Cardiac Pacing, Defibrillation and Resynchronization

A Clinical Approach

David L. Hayes, Samuel J. Asirvatham, Paul A. Friedman, David L. Hayes, Samuel J. Asirvatham, Paul A. Friedman

• Publisher: Wiley-Blackwell
• Year: 2021
• ISBN:
  9781119264019
• Edition: 4
• Topic: Medicine
• Subtopic: Cardiology

A practical and up-to-date guide to pacemaker technology and its clinical implementation

As the field of cardiology continues to advance and expand, so too does the technology and expertise behind today's electrophysiological devices. Cardiac Pacing, Defibrillation and Resynchronization has been assembled by international specialists to give all those caring for patients with heart disorders a clear and informative guide to the pacemakers and clinical methods of today. Now in its fourth edition, this essential resource:

• Explains different methods of pacemaker implementation in a straightforward and easy-to-follow manner
• Explores the most common challenges faced by working clinicians
• Features more than 750 illustrative graphics
• Contains data on the efficacy and long-term outcomes of different device models
• Covers new technology and clinical trial data

Written for cardiologists, cardiac pacing caregivers, and those preparing to take their electrophysiology board examinations, Cardiac Pacing, Defibrillation and Resynchronization offers a complete exploration of electrophysical devices and their vital role in modern-day cardiology.

1
Pacing and Defibrillation : Clinically Relevant Basics for Practice

T. Jared Bunch¹, Suraj Kapa², David L. Hayes², Charles D. Swerdlow^3,4, Samuel J. Asirvatham², and Paul A. Friedman²

¹ University of Utah, Salt Lake City, UT, USA

² Department of Cardiovascular Medicine, Division of Heart Rhythm Services, Mayo Clinic, Rochester, MN, USA

³ Cedars‐Sinai Heart Center at Cedars‐Sinai Medical Center, Los Angeles, CA, USA

⁴ David Geffen School of Medicine, University of California, Los Angeles, CA, USA

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• Anatomy and physiology of the cardiac conduction system
• Electrophysiology of myocardial stimulation
• Pacing basics
  • Stimulation threshold
  • Variations in stimulation threshold
  • Clinical considerations when considering threshold
    • Threshold‐specific programming
  • Sensing
    • Sensing‐specific programming
• Lead design
  • Bipolar and unipolar pacing and sensing
  • Left ventricular and His bundle pacing leads
  • Epicardial leads
  • Defibrillator leads – special considerations
  • Leadless pacemakers
• Pulse generators
  • Pacemaker nomenclature
• Essentials of defibrillation
  • Critical mass
  • Upper limit of vulnerability
  • Progressive depolarization
  • Virtual electrode depolarization
  • Electroporation as a mechanism for defibrillation
  • Defibrillation theory summary
• The importance of waveform
  • Biphasic waveforms
  • Phase duration and tilt
  • Polarity and biphasic waveforms
  • Mechanism of improved efficacy with biphasic waveforms
  • Measuring shock dose
• Measuring the efficacy of defibrillation
  • Threshold and dose–response curve
  • Relationship between defibrillation threshold and dose–response curve
  • Patient‐specific defibrillation threshold and safety margin testing – clinical indications
  • Management of the patient who fails defibrillation testing
  • Upper limit of vulnerability to assess safety margin
  • Practical implications of defibrillator therapies
• Drugs and defibrillators
• Antitachycardia pacing
• Summary
• References

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Anatomy and physiology of the cardiac conduction system

The cardiac conduction system consists of specialized tissue involved in the generation and conduction of electrical impulses throughout the heart. Knowledge of the normal anatomy and physiology of the cardiac conduction system is critical to understanding appropriate utilization of device therapy.

The sinoatrial (SA) node, located at the junction of the right atrium and the superior vena cava, is normally the site of impulse generation (Fig. 1.1). The SA node is composed of a dense collagen matrix containing a variety of cells. The large, centrally located P cells are thought to be the origin of electrical impulses in the SA node, which is surrounded by transitional cells and fiber tracts extending through the perinodal area into the remainder of the right atrium. The SA node is richly innervated by the autonomic nervous system, which has a key function in heart rate regulation. Specialized fibers, such as Bachmann’s bundle, conduct impulses throughout the right and left atria. The SA node has the highest rate of spontaneous depolarization and under normal circumstances is responsible for generating most impulses. Atrial depolarization is seen as the P wave on the surface electrocardiogram (ECG; Fig. 1.1).

Atrial conduction fibers converge, forming multiple inputs into the atrioventricular (AV) node, a small subendocardial structure located within the interatrial septum (Fig. 1.1). The AV node also receives abundant autonomic innervation, and it is histologically similar to the SA node because it is composed of a loose collagen matrix in which P cells and transitional cells are located. Additionally, Purkinje cells and myocardial contractile fibers may be found. The AV node allows for physiologic delay between atrial and ventricular contraction, resulting in optimal cardiac hemodynamic function. It can also function as a subsidiary “pacemaker” should the SA node fail. Finally, the AV node functions (albeit typically suboptimally) to regulate the number of impulses eventually reaching the ventricle in instances of atrial tachyarrhythmia. On the surface ECG, the majority of the PR interval is represented by propagation through the AV node and through the His–Purkinje fibers (Fig. 1.1).

Purkinje fibers emerge from the distal AV node to form the bundle of His, which runs through the membranous septum to the crest of the muscular septum, where it divides into the various bundle branches. The bundle branch system exhibits significant individual variation. The right bundle is typically a discrete structure running along the right side of the interventricular septum to the moderator band, where it divides. The left bundle is usually a large band of fibers fanning out over the left ventricle, forming functional fascicles. Both bundles eventually terminate in individual Purkinje fibers interdigitating with myocardial contractile fibers. The His–Purkinje system has correspondingly less autonomic innervation than the SA and AV nodes.

Because of their key function and location, the SA and AV nodes are the most common sites of conduction system failure; it is understandable, therefore, that the most common indications for pacemaker implantation are SA node dysfunction and high‐grade AV block. It should be noted, however, that conduction system disease is frequently diffuse and may involve the specialized conduction system at multiple sites.

Electrophysiology of myocardial stimulation

Stimulation of the myocardium requires initiation of a propagating wave of depolarization from the site of initial activation, whether from a native “pacemaker” or from an artificial stimulus. Myocardium exhibits “excitability,” which is a response to a stimulus out of proportion to the strength of that stimulus.¹ Excitability is maintained by separation of chemical charge, which results in an electrical transmembrane potential. In cardiac myocytes, this electrochemical gradient is created by differing intracellular and extracellular concentrations of sodium (Na⁺) and potassium (K⁺) ions; Na⁺ ions predominate extracellularly, and K⁺ ions predominate intracellularly. Although this transmembrane gradient is maintained by the high chemical resistance intrinsic to the lipid bilayer of the cellular membrane, passive leakage of these ions occurs across the cellular membrane through ion channels. Passive leakage is offset by two active transport mechanisms, each transporting three positive charges out of the myocyte in exchange for two positive charges that are moved into the myocyte, producing cellular polarization.^2,3 These active transport mechanisms require energy and are susceptible to disruption when energy‐generating processes are interrupted.

The chemical gradient has a key role in the generation of the transmembrane action potential (Fig. 1.2). The mem...