Cardiac Pacing 41 History

Discoveries relating to the identification of the electro-physiological 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 (2). The discovery of the bundle of His is attributed to its namesake, Wilhelm His Jr. (3). 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 (4). He is also credited with being the first to identify clearly the specialized conduction tissues (modified myocytes) that span from the base of 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. 3) (2,5,6).

Fig. 3. Dr. C. Walton Lillehei with the first battery-powered, wearable pacemaker.
Transcutaneous Pacer Device Picture

Fig. 4. Bipolar pacing circuit, including an implantable pulse generator and a pacing lead. Resistances: RC, cathodic lead conductor; RCT, cathode-tissue interface; RT, tissue; RAT, anode-tissue interface; and Ra, anodic lead conductor. Capacitances: CCT, cathode-tissue interface; and CAT, anode-tissue interface. (Tissue includes myocardium and blood.)

Fig. 4. Bipolar pacing circuit, including an implantable pulse generator and a pacing lead. Resistances: RC, cathodic lead conductor; RCT, cathode-tissue interface; RT, tissue; RAT, anode-tissue interface; and Ra, anodic lead conductor. Capacitances: CCT, cathode-tissue interface; and CAT, anode-tissue interface. (Tissue includes myocardium and blood.)

other chapters, a normal myocardial cell has a resting membrane potential of approx -90 mV. The resting membrane potential is dominated by the concentration of potassium. A cellular action potential occurs when the resting membrane potential is shifted toward a more positive value (i.e., less-negative value) to approx -60 to -70 mV. At this threshold potential, the cell's voltage gated sodium channels open and begin a cascade of events. In artificial electrical stimulation (pacing), this shift of the resting potential and subsequent depolarization are 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/cubic centimeter) is required for stimulation of an excitable tissue. The electric field theory requires that a minimum voltage gradient (volts/centimeter) be produced within the myocardium to initiate depolarization (9). These two theories can, in part, be considered related because the passage of current through the tissue (current density theory) will induce a potential difference across the cell membranes because of 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) toward a more positive value until the depolarization threshold is reached.

The impedance (Z) associated with charge transfer from an IPG to the cardiac tissue is composed of resistive (R) and reactive components (XC, capacitive; XL, inductive):

The resistive term R includes the direct current (dc) resistance associated with the conductors internal to the lead (RC, cathodic conductor; RA, anodic conductor), the cathode-tissue interface RCT, the anode-tissue interface RAT, and the tissue itself RT:

4.2. Artificial Electrical Stimulation

In addition to the spontaneous contraction that occurs within the heart, an 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 of managing patients with cardiac arrhythmias and conduction abnormalities (7,8). Pacing induces myocardial contraction through the delivery of an electrical pulse to the patient's heart using an IPG (pacemaker) and a cardiac pacing lead. The cardiac pacing lead acts as the electrical conduit for stimulation and sensing, interfacing with the myocardial tissue. The electrical pulse is delivered in either a bipolar mode (involving cathodal and anodal electrodes on the lead) or in a unipolar mode (with a cathode on the lead and the IPG serving as the anode).

To initiate cardiac depolarization, an action potential must be created on a volume of myocardium. As was described in

The capacitive term XC is the sum of the capacitance of the cathode-tissue interface CCT and the anode-tissue interface CAT.

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. 4 and 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 4 depicts a bipolar pacing circuit in which the cathode and anode both reside on the pacing lead. Figure 5 represents the circuitry associated with a unipolar pacing system. In this case, the circuit is still bipolar, but the anode is the housing of the IPG. The term unipolar refers to the polarity of the lead.

Typical pacing circuit impedances range from 400 to 1500 Q. 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 to 1500 Q), a pacing output of 1.0 V produces currents of 2.5 mA and 0.67 mA.

The most common pacing stimulation waveform used to activate the myocardial tissue electrically is an exponentially decaying square wave. An active recharge is also commonly included at the trailing edge of the stimulation pulse to reduce the postpace polarization on the electrodes by balancing the charge delivered. The stimulating portion of the waveform is characterized by its amplitude (volts) and pulse width (milliseconds). A relationship exists between the required amplitude and pulse width duration for depolarization ("pacing") of the tissue. This relationship, termed a strength-duration curve, is most commonly plotted as shown in Fig. 6.

Additional terminology relating to the strength-duration curve includes the rheobase and chronaxie values. Rheobase is the threshold voltage at an infinitely long pulse width. 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 to ensure a safety margin (9).

4.3. Indications for Pacing

Pacing and defibrillation systems are designed to maintain appropriate cardiac rhythms to maximize both the patient's safety and quality of life. With the exception of cases of sudden cardiac death, for which a defibrillator is clearly required, the determination of when to use a pacing or implantable defibril-lation system can be complex. This section describes the current classification of indications for pacing and provides 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 therapy are commonly classified in the standard American College of Cardiology/American Heart Association (ACC/AHA) format as follows (10):

• Class I: Conditions for which there is evidence or general agreement that a given procedure or treatment is beneficial, useful, and effective.

• Class II: Conditions for which there is conflicting evidence or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.

• Class IIa: Weight of evidence/opinion is in favor of usefulness/ efficacy.

• Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

• Class III: Conditions for which there is evidence or general agreement that a procedure/treatment is not useful/effective and, in some cases, may be harmful.

Cardiac pacing can be used for both temporary and permanent management of heart rhythms and function. Although the permanent pacing systems are the most well known, there are numerous indications for temporary pacing. The most commonly utilized temporary pacing systems are transcutaneous wires stitched directly into the myocardium and connected to an

Info About Heart Failure

Fig. 5. A pacing circuit (unipolar type) that includes an implantable pulse generator and a pacing lead. Resistances: RC, cathodic lead conductor; RCT, cathode-tissue interface; RT, tissue; and RAT, anode-tissue interface. Capacitances: CCT, cathode-tissue interface; and CAT, anode-tissue interface. (Tissue includes myocardium, blood, lungs, etc.)

Fig. 5. A pacing circuit (unipolar type) that includes an implantable pulse generator and a pacing lead. Resistances: RC, cathodic lead conductor; RCT, cathode-tissue interface; RT, tissue; and RAT, anode-tissue interface. Capacitances: CCT, cathode-tissue interface; and CAT, anode-tissue interface. (Tissue includes myocardium, blood, lungs, etc.)

Medtronic Pacemaker Models
Fig. 6. A typical strength-duration curve for cardiac pacing. This particular curve was obtained using a Medtronic model 5076 bipolar pacing lead positioned in the right ventricular apex of a canine. In this plot, chronaxie and rheobase were 0.5 ms and 0.4 V, respectively.

external stimulator. This system can be a small portable unit or a console. Common indications for temporary pacing include postsurgical heart block, heart block following an acute myocardial infarction, pacing for post-/intraoperative cardiac support, and pacing prior to implantation of a permanent pacemaker or during a pulse generator exchange.

The primary indication for the implantation of a permanent pacing system (pacemaker and leads) is to eliminate chronically the symptoms associated with the inadequate CO because of bradyarrhythmias. Typical causes of these bradyarrhythmias 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; or (6) side effect caused by a drug therapy. The type of pacing system employed is dependent on the nature and location of the bradyarrhythmia, the patient's age, previous medical/surgical history, as well as concomitant 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/on the atrium. When management of the ventricular rate is required, a device with ventricular functionality and a ventricular lead is used. When management of the

Table 1

Indications for Permanent Pacing in Sinus Node Dysfunction

Class I 1. Sinus node dysfunction with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms.

In some patients, bradycardia is iatrogenic and will occur as a consequence of essential long-term drug therapy of a type and dose for which there are no acceptable alternatives.

2. Symptomatic chronotropic incompetence.

Class Ila 1. Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy with heart rate less than 40 beats/ min when a clear association between significant symptoms consistent with bradycardia and the actual presence of brady-cardia have not been documented.

2. Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in electrophysiological studies.

Class lib 1. In minimally symptomatic patients, chronic heart rate less than 40 beats/min while awake.

Class III 1. Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate less than 40 beats/min) is a consequence of long-term drug treatment.

2. Sinus node dysfunction in patients with symptoms suggestive of bradycardia that are clearly documented as not associated with a slow heart rate.

3. Sinus node dysfunction with symptomatic bradycardia caused by nonessential drug therapy.

Source: Adapted from ref. 11.

Histoty Cardiac Pacing
Fig. 7. A typical decision tree employed for determining proper therapy when the implantation of a pacemaker for sinus node dysfunction is considered. Adapted from ref. 11. AV, atrioventricular.

rhythms of both the upper and lower chambers of the heart is required, a dual-chamber system is implanted.

Two clinical situations are outlined next to illustrate common indications for pacing as well as the decision tree 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 1, and the decision tree is in Fig. 7 (11). The indications for pacing in an adult with acquired atrioventricular block are found in Table 2, and the decision tree is in Fig. 8 (11).

As an example, a patient with symptomatic chronotropic incompetence would have a class I indication for pacing (Table 1). Because this is related to dysfunction of the sinus node, Fig. 7 would then be used to determine the type of pacing system required. In this situation, rate response (a pacing system that responds to patient activity/exercise) would clearly be desired. If atrioventricular synchrony were also required, a rate-responsive dual-chamber pacemaker would be implanted (most commonly a DDDR system; see Section 4.4 to define this system and Table 3).

Table 2

Recommendation for Permanent Pacing in Acquired Atrioventricular Block in Adults

Class I 1. Third-degree and advanced second-degree atrioventricular block at any anatomical level associated with any one of the following conditions:

a. Bradycardia with symptoms (including heart failure) presumed to be caused by atrioventricular block.

b. Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia.

c. Documented periods of asystole greater than or equal to 3 s or any escape rate less than 40 beats/min in awake, symptomfree patients.

d. After catheter ablation of the atrioventricular junction. There are no trials to assess the outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is the atrioventricular junction modification.

e. Postoperative atrioventricular block that is not expected to resolve after cardiac surgery.

f. Neuromuscular diseases with atrioventricular block such as myotonic muscular dystrophy, Kearn-Sayre syndrome, Erb's dystrophy (limb girdle), and peroneal muscular atrophy, with or without symptoms, because there may be an unpredictable progression of atrioventricular conduction disease.

2. Second-degree atrioventricular block regardless of type or site of block, with associated symptomatic bradycardia. Class Ila 1. Asymptomatic third-degree atrioventricular block at any anatomical site with average awake ventricular rates of 40 beats/min or faster, especially if cardiomegaly or left ventricular dysfunction is present.

2. Asymptomatic type II second-degree atrioventricular block with a narrow QRS. When type II second-degree atrioventricular block occurs with wide QRS, pacing becomes a class I recommendation.

3. Asymptomatic type I second-degree atrioventricular block with intra- or infra-His levels found at electrophysiological study performed for other indications.

4. First- or second-degree atrioventricular block with symptoms similar to those of pacemaker syndrome.

Class IIb 1. Marked first-degree atrioventricular block (more than 0.30 s) in patients with left ventricular dysfunction and symptoms of congestive heart failure in whom a shorter atrioventricular interval results in hemodynamic improvement, presumably by decreasing left atrial filling pressure. 2. Neuromuscular diseases such as myotonic muscular dystrophy, Kearn-Sayre syndrome, Erb's dystrophy (limb girdle), and peroneal muscular atrophy with any degree of atrioventricular block (including first-degree atrioventricular block), with or without symptoms because there may be unpredictable progression of atrioventricular conduction disease. Class III 1. Asymptomatic first-degree atrioventricular block.

2. Asymptomatic type I second-degree atrioventricular block at the supra-His (atrioventricular node) level or not known to be intra- or infra-Hissian.

3. Atrioventricular block expected to resolve and unlikely to recur (e.g., drug toxicity, Lyme disease, or during hypoxia in sleep apnea syndrome in absence of symptoms).

Source: Adapted from ref. 11.

First Degree Atrioventricular Block
Fig. 8. A typical decision tree employed for determining proper therapy when the implantation of a pacemaker for atrioventricular block is considered. Adapted from ref. 11. AV, atrioventricular.

Table 3

NASPE/BPEG Classifications for Pacing and Defibrillation Systems

Table 3

NASPE/BPEG Classifications for Pacing and Defibrillation Systems

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