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CHAPTER 1
Clinically Relevant Basics of Pacing and Defibrillation
T. Jared Bunch, David L. Hayes, Paul A. Friedman
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. In this book, we review how device therapy can be optimally utilized for various forms of conduction system disturbances, tachyarrhythmias, and for heart failure. 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 right atrium proper. 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 the impulse 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 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 likewise 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 physiological 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.
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 and is invariably complex. The right bundle is typically a discrete structure running along the right side of the interventricular septum to the anteriorpap-illary muscle, where it divides. The left bundle is usually a large band of fibers fanning out over the left ventricle, sometimes forming functional fascicles. Both bundles eventually terminate in individual Purkinje fibers interdigitating with myocardial contractile fibers. The His-Purkinje system has little in the way of autonomic innervation.
Because of their key function and location, the SA and AV nodes are the most common sites of conduction system failure; it is therefore understandable 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.
Although the earliest pacemakers were designed to treat life-threatening ventricular bradyarrhythmias, indications have drastically expanded to include conditions that do not specifically involve intrinsic conduction system disease. Guidelines have been developed to provide uniform criteria for device implantation, but the importance of the patient’s clinical status and any extenuating circumstances should also be considered.
Electrophysiology of myocardial stimulation
Stimulation of the myocardium by a pacemaker requires the initiation of a self-propagating wave of depolarization from the site of initial activation, whether from a native “pacemaker” or from an artificial stimulus. Myocardium exhibits abiological property referred to as “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 membrane potential of approximately –90 mV drifts upward to the threshold potential of approximately –70 to –60 mV. At this point, specialized membrane-bound channels modify their conformation from an inactive to an active state, which allows the abrupt influx of extracellular Na+ ions into the myocyte4,5, creating phase 0 of the action potential and rapidly raising the transmembrane potential to approximately +20 mV.6,7 This rapid upstroke creates a short period of overshoot potential (phase 1), which is followed by a plateau period (phase 2) createdby the inward calcium (Ca2+) and Na+ currents balanced against outward K+ currents.8”10 During phase 3 of the action potential, the transmembrane potential returns to normal, and during phase 4 the gradual upward drift in transmembrane potential repeats. The shape of the transmembrane potential and the relative distribution of the various membrane-boundion channels differ between the components of the specialized cardiac conduction system.
Depolarization of neighboring cells occurs as a result of passive conduction via low-resistance intercellular connections called “gap junctions,” with active regeneration along cellular membranes.11,12 The velocity of depolarization throughout the myocardium depends on the speed of depolarization of the various cellular components of the myocardium and on the geometrical arrangement and orientation of the myocytes. Factors such as myocardial ischemia, electrolyte imbalance, metabolic abnormalities, and drugs may affect the depolarization and depolarization velocity.
Pacing basics
Stimulation threshold
Artificial pacing involves delivery of an electrical impulse from an electrode of sufficient strength to cause depolarization of the myocardium in contact with that electrode and propagation of that depolarization to the rest of the myocardium. The minimal amount of energy required to produce this depolarization is called the stimulation threshold. The components of the stimulus include the pulse amplitude (measured in volts) and the pulse duration (measured in milliseconds). An exponential relationship exists between the stimulus amplitude and the duration, resulting in a hyperbolic strength–duration curve. At short pulse durations, a small change in the pulse duration is associated with a significant change in the pulse amplitude required to achieve myocardial depolarization; conversely, at long pulse durations, a small change in pulse duration has relatively little effect on threshold amplitude (Fig. 1.3). Two points on the strength–duration curve should be noted (Fig. 1.4). The rheobase is defined as the smallest amplitude (voltage) that stimulates the myocardium at an infinitely long pulse duration (milliseconds). The chronaxie is the threshold pulse duration at twice the stimulus amplitude, which is twice the rheobase voltage. The chronaxie is important in the clinical practice of pacing because it approximates the point of minimum threshold energy (microjoules) required for myocardial depolarization.
The relationship of voltage, current, and pulse duration to stimulus energy is described by the formula
in which E is the stimulus energy, V is the voltage, R is the total pacing impedance, and t is the pulse duration. This formula demonstrates the relative increase in energy with longer pulse durations. The energy increase due to duration is offset by a decrement in the needed voltage.
The strength–duration curve discussed thus far has been that of a constant voltage system, because contemporary permanent pacemakers are constant voltage systems. Constant current devices are no longer used (Fig. 1.5). It should be recognized, however, that constant current strength–duration curves can also be constructed.13 These strength–duration curves, like constant voltage curves, are hyperbolic in shape, but they have a much more gradual decline in current requirements as the pulse width lengthens. Because of this gradual decline, chronaxie of a constant current system is significantly greater than that in a constant voltage system.
Impedance is the term applied to the impediment to current flow in the pacing system. Ohm’s law describes the relationship among voltage, current, and resistance as
in which V is the voltage, I is the current, and R is the resistance. Although Ohm’s law is used for determining impedance, technically impedance and resistance are not interchangeabl...
