIology of cardiomyopathy Vaillant, Caroline, et al. "Resolution of left bundle branch block–induced cardiomyopathy by cardiac resynchronization therapy." Journal of the American College of Cardiology 61.10 (2013): 1089-1095. Background: LBBB HFREF Does Not Respond to ConvenIonal Treatment • January 2018 Duke study; QRS duraon, EF, and OMT studied on 659 paents • Highest HF hospitalizaon, mortality for LBBB, worst response to OMT (3.5% improvement in EF vs 10% ) Sze, Edward, et al. "Impaired recovery of left ventricular function in patients with cardiomyopathy and left bundle branch block." Journal of the American College of Cardiology71.3 (2018): 306-317. 72 Paents who underwent His Bundle Pacing -
Postural Heart Block*
Br Heart J: first published as 10.1136/hrt.44.2.221 on 1 August 1980. Downloaded from Case reports Br Heart J 1980; 44: 221-3 Postural heart block* PETER E SEDA, JOHN H McANULTY, C JOE ANDERSON From the Department of Medicine, University of Oregon Health Sciences Center, Portland, Oregon, USA SUMMARY A patient presented with orthostatic dizziness and syncope caused by postural heart block. When the patient was supine, atrioventricular conduction was normal and he was asymptomatic; when he was standing he developed second degree type II block and symptoms. The left bundle-branch block on his electrocardiogram and intracardiac electrophysiological study findings suggest that this heart block occurred distal to the His bundle. Orthostatic symptoms are usually presumed to be secondary to an inappropriate distribution of intravascular volume or to autonomic nervous system abnormalities. As shown in this patient, these symptoms may be the result of orthostatic heart block. Ambulatory monitoring may be useful in patients with orthostatic neurological symptoms, particularly when conduction abnormalities are present on the electrocardiogram. Orthostatic neurological symptoms usually result minute and regular, and increased to 90 beats a from inadequate cerebral perfusion caused by minute with some irregularity when he was upright. disturbances of the autonomic nervous system,'-3 The carotid pulse was normal, and there were no ineffective or inappropriate shifts in volume carotid bruits. The cardiac impulse was normal. http://heart.bmj.com/ distribution,4 or drugs.5 We report a patient with The second heart sound was paradoxically split. orthostatic dizziness and syncope caused by inter- There was a grade 2/6 apical systolic murmur. -
How to Define Valvular Atrial Fibrillation?
Archives of Cardiovascular Disease (2015) 108, 530—539 Available online at ScienceDirect www.sciencedirect.com REVIEW How to define valvular atrial fibrillation? Comment définir la fibrillation atriale valvulaire ? ∗ Laurent Fauchier , Raphael Philippart, Nicolas Clementy, Thierry Bourguignon, Denis Angoulvant, Fabrice Ivanes, Dominique Babuty, Anne Bernard Service de cardiologie, faculté de médecine, université Franc¸ois-Rabelais, CHU Trousseau, Tours, France Received 3 June 2015; accepted 8 June 2015 Available online 14 July 2015 KEYWORDS Summary Atrial fibrillation (AF) confers a substantial risk of stroke. Recent trials compar- Atrial fibrillation; ing vitamin K antagonists (VKAs) with non-vitamin K antagonist oral anticoagulants (NOACs) in Valve disease; AF were performed among patients with so-called ‘‘non-valvular’’ AF. The distinction between Stroke ‘‘valvular’’ and ‘‘non-valvular’’ AF remains a matter of debate. Currently, ‘‘valvular AF’’ refers to patients with mitral stenosis or artificial heart valves (and valve repair in North American guidelines only), and should be treated with VKAs. Valvular heart diseases, such as mitral regur- gitation, aortic stenosis (AS) and aortic insufficiency, do not result in conditions of low flow in the left atrium, and do not apparently increase the risk of thromboembolism brought by AF. Post-hoc analyses suggest that these conditions probably do not make the thromboembolic risk less responsive to NOACs compared with most forms of ‘‘non-valvular’’ AF. The pathogenesis of thrombosis is probably different for blood coming into contact with a mechanical prosthetic valve compared with what occurs in most other forms of AF. This may explain the results of the only trial performed with a NOAC in patients with a mechanical prosthetic valve (only a few of whom had AF), where warfarin was more effective and safer than dabigatran. -
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.