IHEU-IHES-IHP Front Matter
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
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. -
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. -
Spontaneous Resolution of Sinoatrial Exit Block and Atrioventricular Dissociation in a Child with Dengue Fever Kaushik J S, Gupta P, Rajpal S, Bhatt S
Case Report Singapore Med J 2010; 51(9) : e146 Spontaneous resolution of sinoatrial exit block and atrioventricular dissociation in a child with dengue fever Kaushik J S, Gupta P, Rajpal S, Bhatt S ABSTRACT her heart rate was regular at 92/min, respiratory rate at Cardiac rhythm abnormalities, including 22/min and blood pressure (BP) at 110/74 mmHg. There ventricular arrhythmia, atrial fibrillation and was a petechial rash over the patient’s back, trunk and atrioventricular block, have been observed upper extremities. The Hess test (tourniquet test) for during the acute stage of dengue haemorrhagic capillary fragility was positive. Systemic examination fever. Atrioventricular or complete heart did not reveal any abnormality. block can be fatal and may require a temporary Investigations revealed normal haemoglobin (12.1 pacemaker. We report a ten-year-old girl who g/dl), haematocrit (35.2%) and leucocyte (6500/cumm) presented with dengue haemorrhagic fever counts, while the platelet count was observed to be with sinoatrial block and atrioventricular low (38000/cumm). Dengue serology was reactive dissociation that had a spontaneous resolution. for immunoglobulin G (IgG) and immunoglobulin M (IgM), suggesting acute primary infection. The liver Keywords: atrioventricular block, enzymes and renal profile, including serum electrolytes, atrioventricular dissociation, dengue were normal. The patient was managed supportively haemorrhagic fever, rhythm abnormality, according to the World Health Organization (WHO) sinoatrial block recommendations for management of dengue Singapore Med J 2010; 51(8): e146-e148 haemorrhagic fever.(3) The following day, the patient was observed to have INTRODUCTION bradycardia (pulse rate 50/min, regular), with normal Dengue fever is a viral infection that is transmitted BP. -
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 -
Cardiac Arrhythmia
Cardiac Arrhythmia How to approach นพ.พินิจ แกวสุวรรณะ หน่วยโรคหัวใจและหลอดเลือด EKG paper is a grid where time is measured along the horizontal axis. Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds. Voltage is measured along the vertical axis Voltage is measured along the vertical axis. 10 mm is equal to 1mV in voltage. The diagram below illustrates the configuration of EKG graph paper and where to measure the components of the EKG wave form P wave Indicates atrial depolarization, or contraction of the atrium. Normal duration is not longer than 0.11 seconds (less than 3 small squares) Amplitude (height) is no more than 3 mm No notching or peaking QRS complex Indicates ventricular depolarization, or contraction of the ventricles. Normally not longer than .10 seconds in duration Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4 R waves are deflected positively and the Q and S waves are negative T wave Indicates ventricular repolarization Not more that 5 mm in amplitude in standard leads and 10 mm in precordial leads Rounded and asymmetrical ST segment Indicates early ventricular repolarization Normally not depressed more than 0.5 mm May be elevated slightly in some leads (no more than 1 mm) PR interval Indicates AV conduction time Duration time is 0.12 to 0.20 seconds QT interval Indicates repolarization time General rule: duration is less than half the preceding R-R interval Sinus Bradycardia Rate40-59 bpm P wavesinus QRSnormal (.06-.12) ConductionP-R normal or slightly prolonged at slower rates Rhythmregular or slightly irregular This rhythm is often seen as a normal variation in athletes, during sleep, or in response to a vagal maneuver. -
Resolution of Left Bundle Branch Block–Induced Cardiomyopathy by Cardiac Resynchronization Therapy
Journal of the American College of Cardiology Vol. xx, No. x, 2013 © 2013 by the American College of Cardiology Foundation ISSN 0735-1097/$36.00 Published by Elsevier Inc. http://dx.doi.org/10.1016/j.jacc.2012.10.053 CLINICAL RESEARCH Resolution of Left Bundle Branch Block–Induced Cardiomyopathy by Cardiac Resynchronization Therapy Caroline Vaillant, MD,* Raphaël P. Martins, MD,*† Erwan Donal, MD, PHD,*† Christophe Leclercq, MD, PHD,*† Christophe Thébault, MD,* Nathalie Behar, MD,* Philippe Mabo, MD,*† Claude Daubert, MD, FACC*† Rennes, France Objectives The study sought to describe a specific syndrome characterized by isolated left bundle branch block (LBBB) and a history of progressive left ventricular (LV) dysfunction, successfully treated by cardiac resynchronization ther- apy (CRT). Background Isolated LBBB in animals causes cardiac remodeling due to mechanical dyssynchrony, reversible by biventricular stimulation. However, the existence of LBBB-induced cardiomyopathy in humans remains uncertain. Methods Between 2007 and 2010, 375 candidates for CRT were screened and retrospectively included in this study if they met all criteria of a pre-defined syndrome, including: 1) history of typical LBBB for Ͼ5 years; 2) LV ejection fraction (EF) Ͼ50%; 3) decrease in LVEF to Ͻ40% and development of heart failure (HF) to NYHA functional class II to IV over several years; 4) major mechanical dyssynchrony; 5) no known etiology of cardiomyopathy; and 6) super-response to CRT with LVEF Ͼ45% and decrease in NYHA functional class at 1 year. Results The syndrome was identified in 6 patients (1.6%), 50.5 years of age on average at the time of LBBB diagnosis. -
Cardiac Rhythms and Arrhythmias Chapter 12 Sinus Node Dysfunction
SECTION II Cardiac Rhythms and Arrhythmias Chapter 12 Sinus Node Dysfunction SAROJA BHARATI, NORA GOLDSCHLAGER, FRED KUSUMOTO, RALPH LAZZARA, RABIH AZAR, STEPHEN HAMMILL, and GERALD NACCARELLI Epidemiology: Nora Goldschlager, Fred Kusumoto, and Rabih Azar Anatomy and Pathology: Saroja Bharati Basic Electrophysiology: Ralph Lazzara Etiology: Nora Goldschlager, Fred Kusumoto, and Rabih Azar Diagnostic Evaluation: Gerald Naccarelli Clinical Electrophysiology: Stephen Hammill Evidence-Based Therapy: Nora Goldschlager, Fred Kusumoto, and Rabih Azar In the early 1900s Keith and Flack identified the sinus due to the decrease in vagal tone that occurs with node as the region responsible for activation of the increasing age. heart.1 Laslett first suggested sinus node dysfunction as Sinus node dysfunction should be suspected when a a cause of bradycardia in 1909, and during the 1950s patient describes symptoms of fatigue, syncope or pre- and 1960s Short, Ferrer, Lown, and others described syncope, or exercise intolerance and is noted to have the clinical spectrum of sinus node dysfunction that is sinus bradycardia or pauses on the 12-lead ECG or dur- commonly called the “sick sinus syndrome resting sinus ing Holter monitoring. In general, symptomatic sinus bradycardia.”2-5 Sinus node dysfunction can have multi- node dysfunction increases with age, with the incidence ple electrocardiographic manifestations including sinus doubling between the fifth and sixth decades of life. pauses, the bradycardia-tachycardia syndrome, and inap- In one study of approximately 9000 patients visiting propriate sinus node response to exercise (chronotropic a regional cardiac center in Belgium, Kulbertus et al. incompetence). estimated that the incidence of sinus node dysfunction is less than 5 per 3000 people older than 50 years of age.9 However, sinus node dysfunction is more com- Epidemiology monly identified today because of an increased elderly population and increased physician awareness. -
View Pdf Copy of Original Document
Phenotype definition for the Vanderbilt Genome-Electronic Records project Identifying genetics determinants of normal QRS duration (QRSd) Patient population: • Patients with DNA whose first electrocardiogram (ECG) is designated as “normal” and lacking an exclusion criteria. • For this study, case and control are drawn from the same population and analyzed via continuous trait analysis. The only difference will be the QRSd. Hypothetical timeline for a single patient: Notes: • The study ECG is the first normal ECG. • The “Mildly abnormal” ECG cannot be abnormal by presence of heart disease. It can have abnormal rate, be recorded in the presence of Na-channel blocking meds, etc. For instance, a HR >100 is OK but not a bundle branch block. • Y duration = from first entry in the electronic medical record (EMR) until one month following normal ECG • Z duration = most recent clinic visit or problem list (if present) to one week following the normal ECG. Labs values, though, must be +/- 48h from the ECG time Criteria to be included in the analysis: Criteria Source/Method “Normal” ECG must be: • QRSd between 65-120ms ECG calculations • ECG designed as “NORMAL” ECG classification • Heart Rate between 50-100 ECG calculations • ECG Impression must not contain Natural Language Processing (NLP) on evidence of heart disease concepts (see ECG impression. Will exclude all but list below) negated terms (e.g., exclude those with possible, probable, or asserted bundle branch blocks). Should also exclude normalization negations like “LBBB no longer present.” -
Hypercalcemia-Induced New Onset Left Bundle Branch Block Mimicking Acute Myocardial Infarction in a Patient with Primary Hyperparathyroidism
Case Report Acta Cardiol Sin 2013;29:188-191 Hypercalcemia-Induced New Onset Left Bundle Branch Block Mimicking Acute Myocardial Infarction in a Patient with Primary Hyperparathyroidism Yu-Tsung Cheng,1 Chieh-Shou Su,1,2 Wei-Chun Chang,1,2 Meng-Hsia Chiang,1,3 Chih-Tai Ting1,2 and Wei-Win Lin1,4 A 78-year-old women with a recent diagnosis of primary hyperparathyroidism presented with vague chest pain, and new onset left bundle block (LBBB) on the electrocardiogram (ECG) mimicking acute myocardial infarction (AMI). LBBB resolved without abnormal Q waves only after correction of hypercalcemia. The cardiac enzymes, including creatine kinase, creatine kinase-MB, and troponin-I were all within normal range. Hypercalcemia provoking ECG changes that mimic acute myocardial infarction is infrequently reported. To our knowledge, this is the first report of hypercalcemia-induced new onset LBBB mimicking AMI. Emergency physicians should include hypercalcemia-induced new onset LBBB on the ECG in the differential diagnosis of AMI. Key Words: Acute myocardial infarction · Hypercalcemia · Hyperparathyroidism · left bundle branch block INTRODUCTION CASE REPORT Acute myocardial infarction (AMI) is an important A 78-year-old female presented to our facility with a differential diagnosis in patients who present with acute 10-year history of hypertension. The patient denied any chest pain and new onset left bundle branch block (LBBB) history of coronary artery disease, diabetes mellitus, or on the electrocardiogram (ECG). Unnecessary treatment hyperlipidemia. She had been hospitalized in another can be harmful in patients who have new onset LBBB institution for a deteriorating level of consciousness and due to conditions other than AMI. -
Intra-His Bundle Block. Clinical, Electrocardiographic, and Electrophysiologic Characteristics
Andréa et al OriginalArq Bras Article Cardiol Intra-His bundle 2002; 79: 532-7. Intra-His Bundle Block. Clinical, Electrocardiographic, and Electrophysiologic Characteristics Eduardo M. Andréa, Jacob Atié, Washington A. Maciel, Nilson A. de Oliveira Jr, Luiz Eduardo Camanho, Luís Gustavo Belo, Hecio Affonso de Carvalho, Leonardo Siqueira, Eduardo Saad, Ana Claudia Venancio Rio de Janeiro, RJ - Brazil Objective - To assess the clinical, electrocardiogra- Atrioventricular block is a conduction disturbance at phic, and electrophysiologic characteristics of patients the axis formed by the atrium, AV node, His bundle, and its (pt) with intra-His bundle block undergoing an electro- branches, which may vary from a mild delay in conduction physiologic study (EPS). (first-degree atrioventricular block) to a conduction block between atria and ventricles (second- and third-degree Methods - We analyzed the characteristics of 16 pt with atrioventricular blocks) 1. second-degree atrioventricular block and symptoms of Atrioventricular block may occur at the 3 following syncope or dyspnea, or both, undergoing conventional EPS. electrophysiological levels: atrioventricular node, within 2 Results - Intra-His bundle block was documented in 16 the His bundle, and below the His bundle . These levels pt during an EPS. In 15 (94%) pt, the atrioventricular block have anatomical correlation with, respectively, the atrioven- was recorded in sinus rhythm; 4 (25%) pt had intra-His tricular node, the penetrating His bundle (within the central Wenckebach phenomenon, which correlated with Mobitz I fibrous body), and nonpenetrating His bundle (out of the (MI) atrioventricular block on the electrocardiogram. Seven central fibrous body). First-degree atrioventricular block (44%) pt had 2:1 atrioventricular block, 2 of whom were usually has a delay in the conduction within the atrioventri- asymptomatic (12.5%). -
Revisiting Electrocardiographic Wolff-Parkinson-White Pattern
The Journal of Medical Research 2020; 6(4): 114-116 Review Article Revisiting Electrocardiographic Wolff-Parkinson-White Pattern JMR 2020; 6(4): 114-116 1 2 July- August Pradnya Brijmohan Bhattad , Vinay Jain ISSN: 2395-7565 1 Resident, Department of Internal Medicine, East Tennessee State University, Tennessee (TN), USA © 2020, All rights reserved 2 Attending Radiologist, Department of Radiology, James H. Quillen Veterans Affairs Medical Center, Mountain www.medicinearticle.com Home, Tennessee (TN), USA Received: 14-06-2020 Accepted: 18-07-2020 Abstract Electrocardiographic features of a short PR interval, a delta wave, and a wide QRS complex constitutes a Wolff- Parkinson-White (WPW) pattern. Asymptomatic electrocardiographic findings are defined as a WPW pattern. Symptomatic patients with these electrocardiographic features have WPW syndrome. WPW syndrome may predispose to arrhythmias such as paroxysmal atrial tachycardia, atrial fibrillation, ventricular tachycardia. Patient’s with WPW syndrome at risk for sudden cardiac death. It is important to recognize the common electrocardiographic characteristics of WPW pattern. The advent of electrophysiological studies (EPS) and radiofrequency ablation has revolutionized the management of WPW syndrome. Keywords: Wolff-Parkinson-White Syndrome, Wolff-Parkinson-White Pattern, Pre-excitation, Accessory pathway. INTRODUCTION Wolff, Parkinson, and White described a patient series in the year 1930 who suffered from paroxysms of tachycardia with classic electrocardiographic findings which has been described as WPW pattern [1]. It is a congenital abnormality in the cardiac conduction system. WPW pattern is a ventricular pre-excitation entity wherein an accessory bypass tract known as the bundle of Kent serves as the connection between the atrial to the ventricular myocardium bypassing the atrioventricular (AV) node [2,3]. -
Adams-Stokes Syndrome Caused by Sinoatrial Block
Br Heart J: first published as 10.1136/hrt.35.10.1002 on 1 October 1973. Downloaded from British Heart Journal, 1973, 35, I002-I008. Adams-Stokes syndrome caused by sinoatrial block Bjarne Sigurd, Gorm Jensen, J0rgen Meibom, and Erik Sand0e From Medical Department B, Rigshospitalet, University of Copenhagen, Denmark Forty-six patients with syncope and/or black-out episodes due to sinoatrial block are presented. Male-to- female ratio was i to i, and mean age at onset of symptoms approximately 63 years in both sexes. Additional heart disease, especially coronary artery disease, was frequently, but not constantly, found. Twenty-five per cent had sinus node dysfunction as the only manifestation of cardiac disease. Ninety per cent had frequent paroxysms of one or several types of a wide spectrum of supraventricular dysrhythmias, which often gave rise to troublesome symptoms in the form of palpitation, fatigue, and/or congestion, but also made it easier to recognize the cardiac origin of the unspecific cerebral symptoms. Cerebral symptoms occurred suddenly and unexpectedly, and often disabled the patients to a severe degree. Drug treatment proved of little value, but pacemaker treatment stopped the cerebral attacks in all the 39 cases in which it was performed. In 3 out of 24 patients pacemaker implantation also abolished the tendency for paroxysms of tachydysrhythmias; in the remaining 2I it allowedfor maximal drug treatment which led to nearly total relieffrom tachydysrhythmias in 17. copyright. Attacks of third-degree sinoatrial block, resulting in Patients cerebral ischaemic symptoms, account for I0 to 20 There were 46 patients with a chronic, intermittent per cent of all cases, in which artificial pacemakers tendency to syncope and/or black-out episodes, assumed are considered necessary (Rasmussen, 197I; Jen- to be caused by paroxysms of third-degree sinoatrial sen et al., I973).