Artificial pacing is generally indicated for the treatment of symptomatic bradycardia of any origin. The two main indications for permanent pacing are failure of impulse formation and
failure of cardiac conduction. Clinically, sick sinus syndrome and complete heart block are the most common indications for pacemakers. The following conditions are class I and IIA indications for a PPM:

Sick sinus syndrome describes an array of clinical disorders resulting from irreversible sinus node dysfunction. This may be manifested by episodes of sinus arrest, sinus pause, or bradycardia secondary to inadequate sinus node automaticity. As a result, episodes of tachyarrhythmias from ectopic atrial foci can occur as well. The diagnosis is made when a correlation is made between a patient’s symptoms and electrocardiographic evidence of bradycardia. Hence, extended ambulatory cardiac telemetry such as 24/48-hour Holter or event monitoring is helpful to make a diagnosis. When episodes of tachycardia and bradycardia coexist, it is often referred to as tachy-brady syndrome. This is one of the most common indications for pacemakers and is characterized by the following:

Chronotropic incompetence is loosely defined as the inability to achieve at least 80% to 85% of an individual’s maximum predicted heart rate (MPHR) at peak exercise. Use of
medications including β-blockers, calcium channel blockers, and antiarrhythmic medications can confound this diagnosis. In these instances, most people have used a modified definition of failure to achieve at least 62% of the MPHR. The presence of chronotropic incompetence has been shown to increase mortality and morbidity especially in those with heart failure. Rate-adaptive pacing is often used in these instances and has been shown to increase peak oxygen consumption during exercise. It is important to point out that not all patients with sick sinus syndrome have chronotropic incompetence and not all patients with chronotropic incompetence have sick sinus syndrome.

First-degree AV block is characterized by a PR interval of greater than 0.20 seconds during normal sinus rhythm (Fig. 8.1). Second-degree AV block is subdivided into two types. Mobitz type I, or Wenckebach block, is characterized by a progressively lengthening PR interval, which occurs until a P wave is not conducted down the AV node and a QRS complex is dropped. The PR interval of the first beat after the blocked P wave is almost always shorter than the PR interval of the beat prior to being blocked. The site of block is usually in the AV node, and the natural history of Mobitz I may or may not involve progression toward complete heart block. Mobitz type II block is characterized by a loss of AV conduction with no progressive lengthening of the PR interval before the sudden dropping of one or more QRS complexes. Additionally, the PR interval of the first beat after the blocked P wave is usually the same as the PR interval of the beat prior to the blocked P wave. The site of block is typically below the AV node and within the His bundle or in the Purkinje system. The natural history of Mobitz II block is often progression toward complete heart block over time. Thirddegree AV block, also called complete heart block, occurs when all electrical activity from the atrium fails to progress into the His-Purkinje system. The site of block can lie in either the AV node or the His-Purkinje system. The atrial and ventricular contractions have no relation with each other, with the atrial rate almost always faster than the ventricular rate. As a result, the QRS complexes seen result from an ectopic focus either from the ventricular myocardium or in an area of the AV node/His-Purkinje system below the site of block. Therefore, the QRS complex may appear wide or narrow, respectively, and typically occur with a rate of 40 to 60 beats per minute.

The term bifascicular block often refers to block in the right bundle and one of the two major fascicles of the left bundle. RBBB with left anterior hemiblock is present when the ECG shows an RBBB with a left axis deviation (usually greater than -60 degrees) in the absence of an inferior myocardial infarction. Complete RBBB with right axis deviation (greater than 90 degrees) is indicative of RBBB and left posterior hemiblock in the absence of a lateral myocardial infarction or evidence of right-sided heart failure. The term trifascicular block is used to describe first-degree AV block in the presence of bifascicular block.

The risk for progression to complete heart block in asymptomatic patients with bifascicular block is low. Further, no clinical characteristics have been identified that accurately predict the risk of development of complete heart block. Therefore, routine PPM implantation in patients with asymptomatic bifascicular block is not recommended. Observations made in the perioperative period have suggested that development of complete heart block during general
anesthesia is also rare; therefore, it is generally not recommended that patients undergo temporary pacemaker insertion before general anesthesia. However, it is advisable to have an external pacemaker available in the operating room. The term trifascicular block is somewhat of a misnomer because, in truth, if all three fascicles (i.e., right bundle, left anterior fascicle, left posterior fascicle) were blocked, the patient would be in complete heart block. Although it is generally agreed that individuals with trifascicular block have a higher risk for sudden death, there is no single clinical variable that predicts a higher risk for complete heart
block during surgery. Small case series have shown that the development of intraoperative complete heart block in asymptomatic patients with trifascicular block is uncommon. Therefore, routine temporary pacemaker insertion before general anesthesia in these patients is not recommended.

Given the complexity of current pacemaker systems, the Intersociety Commission for Heart Disease Resources established a classification code in the 1970s that is now widely accepted. The original nomenclature involved a three-letter identification code, as shown in the first three columns of Table 8.1. In 1980, this code was extended to five letters; the last two letters can be deleted when not applicable. In 1987, this five-letter coding system become known as the NBG pacemaker code after being adopted by both the NASPE (now known as the Heart Rhythm Society) and BPEG. The first letter describes the chamber(s) that the pacemaker can pace, the second letter describes the chamber(s) that it senses, and the third letter describes the response of the pacemaker to sensed intrinsic activity. The last two letters describe additional features such as rate responsiveness that are commonly omitted when not used. For example, a VVI pacing mode paces in the ventricle, can sense intrinsic activity in the ventricle, and inhibits pacing when it senses intrinsic activity. A VOO pacing mode paces in the ventricle but does not sense intrinsic activity nor does it inhibit pacing—it simply paces regardless of the heart’s electrical activity.

Modern pacemakers are programmable into one of three modes of pacing: asynchronous pacing, single-chamber demand pacing, and dual-chamber AV sequential demand pacing.

Asynchronous or fixed-rate (e.g., AOO, VOO, DOO [see section A.5 for details]) modes pace at a programmable preset rate that is independent of the inherent heart rate. They can be atrial, ventricular, or dual-chamber. Competition, pacemaker syndrome, and rarely induction of ventricular arrhythmias are the potential complications when pacing occurs in the presence of intrinsic myocardial electrical activity. Ventricular tachyarrhythmias in those with structural heart disease can theoretically occur because the pacing spike can potentially be delivered during a time when the myocardium is vulnerable to arrhythmogenesis, but this is extremely rare.

Single-chamber demand pacing (e.g., AAI, VVI) paces at a preset rate only when the spontaneous heart rate drops below the programmed preset rate. For example, if this patient’s device was programmed to VVI 70, the device would pace in the ventricle only when the native ventricular rate fell below 70 beats per minute. Once the native ventricular rate resumed above 70 beats per minute, the device would sense this activity and inhibit further pacing. Single-chamber demand pacing in the atrium functions in a similar way but is rarely used alone in the United States.

Dual-chamber AV sequential pacing requires two pacemaker leads, one in the right atrium and one in the right ventricle. The atrium is stimulated to contract first; then, after an adjustable PR interval (also referred to as the AV interval), the ventricle is stimulated to contract if no intrinsic ventricular activity is sensed by the ventricular pacing lead. For example, if this patient’s device was programmed to DDD 70 with an AV interval of 200 milliseconds, the device would begin pacing the atrium first if the intrinsic sinus rate fell below 70 beats per minute. After the atrium has been paced, the device will wait for 200 milliseconds to sense intrinsic ventricular activity. If it does not see intrinsic activity within 200 milliseconds, it will then pace in the ventricle as well. DDD pacemakers can also pace in the ventricle in response to intrinsic atrial activity. For example, if the intrinsic atrial rate was 80 beats per minute, the device would inhibit pacing in the atrium because the base rate was set to 70 beats per minute. But because it is a dual-chamber device programmed to inhibit and trigger pacing in both chambers (i.e., the third “D” in the coding sequence), it will wait 200 milliseconds from the time of the intrinsic atrial activity and watch for intrinsic ventricular activity. If it sees intrinsic ventricular activity (i.e., the atrial signal conducted down the AV node and to the ventricle), it will inhibit ventricular pacing. If it does not see intrinsic ventricular activity occurring within 200 milliseconds from the intrinsic atrial activity, the pacemaker will then “trigger” the ventricular pacing lead to pace the ventricle. Dual-chamber pacemakers programmed to DDI differ slightly from devices programmed to DDD, and the main difference is that AV sequential pacing occurs only when atrial pacing is present. This is in contrast to DDD pacing in which AV sequential pacing is preserved regardless of whether atrial pacing or atrial sensing is occurring. Suppose we have a dual-chamber pacemaker programmed to DDI 70 with an AV interval of 200 milliseconds. If the sinus rate fell below 70 beats per minute, the atrial pacing lead would pace the atrium. After a 200-millisecond interval, if intrinsic ventricular activity was seen by the ventricular lead, then the ventricular lead would be inhibited from pacing the ventricle. If ventricular activity was not seen after 200 milliseconds, the ventricular lead would pace the ventricle. Suppose now that the sinus rate is 80 beats per minute. Because the DDI pacemaker is programmed to 70 beats per minute, no atrial pacing is occurring. Because DDI pacemakers do not track atrial sensed events, ventricular pacing would not be “triggered” after 200 milliseconds by these atrial sensed events and only occur if the ventricular rate fell below the preset rate of 70 beats per minute.

All modern pacemakers have the ability to adjust the pacing rate according to the patient’s level of activity in an effort to obtain a more physiologic response to exercise. This is known as rate-response (adaptive) pacing and is denoted by an “R” in the fourth position of the NBG coding schema. This is often applied in patients with chronotropic incompetence or those with permanent atrial fibrillation who have undergone AV node ablation. Various
activity-detecting systems have been developed to create a reliable rate-responsive pacemaker (e.g., muscle movement, respiratory rate, minute ventilation, central venous temperature, QT interval, myocardial contractility [dP/dt], oxygen saturation and pH in mixed venous blood, and ventricular depolarization gradient), but currently, PPMs used in the United States rely on sensors of motion or changes in minute ventilation through measurements of intrathoracic impedance. Because of the latter phenomenon, patients undergoing general anesthesia who are subjected to mechanical hyperventilation (e.g., neurosurgery) can experience an increase in the rate of pacing. Although it is generally not required to disable rate-responsive features before surgery, pacemaker-induced changes in heart rate resulting from intraoperative hyperventilation or significant motion may sometimes be mistaken for inadequate anesthesia. Hence, it is important that the anesthesia team be aware of the programmed settings of the pacemaker. If reprogramming the device to disable rate-responsive features is not readily available, a magnet may be placed over the pacemaker site to temporarily convert it to asynchronous pacing. Although the response to a magnet may be programmed off in some pacemakers, all properly functioning pacemakers within the United States have magnet-responsive features activated as a default.

Atrial pacing only increases cardiac output by 26% over the cardiac output of ventricular pacing only because atrial contraction contributes to approximately 15% to 25% of the diastolic filling of the ventricle. It has been shown that coronary blood flow increases and coronary resistance decreases during atrial pacing only. Atrial pacing has also been shown to reduce the incidence of atrial fibrillation. Atrial pacing only is seldom used in the United States and often is implanted with the addition of a ventricular pacing lead in the event of AV block.

Ventricular pacing, occurring individually or sequentially with atrial pacing, has been shown to result in dyssynchronous left ventricular electrical activation and mechanical contraction. Under normal circumstances, electrical activation along the His-Purkinje system results in a near simultaneous activation of the entire left ventricle. This allows for efficient contraction and is said to be synchronous. When ventricular pacing is introduced, this results in activation of the right ventricle first, followed by passive activation of the left ventricular free wall. This form of contraction is said to be dyssynchronous and has been shown to potentially worsen congestive heart failure and the left ventricular EF. Prior studies have shown that individuals at greatest risk for developing reductions in EF from right ventricular pacing are those who exhibit ventricular pacing greater than 40% of the time. More recent studies have shown that individuals requiring ventricular pacing for AV block with an EF less than 50% have a 56% risk for developing a composite end point of death, urgent visit for heart failure or left ventricular dilatation over an average of 37 months.