#90804: Antibradycardia Pacemakers

In the normal heart, the heartbeat is initiated by the SA node, which is located in the upper part of the right atrium. The SA is the primary pacemaker of the heart and normally fires at a rate of 60 to 100 impulses per minute. The electrical impulse travels from the SA node through both right and left atria, causing depolarization of the atrium. Complete depolarization takes approximately 80–100 milliseconds (ms). Atrial depolarization is followed by atrial contraction and atrial repolarization. The electrical impulse travels from the atria to the atrioventricular (AV) node, located in the bottom part of the right atrium. The speed of conduction slows in the AV node to allow the atria time to contract and complete ventricular filling. From the AV node, the electrical impulse travels through the bundle of His, located in the septum of the heart between the right and left ventricles. The bundle of His divides into the right and left bundle branches. These branches divide further into the smaller fibers of the Purkinje system. Electrical conduction through the His-Purkinje system is rapid, causing depolarization of both right and left ventricles. Depolarization of the ventricular cells spreads from the apex of each ventricle to the base and moves from the inside layer of the heart (i.e., the endocardium) to the outer layer (i.e., the epicardium). The entire ventricle depolarizes in approximately 80–100 ms. Ventricular depolarization is followed by ventricular contraction and ventricular repolarization [10,11,12].

When an electrical impulse stimulates a cardiac cell, a series of events are initiated that cause the cell to depolarize and repolarize. This generates an action potential that allows the electrical impulse to continue to travel. Ultimately, this process results in the contraction of the cells in the heart [10]. The major events are outlined in this section.

When an electrical impulse stimulates a cardiac cell, the cell depolarizes. Positively charged sodium ions from the extracellular space flood rapidly into the intracellular space. This increases the total number of positively charged ions in the intracellular space, and the charge in the intracellular space becomes less negative. The potential or voltage in the cell increases. This is phase 0 of the development of the action potential.

The flood of sodium ions into the intracellular space stops very quickly. It is followed by a brief and incomplete period of repolarization. This period is mediated by a temporary movement of potassium ions from the intracellular to the extracellular space. This brief period of repolarization is referred to as phase 1 of the action potential.

Phase 2 of the action potential is characterized by a balance of inward and outward movement of ions. Calcium ions move slowly through select channels into the intracellular space while potassium ions move out through multiple channels into the extracellular space. This initiates a slow repolarization and creates a plateau in the action potential. Cardiac contraction is mediated by phase 2.

In phase 3, the calcium channels close. The process of repolarization is accelerated. In phase 4, electrical diastole occurs. Except for the SA node, the heart rests. The SA node begins the process of initiating the next electrical impulse.

After the cardiac cell has depolarized, there is a period of time that the cell cannot generate an action potential in response to another electrical impulse. This is referred to as the absolute refractory period. As the cell continues to repolarize, an effective refractory period occurs, in which the cell can transiently depolarize in response to an electrical impulse but generally will not develop enough of an action potential to propagate the impulse to surrounding cells. As repolarization nears completion, the cell is said to be in a relative refractory period; in this period, a strong electrical stimulus can trigger the cell to depolarize and create another action potential [13].

Electrical events in the cardiac cycle are reflected in the electrocardiogram (ECG) waveform. The P wave represents atrial depolarization. The P-R interval reflects the amount of time from the beginning of atrial depolarization until the onset of ventricular depolarization; it represents the amount of time the electrical impulse takes to travel from the SA node through the AV node. The QRS complex represents the amount of time it takes the ventricles to depolarize. In normal conduction, ventricular depolarization occurs rapidly. This rapid conduction is reflected in a narrow QRS complex. The T wave represents ventricular repolarization. The Q-T interval represents the amount of time that it takes the ventricles to depolarize and repolarize and is measured from the beginning of ventricular depolarization (i.e., start of the QRS complex) to the end of repolarization (i.e., end of the T wave). During the early part of the Q-T interval, the ventricles are completely refractory and unable to respond to another electrical impulse. During the latter part of the interval, the ventricles are only partially refractory and may respond to some impulses. When changes occur in the normal cardiac cycle, the normal ECG waveform is altered to reflect them. For example, prolonged repolarization is reflected in a prolonged Q-T interval. A slowing of conduction from the SA node through the AV node may be reflected in a prolonged P-R interval. Abnormal conduction of the electrical impulse through the ventricles results in a QRS that is wider than usual or bizarre in shape, such as seen with bundle branch block (BBB). Careful analysis of the changes in a patient's ECG can provide valuable information in the diagnosis and treatment of an arrhythmia [10,14].

The pacemaker generator is a small titanium case that contains the electronic circuitry and a power source for the pacemaker. Most generators are small and lightweight. They may range in weight from 1–1 ¾ ounces with average dimensions of 2 inches x 2 inches x ¼ inch. To protect the pacemaker's electronic circuitry from outside interference and to protect the patient from the risk of battery leakage, the components of the generator are sealed in layers of airtight materials [15,16].

Pacemaker Power Source

The power source for pacemaker generators is usually a lithium-iodide battery. Depending on use, a lithium battery typically lasts from 5 to 10 years. As lithium batteries near the end of their battery life, they show predictable, identifiable characteristics that serve as an early warning that the battery is becoming depleted. The early warning allows the physician to schedule the battery change procedure in a timely (as opposed to urgent or emergent) fashion [3,4,15,16,17,18].

Electronic Circuitry

The electronic circuitry that controls the functioning of the pacemaker is also housed in the generator. The circuitry is programmed by the physician when the pacemaker is initially implanted. The programming may be noninvasively changed at later intervals as needed. Four different types of circuits are present: a sensing circuit, a pacing or output circuit, a timing circuit, and a transceiver. The sensing circuit monitors the electrical activity in the heart. The output circuit transforms the electrical energy generated by the pacemaker battery into an electrical pulse that is delivered to the heart to initiate a heartbeat. The strength (or voltage) of the electrical impulse is carefully programmed to provide the proper amount of stimulus to the heart to stimulate depolarization. The timing circuit controls the timing of the artificial electrical impulses that are delivered to the heart by the pacemaker. It is programmed at the time that the pacemaker is implanted; its programming may be adjusted noninvasively as needed to maximize pacemaker function for the individual patient. The transceiver is an electronic device that allows the attending or monitoring physician to "talk" to the electronic circuitry in the pacemaker by way of a specialized programmer. This permits the physician to retrieve data about the pacemaker's current settings and stored data about the pacemaker's functioning. It also allows one to change the programmed settings in the generator noninvasively [3,4].

The pacemaker lead connects the pacemaker generator to the heart. A pacemaker lead serves two main functions: to deliver the pacing impulse created by the pacemaker generator directly to the heart muscle (pacing function), and to relay information about the heart's electrical activity back to the electronic circuitry in the generator (sensing function).

A pacemaker lead consists of an extremely thin, flexible wire that is coated with suitable insulation, usually either silicone or polyurethane. The extreme flexibility of the wire allows the lead to withstand normal body movements without breaking. On one end of the pacemaker lead is a connector pin; this pin attaches the pacemaker lead firmly to the connector block that is located on the outside of the generator. On the other end of the pacemaker's lead is the pacing electrode that is used to deliver the electrical impulse directly to the heart. To work effectively, this electrode must be in direct contact with the heart. A second electrode is also located on the pacemaker lead. It is a sensing electrode designed to monitor and relay information about electrical activity back to the generator.

Pacemaker leads may be attached to the epicardial (outer) or endocardial (inner) surface of the heart. Most permanent pacemaker leads are attached to the endocardium. To hold the pacemaker lead in position inside the heart, the pacemaker lead has a small fixation device at the tip. There are two major types of fixation devices: active fixation and passive fixation. Active fixation devices have a small screw that extends from the end of the pacemaker lead into the endocardium to hold the lead in place. Passive fixation devices have tines (like the tines of a fork) on the end; these tines are designed to become entangled in the trabeculae inside the atria or ventricle to hold the lead in place. In addition to a fixation device, pacemaker leads have a small amount of steroids in a reservoir at the tip of the lead. When the lead is positioned and attached, the steroid is released. The steroid, through its anti-inflammatory action, reduces the amount of inflammation and scar tissue that develop around the tip of the lead. Minimizing scar tissue allows the pacing electrode at the end of the lead to deliver electrical impulses more effectively [3,17,18,19].

In order for the pacemaker to deliver an effective electrical impulse to the heart, a complete electrical circuit must be present. A complete circuit requires both a positive electrode (anode) and a negative electrode (cathode). To provide the complete circuit, pacemaker leads may be designed as either unipolar or bipolar. A unipolar lead contains only a negative electrode, located on the lead tip. The metal casing of the generator acts as the positive pole or anode. A bipolar lead, on the other hand, contains both a positive and a negative electrode. The negative electrode again is located on the tip of the lead; the positive electrode is located several centimeters behind the negative electrode. Because the electrodes are relatively close together on a bipolar lead, the electrical circuit is smaller and is less likely to be disturbed or disrupted by outside electrical interference than a unipolar lead. However, some sources suggest that bipolar leads are more fragile than unipolar leads and more likely to break [16,20].

Depending on the type of pacemaker, one or more pacemaker leads may be used. Single chamber pacemakers, which pace and sense only in the ventricle or only in the atrium, use a single pacemaker lead. Dual chamber systems that are capable of sensing and pacing in both atria and ventricles use two leads. The newer biventricular pacemakers may use three leads: one positioned in the right atrium, a second in the right ventricle, and a third in the left ventricle [20].

In addition to the generator and pacemaker leads, which are implanted inside the person's body, the proper functioning of a permanent pacemaker requires the intermittent use of an external device called a programmer. A pacemaker programmer consists of a relatively portable specialized computer. The technology in the programmer allows the computer to communicate with the pacemaker via the transceiver housed in the pacemaker generator. This process of noninvasive communication is called "interrogation" of the pacemaker. To interrogate an implanted pacemaker, a physician or other person trained in the use of pacemaker programmers holds a wand directly over the generator site. Using remote telemetric communication technology, the wand can transmit data from the pacemaker generator to the programmer. The information retrieved usually includes the current pacemaker settings and some information about past pacemaker function. In addition, data about the status of the battery and remaining battery life may also be obtained. The retrieved data may be printed for later analysis and/or documentation in the patient's medical record. Changes in pacemaker settings may also be transmitted from the pacemaker programmer through the wand to the generator. This permits the physician to adjust settings based on analysis of the pacemaker's past functioning and the assessment of the patient's current status [17,18].

When the heart's normal rhythm is interrupted, the pacemaker can initiate a heartbeat by pacing the heart. Using power from its battery, the pacemaker generator creates a tiny electrical signal or impulse. This impulse is sometimes called a pacing pulse, pacing impulse, or pace. The impulse is conducted through the pacing lead to the electrode on the tip. The impulse is discharged through the electrode directly into the surrounding cells of the heart. If delivered at the right time and the proper voltage, the impulse causes the surrounding cells to depolarize, thus initiating a heartbeat. As discussed, the output circuit in the pulse generator is responsible for generating an impulse that has enough voltage to trigger depolarization. At the time of implantation, the amount of electrical energy needed to depolarize the heart is carefully determined. This is sometimes referred to as the pacing threshold or the stimulation threshold. Once the pacing threshold has been established and programmed into the pacemaker generator, the pacemaker pacing function is tested to ensure that the amount of voltage delivered in each pacing impulse can successfully trigger depolarization. If the pacing impulse successfully triggers depolarization and initiates a heartbeat, the pacemaker is said to have effectively achieved "capture." Depending on the patient's specific conduction abnormality, pacing impulses may be delivered to the atria, the ventricles, or both. The rate and timing of the pacing impulses will vary with the pacemaker's programmed settings. The frequency of paced beats depends on the patient's underlying rhythm. In some instances, when the patient has a severe conduction abnormality, the pacemaker will pace the heart 100% of the time. If the patient's conduction problem is only intermittent, the pacemaker will fire only when needed. The ability of the pacemaker to pace the heart only when needed is referred to as "demand" pacing. Demand pacing prevents the pacemaker from competing with the heart's own intrinsic rhythm and reduces the risk that the pacing impulse will fall at a vulnerable point in the cardiac cycle and throw the heart into a chaotic rhythm. Demand pacing enables the heart to maintain a minimum rate and prevents long pauses without an effective heartbeat, maintaining cardiac output and cerebral circulation [17,19,20].

For the pacemaker to deliver a pacing impulse on demand, the generator must recognize or sense when the beat is needed. Sensing occurs when the pacemaker monitors and recognizes electrical activity in the heart. As previously noted, the pacemaker lead is equipped with both a sensing function and a pacing function. The sensing function monitors for depolarization in a specific region of the heart; if depolarization occurs, the sensing electrode transmits that information back through the pacemaker lead to the sensing circuit in the generator. The generator processes the information and responds according to its programmed parameters. For the pacemaker to recognize electrical activity in the heart correctly, the sensing threshold must be carefully established and programmed. The sensing threshold is defined as the largest electrical signal (ventricular or atrial) that can be consistently recognized by the sensing circuit. Sensing thresholds that are set too high or too low will result in improper functioning of the pacemaker's pacing function. Depending on the type of pacemaker, sensing may occur only in the atria, only in the ventricles, or in both the atria and the ventricles. The sensing function prevents the pacemaker from competing with the heart's own rhythm. It also permits the pacemaker to perform the more complex functions required by dual chamber and rate responsive pacemakers [17,18,19,21].

The timing function works interactively with the pacing and sensing functions of the pacemaker to ensure that a pacing impulse is delivered to the heart when it is needed, according to the pacemaker's programmed parameters. The timing function is very complex; it controls a variety of intervals that are involved in a pacing cycle. The specific intervals that are programmed depend on the type of pacemaker and its parameters. The timing function common to all types of demand pacemakers is the low rate limit setting. The low rate limit setting is the rate at which the pacemaker will pace the heart when the heart fails to initiate its own beat. This setting is usually expressed in terms of bpm and is often set at a rate of 50–70 bpm. To program the low rate setting limit, a low rate setting timing interval is used. This timing interval defines the maximum length of time that may occur between two paced beats, an intrinsic beat and a paced beat, or two intrinsic beats. The interval is based on the low rate limit; if the low rate limit is set at 60 bpm, a heartbeat (either paced or intrinsic) should occur approximately every second. If the low rate limit is set at 50 bpm, a heartbeat should occur approximately every 1.2 to 1.3 seconds. If the end of the timing interval is reached and no heartbeat occurs, the generator sends a pacing impulse to the heart. The sequence of events is [20]:

In the past, a drawback of many permanent pacemakers was the inability of the devices to increase the rate of pacing to meet increased metabolic demands of the body. Only one pacemaker, the dual chamber pacemaker (coded DDD), had the ability to vary pacing rates. However, in order for the dual chamber pacemaker to increase its rate, the patient's SA node had to be functioning normally. Because many people who required pacemaker therapy did not have intact SA node function, this DDD capability was of limited value. To provide an artificial substitute for the chemical, neural, and hormonal factors that normally increase the heart rate by stimulating the SA node, researchers developed a rate adaptive or rate responsive feature for permanent pacemakers. With the rate responsive feature, the pacemaker can increase or decrease its pacing rate in response to an identifiable parameter that reflects increased activity or increased metabolic demands. In an attempt to identify the most accurate and stable indicator for rate changes, researchers initially explored a wide variety of indicators, including minute ventilation, body temperature, changes in pH, changes in venous oxygen saturation in the body, increased stroke volume, changes in force of contraction, changes in respiratory rate, changes in skeletal muscle activity, and increased body motion. Activity is the most commonly employed rate indicator. The activity sensor is a piezoelectric crystal (i.e., vibration sensor) or accelerometer (i.e., acceleration sensor) that senses vibration from motion. When the activity sensor detects increased activity, the generator responds by increasing the pacing rate according to programmed parameters. When the activity sensor detects that activity has decreased, the generator is programmed to respond by lowering the rate to a preset level. Careful programming is a critical task to ensure that the rate responsive feature functions appropriately. To facilitate optimal programming, the software in newer generators allows for initial programming of the rate response along with subsequent automatic adjustments of the parameters. These generators also have the capability for physicians to retrieve data from the pacemaker to assess the adequacy/functioning of the rate responsive programming. In addition to a low rate limit and a low rate interval setting, a rate responsive pacemaker is programmed with a high rate limit setting. This high rate limit is the highest or fastest rate at which the pacemaker will pace the heart in response to data from the rate responsive sensor that an increase in heart rate is needed. In addition, the rate responsive feature is programmed with tiered rates correlated to activity levels. This often includes the resting rate and the average daily living rate. The rate responsive feature can be included in most types of demand pacemakers (single or dual chamber). Inclusion of the rate responsive feature involves additional costs, both for the sensor and for the programming. However, the benefits of rate responsive pacing as compared to nonrate responsive function include an improved ability to complete activities of daily living, provision of a heart rate that is appropriate (i.e., neither too fast nor too slow) for a given activity level, increased quality of life for the person who requires permanent pacing, and increased activity tolerance [18,22,23].

Pacemakers are now available with a programmable feature referred to as the "magnet mode." When programmed "on," the magnet mode allows the programmed functioning of the pacemaker to be altered temporarily by the direct, noninvasive application of a magnet over the pacemaker generator [15]. A pacemaker's specific response to the application of a magnet is established by the pacemaker manufacturer and will vary among different pacemaker types and brands. Generally, the expected response of a given pacemaker to application of a magnet should be known before the magnet is applied. Application of a magnet to a single chamber pacemaker always results in a change in pacing mode from demand to asynchronous pacing. In asynchronous mode, the sensing function is temporarily turned off, and the pacemaker generator is programmed to deliver a pacing impulse through the pacing lead at a regular interval and rate that do not vary. The term "magnet rate" is sometimes used to describe the rate at which the pacemaker paces the heart during the application of the magnet. The magnet rate may be used to evaluate the status of the pacemaker battery. As the battery voltage declines, the magnet rate will change. It is important to know the magnet rate for each specific pacemaker, as magnet rates vary greatly from manufacturer to manufacturer and even from one device to another produced by the same manufacturer [15,20,21].

In addition to the pacing and sensing thresholds, there are several key settings that must be programmed appropriately for an AAI pacemaker to work correctly. These include [20]:

Normal pacing patterns that may be seen with an AAI pacemaker include:

In addition to the pacing and sensing thresholds, programmable settings for VVI/VVIR pacemaker include [20]:

Normal pacing patterns that the patient may have with VVI/VVIR pacemaker include:

Normal pacing patterns seen with a DDD pacemaker include:

Settings that are programmed for the DDD/DDDR pacemaker include [4,17,18,22]:

Normal pacing patterns seen with a VDD pacemaker include:

Programmed settings for a VDD pacemaker include [4,20,22]:

Sinus node dysfunction occurs when the SA node is unable to pace the heart normally. Referred to as sick sinus syndrome, sinus node dysfunction encompasses a group of disorders that include [30]:

Signs and symptoms of sinus node dysfunction include [30,31]:

Associated clinical signs and symptoms include [22,27,31,32,33]:

Underlying Causes

According to the American College of Cardiology/American Heart Association, in patients with symptoms that are directly attributable to sinus node dysfunction, permanent pacing is indicated to increase heart rate and improve symptoms.

(https://www.hrsonline.org/clinical-resources/2018-accahahrs-guideline-evaluation-and-management-patients-bradycardia-and-cardiac-conduction Last Accessed: August 30, 2023)

Strength of Recommendation: I (Benefit>>>Risk)

One of the most common causes of sinus node dysfunction is the normal aging process. As a person ages, a decrease occurs in the number of specialized cells that are present in the SA node and able to depolarize spontaneously and initiate a heartbeat. At the same time, an increase occurs in the amount of collagen tissue that is unable to generate or conduct an electrical impulse in the SA node. As a result, the ability of the SA node to act effectively as the pacemaker of the heart decreases. Another major cause of sinus node dysfunction is inferior wall MI. Cardiomyopathy, a condition in which the heart's ability to pump blood adequately is impaired, may also lead to sinus node dysfunction. Other cardiovascular diseases associated with sinus node dysfunction include hypertension, valvular heart disease, and coronary artery disease. Noncardiac causes of sinus node dysfunction include hypothyroidism, sleep apnea, and electrolyte imbalances. More rarely, conditions such as muscular dystrophy and amyloidosis may cause sinus node dysfunction [3,31].

Class I Indications for Pacemaker Implantation in Sinus Node Dysfunction

According to the, dual-chamber pacing (DDD) or single-chamber atrial pacing (AAI) is recommended over single-chamber ventricular pacing (VVI) in patients with sinus node dysfunction and intact atrioventricular conduction.

(https://www.nice.org.uk/guidance/cg109 Last Accessed: August 30, 2023)

Level of Evidence: A (Data derived from multiple randomized clinical trials or meta-analyses)

For persons with sinus node dysfunction, class I indications for permanent pacemaker implantation according to the updated ACCF/AHA guidelines include [28]:

Symptomatic chronotropic incompetence with sinus node dysfunction was previously considered a class I indication but was downgraded to class II in the 2018 guidelines update [28].

Another common cause of symptomatic bradycardia is third-degree (or complete) AV block. Third-degree AV block occurs when none of the impulses generated by the SA node are conducted through the AV node. Sinus node function is often normal; however, conduction abnormalities at the level of AV junction or below the AV junction in the bundle of His/bundle branch region prevent the sinus impulse from reaching the ventricles [34]. The ventricles are paced by an escape rhythm. The type and effectiveness of the escape rhythm depends on the location of the conduction abnormality. If the problem occurs high in the AV node, a junctional escape rhythm may pace the ventricles. Junctional escape rhythms are characterized by a normally configured QRS complex and a heart rate of 45–60 bpm [34]. Junctional escape rhythms are often effective in maintaining an adequate cardiac output. If the conduction abnormality occurs lower in the ventricular conducting system (i.e., at the level of the bundle branches or below), a ventricular escape rhythm may emerge as the pacemaker of the heart. Ventricular escape rhythms are characterized by a widened, bizarre-appearing QRS complex and a heart rate of 30–40 bpm [34]. Persons frequently develop symptoms of decreased cardiac output and diminished cerebral blood flow with a ventricular escape rhythm. The defining ECG characteristics of complete AV block include [34]

In addition to identifiable ECG changes, signs and symptoms associated with complete heart block include [34]:

Underlying Causes

A major cause of complete AV block is MI. A branch of the right coronary artery usually provides the blood supply for the AV node and the bundle of His. An inferior wall MI can result in damage and impaired conduction through the node and the bundle of His. A branch of the left anterior descending (LAD) artery provides blood supply to the right and left bundle branches; an anterior wall MI may result in blocked conduction through this part of the ventricular conducting system. The development of chronic AV block has been linked with other cardiac causes, including valvular heart disease, congenital heart disease, coronary artery disease, myocarditis, and cardiomyopathies. Complete heart block may develop following cardiac surgery. Antiarrhythmic medications, such as digoxin, calcium channel blockers, beta blockers, and amiodarone, may also cause complete heart block. Older adults have an increased risk of developing heart block. Although the AV node is relatively unaffected by the aging process, both the bundle of His and the bundle branches gradually lose the ability to conduct impulses effectively as a person ages. In addition, elderly individuals are often more susceptible to the effects of antiarrhythmic medications and other medications known to influence cardiac rhythm. Finally, complete heart block may be caused by radiofrequency ablation (RFA). RFA of the AV node is an interventional procedure performed to manage a variety of tachyarrhythmias that are refractory to pharmacologic therapy. With RFA, the conducting cells in the AV node are destroyed and complete heart block results [3,34,35].

Class I Indications

According to the 2018 ACCF/AHA guidelines, the indications for permanent pacemaker implantation for the person with third-degree heart block include [28]:

Second-degree heart block occurs when impulses from the SA node are intermittently blocked at the level of the AV node or below. Some atrial impulses are conducted, and some are not. There are two types of second-degree heart block: Mobitz type I and Mobitz type II. Mobitz type I, also known as Wenckebach, is characterized by a P-R interval that gradually lengthens until a P wave is blocked. The pattern of gradual lengthening of the P-R interval then repeats. Mobitz type I is associated with inferior wall MIs, digitalis toxicity, and administration of calcium channel blockers or beta blockers. It may also occur for a period of time following cardiac surgery. Mobitz type II is characterized by an intermittent block of the atrial impulse; however, unlike the pattern seen in Mobitz type I, the P-R interval for conducted beats remains the same. In Mobitz type II, the conduction block occurs in or below the bundle of His. It is associated with anterior wall MIs. When it occurs after an MI, it is often an indication of a poor long-term prognosis for the patient. Mobitz type II may progress to the development of complete heart block [35,36].

Signs and Symptoms

Clinical signs and symptoms depend in large part on how often the atrial impulses fail to be conducted to the ventricles. Blocked P waves that occur every second or third beat can result in a severe bradycardia, with resulting symptoms of decreased cardiac output and diminished cerebral circulation [35,36].

Class I Indications

According to the 2018 ACCF/AHA guidelines, patients with transient or reversible causes of AV block (e.g., Lyme carditis, drug toxicity) should have medical therapy and supportive care, including temporary transvenous pacing if necessary, before determination of the need for permanent pacing [28]. Permanent pacing is a class II recommendation [28].

According to the 2018 ACCF/AHA guidelines, atrial fibrillation is an indication for permanent pacemaker implantation in patients who have new postoperative sinus node dysfunction, or AV block associated with symptoms, or hemodynamic instability that does not resolve after surgery for atrial fibrillation [28]. Permanent pacing is not indicated for the prevention of atrial fibrillation in patients without any other indication for implantation [28].

Clinical signs and symptoms indicative of hypersensitive carotid sinus syndrome include syncope, blurred vision, and lightheadedness or confusion when the patient sits or stands. These symptoms may be most pronounced during movement of the patient's head or neck. Some persons may be able to identify factors that trigger the onset of an episode, including turning the head, wearing tight clothing around the neck, shaving, and hyperextending the neck. Other patients are unable to identify any specific precipitating event. Syncopal episodes are transient, lasting only several minutes. A basic screening measure for hypersensitive carotid sinus syndrome is carotid sinus massage, which may cause/precipitate the patient's symptoms. More definitive testing is done using a tilt-table test [19,20,21,22,38]. The 2018 ACCF/AHA guidelines contain no class I indications for permanent pacing in persons with carotid sinus hypersensitivity syndrome [28].

Examples of medications commonly associated with the development of conduction abnormalities are outlined in Table 2. When possible, drug-induced arrhythmias are treated by changing the dosage and/or type of antiarrhythmic medication prescribed. In some cases, dosage reduction or a switch to another medication corrects the conduction abnormality. In other cases, however, it is not possible to find an antiarrhythmic agent (or combination of agents) that is effective in managing the patient's arrhythmia and does not cause additional conduction problems and significant bradycardia. Use of a permanent pacemaker is often indicated in these patients to counteract the bradycardia caused by the antiarrhythmic therapy. Other noncardiovascular medications, especially when given in conjunction with cardiovascular medications, may cause arrhythmias. Cardiovascular medications given in management of coronary artery disease or hypertension may also have proarrhythmic side effects [19,40].

Indications for permanent pacemaker implantation for the management of persons who have drug-induced conduction abnormalities include sinus node dysfunction with symptomatic bradycardia induced by necessary long-term pharmacologic therapy for which there is no acceptable alternative [28].

The American College of Cardiology/American Heart Association asserts that for patients with tachy-brady syndrome and symptoms attributable to bradycardia, permanent pacing is reasonable to increase heart rate and reduce symptoms attributable to hypoperfusion.

(https://www.hrsonline.org/clinical-resources/2018-accahahrs-guideline-evaluation-and-management-patients-bradycardia-and-cardiac-conduction Last Accessed: August 30, 2023)

Strength of Recommendation: IIa (Benefit>>Risk)

As pacemaker technology continues to advance, and as medical research continues to refine knowledge of the link between normal cardiac conduction and the successful management of cardiovascular disease and its symptoms, the indications for permanent pacemaker implantation will also continue to advance. The ACCF/AHA note that there are certain conditions that permanent pacemaker implantation may benefit; however, the guidelines caution that expert opinion and strength of clinical evidence to support the use of permanent pacemakers in the management of these conditions are controversial. Medical conditions that may benefit from permanent pacemaker implantation include [28]:

The 2018 ACCF/AHA guidelines note that implantation of a permanent pacemaker is not indicated for the management of some medical conditions. Conditions for which pacemaker therapy has not been found to be beneficial, useful, or effective, and which may cause harm include [28]:

Thorough assessment of the patient's symptoms is necessary to determine if the symptoms are correlated with the occurrence of the arrhythmia. Begin by identifying the primary reason that the patient has sought medical care. Listen for a history of a recent fall, recurrent unexplained falls, fainting spells, or periods of "black out." Ask the patient's family if he or she has had any unexplained periods of confusion. Determine when the symptom occurred, what the person was doing, what (if anything) appeared to trigger the event, how long it lasted, and what (if anything) relieved the symptom. Also question the patient about any associated symptoms, including increased fatigue with no change in daily activities, shortness of breath, activity intolerance, or other signs of congestive heart failure. Determine how often symptoms occur: daily, weekly, or less frequently. Also obtain data about the patient's "usual" lifestyle; inquire about the patient's normal activity level, exercise tolerance, and ability to perform normal activities of daily living. Also determine if the patient has recently experienced any exacerbation or worsening of previous symptoms; examples include increasing frequency of angina attacks in a patient with coronary artery disease or decreasing activity tolerance in a person with congestive heart failure.

Specifically question the patient about the current medications that he or she is taking, with special attention to any cardiovascular medications. As noted, many antiarrhythmic medications prescribed to control tachyarrhythmias may cause a symptomatic bradycardia. In addition, medications that are prescribed to manage other cardiovascular conditions, such as hypertension and coronary artery disease, can affect the electrical conducting system in the heart and cause symptomatic bradycardia. Also inquire about any other medications the patient may be taking. A wide variety of medications, such as tricyclic antidepressants, lithium, and phenothiazines, can interact with cardiovascular medications or antiarrhythmic medications to create bradyarrhythmias. Also assess the patient's medication history. Determine if any other cardiovascular medications have been prescribed for the patient at one time and why those medications were changed or discontinued. If indicated, consider obtaining serum drug levels for medications such as digoxin or procainamide to determine if toxicity is present. Toxic levels of some antiarrhythmics may result in bradycardia [19].

Finally, obtain information about the patient's medical history. Specifically inquire about any history of cardiovascular diseases, including coronary artery disease, previous MI, congestive heart failure, cardiomyopathy, hypertension, valvular heart disease, and any previous history of cardiac conduction problems. Determine if the patient has any history of interventional cardiovascular procedures, such as coronary angioplasty, coronary artery bypass surgery, valvular heart surgery, or electrophysiology interventions such as radiofrequency ablation. The presence and type of concurrent cardiovascular disease may influence the type of pacemaker selected and its programming.

When a patient does not speak the same language as the clinician, a professional interpreter should be consulted to ensure accurate communication. A systematic review of the literature has shown that the use of professional interpreters provides better clinical care than the use of "ad hoc" interpreters, with the former improving the quality of care for patients with limited English language skills to a level equal to that for patients with no language barriers [41]. Use of professional interpreters has been associated with improvements in communication (errors and comprehension), utilization, clinical outcomes, and satisfaction with care [41]. Individuals with limited English language skills have indicated a preference for professional interpreters rather than family members [42].

The traditional method of assessing a patient's heart rhythm is a 12-lead ECG. It is inexpensive, noninvasive, and readily performed in any healthcare setting or physician's office. Unfortunately, for persons with symptomatic bradycardia, this diagnostic tool has limited value. Typically, an ECG only records about 12 seconds of data. Because symptoms may be transient and occur intermittently, the ECG may not capture the patient's heart rhythm at the time that the symptoms are occurring. The patient may or may not have symptoms during an office or clinical visit. The ECG is considered a passive diagnostic tool; it only records the rhythm occurring at the time the tracing is done. It does nothing to actively precipitate an occurrence of arrhythmia [18,27].

To facilitate documentation of the patient's heart rhythm at the exact time that the patient is experiencing symptoms, researchers have developed another type of ECG monitoring called ambulatory electrocardiography, or AECG. This type of monitoring may be done over a longer period of time and in a setting outside the hospital, clinic, or physician's office. Three types of AECG monitoring are available: Holter monitors, event monitors, and implanted event monitors. The earliest AECG monitor developed, the Holter monitor, is a small, portable, battery-powered device that is worn by the patient for a period of 24 to 48 hours. Electrodes connected to the monitor are attached and taped to the patient's chest. A belt or shoulder strap holds the monitor in position. The patient is not allowed to bathe or shower during the period of the test. Otherwise, the patient is encouraged to perform his or her usual daily activities. The patient is instructed to keep a diary to document the occurrence, type, and time of any symptoms that he or she experiences [43]. In some cases, if the patient is elderly or might otherwise have problems completing a written log, a family member is asked to assist the patient to document the occurrence of any symptoms. Holter monitoring is a noninvasive procedure with little to no associated risk to the patient. The device may be applied in a physician's office, outpatient clinic, or inpatient hospital unit. A Holter monitor may be useful for persons who experience symptoms on a daily (or more frequent) basis; it is also useful for persons whose symptoms are severe enough to cause loss of consciousness or severe disorientation [43]. Persons with these severe symptoms would not be able to operate some of the more complex forms of AECG. The disadvantage to Holter monitoring is that it may fail to capture a symptomatic period or a period of bradyarrhythmia. Many people's symptoms occur less frequently than every day; longer periods of ambulatory monitoring are required to capture the necessary period of time [18]. Wireless Holter monitors have a longer recording time than standard Holter monitors. Using wireless cellular technology, these monitors record the heart's electrical activity for a preset amount of time and then send the recorded data to the patient's physician. Wireless Holter monitors work for days or even weeks, until signs or symptoms of a heart rhythm problem occur. They are usually used to detect infrequent symptoms. The downside to wireless monitors is that the patient must remember to write down the time symptoms occurred so that his or her physician can match it to the recording. These monitors also have a short battery life and are more expensive than a Holter monitor or an event monitor [43].

Implantable cardiac monitors are also available to serve as long-term Holter monitors [44]. These monitors allow long-term ECG monitoring without external leads connected to a recording device. They use a wireless, implantable system to help diagnose cardiac arrhythmias and the causes of syncope. Implantable cardiac monitors can be programmed to automatically record when defined triggers are activated or can be activated manually by the patient [44].

Advances in technology have resulted in the development of an AECG device known as an event recorder. An event recorder may be used for monitoring the patient's heart rhythm over a one- to two-month period; it is helpful in documenting arrhythmias and episodes of symptoms that occur more infrequently (such as weekly or monthly). There are several types of event recorders. Post-event recorders are among the smallest event monitors—about the size of a thick credit card. They can be worn by the patient like a wristwatch or carried in a pocket. They have no wires connecting them to chest sensors. The patient must hold the device to the chest when a symptom is felt. Post-event recorders only record what happens after started by the patient, so they may miss a heart rhythm problem that occurs before and during the onset of symptoms. Additionally, it may be difficult for the patient to start the device while experiencing symptoms [43,45]. Autodetect recorders are also small—about the size of the palm of the hand. They do have wires connecting them to chest sensors. These recorders need not be started by the patient. They detect abnormal heart rhythms and automatically record and send the data to the patient's physician [43,45]. Pre-symptom memory loop recorders (also called continuous loop event recorders) are the size of a pager. They are worn constantly, either clipped to a belt or carried in a pocket. A loop recorder records the patient's heart rhythm continuously, but it only stores and saves the data when "instructed" to do so by the patient [43,45]. When the event monitor is applied, the patient is told to depress a switch on the recorder any time he or she feels symptoms. When the switch is activated, the recorder automatically stores a few minutes of data from before, during, and after the onset of symptoms, making it possible for the patient's physician to see even very brief changes in heart rhythm [43,45]. This type of event recorder is indicated for persons whose symptoms are so brief and fleeting that they would disappear before any type of recording device could be attached. The loop recorder may also be used for persons whose symptoms cause loss of consciousness (or near loss of consciousness) as long as the person is not severely disoriented upon returning to consciousness and can still depress the event switch on the outside of the recorder. The data obtained by the event recorder can be readily transferred to a physician via telephone for analysis.

Another type of external event recorder is only attached when the patient experiences symptoms. During a clinic visit, physician appointment, or prior to discharge from an inpatient hospital stay, the patient is given the recorder and instructed on how to apply the electrodes. Commonly, the electrodes attach as bracelets, finger clips, or patches applied under the arms. When the device is attached to the patient, it records and stores ECG data. This type of event recorder is indicated for persons whose symptoms last long enough to permit attachment of the device; it is not indicated for persons who experience loss of consciousness or near loss of consciousness during an episode. To capture the data, the patient should be capable of finding and applying the device during symptomatic episodes. As with the loop recorder, data recorded and stored by this type of event monitor may be readily transmitted to a physician via telephone for analysis [17,18,46].

An event monitor that may be implanted under the skin has also been developed. Implantation of this device is a minor procedure that takes approximately 20 minutes and may be performed under local anesthesia. To implant the event recorder, a physician trained in the procedure makes a short (roughly ¾ inch) incision in the subclavian area and creates a small pocket to hold the monitor. Risks include the usual risks associated with a minor surgical procedure (i.e., primarily the risk of infection and reactions to the local anesthesia) [45]. No significant morbidity has been associated with use of the actual device. The implanted event monitor may remain in place for up to 14 months, until the necessary data is obtained or the end of battery life occurs. Implanted event recorders are continuous loop recorders. Like the external loop recorders, the implanted device continuously records the patient's ECG rhythm. In some instances, the device may be programmed to automatically store ECG information during a fainting or syncopal episode. Additionally, the patient may be instructed to depress a switch when he or she feels symptoms. When the switch is activated, a small amount of data about the heart rhythm at that time is stored. Family members may be instructed on how to activate the switch in the event that the patient is unable to do so. The implanted recorder can only store a certain amount of recorded data; when it is "full," the physician may clear the stored information. In general, the patient should be instructed to contact his or her physician for an appointment shortly after he or she has experienced a symptomatic episode.

In general, patients may continue with their usual daily activities during the period of time that the event monitor is implanted. However, there are a few precautions that the patient should know about at the time of implantation. These include [17]:

Mobile cardiac telemetry (MCT) monitoring represents a development in cardiac monitoring. The MCOT patch system consists of a sensor that the patient attaches to replaceable patches (placed near the heart) and a monitoring device that resembles a cell phone. The system conducts a beat-by-beat analysis of the patient's heart activity. Cardiac events are detected even if the patient is asymptomatic. The patient can also record symptoms as felt using the monitor. The recordings are transmitted to a central surveillance center where certified cardiac technicians perform real-time analysis. Patients are monitored 24 hours per day, seven days per week. Clinical reports are made available to the patient's healthcare professional both during and at the end of the monitoring period [47,48,49].

Outcomes from AECG Monitoring

Optimally, the data from AECG monitoring would clearly confirm the need for a pacemaker or definitively rule it out. In reality, several different outcomes may occur:

Due to the costs involved in the use of AECG monitoring, the ACCF, the AHA, and the HRS have established national guidelines for its use [46,50]. According to these guidelines, AECG is indicated for persons with documented or suspected bradycardia or conduction disorders [50]. Cardiac rhythm monitoring is useful to establish a correlation between heart rate or conduction abnormalities with symptoms, with the specific type of cardiac monitor chosen based on the frequency and nature of symptoms, as well as patient preferences [50]. The intermittent nature of most symptomatic bradycardia and conduction disorders often necessitates a more prolonged form of electrocardiographic monitoring to correlate rhythm disturbances with symptoms. For patients with daily symptoms, a 24- or 48-hour continuous ambulatory ECG (Holter monitor) is appropriate and, in active individuals, may help identify the presence or absence of chronotropic incompetence. Less frequent symptoms are best evaluated with more prolonged AECG that can be accomplished with a broad array of modalities, as previously discussed. The yield of ambulatory monitoring for significant bradyarrhythmias varies according to the population studies but is typically less than 15% [50]. The guidelines support the trend toward the development and use of AECG devices that permit longer periods of monitoring to facilitate correlation of symptoms with arrhythmias for persons with infrequent episodes [46,50].

Electrophysiology testing (EPS) is not generally the first diagnostic method of choice when evaluating a patient for the presence of symptomatic bradycardia. However, under certain conditions, EPS may be performed in order to aid in the management of the patient, such as patients with tachy-brady syndrome or when the initial noninvasive evaluation is nondiagnostic; EPS can document the mechanism and location of the tachyarrhythmia [50]. It can also determine if ablation of some area involved in the tachyarrhythmia can help control the rapid heart rate. EPS may be used to evaluate a patient for the presence of retrograde conduction. As will be discussed further, retrograde conduction (i.e., conduction that spreads from the AV node back into the atria) can interfere with optimal pacemaker functioning, and certain types of pacemakers are contraindicated in the presence of retrograde conduction. EPS may also be used to evaluate the extent of bundle branch block present in selected patients [19].

When hypersensitive carotid sinus syndrome is thought to be responsible for syncopal episodes, a tilt-table test may be used to confirm the diagnosis. Tilt-table tests are often performed in the cardiac catheterization laboratory. The patient is placed on a table that can tilt up to 80 degrees upright; safety straps are applied to prevent the patient from slipping and injuring him/herself during the test. An IV access is started to permit the rapid administration of IV medications or fluids should those be indicated during the test. Continuous ECG and blood pressure monitoring are performed, and the use of continuous intra-arterial blood pressure monitoring via placement of an arterial line is recommended. The purpose of the tilt test is to create the physiologic environment required to trigger vasovagal syncope. The patient is tilted from a supine position to a 70-degree angle. Patients who suffer from vasovagal syncope experience a decrease in venous return followed by a decrease in the left ventricular filling pressure when they are tilted to an upright position. The sequelae can include hypotension, bradycardia, and syncope. In addition to confirming the presence of a vasovagal syncope, a tilt-table test can also help to differentiate the major contributing cause. Permanent pacemaker implantation is indicated for syncope due to a mixed cardio-inhibitory/vasodepressor response [17,21].

After the decision is made to implant the pacemaker and the specific type of pacemaker is selected, the patient is scheduled for pacemaker implantation. The length of stay for pacemaker implantation is generally very short and often involves only an overnight stay in an acute care facility. Some institutions are exploring the option of implanting pacemakers on an outpatient basis; however, this practice is not yet widespread [51]. Pacemaker implantation may be safely performed in either the cardiac catheterization laboratory or the operating room. The selection of the specific site is based on an evaluation of which site will provide the best outcome and most cost-effective method for the individual patient. Some patients, such as patients who are confused, uncooperative, or have special medical needs, require the use of general anesthesia; pacemaker implantation for these patients should occur in the operating room. Implantation for patients who do not require general anesthesia but who can be managed with moderate sedation/analgesia may be performed in the cardiac catheterization lab [19,22].

Unless the patient's medical status requires hospital admission for management prior to pacemaker implantation, the patient may be admitted to the hospital on the morning of the procedure. The patient should be NPO for six to eight hours prior to the procedure. Basic preimplantation laboratory work is obtained, including a complete blood count, serum electrolytes, blood urea nitrogen (BUN), creatinine, prothrombin time (PT), partial thromboplastin time, and a urinalysis. A baseline 12-lead ECG, alveolar pressure (PA), and lateral chest x-ray are also obtained. Baseline vital signs and physical assessment are performed and documented. In the past, if the patient had been taking warfarin or similar anticoagulant drugs, the patient would have been instructed to discontinue taking them for several days in advance of the procedure to permit his/her' PT and international normalized ratio (INT) to return close to normal values in order to reduce the risk of excessive bleeding during the implantation. Patients at high risk for thromboembolic events might have been admitted to the hospital for temporary IV heparin therapy. However, a strategy of implanting devices during uninterrupted warfarin therapy appears to have a lower bleeding risk than a strategy of temporarily discontinuing warfarin and bridging with heparin [52].

The planned site for the pacemaker generator (usually the right or left subclavicular area) is scrubbed and shaved according to institutional protocol. The patient's dominant arm is identified; generally, pacemaker generators are implanted on the nondominant side. Informed consent should always be obtained. The patient may receive a mild sedative prior to leaving for the catheterization lab or operating room. Additional sedation and/or analgesics will be administered during the procedure. Generally, the patient is instructed to continue taking his/her routine medications prior to implantation. Due to the patient's NPO status, doses of insulin or oral hypoglycemic agents may need to be temporarily reduced or held.

Education for the patient and his or her family begins in the preoperative period and continues throughout the patient's life. The focus of patient education in the preoperative period is on addressing the patient's immediate questions and concerns and providing the patient and family with information about what to expect during implantation and in the period immediately following implantation. Many patients are very anxious about undergoing pacemaker implantation. They may express fears of "being dependent on a machine" to stay alive. Some may have heard a variety of "old wives' tales" about pacemakers from friends or relatives. Or, they may have known of a family member "years ago" who had a pacemaker implanted that did not work "right," and the person died. Some people have specific concerns about how a permanent pacemaker may interfere with their normal activities or ability to use certain types of equipment. Responding to any concerns or questions that the patient has during the preoperative period is very important. Providing specific information about what the patient can expect before, during, and immediately after pacemaker implantation can also help to reduce the patient's anxiety. The following topics are often helpful to cover in the preoperative period:

Allow time for the patient and family to ask questions and clarify concerns. The AHA, the Heart Rhythm Society, and various patient education sites provided by pacemaker manufacturers may be recommended as helpful educational sources (Resources).

Complications that may develop following permanent pacemaker implantation include bleeding into the pacemaker generator pocket, hemothorax, pneumothorax, and dislodgment of the pacemaker leads. Upon return to the floor, the patient's vital signs are monitored periodically. Continuous ECG monitoring is initiated. Spot checks of the patient's oxygen saturation level may be performed as needed. The pacemaker pocket site is assessed frequently for signs of excessive bleeding or swelling; if these are present, the physician should be notified immediately. A PA and lateral chest x-ray is taken to evaluate the positioning of the pacemaker leads as well as to rule out the presence of either a hemothorax or a pneumothorax [18].

Patients often experience pain at the pacemaker implantation site. Depending on multiple factors, patients may describe pain as mild to very severe. The patient's pain level should be routinely assessed using a 10-point pain scale (1 for least, 10 for worst). The physician's orders should include analgesic medications; prescribed medications may range from acetaminophen to stronger narcotic analgesics. The effectiveness of pain medication should be assessed and documented. Any complaint of increasing pain despite adequate analgesic medication should be carefully investigated; increased pain in the pacemaker pocket may be an indication that bleeding is occurring into the pocket.

Early complications associated with permanent pacemaker implantation include infection of either the incision site or the pacemaker pocket and accidental dislodgment of the pacemaker leads. To lessen the risk of infection, the patient should avoid getting the incision site wet. The site should also be routinely inspected for signs of redness, warmth, or drainage. During the patient's hospital stay, a dressing should be maintained over the incision site as ordered by the physician; if the dressing becomes dislodged or saturated with blood during this initial period, it may be changed using sterile technique. To lessen the risk of lead dislodgment, the patient should be instructed to limit movement of the affected arm and cautioned to avoid extending the arm above the level of the shoulder. Use of a sling on the affected arm can serve to promote comfort and remind the patient to limit use of that arm [3].

Assessing the patient's heart rate is a basic method for screening for proper pacemaker function that can be readily performed and requires no specialized ECG interpretation skills. If a permanent pacemaker is functioning correctly, the patient's heart rate should never drop to significantly less than the low rate setting on the pacemaker. A drop of one to two beats is not considered "significant" and may occur normally following pacemaker implantation; however, a rate that drops significantly may indicate a pacemaker malfunction [20].

Practice Exercise: Evaluating Heart Rates

Using the provided information regarding pacemaker codes and low heart rate settings, evaluate the heart rates in the following case examples.

Patient Z has a VVI pacemaker implanted for the management of chronic atrial fibrillation with a slow ventricular response. The low rate setting on the pacemaker is 60 bpm. When Patient Z's heart rate is checked, a reading of 58 bpm is obtained. Does this represent normal pacemaker function for this patient?

Answer and Rationale: Yes. The low rate setting on Patient Z's pacemaker is 60 bpm; a 1–2 bpm drop in heart rate may occur normally following the implantation and initial programming of the pacemaker. Patient Z's heart rate falls within the expected parameters for normal functioning of his pacemaker.

Patient Y also has a VVI pacemaker implanted for management of infrequent long pauses. The low rate setting for Patient Y's pacemaker is 50 bpm. The nursing assistant records a heart rate of 44 bpm for Patient Y. Does this represent normal functioning of Patient Y's pacemaker?

Answer and Rationale: No. Patient Y's pacemaker is programmed to deliver a pacing impulse as needed to maintain her heart rate at a rate of at least 50 bpm. A heart rate of 44 bpm is significantly less than the low rate setting programmed for the pacemaker and indicates a possible pacemaker problem.

Patient X also has a VVI pacemaker implanted for management of intermittent severe bradycardia. His underlying rhythm is atrial fibrillation. The low setting on his pacemaker is 55 bpm. The nursing assistant records his heart rate as 76 bpm. Does this represent normal pacemaker functioning?

Answer and Rationale: Yes. Patient X has only intermittent periods of bradycardia. A heart rate of 76 bpm most likely reflects his intrinsic heart rate and rhythm when he is not experiencing bradycardia. To confirm this assessment, his rhythm on telemetry is checked and it is clear that Patient X is indeed in his usual baseline rhythm with only intermittent paced beats present.

When a patient has a pacemaker that is capable of increasing the heart rate in response to changes in activity or metabolic demands, the assessment of the patient's heart rate as an indicator of pacemaker function becomes more complex. Appropriate assessment involves both counting a pulse rate and analyzing the patient's ECG image. General guidelines to follow when evaluating a heart rate for proper upper rate limit functioning include:

Pacemakers that have the capability of increasing the pacing rate in response to the body's needs include any pacemaker with the rate responsive feature as well as dual chamber pacemakers in persons with intact sinus node function [20].

Practice Exercise

Using this information on low and upper rate limit settings and pacemaker coding, evaluate the heart rates for the following patients.

Patient W has an AAIR pacemaker implanted to manage severe bradycardia associated with sick sinus syndrome. The low rate setting on the pacemaker is 60 bpm, and the high rate setting is 120 bpm. Patient W's resting heart rate is 60 bpm, but his heart rate increases to 96 bpm during ambulation. According to Patient W's telemetry, he is 100% paced when he is at rest and when he is ambulating. Does this represent normal pacemaker function?

Answer and Rationale: Yes. At rest, Patient W's heart rate matches the low rate setting programmed for his pacemaker. An AAIR pacemaker is programmed to increase the rate of pacing with changes in activity. When patient W increases his activity by walking, his paced rate increases accordingly. The paced rate with activity does not exceed the programmed upper rate limit setting.

Patient U has dual chamber pacemaker implanted for management of third-degree AV block; her sinus node function is normal. The rate limit settings are 60 bpm (low) and 120 bpm (high). When Patient U is sitting out of bed reading, her heart rate is 64 bpm. When she works with physical therapy, her heart rate is 110 bpm. Telemetry monitoring shows that her rhythm is consistently 100% paced. Does this reflect normal pacemaker function for this patient?

Answer and Rationale: Yes. For a person with intact sinus node functioning, the dual chamber pacemaker is programmed to track the patient's SA node firing and pace the ventricles at the same rate as long as the sinus node fires at or above the programmed low rate setting on the pacemaker. The paced rate should not exceed the upper rate limit setting. A paced rate of 64 bpm at rest and a paced rated of 110 bpm with activity fall within normal functioning for this dual chamber pacemaker.

Patient V has a VVIR pacemaker implanted. The low rate setting is 60 bpm with a high rate of 120 bpm for rate responsive pacing. Patient V contacts a nurse in the middle of the night and states that she feels like her "heart is pounding." Her heart rate is 110 bpm. Patient V's blood pressure, heart rate, and temperature are normal. Patient V shows no clinical signs that would indicate an increased metabolic demand or a need for an increased heart rate. Telemetry shows that her heart rhythm is 100% paced at a rate of 110 bpm. Does this reflect normal pacemaker function for this patient?

Answer and Rationale: No. The rate responsive programming is designed to increase the patient's heart rate in response to activity or increased metabolic demands. At rest, Patient V's paced rate should not be less than 60 bpm but not markedly greater than 60 bpm. A resting paced rate of 110 bpm indicates a possible problem with the rate responsive sensor or programming.

Patient T has a DDDR pacemaker placed for management of sick sinus syndrome with chronotropic incompetence. Patient T is a man, 84 years of age, who has a history of coronary artery disease and moderate congestive heart failure. The low rate setting on the pacemaker is 60 bpm with an upper rate limit for activity response set at 120 bpm. Patient T's heart rate at rest is 60 bpm. When he walks in the hall, his heart rate increases to 120 bpm and he complains of dizziness, shortness of breath, and chest pain. Telemetry shows that his rhythm is consistently 100% paced. Is Patient T's pacemaker functioning properly?

Answer and Rationale: Yes. With a DDDR pacemaker, the pacemaker should pace the patient at the low rate setting when the patient is at rest. Patient T's low rate setting is 60 bpm and his heart rate at rest is also 60 bpm. With activity, a DDDR pacemaker should increase its rate of firing but should not exceed the programmed high rate setting. Patient T's high rate setting is 120 bpm, and his heart rate with activity is also 120 bpm. The pacemaker is functioning normally as programmed; however, because Patient T experiences symptoms with the high rate setting, the programming may need to be adjusted. Elderly patients with underlying cardiovascular disease may require a lower rate for the high rate setting.

To calculate a heart rate from a rhythm strip, you should first recall a few basic facts about ECG recordings. ECG tracings are recorded on grid paper that is laid out in small and large squares. Vertical lines measure amplitude or voltage. Horizontal lines measure time. When ECGs are recorded at the standard speed of 25 mm/sec, the large and small squares may be used to calculate heart rates, measure intervals, and compute the length of a pause between two beats. On ECG recording paper, each small square is 1 mm on the longitudinal axis. This represents 0.04 seconds (or 40 ms); see "A" on Strip 1. Each large square is made of five small squares and is 5 mm on the X and Y axes. On the horizontal line, each large square represents 0.20 sec (or 200 ms); see "B" on Strip 1. Five large squares on the horizontal line represent one second.

Image 1

 

There are several ways to estimate a heart rate from a rhythm image.

Method 1

Identify a six-second period of time on the image. Some ECG recording machines place a "hash mark" on top of the grid at three-second intervals. You can also identify a six-second period by counting off large squares on the recording paper. Five large squares measure one second, and therefore, 30 large squares make a six-second strip (Strip 2).

Image 2

 

Start at the beginning of the six-second period and count the number of complete QRS complexes that fall within that time period. Multiply the number of QRS complexes in six seconds by 10. This gives you an estimated heart rate for one minute.

In Strip 2, there are almost 15 complete QRS complexes within the six-second period. Fourteen to fifteen complexes multiplied by 10 equals a heart rate of approximately 140–150 bpm.

Method 2

If the heart rate is regular, it may be calculated by using "the rule of 300." This method also works well for extremely slow or extremely fast heart rates. It is also useful to estimate rates when the patient's rhythm and rate change abruptly in a brief period of time. To estimate a heart rate using the rule of 300, follow these steps:

Using the example in Strip 3, the R-R interval between 1 and 2 contains five large squares. Three hundred divided by five gives an estimated rate of 60 bpm.

Image 3

 

To determine if pacemaker spikes are occurring when and where they should, several basic steps should be followed. Based on the type of pacemaker, determine if a pacemaker spike should occur before the P wave, the QRS complex, or both:

Carefully analyze each paced beat present on the ECG tracing to determine if the pacemaker spike occurs at the correct place. Low voltage spikes may be difficult to identify on a rhythm image. Adjusting the settings on the monitor, changing monitoring leads, or adjusting the position of the monitoring electrodes on the patient may be necessary to make the spikes more readily visible on a rhythm image.

Carefully analyze each pacer spike present on the ECG tracing to ensure that the spike is followed by depolarization of the appropriate chamber of the heart. Atrial pacing spikes should be followed by a paced P wave, and ventricular pacing spikes should be followed by a paced QRS complex. Paced beats often have a different configuration from normal beats. Depending on the location of the atrial pacing lead, a paced P wave may appear almost normal or it may have a flattened, abnormal configuration. Because the ventricular pacing lead is generally positioned in the right ventricle, paced QRS complexes generally show a left bundle branch block configuration. This occurs because the wave of depolarization from a paced impulse begins in the right ventricle and spreads across to the left ventricle and down toward the base of the heart. A pacer spike that is not followed by appropriate depolarization may indicate a problem in the pacemaker's ability to trigger depolarization. On Strips 1, 5, and 6, note the presence and the configuration of paced P waves and paced QRS complexes.

Carefully assess the ECG strip for the presence of random pacemaker spikes. Spikes are considered random if they appear anywhere in the tracing besides the programmed location. Random pacing spikes may indicate a problem with the sensing function of the pacemaker.

Finally, carefully assess the ECG strip to verify that none of the intervals between any two consecutive beats exceeds the timing interval for the low rate setting. An interval or a pause that exceeds the programmed timing interval may indicate a problem with the sensing or pacing function of the pacemaker.

When a patient is experiencing abnormally long pauses between effective heartbeats, it is often useful to calculate how long the pause lasts. By counting the squares between the R waves of two beats separated by a pause, the length of the pause in seconds or milliseconds can be determined. Find the beats marked A and B in Strip 4. Note that there are approximately 11.5 large squares between those two beats. According to this strip, the patient went for a little more than 2 seconds (11.5 x 0.20 seconds is 2.3 seconds) without an effective heartbeat.

Image 4

 

When evaluating normal pacemaker function as well as normal cardiac conduction, it is necessary to measure various intervals. Generally, because most intervals are very short, the small squares are used to estimate any given interval. This can include:

Image 5

 

Image 6

 

Before moving on to assessing the patient's response to pacemaker therapy, take a few minutes and complete the following practice exercise.

Example 1

Patient S has a VDD pacemaker implanted. The low rate setting is 60 bpm; the high rate setting is 100 bpm. Analysis of the rhythm strip indicates that the heart rate is 85 bpm. Pacer spikes are presently in front of each QRS complex. Each QRS complex is wider than normal and reflects a left bundle branch block pattern. There is no pause between any two beats that exceeds the programmed timing interval for the low rate setting. Sinus P waves are present; all P waves are followed by a paced QRS complex. All pacer spikes are followed appropriately by a QRS complex, and there are no random spikes. Does this data reflect normal VDD pacemaker function?

Answer and Rationale: Yes. A paced heart rate of 85 bpm falls within the programmed parameters of this patient's pacemaker. A VDD pacemaker is programmed to sense atrial activity and pace the ventricles in response (up to the limit of the high rate setting). The presence of sinus P waves followed by appropriately paced QRS complexes indicates that the pacemaker is sensing and pacing as programmed.

Example 2

Patient R has a DDD pacemaker implanted for management of intermittent second-degree heart block. The low rate setting is 60 bpm; the high rate setting is 110 bpm. Patient R's rhythm strip indicates a heart rate of 72 bpm. Sinus P waves are present at a regular interval. Some P waves are followed by a ventricular pacing spike and a paced QRS complex; other P waves are followed by a normal QRS complex. There are P waves in front of every QRS; every P wave is followed by either the patient's normal QRS complex or a paced QRS complex. The paced QRS complexes are broad and show a left bundle branch block pattern. The native QRS complexes are narrow. There are no random pacemaker spikes present in this tracing; every ventricular spike is followed by a paced QRS. Does this reflect normal DDD pacemaker function for this patient?

Answer and Rationale: Yes. With second-degree heart block, Patient R has normal sinus node function. The conduction abnormality lies in the AV node. The DDD pacemaker is programmed to sense the patient's sinus node activity and pace the ventricles in correct sequence at that same rate. A heart rate of 72 bpm falls within the programmed rate parameters for this pacemaker.

Example 3

Patient Q has a VVI pacemaker implanted for the management of symptomatic bradycardia caused by atrial fibrillation with a slow ventricular response. The low rate setting is 60 bpm. Does Strip 7 represent normal VVI pacemaker functioning for this patient?

Image 7

 

Answer and Rationale: Yes. A VVI pacemaker is programmed to pace the heart when the heart's rate is either too slow or too irregular. With a low rate setting of 60 bpm, the interval between any two beats should not exceed approximately one second (or five squares). In this strip, beats 1 and 2 are paced beats at a rate of 60 bpm; beat 3 is the patient's beat, followed by a paced beat 1 second later. The fifth beat comes before the end of the programmed timing interval and is not paced; the sixth beat is paced and occurs at the end of one second.

In some cases, unraveling an apparent pacemaker malfunction requires skills and great attention. For example, Patient O is admitted for overnight monitoring following a percutaneous coronary angioplasty (PTCA) with stent placement. Patient O has a history of previous coronary artery bypass surgery and radiofrequency ablation with permanent pacemaker placement for management of atrial fibrillation refractory to medications. According to Patient O's medical records, his pacemaker is a VVIR. Following his admission to the hospital, Patient O's vital signs remain stable and he shows no signs of complications from the PTCA. Telemetry monitoring shows his heart rhythm is 100% paced at a rate that varies from 70–100 bpm depending on his activity. That evening, Patient O complains of chest pain and shortness of breath. His heart rate is 50 bpm, but his blood pressure is unchanged. The telemetry monitor indicates that Patient O's rhythm is 100% paced at a rate of 50 bpm. There is no evidence of pacemaker malfunction; there are no random pacemaker spikes or long pauses. Because Patient O is symptomatic, the physician is notified. By the time the physician arrives, the patient's paced rate has increased to 98 bpm. The physician interrogates the pacemaker generator to determine the programmed settings. The interrogation confirms that the pacemaker is programmed for a low rate limit setting of 70 bpm and a high rate responsive limit of 110 bpm. However, the interrogation produces an additional piece of information: at the time of insertion, the pacemaker had been programmed with a "sleep mode." With a sleep mode setting, the pacemaker was programmed to reduce the paced rate at a specific time in the evening and resume the more rapid rate at a preset time in the morning. The sleep mode rate is 50 bpm, and its programmed time of onset is 8:30 p.m. Because the patient experienced symptoms of decreased cardiac output at a heart rate of 50 bpm, the physician programs the sleep mode to "off." The patient experiences no further problems. What is the lesson? Not all apparent pacemaker malfunctions are due to problems with the generator or the pacing leads. Sometimes the "problem" is not a pacemaker malfunction, but a mismatch between the patient's needs and the programmed settings.

At the time that a pacemaker is implanted, a temporary identification card is issued. This card lists specific information about the patient's pacemaker, including the type of pacemaker, manufacturer, date of insertion, and healthcare provider information. All patients should receive the card before discharge. Explain that the device manufacturer will mail a permanent card to the patient within a few weeks following discharge. Instruct the patient to always carry the pacemaker identification card and encourage a family member to keep and carry an additional copy. Explain that the card contains vital information that a physician would need to know to accurately assess the patient and the pacemaker function in the event of a problem [51].

Instruct the patient and family to let all other medical healthcare providers, including dentists, know that the patient has a permanent pacemaker. Some medical and dental procedures may temporarily affect the functioning of the pacemaker and will need to be modified. Other procedures, such as magnetic resonance imaging (MRI), are contraindicated for a person with a permanent pacemaker (Table 4) [53,54].

The patient or a family member should be taught how to check the patient's pulse. When teaching a patient to check his/her pulse, consider covering these points:

The American Society of Anesthesiologists recommends the anesthesiologist, patient, referring physician, and radiologist confer to determine whether the patient has been screened for implanted devices (e.g., pacemakers, cardioverter defibrillators) prior to conducting magnetic resonance imaging.

(https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2091587 Last Accessed: August 30, 2023)

Level of Evidence: Expert Opinion/Consensus Statement

Many tools and electronic devices use both electricity and magnets. The combination creates an electromagnetic field around the device. The size and strength of the field varies with the device. A large piece of equipment, such as an MRI machine or an arc-welding device, generates a very strong, powerful electromagnetic field. Household items, such as microwave ovens, mixers, and electric blankets, generate a very weak electromagnetic field. When the functioning of one electronic device disrupts or interferes with the normal functioning of another device, electromagnetic interference is said to occur. A strong electromagnetic field can disrupt the functioning of a permanent pacemaker. When electromagnetic interference occurs, the settings on the pacemaker may be altered. Sensing function may be lost, and the pacing rate may revert to the magnet mode rate. The patient may experience signs and symptoms, such as dizziness, light-headedness, or a rapid heart rate. Electromagnetic interference does not permanently damage pacemaker function. To relieve the symptoms and restore normal pacemaker function, persons with pacemakers may simply move away from the offending equipment and sit down and rest until symptoms disappear [53,54].

Many patients and their families have heard a mix of accurate and inaccurate information about the impact of electromagnetic interference on the functioning of a pacemaker [53,54]. Others may be unaware of the potential risk of electromagnetic interference from the use of relatively common items. Careful, precise instructions can both help relieve the patient's anxiety and prevent unnecessary disruption of pacemaker function from electromagnetic interference. Some pacemakers are called "MR conditional," "MRI conditional," or "MRI ready" [54]. This means that they are designed to allow the patient to safely undergo an MRI scan under certain conditions, due to safeguards in the system's design that protect it from the risks of electromagnetic interference [54].

Three major areas to cover with the patient and the family are: use of cell phones, use of normal household equipment, and airport security and commercial antitheft screening devices.

Some studies have shown that cell phones may not adversely affect pacemaker functioning. However, as technology continues to advance and the use of digital technology grows, it is prudent to instruct patients to use some precautions when using or carrying a cell phone, including maintaining a distance of 6 inches between cell phones and the device. Consider covering the following points [53,54]:

Generally, a person with a permanent pacemaker can safely use normal household electrical devices as long as those devices are in good repair and properly grounded. A few devices that, when used as intended, carry no known risk to implanted cardiac devices include [23,53,54]:

As noted, electrical equipment in poor condition or improperly grounded may produce electromagnetic interference, and these devices are contraindicated in patients with implanted cardiac devices. The use of magnetic mattresses or chairs is also contraindicated [54].

With the heightened emphasis on security checks at airports, patients and families may have concerns about getting through airport security. Studies have shown that while airport security devices do not damage pacemakers, the security devices will detect the implanted metal and trigger the alarm. To facilitate clearance through airport security, instruct patients to [53,54]:

Commercial antitheft devices are commonly used in many department stores in the United States. As noted, these devices have the potential to temporarily disrupt the functioning of the pacemaker. Instruct the patient to walk through the security-screening device at a reasonable pace; also instruct the patient to avoid lingering in the area around the antitheft devices [53,54].

The pacemaker pocket site should be carefully assessed for indications of impaired healing or signs of complications. Complications that may occur include infection in the pacemaker pocket, development of a hematoma in the pocket site, or erosion of the generator or the pacemaker lead through the tissue and skin [15]. Persons with diabetes are more at risk to develop an infection in the pacemaker pocket. Persons taking anticoagulants are at risk to form a hematoma in the pacemaker pocket [15,19]. Signs of impaired healing may include:

While not common, infection, hematoma, and erosion are serious complications that may require surgical revision or removal of the pacemaker [19]. Erosion also generally requires systemic antibiotics. In many cases, hematomas may be treated with direct pressure and observation [15].

A chest x-ray is performed to verify that the pacemaker leads remain correctly positioned. A 12-lead ECG with and without a magnet is done to evaluate pacemaker function. The pacemaker generator may be interrogated, and data obtained. Often, the sensing and pacing thresholds are tested. By the time of the first follow-up visit, the inflammation associated with implantation of the leads has resolved, and the programmed thresholds may need to be revised [19].

During either the initial follow-up visit or a subsequent visit, the patient's underlying rhythm should be determined and the extent of the patient's dependence on the pacemaker should be assessed. A person is considered "pacemaker dependent" if he/she requires the proper functioning of the pacemaker in order to perform activities of daily living. Persons who are pacemaker dependent often have very little effective underlying or intrinsic heart rhythm. Abrupt cessation of pacing often results in significant hemodynamic compromise. Persons who are pacemaker dependent may require more frequent follow-up, as pacemaker failure would have severe consequences requiring emergency intervention [21].

Adequate clinical documentation is vital for the effective long-term management of a person with a permanent pacemaker. Accurate evaluation of the pacemaker's function can only occur when the pacemaker type and programming are known. Current patient demographics are needed in the event that a device recall occurs, and patient notification is required. Recommended information to document in the patient's file includes [19]:

Before the end of the first follow-up visit, the patient and family should receive detailed instructions about long-term follow-up. This should include the schedule for both TTM and direct evaluation visits. The patient should receive the equipment required to perform TTM at home. In addition, the patient and a family member should be instructed in the procedures for contacting the TTM facility and performing the monitoring. Written instructions should supplement verbal instructions and demonstration of the equipment. Contact numbers for both the TTM center and the follow-up pacemaker clinic should be provided.

Preoperative preparation of the patient for transvenous insertion of a biventricular pacemaker is very similar to the preparation previously discussed for antibradycardia pacemakers. The same precautions and patient education are applicable in this case.

In addition to the usual risks associated with pacemaker implantation, implantation of a biventricular pacemaker carries additional risks specifically related to the left ventricular lead placement, including dissection or perforation of the coronary sinus [81]. Although these complications have been rare, their occurrence results in significant morbidity and mortality [7].

Care of the patient following successful biventricular pacemaker implantation is similar to that for patients who have undergone antibradycardia pacemaker implantation. Vital signs are monitored, and the pacemaker pocket is assessed for signs of bleeding or hematoma formation. The patient's ECG is continuously monitored to evaluate the pacemaker's function. Due to the sophistication of today's pacemakers and the complexity of the programming involved, the assessment and evaluation of biventricular pacing is the responsibility of a specially trained physician [71]. Nurses caring for the patient in the postoperative period should be alert to signs and symptoms that indicate a potential problem with the pacemaker, its leads, or its programming. Pertinent signs and symptoms include [69,83,94]:

Practice Exercise

Patient AA has had a dual chamber biventricular pacemaker implanted. The patient required both antibradycardia pacing for sick sinus syndrome and biventricular pacing for CRT. The programmed rate parameters are 50 bpm (low rate setting) to 120 bpm (high rate setting). The device does not include an ICD. Patient AA is placed on telemetry, and it is determined that she is 100% AV paced. Several hours later, Strip 12 is obtained. Does this strip show normal biventricular pacing function? Why or why not? What action should be taken?

Image 12

 

Answer: This strip does not show appropriate biventricular pacing. Pacer spikes in front of the P wave indicate that the atria are being paced. However, there are no pacemaker spikes in front of the QRS complexes; the ventricles are not being paced. In biventricular pacing, the ventricles should be paced 100% of the time. The physician should be notified. Evaluation of the programmed settings and pacemaker functioning is indicated.

When Left Ventricular Lead Placement Is Unsuccessful

On occasion, the physician will be unable to successfully position the left ventricular lead through a transvenous approach. Medical management options include:

Prior to the patient's discharge, the physician will evaluate the effectiveness of the pacemaker's programmed settings. An echocardiogram may be performed to assist the physician in identifying and programming optimal settings for each patient [71].

Discharge Education

Key points in discharge education following biventricular pacemaker implantation include [69,71,94]:

Patient BB is a woman, 74 years of age, who presents to her physician's office with complaints of dizziness and recent unexpected falls. She reports that she experiences symptoms once every week or so. When questioned about her falls, she states that she thinks she "blacks out for a second" but "comes to fast" and "knows where she is." She denies any injury from the falls. On admission, her blood pressure is 154/86 mm Hg, her heart rate is 68 bpm and irregular, and her respiratory rate is 14. Patient BB is alert and oriented, and does not appear to be in any distress. A 12-lead ECG shows that the patient is in atrial fibrillation at a controlled rate. A review of Patient BB's medical record shows that she has persistent atrial fibrillation. Past attempts at pharmacologic and electrical cardioversion have failed, and Patient BB remains on low dose antiarrhythmic therapy for rate control and on warfarin for anticoagulation. She has a history of hypertension, coronary artery disease, and percutaneous transluminal angioplasty (PTCA) for placement of two stents. She also has a history of a mitral valve replacement with an artificial valve. Patient BB lives alone in a senior citizen apartment complex; she participates in the social life of the community and takes frequent walks outside in good weather. Her favorite hobby is window-shopping at the mall.

Comments and Rationale: Complaints of dizziness and frequent, unexplained falls are symptoms commonly associated with symptomatic bradycardia. Symptomatic bradycardic episodes are often transient and difficult to capture either on 12-lead ECG or during routine vital sign checks. Due to Patient BB's age, she is at risk to develop symptomatic bradycardia as a result of age-related changes in the cardiac conduction system. She is also more likely to develop conduction abnormalities from antiarrhythmic therapy and medications prescribed to manage hypertension.

The physician orders AECG monitoring for Patient BB. A continuous loop event recorder is selected, and the patient is instructed on its use. She is also instructed to contact the physician when she has experienced one of her symptomatic episodes.

Comments and Rationale: A continuous loop event recorder may be used to document arrhythmias that occur relatively infrequently. This type of AECG is worn continuously; the patient is instructed to depress a switch when he or she feels symptoms. Although Patient BB appears to lose consciousness briefly during her episodes, she is not severely disoriented when she returns to consciousness and would be able to depress the switch in time to signal the device to save the data. Data from the AECG may be transmitted via telephone for analysis.

Approximately 10 days after Patient BB begins wearing the AECG, she experiences another symptomatic episode. Following instructions, she depresses the switch on the recorder. When the episode has ended, she contacts her physician and follows instructions to transmit the data from the AECG via telephone. Analysis of the transmitted data shows that Patient BB is experiencing episodes of severe bradycardia; her ECG tracing shows that she has pauses that last several seconds without an effective heartbeat; during these episodes, her heart rate drops to well less than 60 bpm. See Strip 13.

Image 13

 

A diagnosis of symptomatic bradycardia caused by atrial fibrillation with a slow ventricular response is established. Patient BB is referred for pacemaker implantation. Based on a thorough assessment, the physician chooses to implant a VVIR pacemaker.

Comments and Rationale: The definitive diagnosis of symptomatic bradycardia requires that the patient's symptoms of decreased cerebral blood flow and bradyarrhythmia be correlated and documented. For some persons with atrial fibrillation and a slow ventricular response, modifying the prescribed antiarrhythmic therapy may be sufficient to resolve the bradycardic episodes. However, this patient's antiarrhythmic therapy is already low dose and cannot be effectively reduced or altered. Implantation of a permanent pacemaker is indicated. A VVI (or VVIR) is the pacemaker of choice for persons with chronic atrial fibrillation; because a VVI pacemaker does not sense or pace in the atria, it cannot be confused by the chaotic atrial activity that occurs in atrial fibrillation. As Patient BB has an active lifestyle, the rate adaptive feature could be indicated. This will allow the pacemaker to pace her heart at a higher rate when she is engaged in increased activity.

The physician instructs Patient BB to discontinue taking her warfarin two days in advance of her admission to the hospital. When the patient is admitted to the hospital, her INR remains elevated. A continuous heparin drip is initiated and partial thromboplastin times (PTTs) are monitored; the heparin drip is adjusted to maintain the PTT in the desired range. Preoperative lab work, ECG, and chest x-ray are completed. Preoperative education is begun. Two days after admission, Patient BB's INR has dropped to the desired level, and pacemaker implantation is scheduled for the next day. Preoperative preparation is completed; Patient BB is made NPO overnight, and her heparin drip is discontinued. The following morning, Patient BB is taken to the cardiac catheterization lab. Under sedation and local anesthesia, the pacemaker is implanted. The low rate setting is programmed at 60 bpm, and the upper rate limit for rate adaptation is set at 120 bpm.

Comments and Rationale: To reduce the risk of bleeding during and after implantation, warfarin is discontinued prior to the procedure, and the patient's INR is allowed to return to near normal. However, because of Patient BB's chronic atrial fibrillation and artificial heart valve, she is at high risk for thromboembolic events. To reduce this risk, she is admitted to the hospital several days before the implantation is scheduled and placed on a heparin drip. To limit the risk of bleeding during the procedure, the heparin drip is discontinued four to six hours before the procedure. However, as previously stated, a strategy of implanting devices during uninterrupted warfarin therapy appears to have a lower bleeding risk than a strategy of temporarily discontinuing warfarin and bridging with heparin. Because the patient has no special needs, the cardiac catheterization lab is an appropriate site for the pacemaker implantation.

Following Patient BB's return to her room, she is placed on continuous telemetry monitoring. Her vital signs are monitored periodically, and the pacemaker pocket site is inspected for signs of excessive swelling or bleeding. She is instructed to limit use of the arm on the same side as the pacemaker generator, and she receives analgesic medications as prescribed for pain management. A chest x-ray is done, and a 12-lead ECG (with and without magnet) is completed. Patient BB's vital signs remain stable; the pacemaker generator site shows no signs of excessive bleeding or swelling. Telemetry monitoring obtains Strip 14.

Image 14

 

Comments and Rationale: The most common complications in the immediate postoperative period are bleeding or swelling in the pacemaker pocket and accidental dislodgment of the pacemaker lead. A chest x-ray is performed to verify lead position; a 12-lead ECG is used to evaluate pacemaker function. Strip 14 shows normal VVIR pacemaker function. The strip shows a heart rate of approximately 70 bpm; this falls within the lower and upper rate limits of Patient BB's pacemaker. Ventricular pacer spikes are present in front of each QRS complex. The QRS complex shows the typical configuration for a paced QRS. Each pacer spike is followed by a paced QRS; there are no random pacemaker spikes or excessive pauses between beats.

Prior to Patient BB's discharge, she receives information on incision line care and precautions to consider. She receives her temporary pacemaker identification card and is instructed to carry the identification card at all times. She is taught how and when to count her pulse and when to notify the physician. The nurse provides the patient with additional written materials, including the patient education handbook supplied by the pacemaker manufacturer. Patient BB expresses concerns about using cellular phones and flying; the nurse provides specific information about the use of cellular phones and how to manage airport security. Patient BB is discharged home; she has a follow-up appointment one week following discharge.

Comments and Rationale: The major focus of patient education just prior to discharge is on prevention of infection and prevention of accidental dislodgment of the pacemaker leads. Specific patient and family concerns should be addressed. Because patients and families frequently think of additional questions following the patient's discharge, the use of written materials provides a resource for them to use at home. Additional patient education will occur during the follow-up visit.

Patient CC, a man 56 years of age who has a DDD pacemaker, calls the TTM center to report that his heart rate is 30 bpm and that his preimplantation symptoms of dizziness, shortness of breath, and light-headedness have reoccurred. Patient CC's pacemaker was implanted approximately two years earlier for management of third-degree heart block. The rate settings on the DDD pacemaker are 60 bpm (low) and 120 bpm (high). Up to this point, the patient has experienced no problems with his pacemaker. Following instructions from the TTM center, Patient CC transmits a recording of his heart rhythm without application of a magnet.

Comments and Rationale: A heart rate that drops to dramatically less than the low rate setting coupled with a return of preimplantation symptoms is indicative of pacemaker malfunction. Malfunctions that may occur during the mid-life of a pacemaker include damage to the pacemaker lead or its insulation. TTM may be used to identify indications of pacemaker malfunction.

The TTM center receives Strip 15. The center immediately notifies Patient CC to report to the emergency department of his local hospital.

Image 15

 

Comments and Rationale: Strip 15 shows a pause of approximately three seconds. The pause is followed by an escape beat. As there are no pacemaker spikes present during the pause, the pacemaker malfunction appears to be failure to fire. Patient CC should obtain immediate medical care.

Upon Patient CC's arrival in the emergency department, he is placed on continuous telemetry monitoring. The monitoring initially shows a heart rate of 60 bpm. Telemetry interrogation of the pacemaker shows indications of probable lead fracture. A chest x-ray confirms the presence of a lead failure. The patient is admitted to a telemetry unit for monitoring and revision of his pacemaker. On the acute care unit, Patient CC is again placed on continuous telemetry monitoring. Telemetry monitoring shows a paced rhythm with intermittent missed beats and an isolated two- to three-second pause. An external noninvasive pacemaker is made available. Preoperative lab work is completed, and the patient is kept NPO. Patient CC is taken to the catheterization lab, and the broken lead is replaced.

Comments and Rationale: Telemetry interrogation can retrieve data that reflects the functioning of the pacemaker leads. Fracture of a pacemaker lead may often be seen on a PA and lateral chest x-ray. Fracture of a lead may result in the pacemaker's inability to deliver a pacing impulse to the heart when needed. Due to the length of Patient CC's pauses and the bradycardic rate of his escape rhythm, equipment for externally pacing the heart should be readily available. Replacement of the pacemaker lead is indicated to correct the pacemaker malfunction.

Following revision of the lead, the patient returns to the inpatient unit. His vital signs are monitored periodically, and the generator pocket site observed for bleeding or swelling. He is placed on continuous telemetry monitoring, and his rhythm is monitored for signs of proper pacemaker functioning. His rate settings remain at 60 bpm (low) and 120 bpm (high). Strip 16 is obtained and documented.

Image 16

 

Comments and Rationale: Strip 16 shows normal DDD pacemaker functioning. The patient's SA node is firing normally, and the pacemaker is pacing the ventricles at the same rate. The heart rate is approximately 100 bpm, which is somewhat high but within the rate limit setting of the pacemaker. Each pacemaker spike falls at the appropriate place, and each spike is followed by a QRS complex. Each QRS complex shows the typical configuration for a paced QRS complex. There are no random pacer spikes, and there are no pauses that exceed the interval allowed by the timing interval for the low rate limit setting.

As previously discussed, Patient N, a man 66 years of age, presented to his physician's office complaining of increased shortness of breath, rapid weight gain in the last three to four days, and an inability to perform his usual daily activities due to fatigue. Patient N has a history of MIs, coronary artery bypass surgery, acute coronary syndrome, multiple stent placements, and heart failure. Until recently, Patient N's heart failure has been well managed through the use of medications and diet. However, in the last month, the patient has been admitted to the local hospital twice for management of his heart failure symptoms. Based on an assessment of Patient N's status, the physician decides to admit him to the hospital for further management of his heart failure and evaluation for possible biventricular pacemaker implantation.

Comments and Rationale: Heart failure is a progressive, debilitating disease characterized by increasing symptoms, loss of function, and frequent admissions to the hospital for symptom management. Research has shown that neurohormonal mechanisms in the body contribute to this pattern of increased symptoms and worsening disease. Biventricular pacing has been found to be an effective therapy for the management of heart failure in selected patients.

Patient N's admitting ECG reveals that he is in normal sinus rhythm, with a QRS duration of 150 ms. An echocardiogram shows an ejection fraction of 25% as well as abnormal findings consistent with ventricular dyssynchrony. Based on the patient's symptoms, the physician determines that he is in NYHA functional class III heart failure. A review of Patient N's medications shows that he is receiving optimal doses of recommended medications for the management of heart failure. The physician recommends the implantation of a biventricular pacemaker ICD.

Comments and Rationale: Patient N meets the eligibility criteria for implantation of a biventricular pacemaker: an ejection fraction of 35% or less, NYHA Class III to Class IV heart failure, symptomatic despite optimal medical therapy, and a QRS duration of greater than 120 ms. In addition, the patient's ECG demonstrates additional clinical findings that are indicative of ventricular dyssynchrony. Patient N also meets criteria, based on clinical trial data, for the implantation of an ICD: has a history of ischemic heart disease, is at least 40 days post MI, has a left ventricle ejection fraction less than or equal to 30%, NYHA class II or III symptoms despite optimal medical therapy, and can reasonably be expected to survive with a good functional status for more than one year.

Patient N undergoes successful transvenous implantation of a biventricular pacemaker ICD in the cardiac catheterization lab. Upon return to the floor, his vital signs are stable. He is drowsy but responds appropriately to verbal stimuli. The pacemaker pocket shows no signs of bleeding or hematoma formation. Continuous telemetry monitoring is initiated and Strip 17 is obtained.

Image 17

 

Comments and Rationale: Strip 17 does not show any evidence of pacing problems; each beat is initiated by a P wave, and each beat is followed by a paced QRS complex. Every QRS is paced, and the rate falls within the rate setting programmed for the pacemaker.

Key points of care following implantation of a biventricular pacemaker ICD include assessment of vital signs, continuous monitoring of ECG rhythm, and assessment of the pacemaker pocket for signs of bleeding or hematoma formation. Although definitive diagnosis of pacing problems requires the expertise of a specially trained physician, continuous telemetry monitoring can identify clues that suggest a problem might exist.

About four hours after Patient N's return from the catheterization lab, he indicates that he has become extremely short of breath. His status is assessed. His blood pressure remains within his usual range. His heart rate is 100 bpm, and he remains 100% ventricularly paced on telemetry. His oxygen saturation has fallen to 88% on 2 liters nasal cannula. He has increased crackles and wheezes bilaterally in his lung bases. The physician is notified and orders a portable chest x-ray and a dose of IV furosemide. Patient N verbalizes distress regarding the recurrence of his symptoms, asking if this means "the pacemaker is not going to help."

Comments and Rationale: Shortness of breath following pacemaker implantation in a patient with severe heart failure may be an indication that a pneumothorax has developed as a complication of the procedure, or it may indicate that the patient is experiencing some volume/fluid overload. A chest x-ray can be used to confirm or rule out the presence of a pneumothorax. IV furosemide is a treatment of choice of an acute episode of volume overload. Volume overload postimplantation in a patient with heart failure may occur from a combination of factors, including physiologic stress of the procedure, anxiety, disruption in normal medication times, and the administration of even small amounts of IV fluid during the procedure. It is appropriate to reassure the patient that the occurrence of his symptoms at this point in his hospitalization is not an indication that CRT will be ineffective.

In response to the IV furosemide, Patient N diureses well and his acute episode of dyspnea resolves. He develops no further acute episodes and is discharged home two days later. In addition to the usual discharge instructions for patients with newly implanted pacemakers, Patient N is instructed to adhere to his prescribed medication therapy, diet restrictions, and lifestyle changes. He is advised to identify the level of his symptoms and activity; it is suggested that he keep a diary noting even small improvements. He is instructed to report increasing signs and symptoms of heart failure to his physician and to make sure to keep his follow-up appointments for the evaluation of his device. Because Patient N also has an ICD, specific ICD discharge instructions are also included.

Comments and Rationale: Persons with biventricular pacemakers should understand that the pacemaker does not replace previously prescribed medical therapies, and that just because their symptoms decrease, they cannot stop taking their medications or adhering to their diet restrictions and recommended lifestyle changes. Improvement in activity tolerance and symptom reduction may occur very gradually. Instructing the patient to note his/her baseline level of symptoms/activity and to record every improvement, no matter how small, can encourage the patient that CRT is working. Recurring or increased signs of failure can be an indication that resynchronization has been lost and should be reported immediately to the physician.

At Patient N's six-month follow-up appointment, he tells the physician that he has noticed little improvement in the amount of activity that he can do. With questioning, the patient admits that he has not been re-hospitalized for management of his heart failure symptoms in the last six months and that his ICD has not fired. The physician interrogates the device and obtains an echocardiogram to evaluate the effectiveness of the programming. The physician also reviews Patient N's current medications, with special emphasis on the dosages of his beta blockers and ACE inhibitors. The physician also questions the patient about his daily activities and what steps he has taken to gradually improve his physical conditioning. Based on this assessment data, the physician decides to increase Patient N's ACE inhibitor dose and to prescribe a structured activity program designed to increase his exercise tolerance.

Comments and Rationale: Some people respond more slowly than others to biventricular pacing. Measures that can improve the patient's response include "fine tuning" the device's programming, decreasing symptoms by increasing neurohormonal blockade through increased medication doses, and employing measures to help the patient slowly, carefully increase his/her activity in small steps.