Cardiac Arrhythmia Management E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Cardiac Arrhythmia Management: A Practical Guide for Nurses and Allied Professionals provides a much-needed resource for nurses and other professionals who work directly with patients being treated for cardiac arrhythmias. Comprehensive in scope, the book covers cardiac arrhythmia conditions and the issues surrounding implantable devices from implant surgery to remote monitoring and troubleshooting. Edited by a team of doctors and nurses, the book addresses key patient management issues in a practical way. Fundamentals for understanding the anatomy and physiology of cardiac arrhythmias and the technology behind cardiac devices are covered in preliminary chapters followed by more specific chapters devoted to cardiac conditions and treatments. Both novices and experienced health professionals will find the book useful and easy to use on a day-to-day basis.
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Veröffentlichungsjahr: 2011
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Contents
Copyrigiht
Dedications
Foreword1
Foreword2
preface
Contributors
Section 1: Basics of Cardiac Anatomy and Electrophysiology
1.1 Cardiac Anatomy, Physiology, Electrophysiology, and Pharmacology
ANATOMY OF THE CARDIAC CONDUCTION SYSTEM
CARDIAC ACTION POTENTIAL
DRUGS FOR CARDIAC ARRHYTHMIAS
1.2 Diagnostic Testing for the Arrhythmia Patient
INTRODUCTION: APPROACH TO THE ARRHYTHMIA PATIENT
RHYTHM ASSESSMENT AND DIAGNOSIS
Section 2: Supraventricular Tachycardia: Diagnosis and Management
2.1 AVNRT, AVRT, and AtrialTachycardia: Diagnosis and Treatment
INTRODUCTION
CLINICAL AND ELECTROCARDIOGRAPHIC PRESENTATION OF SVT
AVNRT
AVRT
ATRIAL TACHYCARDIA
2.2 Atrial Fibrillation and Flutter: Diagnosis and Treatment
INTRODUCTION
AF EPIDEMIOLOGY AND PREVALENCE
THE COST OF AF
ETIOLOGY OF AF
DIAGNOSIS OF AF
MEDICAL MANAGEMENT OF AF
RHYTHM CONTROL
CATHETER-BASED MANAGEMENT OF AF
ATRIAL FLUTTER
CONCLUSION
2.3 Ventricular Tachycardia Associated with Cardiomyopathies: Diagnosis and Treatment
INTRODUCTION
DEFINITIONS AND CLASSIFICATIONS OF VENTRICULAR ARRHYTHMIAS
BASIC CELLULAR ELECTROPHYSIOLOGY
MECHANISMS OF VT
DEFINITIONS AND CLASSIFICATIONS OF CARDIOMYOPATHY
PATIENT MANAGEMENT
TREATMENT OPTIONS FOR VT ASSOCIATED WITH CARDIOMYOPATHIES
SUMMARY
2.4 Ventricular Tachycardia in Structurally Normal Hearts
INTRODUCTION
GENERAL FEATURES
OUTFLOW TRACT VT
ILVT
LQTS
BRUGADA SYNDROME
CONCLUSION
Section 3: Implantable Device Management
3.1 Basics of Pacing and Defibrillation: Indications and Components
COMPONENTS OF PACEMAKERS, ICDS, AND CRTS
3.2 Device Implantation and Perioperative Care
INTRODUCTION
THE FACILITY
DOCUMENTATION OF HARDWARE
INTRAOPERATIVE MONITORING
PREPARING THE PATIENT
SEDATION AND ANALGESIA
PERIOPERATIVE ANTIBIOTICS
POCKET SITE
VENOUS ACCESS
LEAD INTRODUCTION AND POSITIONING
DFT TESTING
IMPLANTATION OF RESYNCHRONIZATION DEVICES
DEVICE REPLACEMENT
POSTOPERATIVE CARE
COMPLICATIONS
CONCLUSIONS
3.3 Pacemaker Timing Cycles, Programming, and Troubleshooting
PACEMAKER TIMING CYCLES
WHAT IS CAPTURE AND SENSING?
PACEMAKER INTERVAL TIMERS
PACEMAKER SENSING INTERVALS
PACEMAKER MODES
MISCELLANEOUS PACEMAKER BEHAVIORS
SYSTEMATIC APPROACH TO PACEMAKER ECG INTERPRETATION
PACEMAKER FOLLOW-UP
SPECIAL CONSIDERATIONS FOR PACEMAKER PROGRAMMING
TROUBLESHOOTING
COMPLICATIONS OF LONG-TERM PACING
3.4 Cardiac Resynchronization Therapy
EPIDEMIOLOGY
ELECTROMECHANICAL DYSSYNCHRONY
CRT
CLINICAL TRIALS SUMMARY
CRT, AF, AND HF
FORCED RV PACING, HF, AND CRT
SUDDEN DEATH IN HF PATIENTS
IMPLANTATION OF CRT
OPTIMIZATION OF CRT
(RESPONDERS AND NONRESPONDERS
SUMMARY
3.5 ICD Follow- Up and Troubleshooting
INTRODUCTION
ROUTINE ICD FOLLOW-UP
ICD INTERROGATION
DEVICE DIAGNOSTICS
ROUTINE DEVICE FOLLOW-UP
DOCUMENTATION
REMOTE FOLLOW-UP
TROUBLESHOOTING
OTHER CONSIDERATIONS
SUMMARY
3.6 Pacemaker and ICD Follow-Up
INTRODUCTION
TYPES OF FOLLOW-UP
FREQUENCY OF FOLLOW-UP AND TRACKING PATIENTS
FOLLOW-UP PROCEDURES
3.7 Family Matters: Research and Clinical Management of Psychosocial Issues for ICD Patients and Their Partners
HEART PARTNERS: RESEARCH AND CLINICAL MANAGEMENT OF PSYCHOSOCIAL ISSUES FOR ICD PATIENTS AND THEIR PARTNERS
PSYCHOSOCIAL IMPACT FOR ICD PATIENTS: COMMON PROBLEMS IN ICD PATIENTS
SOCIAL SUPPORT AND THE PSYCHOSOCIAL IMPACT OF THE ICD ON PARTNERS: MORE ANXIETY THAN PATIENTS?
CLINICAL MANAGEMENT OF ICD PATIENTS AND PARTNERS TO OPTIMIZE OUTCOMES
CONCLUSION
3.8 Management of Device Recalls
INTRODUCTION
DEFINITION OF RECALL
READINESS FOR THE RECALL
STEPS TO TAKE UPON NOTIFICATION OF RECALL
AFTER THE INITIAL POSTNOTIFICATION VISIT
CONCLUSION
3.9 Device Evaluation in Special Circumstances
ACUTE PRESENTATIONS
PERIPROCEDURAL EVALUATION
POSTMORTEM EVALUATION
CONCLUSION
Section 4: Syncope and Sudden Cardiac Death
4.1 Diagnosis and Management of Syncope
INTRODUCTION
EPIDEMIOLOGY AND SIGNIFICANCE
CLASSIFICATION OF SYNCOPE
MECHANISMS OF BLOOD PRESSURE CONTROL
ANS DISORDERS OF OI
NCS
CSH
POTS
PAF and MSA
DIAGNOSTIC EVALUATION OF SYNCOPE
TREATMENT
CONCLUSION
4.2 Sudden Cardiac Death
INTRODUCTION
ETIOLOGIES OF SCD
MECHANISMS OF SCD
ICD
REVIEW OF THE LITERATURE
RISK STRATIFICATION
THERAPEUTIC CONSIDERATIONS
CONCLUSION
Section 5: Care of the Pediatric Arrhythmia Patient
5.1 Care of the Pediatric Patient with a Device
PACEMAKERS
ICDS
CARDIAC RESYNCHRONIZATION THERAPY
CARE AND FOLLOW-UP
5.2 Care of the Pediatric Patient with SVT
INTRODUCTION
CLINICAL MANIFESTATIONS
DIAGNOSTIC TOOLS
CLINICAL AND ECG PATTERNS OF SVT (SEE TABLE 5.2.2)
PREVENTIVE MANAGEMENT AND TREATMENT
PROGNOSIS
COMPLICATIONS
CONCLUSION
Section 6: Additional Topics in Cardiac Arrhythmia Management
6.1 EP Mapping System Technologies
INTRODUCTION
CARTO MAPPING SYSTEM
ENSITE MAPPING SYSTEM
ABLATION TECHNOLOGY
CONCLUSION
6.2 Procedural Sedation in the Electrophysiology Lab
INTRODUCTION
NURSING CARE OF PATIENTS UNDERGOING PROCEDURAL SEDATION
PATIENT MONITORING DURING PROCEDURAL SEDATION
DOCUMENTATION
POTENTIAL COMPLICATIONS DURING PROCEDURAL SEDATION
SUMMARY
6.3 Ethical Issues in Cardiac Electrophysiology Practice: A Guide for Clinicians
INTRODUCTION
PRINCIPLES OF ETHICS
ETHICAL ISSUES IN IMPLANTABLE CARDIAC DEVICE-RELATED CLINICAL PRACTICE
AVOIDING ETHICAL DILEMMAS IN CARDIAC ELECTROPHYSIOLOGY PRACTICE
ETHICS CONSULTATION
CONCLUSIONS
ACKNOWLEDGEMENT
Index
This edition first published 2011 © 2011 by Blackwell Publishing, Ltd.
Chapters 2.1 and 6.3 © Mayo Foundation for Medical Education and Research
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Library of Congress Cataloging-in-Publication Data
Cardiac arrhythmia management : a practical guide for nurses and allied professionals / edited by Angela Tsiperfal ... [et al.].
p. ; cm.
Includes bibliographical references and index.
ISBN 978-0-8138-1667-8 (pbk. : alk. paper)
1. Arrhythmia–Treatment. 2. Arrhythmia–Diagnosis. I. Tsiperfal, Angela.
[DNLM: 1. Arrhythmias, Cardiac–therapy. 2. Arrhythmias, Cardiac–diagnosis. WG 330]
RC685.A65C23 2011
616.1’28–dc22
2010042172
Disclaimer
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Dedications
To my husband Boris, my son Feliks, and my parents for their encouragement, love, support, and many sacrifices. To all my teachers for their wisdom and inspiration.
Angela Tsiperfal
To Gary, Lucas, and Briana for their love and willingness to support my professional endeavors. To my Stanford Arrhythmia colleagues for providing daily inspiration to seek new knowledge and challenge ourselves to always provide excellent care to patients.
Linda K. Ottoboni
To my mentors Afaf Meleis, RN, DSC and Andrea Natale, MD who were my inspiration.
Salwa Beheiry
To my wife Rola and my children Maya, Dana, and Mohammad for their patience, love and support. To my parents for their constant guidance. To my teachers and mentors for their inspiration. To the nurses and technicians who I am privileged to work with and learn from every day.
Amin Al-Ahmad
To my family and my staff for the endless patience and the unwavering support.
Andrea Natale
To my loving wife, Gloria, and my wonderful daughters, Margaret and Katie. To the fantastic nurses, technicians, fellows, and colleagues, with whom I feel privileged to work.
Paul J. Wang
Foreword by N.A. Mark Estes III
Over the last three decades, we have witnessed a remarkable expansion and maturation of the fields of cardiac electrophysiology, ablation, pacing, and defibrillation. This has resulted in a core of highly skilled nurses, physician assistants, technicians, and industry-employed allied professionals assuming a larger and increasing important role in the clinical care of patients with arrhythmias. Given the considerable progress in the clinical evaluation and management of patients, the need has emerged for a comprehensive educational resource to ensure the highest quality of care. CardiacArrhythmia Management: A Practical Guide forNurses and Allied Professionals merits particular recognition as it uniquely fulfills this need. It represents a timely and novel contribution that should be considered essential for all health care professionals involved in the care of patients with heart rhythm disorders.
Amin Al-Ahmad, MD, Paul J. Wang, MD, Andrea Natale, MD, Angela Tsiperfal, RN, NP, Linda Ottoboni, RN, MS, and Salwa Beheiry, RN, as editors, have masterfully selected topics and authors to produce an essential educational resource. All sections, including those on anatomy, physiology, arrhythmia mechanisms, pacemakers, defibrillators, pediatric arrhythmias, syncope, sudden death, and ethical issues, are superbly written by leading clinical educators. The case-based approach supplements the didactic materials. This allows the practical application of both clinical and technical knowledge to the individual case. As always, this markedly enhances information retention and clinical utility.
The editors and authors are to be congratulated for producing this unique, practical, and comprehensive book. All interested in improving their knowledge and skills related to arrhythmias, ablation, pacing, and defibrillation should consider it an essential resource. With mastery of its content, all health care professionals will meaningfully improve their ability to ensure optimal patient outcomes.
N.A. Mark Estes III, MD, FHRS, FACC, FAHA
Director, Tufts Cardiac Arrhythmia Center,
Tufts Medical Center, Boston, MA
Professor of Medicine,
Tufts University School of Medicine
Past President, Heart Rhythm Society
Chairman, Council on Clinical Cardiology,
American Heart Association
Foreword by Rosemary S. Bubien
The role of allied professionals in providing care to patients with cardiac rhythm management devices is constant yet dynamic. While this statement may seem paradoxical, its truth is self-evident to all who work in this rapidly growing subspecialty within cardiology.
One has only to look at the history of cardiac electrophysiology to discern the truth of constancy amid innovation. Today’s devices are a testament to the visions of scientists who, working in concert with engineers and medical professionals, have produced devices that are life saving and life enhancing. Innovative catheter-based technologies and cardiac rhythm management devices present new challenges. As visions become reality and theory is applied to clinical practice, new operational features are assessed, evaluated, and integrated to ensure the provision of safe, optimal patient care. Our goal always has and always shall be providing safe and optimal patient care. Daily, we strive to incorporate how to best assess available evolving therapies and an everexpanding array of physiologically based device features and device-based diagnostic data as we evaluate patients “in person” and “remotely.” Efforts to contain health care costs impact us and we are expected to be not only proficient but also efficient. We seek to apply scientific principles as we navigate and plum the depths of devices, their programmers, and remote Web sites to evaluate data and ensure devices are optimally programmed to meet the needs of individual patients. How to assess and address the unique challenges of device-based care permeate this text, which integrates the theoretical and the practical. In this regard, the text for allied professionals espouses and exemplifies the standards of professional practice for allied professionals in pacing and electrophysiology (Gura et al. 2003).
Devices represent only one of the varied therapy options. The challenges to understand and apply technology to the management of life-threatening/life-altering arrhythmias in patients are vast. A thorough understanding of arrhythmia mechanisms provides an essential foundation for identifying the most appropriate technique for patient treatment. Advanced diagnostic testing creates additional patient-specific information that results in an optimal treatment decision. Within the electrophysiological procedure and ablation, innovative technological achievements have simplified arrhythmia location, improved catheter ablative therapy techniques, and reduced patient complications. All of these are outlined in the text so that caregivers can deliver improved patient care with an understanding of the pathophysiology and biomedical technology. One must also consider the “care” in patient care. We strive to do so while acknowledging the unique human qualities and quirks of our patients, recognizing that the ordinary and mundane to one person may represent the unique, provoking anxiety and distress to others.
The authors and editors of this text provide exemplary material designed to teach us how to utilize technology to enable each of our patients to derive maximum benefit.
Rosemary S. Bubien,
RN, MSN, FAHA, FHRS, CCDS
REFERENCE
Gura MT, Bubien RS, Belco KM, et al. 2003. Policy statement. North American Society of pacing and electrophysiology standards of professional practice for allied professionals in pacing and electrophysiology. PACE 26: 127–131.
Preface
The field of cardiac arrhythmias has evolved greatly over the past several decades. This field involves direct patient management of patients who have implantable cardiac devices such as pacemakers or implantable cardioverter defibrillators. In addition, the role of catheter ablation in these patients has expanded over the past few years for arrhythmia management. The front line in management of arrhythmia patients is often nursing or allied professional staff that works closely with cardiologists and cardiac electrophysiologists.
This aim of this book is to be a comprehensive reference for allied professionals in a very specialized field. The book is divided into six sections that cover the variety of topics in the field of arrhythmia management, from the most basic to the complex. Each chapter was written and edited by experts in the field and was the collaboration of electrophysiologists and allied professionals.
Our goal is to provide the fundamentals and nuances in management of cardiac arrhythmia devices, as well as arrhythmia management for patients who undergo radiofrequency ablation procedures.
We hope that this book will be used by both experienced and novice nurses and allied professionals. We also hope this book may be useful for those preparing for any examination of competency in the field and will be valuable as a learning guide as well as a useful resource on a day-to-day basis. We hope that this book will contribute to the improvement in care of the arrhythmia patient.
Angela Tsiperfal
Linda K. Ottoboni
Salwa Beheiry
Amin Al-Ahmad
Andrea Natale
Paul J. Wang
Contributors
Amin Al-Ahmad, MD, FACC, FHRS
Director, Cardiac Electrophysiology
Laboratory
Associate Director, Arrhythmia Service
Stanford University Medical Center
Stanford, CA
Samuel J. Asirvatham, MD
Professor of Medicine
Division of Cardiovascular Diseases
Department of Pediatrics and Adolescent Medicine
Mayo Clinic
Rochester, MN
Salwa Beheiry, RN, CCRN
Director, Electrophysiology Services
California Pacific Medical Center
San Francisco, CA
Christie Benton, RN
Electrophysiology Nurse Clinician
Department of Cardiovascular Sciences
East Carolina University
Greenville, NC
Deepak Bhakta, MD, FACC, FHRS
Associate Professor of Clinical Medicine
Krannert Institute of Cardiology
Indiana University School of Medicine
Indianapolis, IN
David J. Bradley, MD
Associate Professor of Pediatrics
Director of Pediatric Heart Rhythm Service
University of Michigan Congenital Heart
Center
Ann Arbor, MI
Traci Buescher, RN
Heart Rhythm Services
Division of Cardiovascular Diseases
Mayo Clinic
Rochester, MI
Christine C. Chiu-Man, MSc
EP Pacemaker Technologist
The Labatt Family Heart Center
The Hospital for Sick Children
Toronto, ON, Canada
Kelly Collardey, MSN, RN, CPNP-PC, PCNS-BC
Pediatric Nurse Practitioner
Pediatric Heart Rhythm Service
University of Michigan Congenital Heart
Center
Ann Arbor, MI
Kelly J. Cook, RN, MS, ACNP-BC
Nurse Practitioner
Cardiac Electrophysiology and Arrhythmia
Service
Stanford Hospital and Clinics
Stanford, CA
Laura De Souza, BSc
The Labatt Family Heart Center
The Hospital for Sick Children
Toronto, ON, Canada
Laurence M. Epstein, MD
Chief, Cardiac Arrhythmia Service
Brigham and Women’s Hospital
Associate Professor of Medicine
Harvard Medical School
Boston, MA
Lynne D. Foreman, RN, BSN, FHRS
Krannert Institute of Cardiology
Indiana University School of Medicine Indianapolis, IN
Blair P. Grubb, MD, FACC
Professor of Medicine and Pediatrics
Director, Cardiac Electrophysiology Service
Cardiovascular Medicine
Health Science Campus
University of Toledo College of Medicine
Toledo, OH
Melanie Turco Gura, RN, MSN, CNS, CCDS, FHRS, FAHA
Director, Pacemaker and Arrhythmia Services
Northeast Ohio Cardiovascular Specialists
Akron, OH
Debra Hanisch, RN, MSN, CPNP, CCDS, FHRS
Nurse Practitioner
Children’s Heart Center
Lucile Packard Children’s Hospital at Stanford
Palo Alto, CA
Steven C. Hao, MD FACC FHRS
Atrial Fibrillation and Complex Arrhythmia
Center
Sutter Pacific Medical Foundation San
Francisco, CA
Munther K. Homoud, MD
Codirector, Cardiac Electrophysiology and
Pacemaker Laboratory
Tufts Medical Center
Associate Professor of Medicine
Tufts University School of Medicine
Boston, MA
Richard H. Hongo, MD
Atrial Fibrillation and Complex Arrhythmia
Center
California Pacific Medical Center San Francisco, CA
Henry H. Hsia, MD, FACC
Cardiac Electrophysiology and Arrhythmia
Service
Stanford University
Stanford, CA
D. Randolph Jones, MD
Heart Rhythm Center
Providence St. Vincent Medical Center
Portland, OR
Beverly L. Karabin, RN, PhD, CNP
Associate Professor School of Nursing
Nurse Practitioner, Division of Cardiology
Autonomic Disorders Clinic
University of Toledo Medical Center
University of Toledo
Toledo, OH
Kari Kirian, MA
Department of Psychology
East Carolina University
Greenville, NC
Aimee Lee, RN, MS, CNS
Cardiovascular Medicine
Stanford Hospital and Clinics
Stanford, CA
William R. Lewis, MD
Associate Professor of Medicine, Case Western
Reserve University
Chief of Clinical Cardiology, Metro Health
Medical Center
Cleveland, OH
Melanie E. Marshall, RN
Clinical Research Coordinator
Cardiac Arrhythmia Center
Tufts Medical Center
Boston, MA
Melissa Matchett, PsyD
Department of Psychology
East Carolina University
Greenville, NC
Katie Morganti, MS, NP, RN, ACNP
Cardiac Arrhythmia Service
Massachusetts General Hospital
Boston, MA
Paul S. Mueller, MD
Chair, Division of General Internal Medicine
Codirector, Program in Professionalism and Ethics
Associate Professor of Medicine
Mayo Clinic
Rochester, MN
Andrea Natale, MD, FACC, FHRS
Executive Medical Director
Texas Cardiac Arrhythmia Institute
St. David’s Medical Center
Austin, TX
Rajasekhar Nekkanti, MD
Cardiac Electrophysiology
Associate Director, Cardiology Fellowship
Program
Department of Cardiovascular Sciences
East Carolina University
Greenville, NC
Anders Nygren, MD
Department of Pediatric Cardiology
The Queen Silvia Children’s Hospital
Gothenburg, Sweden
Linda K. Ottoboni, RN, MS, FHRS, CCDS
Arrhythmia Nurse Coordinator
Sanford Hospitals and Clinics
Stanford, CA
Laurie Racenet, RN, MSN, ANP, CCDS, CEPS
Alaska Heart Institute
Anchorage, AK
Kimberly Scheibly, RN, MS, CNS
Guest Lecturer
UCSF Medical Center
San Francisco, CA
Samuel F. Sears, PhD
Professor
Department of Psychology
Department of Cardiovascular Sciences
East Carolina University
Greenville, NC
Julie B. Shea, MS, RNCS, FHRS, CCDS
Nurse Practitioner
Cardiac Arrhythmia Service
Brigham and Women’s Hospital
Boston, MA
Craig A. Swygman, CVT, CEPS
Heart Rhythm Center
Providence St. Vincent Medical Center
Portland, OR
Angela Tsiperfal, MS, RN, NP
Electrophysiology
Stanford University Medical Center
Stanford, CA
Paul J. Wang, MD, FACC, FHRS
Professor of Medicine
Director, Cardiac Arrhythmia Service and
Cardiac Electrophysiology
Laboratory Stanford University
Stanford, CA
Charles L. Witherell, ACNS- BC, MSN
Clinical Nurse Specialist
Cardiac Electrophysiology
UCSF Medical Center
San Francisco, CA
Paul Zei, MD PhD
Clinical Associate Professor
Department of Medicine, Cardiovascular
Division
Stanford University
Stanford, CA
Section 1
Basics of Cardiac Anatomy and Electrophysiology
1.1
Cardiac Anatomy, Physiology, Electrophysiology, and Pharmacology
Linda K. Ottoboni, Aimee Lee, and Paul Zei
Electrical stimulation is the key in initiating the sequence of events that result in cardiac contraction, the ultimate measure of cardiac performance. The inherent pacing properties that are required to generate an electrical impulse, the intrinsic conduction pathways that move depolarization from the initial impulse throughout the entire cardiac muscle, and finally, the patterns of depolarization that create an optimal squeeze of the cardiac muscle are the result of the electrical conduction system and mechanical system functioning synchronously. Impulse generation and dispersion to all areas of the heart muscle via cell-to-cell activation and via electrical pathways must be well understood to comprehend the complexity of electrical conduction and the strategies for treating conduction abnormalities. This chapter will provide an overview of cellular physiology, electrical physiology, the anatomy of the conduction system, and the medications that can be used to treat conduction abnormalities. A thorough understanding of the normal anatomy and physiology of the conduction system will enable the allied professional to understand the rationale for utilizing specific arrhythmia treatment modalities, whether it be medications, ablations, or devices.
ANATOMY OF THE CARDIAC CONDUCTION SYSTEM
The anatomy of the conduction system is composed of electrical tracts within the myocardium. This electrical network is strategically arranged in the nodes, bundles, bundle branches, and branching networks of fascicles. The cells that form these structures lack contractile capability but can generate spontaneous electrical impulses and alter the speed of electrical conduction throughout the heart. The sinoatrial (SA) node, internodal tracts, atrioventricular (AV) node, bundle of His, right bundle, left bundle, anterior and posterior fascicles, and the Purkinje fibers are all the necessary conduction routes established throughout the cardiac muscle (Fig. 1.1.1). Normal conduction utilizes this electrical conduction system to expedite transmission of the electrical impulse from the top of the heart to the bottom. Abnormal conduction or arrhythmias are the result of an arrhythmogenic site or region that interferes, alters, or bypasses the normal conduction circuit. Therefore, a comprehensive understanding of normal conduction provides a foundation for better understanding the mechanisms present in abnormal conduction or arrhythmias.
Figure 1.1.1 Anatomy of the conduction system.
Anatomically, the SA node is subepicardially located in the left upper corner of the right atrium, near its junction with the superior vena cava. The SA node is the native pacemaker site within the heart and is composed of cells capable of impulse formation or “pacing.” Pacing cells within the SA node independently move to a threshold potential, thereby initiating depolarization. The SA node establishes the intrinsic heart rhythm between 60–100 pulses per minute but is influenced by the autonomic nervous system to meet the changing requirements of the body (Fig. 1.1.2). The region of the sinus node has numerous nerve endings and is predominantly regulated by the parasympathetic system or acetylcholine at rest and the sympathetic tone is mediated with the release of norephinephrine to meet increased energy requirements.
The sinus node lies near the central artery whereby it obtains its blood supply from the right coronary artery 55–65% of the time, while in 35–45% the left circumflex provides blood flow (Anderson et al. 1979). The function of the sinus node may be jeopardized if the blood supply is reduced due to coronary artery disease or an increase in fibrous tissue with maturity, resulting in fewer SA cells available for impulse formation within the sinus node (Davies and Pomerance 1972).
Figure 1.1.2 Pacing rates associated with pacing sites within conduction system.
Once the impulse is initiated within the SA node, it not only travels cell to cell through the atrium but also utilizes more specialized, expedient pathways known as internodal tracts (Fig. 1.1.1). The Bachmann’s bundle moves away from the SA node anteriorly around the superior vena cava and then bifurcates with one branch leading from the right to the left atrium, while the other branch descends along the interatrial septum into the anterior portion of the AV node (fast pathway). The Wenckebach’s tract transfers the stimulus from the superior region of the SA node, posterior to the superior vena cava, and travels through the atrial septum to the AV node, while the third pathway (Thorel’s) is responsible for moving the impulse inferiorly and posteriorly along the coronary sinus, arriving into the posterior portion of the AV node (slow pathway).
Once atrial depolarization is completed, depolarization moves into the AV node via the internodal tracts previously described or via cell-to-cell conduction. Normally, the structure of the AV node is the only conduction route from the atrium to the ventricle because the chambers are separated by fibrous and fatty tissue that is nonconductive. The primary function of the AV node is to slow electrical conduction adequately to synchronize atrial contribution to ventricular systole. The AV node is also capable of rescue pacing when the SA node fails and will provide a heart rate of 40–60 bpm (Fig. 1.1.2). By contrast, an ectopic site within the AV node is capable of pacing competitively against the SA node to produce arrhythmias or junctional tachycardias greater than 100 bpm.
The fast and slow pathways of the AV node are anatomical as well as functional structures. Slow pathway physiology is not seen in every individual. The fast pathway conducts more quickly but has a longer refractory period or recovery period. By contrast, the slow pathway conducts more slowly but has a shorter refractory or recovery period. Conducted impulses commonly travel along the fast pathway through the AV node, but with increased heart rates or the presence of a premature stimulus, the fast pathway may be unable to transmit because it is unable to recover fast enough to transmit the stimulus or be “refractory.” Because the slow pathway has a shorter effective recovery time or is able to recover more quickly, it is able to transmit a signal down the slow pathway while the fast pathway is still recovering. The timing of recovery and the ability or inability to transmit a signal can result in a reentrant tachycardia (Fig. 1.1.3). Reentry is the result of a circuit that is initiated by a signal, often early, being blocked and forced to move in the opposite direction. When the electrical signal conducts back toward the area of block, the structure has had time to recover and is now able to transmit the signal in the opposing direction. Hence, the critical timing sequence of the signal being transmitted creates an independent reentrant circuit.
Figure 1.1.3 Reentry of the fast and slow pathways.
Once the activation through the AV node occurs, depolarization travels to the common bundle of His (also called His bundle or common bundle). The region where the AV node (node of Tawara) and the His bundle join can be termed the triangle of Koch. Anatomically, the triangle of Koch includes the coronary ostium, the tendon of Todaro, and the tricuspid valve annulus along the septal leaflet. The AV node is approximately 5–6 mm long and 2–3 mm wide, and 0.5–1.0 mm thick, although there is some discrepancy in what is included in the AV node (Hecht et al. 1973; Becker and Anderson 1976). The blood supply of the AV node is the AV nodal artery and is usually dual supplied by the right coronary artery in 90% of the patients and the remaining 10% receive blood from the left circumflex coronary artery. Similar to the SA node, there is evidence of a generous autonomic innervation of the AV node, and therefore, the autonomic nervous system influences the rate of conduction through the AV node. AV nodal conduction abnormalities arise from altered blood supply, change in autonomic tone, increased fibrous tissue replacing AV nodal tissue, and an alteration in the normal conduction route.
Once depolarization moves through the bundle of His, it branches out to the right and left bundle branches. The right bundle branch remains compact until it reaches the right distal septal surface, where it branches into the interventricular septum and proceeds toward the free wall of the right ventricle. Because the left ventricle is larger in size, the left bundle branch moves conduction down the left septum and then bifurcates into a posterior and anterior descending fascicle. The left fascicles extend to the base of the papillary muscles and the adjacent myocardium, while the right bundle stays along the interventricular septum superficially within the endocardium (see Fig. 1.1.1).
The final destination is the arrival into the complex network of the specialized Purkinje fibers, capable of independently pacing at a rate of 20–40 bpm if needed along with rapid conduction (Fig. 1.1.2). Once the impulses arrive at the Purkinje fibers, they proceed slowly from the endocardium to epicardium throughout the left and right ventricles. This assures earlier activation at the apex of the heart, the sequence necessary to achieve the most efficient cardiac pumping, which is the intended outcome of cardiac depolarization.
CARDIAC ACTION POTENTIAL
The conduction system is composed of two distinctly different cells, pacing cells and nonpacing cells. “Pacing” cells are specialized cells with automaticity, meaning that they can move to a threshold potential independently and propagate or spontaneously initiate an impulse. The specialized cells with automaticity reside within the SA node, AV node, and the Purkinje fibers. All the rest of the cardiac cells, myocytes, are “nonpacing cells” or conducting cells, which means they can be stimulated by an electrical impulse arriving at the cell and then conduct or transmit the impulse from one cell to another cell once the cell is stimulated. Therefore, cardiac cells are unable to initiate an impulse contrary to pacing cells.
Cells have the property of pacing or conductivity due to the electrical charge or voltage on the inside of the cell compared with the voltage on the outside of the cell. If the electrical charge inside the cell is less than the charge on the outside, the transmembrane potential is “negative.” By contrast, if the electrical charge is greater inside the cell than outside the cell, the transmembrane potential is “positive.” Depolarization occurs when the transmembrane potential is positive, while repolarization restores the cell to its negative state, making it available to accept an electrical stimulus in its negative or resting state. Pacing cells are able to depolarize independently, in contrast to a nonpacing cell, which is dependent on an outside stimulus to initiate depolarization.
The transmembrane potential is altered by ions moving in and out of the cell across the cellular membrane. Ion movement is the result of the selective permeability of ion channels distributed along the cell membrane. The movement of the Na+, K+, and Ca2+ ions are the most predominant throughout the cardiac action potential. These ions move in or out of the cell as a result of a change in concentration gradient, electrical gradient, ion pumps, and altered membrane permeabilities (Table 1.1.1). Alterations in permeability to specific ions are most often regulated by voltage-gated channels that will open or close depending on the current measured between the inside and the outside of the cell, but there are additional properties that are responsible for moving ions in and out of the cell (Table 1.1.2). Some of these ion shifts occur passively, while other transport mechanisms require energy at the cellular level. The ion “pumps” or ion transfers that require energy will be at risk in the event that the cell does not have an energy source or is oxygen deprived, for example, ischemia provides an opportunity for arrhythmias to occur.
Table 1.1.1 Fundamentals of ion transport.
Table 1.1.2 Ion-specific channel characteristics.
Phases of the Cardiac Action Potential
The cardiac action potential of the “nonpacing” cell consists of five phases:
Phase 0—rapid depolarizationPhase 1—early rapid repolarizationPhase 2—plateau phasePhase 3—repolarizationPhase 4—resting phaseThe cell moves from one phase to another very quickly with the entire process occurring within milliseconds. Although we describe each specific phase, the transition from one phase to another is dynamic and seamless. The action potential takes a round-trip journey in that the signal is able arrives at baseline (phase 4) and is able to travel to the destination (depolarization — phase 0). Then, the action potential is able to return back to home (repolarization—phases 1–4) and prepare to depart from home or baseline (resting—phase 4) once again. What actually occurs at each phase is described below.
Phase 0—Rapid Depolarization
When an electrical impulse arrives at the cell, the membrane potential shifts from approximately −90 to −60v and reaches “threshold” potential. The shift in voltage triggers the “voltage-gated” sodium channels to open and the permeability of the plasma membrane to sodium ions (PNa+) increases, thereby resulting in rapid movement of sodium ions from extracellular to intracellular along their electromechanical gradient. Positively charged Na+ ions shift from the outside of the cell to the inside of the cell, causing the membrane potential to become more positive, now to approximately 0 mV (Fig. 1.1.4). The “fast” sodium channels inactivate within a few milliseconds, decreasing permeability of the cellular membrane to Na+ and preventing any further voltage increase.
Figure 1.1.4 Phase 0—rapid depolarization. Sodium moving into the cell quickly increases the intracellular charge, creating a positive transmembrane potential.
Figure 1.1.5 Phase 1—early rapid repolarization. Potassium channel (Ito—transient outward current) opens briefly, moving K+ outside the cell, resulting in a less positive intracellular charge.
Phase 1 — Early Rapid Repolarization
Transient outward K+current, Ito, is turned on briefly by depolarization and drives the potassium out of the cell. This transient outward current rapidly inactivates, so the rapid outward current is brief, resulting in a slightly reduced intracellular charge as the positively charged K+ ions move outside of the cell (Fig. 1.1.5).
Phase 2 — Plateau Phase
The following ions are in motion in phase 2:
Calcium moves slowly to the inside of the cell through the ICa-L channel (inward calcium channel)Potassium moves to the outside of the cell with the voltage and concentration gradient in an effort to equalize the voltage and the concentration of K+ within the inside and the outside of the cellThree sodium ions are moving into the cell in exchange for one calcium ion moving out of the cellThe cumulative, simultaneous movement of these ions results in a stable voltage along the membrane or a “plateau phase” (Fig. 1.1.6).Phase 3 — Final Repolarization
In final repolarization, potassium diffuses to the outside of the cell with the increased permeability along the cell membrane with potassium channels opening and due to the movement caused by the concentration gradient. These voltage-dependent potassium channels are delayed rectifier currents and are slowly activating outward currents (IKur, IKr, IKs). Concurrently, Ca2+ channels close, so the inward movement of calcium stops, while potassium continues to move outside of the cell and allows the membrane potential to go back to a negative resting membrane potential. Ion movement includes the following:
Inactivation of the ICa -L stops Ca2+ entry into cellDelayed rectifier K+ currents, IKs (slow), IKr (rapid), and IKur (ultrarapid), moving K+ to the outside of the cell, while inwardly rectifying currents, IKI and IKAch, result in the movement of positive charges out of the cell.Potassium conductance falls to plateau levels as a result of the inward rectification, membrane conductance changes with voltage (K+ channels are open at negative potentials but closed at less negative or positive voltages) (Fig. 1.1.7)Figure 1.1.6 Phase 2—plateau phase. Stable charge created by equivalent ion movement to the inside and to the outside of the cell.
Phase 4—Resting Membrane Potential
The cardiac action potential relies on the cell to adequately prepare for depolarization in the resting phase. It is during the cardiac cell resting phase that the intracellular potential is −50 to − 95 v relative to the measured voltage outside of the cell, making it negative. During resting phase, there are more potassium ions within the cellular membrane (intracellular), while the majority of sodium and calcium ions are kept on the outside of the cell membrane (extracellular).
Although phase 4 is referred to as “resting” phase, the negative intracellular voltage is the result of ion movement related to a combination of complex systems that include the opening of selective ion channels, altering membrane permeability, concentration gradients, electrogenic gradients, and active ion pumps (Fig. 1.1.8). This phase includes the sodium-potassium pump, which requires energy, thus it relies on oxygenation to the area to maintain resting phase. Maintaining the resting membrane potential of −90 to −100 mV allows the cell to be ready to accept an outside stimulus or to be depolarized.
Action Potential of Pacemaker Cells (Slow Response)
The unique quality of the pacing cells is that they have the capability of reaching depolarization independently. Therefore, they can initiate a stimulus as opposed to being able to only conduct or transmit a stimulus. The specialized cells with automaticity reside within the SA node, AV node, and the Purkinje fibers. Their inherent pacing rate of the specialized cells is most rapid in the sinus node while slowest in the ventricles. This provides rescue pacing if the higher pacing sites fail, for example, the AV node will pace at a rate of 40–60 bpm in the absence of the sinus node firing at a rate of 60–100 bpm (Fig. 1.1.2). As mentioned previously, the intrinsic pacing rate is greatly influenced by the balance between the sympathetic and parasympathetic autonomic nervous system.
Figure 1.1.7 Phase 3—final repolarization. Potassium efflux is the essential ion movement.
Figure 1.1.8 Phase 4—resting phase. 1. Open, inward rectifying K+ channels, IKI, moving potassium to the inside of the cell. 2. Three Na+ ions move to the outside of the cell while two K+ ions are transferred to the inside of the cell by the active Na+/K+ pump. 3. With the negative transmembrane potential, the Na+/Ca2+ exchanger is exchanging three Na+ ions to the inside of the cell while moving one Ca2+ ion outside the cell. 4. Plasma membrane calcium (PMCA) pump removes calcium.
Figure 1.1.9 Action potential of pacing cell.
The ability to “pace,” propagate, or initiate a signal is the result of independent ion shifting within the cell through specialized ion channels that are only available within the pacing cell structure. Phase 4 and phase 0 in the pacing cells are the most distinctly different phases when compared with cardiac cells (Fig. 1.1.9). The unique characteristics of the pacing cell are described in detail below.
Phase 4—Diastolic Depolarization of the Pacing Cell
Automaticity of the pacing cell is the result of ions shifting to achieve a net gain in intracellular positive charges during diastole. This ion movement allows the cell to independently reach a “threshold” potential. There are a number of differences between the action potential of the pacing cell and the cardiac cell that allow this to be achieved. First, the transmembrane potential of the pacing cell does not return to the same negative membrane potential as the cardiac cell in resting phase. Instead, the voltage of the cell at the onset of phase 4 is −40 to −70. This is the result of the presence of the If channel, pacemaker or “funny” current, which is a current activated by hyperpolarization and causes Na+ and K+ to enter the cell, thus allowing the cell to independently move to depolarization. Automaticity is dependent on a combination of the If channel, the deactivation of IKI current, and the transient inward calcium current, ICa-T. The If channel moves Na+ and K+ into the cell to offset the deactivation of IKI current, which causes an inward K+ current. The ICa-T current is limited to pacing cells exclusively and the opening of this calcium current allows calcium to move slowly into the cell, moving the charge inside of the cell to −30 and −40, resulting in “threshold” potential, and finally, opening of the fast Na+ channels for depolarization to occur.
Phase 0—Depolarization of the Pacing Cell
The significant contrast of the pacemaker cell and the cardiac cell during phase 0 is the absence of a stimulus to alter the transmembrane potential in the pacing cell. The cell itself moves from a transmembrane potential of −60 to “threshold potential” by a slow, inward current rather than a fast inward Na current, as described above. The discharge rate of the sinus node normally exceeds the discharge rate of the other potentially automatic pacemaker sites, and therefore, maintains the dominant rate. It is also more sensitive to the effects of norephinephrine (sympathetic) and acetycholine (parasympathetic) so it provides the best physiological heart rate. The lower, alternative pacing sites in the AV node and Purkinje fibers provide an electrical stimulus in the absence of an intact sinus node. The complex intrinsic pacing capability of the heart is essential in providing optimal blood flow and meeting the oxygen demands of the body during times of increased physical activity and/or increased stress.
DRUGS FOR CARDIAC ARRHYTHMIAS
Cardiac arrhythmias generally result from an abnormality in the rate, rhythm, or conduction of an electrical impulse in the heart (Perry and Illsley 1986). These abnormalities are disturbances in normal impulse initiation (automaticity), impulse conduction, or both. Various antiarrhythmic agents affect intracellular and extracellular concentrations of sodium, potassium, calcium, and magnesium. The balance of all these molecular components have varying effects on the electrophysiology of the heart and are critical to controlling arrhythmias with antiarrhythmic medications. In general, antiarrhythmic medications are available to treat tachyarrhythmias. There are no currently available medications to treat bradyarrhythmias effectively, particularly in oral form.
The classification of antiarrhythmic agents is discussed below, with emphasis on the particular electrophysiological action of each drug classification. Several of the drugs studied had more than one of the four actions, so that it deserves emphasis that the classification is not so much categorization of drugs in accordance with chemical structures or physical properties, but describes four ways in which abnormal cardiac rhythms can be corrected or prevented (Vaughan Williams 1984). Based on the Vaughan Williams classification, there are four main classes of antiarrhythmic medications (Tables 1.1.3 and 1.1.4). Although much maligned, the Vaughan Williams classification system is still the most commonly used by those in the medical field worldwide. Because the antiarrhythmic drugs usually target a specific ion and either block or enhance its movement in or out of the cell, there are electrocardiogram (ECG) changes that may be evident as a result of that (see Table 1.1.5).
The classes are further simplified and subdivided based on the primary electrophysiological effect of either their ability to convert the rhythm or control the rate (Table 1.1.6). Class I and class III drugs are more effectively utilized to prevent arrhythmias and maintain sinus rhythm. Class IV drugs provide rate control with the primary goal of reducing conduction through the AV node, while class II drugs are used to reduce heart rate and maintain sinus rhythms in those patients who have arrhythmias that are triggered by catecholamines. The discussion below describes each group in more detail.
Class I Drugs: Sodium Channel Blockade
The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting or altering phase 0 depolarization (Fig. 1.1.4). Their dominant electrophysiological property has been related to their ability to reduce the maximal rate of depolarization in cardiac muscle. A reduction in the rate of depolarization by therapeutic concentrations of these drugs has been found to be associated with an increase in the threshold of excitability, a depression in conduction velocity, and a prolongation in the effective refractory period (Singh 1978). Three different subgroups, class IA, IB, and IC, have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dissociation from the channel receptor (Snyders et al. 1991).
Table 1.1.3 Drug effects on ECG.
The major drugs with class IA classification are quinidine, procainamide, and disopyramide. These drugs depress phase 0 (sodium-dependent) depolarization, thereby slowing conduction. They also have moderate potassium channel blocking activity (which tends to slow the rate of repolarization and prolong action potential duration [APD]), anticholinergic activity, and depress myocardial contractility. At slower heart rates, when use-dependent blockade of the sodium current is not significant, potassium channel blockade may become predominant (reverse use dependence), leading to prolongation of the APD and QT interval and increased automaticity.
Table 1.1.4 Specifics of each drug classification.
Table 1.1.5 Antiarrhythmic drug effects on the ECG.
The class IB drugs include lidocaine, mexiletine, and tocainide. They have less prominent sodium channel blocking activity at rest but effectively block the sodium channel in depolarized tissues. This group tends to bind in the Na+ channel inactivated state (which follows the fast channel opening in phase 0 depolarization) and dissociate from the sodium channel more rapidly than other class I drugs. As a result, they are more effective with tachyarrhythmias than with slow arrhythmias.
The class IC drugs, flecainide and propafenone, block both the open and inactivated sodium channels and thus, slow conduction. They dissociate slowly from the sodium channels during diastole, resulting in increased effect at more rapid rate (use dependence). This characteristic is the basis for their antiarrhythmic efficacy, especially against supraventricular arrhythmia. Use dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia.
Table 1.1.6 Common drugs for atrial fibrillation and supraventricular arrhythmias.
Class II Drugs: Beta Blockade (Antagonists)
Hyperactivity of the sympathetic nervous system has been recognized for many years as a factor in the genesis of cardiac arrhythmias. The class II drugs, such as atenolol, metoprolol, carvedilol, act by inhibiting sympathetic activity, primarily by causing beta blockade. Their principal electrophysiological effect on heart muscle in clinically relevant concentrations is the depression of phase 4 depolarization (see Fig. 1.1.8), resulting in a reduced heart rate. Only in very high concentrations do these drugs exert effects on other parameters, such as the upstroke velocity of the phase 0 of the action potential (Singh 1978). Beta agonists or catecholamines (i.e., epinephrine and norepinephrine) are endogenous, neurohormonal substances that mediate diverse physiological and metabolic responses in man by interaction with adrenergic receptors (beta receptors) in various tissues. As a result of this, beta agonists potentiate positive chronotropic (increased heart rate) and inotropic (increased contractility) actions. By contrast, beta adrenergic antagonists’ main therapeutic effect is to slow the heart rate and decrease myocardial contractility. They reduce sinus rate, especially when sympathetic control of the heart is dominant, as during exercise. They have less effect on heart rate in an individual at rest. They also decrease the rate of spontaneous depolarization of ectopic pacemakers, slow conduction in the atria and AV node, and increase the refractory period of AV node.
Class III Drugs: Potassium Channel Blockade
Class III drugs, amiodarone, ibutilide, dofetilide, sotalol, azimilide, and dronedarone, block the potassium channels, thereby prolonging repolarization, the APD, and the refractory period (Arnsdorf et al. 2009; see Fig. 1.1.7). These changes are manifested on the surface ECG by prolongation of the QT interval, providing the substrate for torsade de pointes, a polymorphic ventricular tachycardia. Amiodarone is an exception, with very little proarrhythmic activity. Amiodarone has since been found to be a potent antiarrhythmic drug in the clinic, but although it does prolong the QTc (corrected QT) interval on the ECG in patients, ventricular arrhythmias have not been encountered during prolonged periods of treatment in large numbers of patients (Singh 1978; see Table 1.1.5).
Amiodarone—Among available antiarrhythmics, amiodarone (Cordarone and others) is the most effective for prevention of atrial fibrillation and of ventricular tachycardia or fibrillation. The antiarrhythmic actions of amiodarone can be attributed to its property of inhibiting adrenergic stimulation (alpha and beta blocking properties), its effects on sodium, potassium, and calcium channels, its ability to prolong the action potential with consequent lengthening of the effective refractory period in myocardial tissue and decreasing AV nodal conduction and sinus node function. Multiple clinical trials have indicated that amiodarone is the most potent antiarrhythmic agent for the control of refractory ventricular tachyarrhythmias and for the prophylaxis of recurrent supraventricular tachyarrhythmias, including atrial fibrillation or flutter complicating the Wolff–Parkinson–White syndrome. Amiodarone is well tolerated by most patients, but there are several potential side effects that need to be monitored for closely.Dronedarone—This is one of the newer class III antiarrhythmic drugs and is a “cousin” to amiodarone; it is indicated for the treatment of atrial arrhythmias. The primary differences compared with amiodarone are attributable to the lack of iodine in the molecular structure, along with a reduced half-life due to its less hydrophobic nature. As a result, it may be associated with fewer long-term complications compared with amiodarone. Its efficacy can be evaluated more quickly, as achieving therapeutic levels is not reliant on a “loading” regimen; rather it is given twice daily, with steady state achieved usually within 3–7 days.Sotalol—Sotalol is a racemic mixture of D-sotalol and L-sotalol; both isomers have similar class III antiarrhythmic effects, while the L-isomer is responsible for virtually all of the beta blocking activity. Sotalol contains both beta adrenoreceptor blocking (class II) and cardiac APD prolongation (class III) properties. The noncardioselective beta-blocking effect of sotalol (increased sinus cycle length, slowed heart rate, decreased AV nodal conduction, and increased AV nodal refractoriness) occurs at oral doses as low as 25 mg/day. The class III effects (prolongation of the atrial and ventricular monophasic action potentials, and effective refractory prolongation of atrial muscle, ventricular muscle, and AV accessory pathways in both the antegrade and retrograde directions) are seen only at oral doses ≥ 160 mg/day. Sotalol should be initiated and doses increased in a hospital with facilities for cardiac rhythm monitoring and assessment, as proarrhythmic events can occur after initiation of therapy and with each upward dosage adjustment.Dofetilide—Dofetilide has no effect on sodium channels, adrenergic alpha receptors, or adrenergic beta receptors. It increases the monophasic APD and effective refractory period of the myocyte, thereby terminating reentrant tachyarrhythmias and preventing their reinduction (Roukoz et al. 2007). The increase in the QT interval is a function of prolongation of both effective and functional refractory periods in the His-Purkinje system and the ventricles. Changes in cardiac conduction velocity and sinus node function have not been observed in patients with or without structural heart disease. PR and QRS width remain the same in patients with preexisting heart block and or sick sinus syndrome. Dofetilide is generally well tolerated but like other antiarrhythmic agents in its class, torsades de pointes may be induced as a consequence of therapy. Therefore, it should be initiated and doses titrated while in a hospital with facilities for cardiac rhythm monitoring and assessment.Class IV Drugs: Calcium Channel Blockade (Antagonists)
As a class, calcium channel antagonists do not increase the effective refractory period of the atria, ventricle, His-Purkinje fibers, or the accessory pathways in the heart. The dominant effect of calcium channel antagonists is slowing of conduction in the AV node with the prolongation of the AV nodal refractory period (Singh et al. 1983). Selective calcium channel antagonists, such as verapamil and diltiazem, have been found to have some antiarrhythmic activity. They preferentially affect slow-response myocardial tissue rather than fast-response tissue. Slow-response tissues (the SA and AV nodes) depend on calcium currents to generate slowly propagating action potentials. By contrast, fast-response myocardial tissues (the atria, specialized infranodal conducting system, the ventricles, and accessory pathways) depend on sodium channel currents. Verapamil is the prototype calcium antagonist and has the most clearly defined antiarrhythmic properties (Singh et al. 1983). Verapamil, as well as diltiazem, terminate paroxysmal supraventricular tachycardia and slow the ventricular response in atrial flutter and fibrillation. They also have prophylactic value in preventing recurrences of paroxysmal supraventricular tachycardia and controlling the ventricular response in atrial flutter and fibrillation during long-term oral therapy. They play a much more limited role in the treatment of ventricular arrhythmias (Singh et al. 1983).
Antiarrhythmic drugs are available as one treatment option for controlling arrhythmias. As you can see, there are a variety of medications available to treat the full spectrum of tachyarrhythmias. Each clinician may prefer one agent over the other, and a particular patient’s arrhythmia control and tolerance of medications may vary considerably. Therefore, the use of antiarrhythmics in patient management may not be straightforward and may require increased patient surveillance. Additional methods of treatment, that is, ablation, may be utilized as an adjunct to medication and provides the patient with additional options for controlling arrhythmias.
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1.2
Diagnostic Testing for the Arrhythmia Patient
Angela Tsiperfal, Paul J. Wang, and Amin Al-Ahmad
INTRODUCTION: APPROACH TO THE ARRHYTHMIA PATIENT
The diagnosis of cardiac rhythm disorders depends on the accurate documentation of the abnormal rhythm, usually in association with symptoms. Rhythm disorders can be very infrequent, occurring a few times a year or can be constant, such as in persistent atrial fibrillation. Thus, the challenge of diagnosis of arrhythmias depends a great deal on the appropriate selection of diagnostic tools. An accurate diagnosis of arrhythmia allows prompt and appropriate treatment. While the “gold” standard for obtaining a diagnosis is demonstrating a rhythm abnormality associated with symptoms, this is not always possible. Often, the use of multiple diagnostic tests in addition to the history and physical examination may yield a likely diagnosis. In addition, in some cases, the risk of waiting to document an arrhythmia may be too great. For example, patients with syncope who may be at high risk for ventricular arrhythmias may be best served by placement of an implantable cardioverter defibrillator (ICD; based on the appropriate guidelines) rather than waiting to document the ventricular arrhythmia that likely caused the syncope and placing the patient at significant risk (Miller et al. 2004; Zipes and Miles 2004).
