Discoveries relating to the identification of the electrophysiological properties of the heart and the ability to induce cardiac depolarization through artificial electrical stimulation are relatively recent. Gaskell, an electrophysiologist, coined the phrase heart block in 1882 and Purkinje first described the ventricular conduction system in 1845. Importantly, Gaskell also related the presence of a slow ventricular rate to disassociation with the atria [4]. The discovery of the bundle of His is attributed to its namesake, Wilhelm His Jr. [5]. He described the presence in the heart of a conduction pathway from the atrioventricular node through the cardiac skeleton that eventually connected to the ventricles. Tawara later verified the existence of the bundle of His in 1906 [6]. He is also credited with being the first to clearly identify the specialized conduction tissues (modified myocytes) that span from the atrial septum to the ventricular apex, including the right and left bundle branches and Purkinje fibers.

The first known instance of electrical resuscitation of the heart was by Lidwell in 1929. Further, Hyman produced the first device for emergency treatment of the heart in 1932. Paul Zoll performed the first clinical transcutaneous pacing in 1952. Importantly for the pacing industry, the first battery-powered pacemaker was developed by Earl Bakken and used in postsurgical pediatric patients by C. Walton Lillehei in 1957 at the University of Minnesota (Fig. 30.3) [4, 7, 8]. Also see Chap. 25.

In addition to the spontaneous contraction that occurs within the heart, artificial electrical stimulus (cardiac pacing) can be used to initiate myocardial contraction. This stimulation, in the form of cardiac pacing, is routinely performed as a means to manage patients with cardiac arrhythmias and conduction abnormalities [9, 10]. Pacing induces myocardial contraction through the delivery of an electrical pulse to the patient’s heart using an IPG and a cardiac pacing lead. The cardiac pacing lead acts as the electrical conduit for both stimulation and sensing, thus interfacing with the myocardial tissue. The electrical pulse is delivered either in a bipolar mode (involving cathodal and anodal electrodes on the lead) or in a unipolar mode (with a cathode on the lead and the metallic housing of the IPG serving as the anode).

To initiate depolarization, an action potential must be created on a given volume of myocardium. As was described in previous chapters, a normal myocardial cell has a resting membrane potential of approximately –90 mV. The resting membrane potential is dominated by the concentration of potassium (K). A cellular action potential occurs when the resting membrane potential is shifted towards a more positive value (i.e., less negative value) to approximately –60 to –70 mV. At this threshold potential, the cell’s voltage-gated Na channels open and begin a cascade of events. In artificial electrical stimulation (pacing), this shift in the resting potential and subsequent depolarization is produced by the pacing system.

Two theories describe the mechanism by which artificial electrical stimulation initiates myocardial depolarization. The Current Density Theory states that a minimum current density (amps/cm³) is required for stimulation of an excitable tissue. The Electric Field Theory requires that a minimum voltage gradient (volts/cm) be produced within the myocardium to initiate depolarization [11]. These two theories can, in part, be considered related, since the passage of current through the tissue (Current Density Theory) will induce a potential difference across the cell membranes due to the limited conductivity of the tissue. Similarly, the creation of a potential within the tissue (Electric Field Theory) will also induce a current. Regardless of the theoretical position taken regarding stimulation, the requirement for artificial stimulation is the shifting of the resting membrane potential from its normal value (typically –90 mV) towards a more positive value, until the depolarization threshold is reached.

The impedance associated with charge transfer from an IPG to the cardiac tissue is comprised of resistive (R) and reactive components (X _C = capacitive; X _L = inductive):
The resistive term (R) includes the DC resistance associated with the conductors internal to the lead (R _C = cathodic conductor; R _A = anodic conductor), the cathode–tissue interface (R _CT), the anode–tissue interface (R _AT), and the tissue itself (R _T):
The capacitive term (X _C) is the sum of the capacitance of the cathode–tissue interface (C _CT) and the anode–tissue interface (C _AT).
The inductance within the conductors and circuit is extremely small and this term is typically neglected. Ignoring inductance, the resulting equation for lead impedance is:
Schematic representations of the circuitry for bipolar and unipolar pacing systems are shown in Figs. 30.4 and 30.5. In these figures, the electric circuit for the delivery of energy to the myocardium is described as a simple RC circuit in which the IPG acts as the voltage/charge source and the lead conductors, electrodes, and cardiac tissue act as the load. Figure 30.4 depicts a bipolar pacing circuit in which the cathode and anode both reside on the pacing lead. Figure 30.5 represents the circuitry associated with a unipolar pacing system. In this case, the circuit is still bipolar but the anode is the metallic housing of the IPG; the term unipolar refers to the polarity of the lead.

Typical pacing circuit impedances range from 400 to 1500 Ω. Approximately 80 % of the total impedance is at the tissue interface; as an example, this will result in a 0.8 V drop at the tissue interface when a 1.0 V pacing pulse amplitude is used. Using the aforementioned impedances (400–1500 Ω), a pacing output of 1.0 V produces currents of 2.5 mA and 0.67 mA, respectively.

To date, the most common pacing stimulation waveform used to electrically activate the myocardial tissue is an exponentially decaying square wave. An active recharge is also commonly included at the trailing edge of the stimulation pulse to reduce the post-pace polarization on the electrodes by balancing the charge delivered. The stimulating portion of the waveform is characterized by its amplitude (volts) and width (milliseconds). A relationship exists between the amplitude and pulse width that will be required for depolarization (pacing) of the tissue. This relationship, termed a strength-duration curve is most commonly plotted as shown in Fig. 30.6.

Terminology relating to the strength-duration curve includes the rheobase and chronaxie values. Rheobase is the threshold voltage at an infinitely long pulse width, and chronaxie is the threshold pulse width at two times the rheobase voltage. The output of a clinical IPG is commonly set at twice the voltage threshold corresponding at the chronaxie pulse width, thus insuring a safety margin [11].

Pacing and defibrillation systems are designed to maintain appropriate cardiac rhythms to maximize the patient’s safety and quality of life. With the exception of cases of sudden cardiac death where an external defibrillator is clearly required, the determination of when to use a pacing or implantable defibrillation system can be complex. This section will describe the current classification of indications for pacing and provide a few practical examples of these indications and the decision process associated with choosing the appropriate system for a given patient’s condition.

The indications for either pacing or defibrillation therapies are commonly classified in the standard ACCF/AHA/HRS (American College of Cardiology Foundation/American Heart Association/Heart Rhythm Society) format as follows [2]:

For each classification listed above, a Level of Evidence is also referenced: Level A—multiple populations evaluated with data derived from multiple randomized clinical trials or meta-analyses; Level B—limited populations evaluated with data derived from a single randomized trial or nonrandomized studies; and Level C—very limited populations evaluated and only consensus opinions of experts, case studies, or standards of care.

Cardiac pacing can be used for both temporary and permanent management of heart rhythm and function. Although the permanent pacing systems are the most well known, there are numerous indications for temporary pacing. The most common temporary pacing systems utilize transcutaneous wires that are stitched directly into the myocardium and connected to an external stimulator. The stimulator is usually a small portable unit, but it can be a console. Common indications for temporary pacing include: postsurgical heart block, heart block following an acute myocardial infarction, pacing for post- or intra-operative cardiac support, pacing prior to implantation of a permanent pacemaker, and/or pacing during a pulse generator exchange.

The primary indication for the implantation of a permanent pacing system (pacemaker and leads) is to chronically eliminate the symptoms associated with the inadequate cardiac output due to bradyarrhythmias. Typical causes of these bradyarrhythmia are: (1) sinus node dysfunction; (2) acquired permanent or temporary atrioventricular block; (3) chronic bifascicular or trifascicular block; (4) hypersensitive carotid sinus syndrome; (5) neurocardiogenic in origin; and/or (6) a side effect due to a drug therapy. The type of pacing system to be employed is dependent on the nature and location of the arrhythmia, the patient’s age, previous medical/surgical history, as well as additional medical conditions.

For conditions related to dysfunction of the sinoatrial node, an IPG with atrial features is commonly used in combination with a lead placed in (or on) the atrium. When management of the ventricular rate is required, a device with ventricular functionality and a ventricular lead are used. When management of the rhythms of both the upper and lower chambers of the heart is required, a dual-chamber system is implanted.

Two clinical situations are outlined below to illustrate common indications for pacing, as well as the decision tree that is often used to determine the type of pacing system for the particular indication. The indications for pacing in a patient with sinus node dysfunction are found in Table 30.4 [2] and the decision tree in Fig. 30.7 [12]. The indications for pacing in an adult with acquired atrioventricular block are found in Table 30.1 and the decision tree in Fig. 30.8 [2]. As an example, a patient with symptomatic chronotropic incompetence would have a Class I indication for pacing (Table 30.4). Since this is related to dysfunction of the sinus node, Fig. 30.7 would then be used to determine the type of pacing system required. In this situation, a rate response system (a pacing system that responds to patient activity/exercise) would clearly be desired. If atrioventricular synchrony were also required, a rate-responsive ventricular pacemaker would be implanted (mostly commonly a DDDR system; see the next section on the standard coding system and Table 30.2).

In order to describe the function of a pacing system in a standardized manner, the North American Society of Pacing and Electrophysiology (NASPE) and British Pacing and Electrophysiology Group (BPEG) had developed a standard coding system [3]. This code describes the pacing system’s functionality using a multi-letter designation. The first four letters are typically used, although this practice is evolving as new pacing features and indications are being developed. In the four letter code system, the first letter indicates the pacing activity (A = atrial pacing, V = ventricular pacing, D = dual-chamber pacing, O = no pacing), the second letter indicates sensing (A = atrial sensing, V = ventricular sensing, D = dual-chamber sensing, O = no sensing), the third letter indicates the reaction to a sensed event (I = inhibit pacing, T = trigger pacing, D = inhibit and trigger, O = no reaction to sensing), and the fourth letter is used to describe unique device functionality (R = rate responsive, for example). Thus, a VVIR system would pace the ventricles (V—), sense ventricular activity (-V–), inhibit or withhold pacing upon detection of a sensed event in the ventricle (–I-), and provide rate response to manage chronotropic incompetence (—R). See Table 30.2 for a more complete explanation of the coding system.

The IPG is an implantable computer with an integral pulse generator and battery. The componentry is typically encased within a hermetically sealed stamped titanium housing with the battery taking up approximately half of the device volume. The most common battery chemistry used in modern pacemakers is lithium iodide. Device longevity is typically 8–10 years, but may vary significantly depending on system utilization (Fig. 30.9). Electrically insulated feedthroughs connect the internal circuitry to an external connector block, which acts as the interface between the internal circuitry of the IPG and the leads. Typically today, the connector block consists of a molded polyurethane superstructure which houses metallic contacts. The contacts may be simple machined blocks or “spring-type” metallic beams. Most connector blocks employ set screws to ensure permanent retention of the leads and these may also enhance electrical contact. A cutaway view of an IPG can be found in Fig. 30.10, and the scheme for connection between the IPG and the leads is shown in Fig. 30.11 and online Video 30.13. In addition to the standard IS-1 and DF-1 connectors shown in Fig. 30.11, a new standard connection scheme is now available. The so-called DF-4 connector is an in-line quadripolar connector that includes electrical connections for both the pacing and defibrillation electrode circuits. The new connector is documented in ISO 30186:2010 (Active implantable medical devices—Four-pole connector system for implantable cardiac rhythm management devices—Dimensional and test requirements).