The use of pacemaker therapy in the clinical management of persons with heart disease is well-established. It is estimated that more than 250,000 persons in the United States have a pacemaker implanted each year, and more than 700,000 pacemakers are implanted worldwide [1]. As the American population continues to age, the incidence of elderly persons requiring permanent pacemaker therapy is likely to increase, as more than 80% of patients requiring pacemaker therapy each year are 60 years of age or older [2].

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].

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].

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].

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].

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].

The first letter in the pacemaker code (i.e., the "first position") identifies which chamber(s) of the heart are paced by the pacemaker. "A" refers to atrium, "V" to ventricle, and "D" to both atrium and ventricle (or "dual") [15,25].

A single chamber ventricular pacemaker consists of a generator and a single pacing/sensing lead. The pacemaker lead is usually passed transvenously into and through the right atrium into the right ventricle, where it is attached to the wall of the right ventricle. VVI/VVIR pacemakers are capable of sensing and responding to electrical activity in the ventricles. The single lead positioned in the right ventricle is capable of sensing the heart's electrical activity and of delivering a pacing shock to the muscle of the right ventricle to trigger depolarization. The VVI/VVIR pacemaker is programmed to sense when the heartbeat drops to less than the programmed low rate setting. When needed, the pacing lead delivers a pacing impulse to the right ventricle; the right ventricle depolarizes, and the wave of depolarization spreads to the left ventricle. Depolarization of the ventricles is followed by normal contraction. When the VVI/VVIR pacemaker senses a normal ventricular depolarization impulse, the generator is inhibited and refrains from delivering a pacing impulse to the ventricles. Because a VVI/VVIR pacemaker neither paces nor senses in the atrium of the heart, there can be a loss of the normal AV synchrony. Remember that in normal conduction, the impulse coming from the SA node is slowed at the AV node to permit the atria to contract and complete ventricular filling. With a VVI/VVIR pacemaker, atrial contraction is not synchronized with ventricular contraction, and active ventricular filling may not occur. Cardiac output can drop. For persons with congestive heart failure, the loss of AV synchrony can increase signs of reduced cardiac output and heart failure. Because VVI/VVIR pacemakers do not sense or pace in the atrium, they are often the pacemaker of choice for persons with atrial fibrillation or atrial flutter (i.e., chaotic atrial arrhythmias), which could confuse the pacemaker. VVI/VVIR pacemakers are rarely used if the patient's SA node is functioning due to loss of AV synchrony. The rate responsive feature may be included in a ventricular demand pacemaker [3,4,22].

As noted, the major signs and symptoms of symptomatic bradycardia are syncope, near syncope, confusion, light-headedness, and/or dizziness during a bradyarrhythmia. In addition to the major definitive symptoms of cerebral hypoperfusion, persons with symptomatic bradycardia may also experience hypotension, fatigue, signs of congestive heart failure, shortness of breath, and exercise intolerance. Specific diagnosis of symptomatic bradycardia can be challenging. The bradyarrhythmia and the symptoms should occur simultaneously, and their simultaneous occurrence should be clearly documented through appropriate diagnostic tests [3].

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]:

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

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].

Atrial fibrillation is an atrial arrhythmia characterized by an absence of normal P waves and an irregularly irregular ventricular response. In atrial fibrillation, the heartbeat is not initiated by the depolarization of the SA node. Instead, chaotic electrical activity is present in the atria. This chaotic electrical activity is reflected by fibrillation waves on the ECG tracing; they occur at excess of 400 bpm and are ineffective in depolarizing the atria. Some fibrillation waves are conducted to the AV node; some are conducted through the AV node, while others are blocked. Atrial fibrillation with slow ventricular response is defined as atrial fibrillation with an average ventricular response of less than 60 bpm. It may be induced by medications (e.g., antiarrhythmics) used to control tachyarrhythmia as well as catecholamine excess, hemodynamic stress, atrial ischemia, atrial inflammation, metabolic stress, and neurohumoral cascade activation [37]. Atrial fibrillation is present in 30% to 50% of patients undergoing valve surgery and is associated with reduced survival and increased risk of stroke [28]. Successful surgical correction of atrial fibrillation is associated with improved patient survival compared with patients who have recurrent atrial fibrillation. The 2018 ACCF/AHA guidelines address pacing after surgery for atrial fibrillation [28].

Hypersensitive carotid sinus syndrome is a noncardiovascular, neurogenic cause of syncope. It is an extreme reflex that occurs in response to carotid sinus baroreceptor stimulation. To understand the pathophysiology of the syndrome, it is important to understand the normal physiology related to carotid stimulation. Normally, when pressure is exerted on the carotid sinus, the baroreceptors in the wall of the carotid sinus are stimulated. Stimulation of the baroreceptors results in vagal stimulation and a subsequent slowing of the heart. This response is normal; however, some individuals may have an exaggerated response. There are three types of hypersensitive carotid sinus syndrome. The first, called the cardio-inhibitor reflex, comprises 70% to 75% of cases and results from increased parasympathetic tone and decreased sympathetic tone; the person may experience significant bradycardia and hypotension. The second type, vasodepressor carotid hypotension, comprises 5% to 10% of cases and is characterized by reduced peripheral vascular resistance caused by a decrease in sympathetic tone, resulting in hypotension. The heart rate may or may not drop. The third type is a mix of the first two and comprises 20% to 25% of cases [38]. Patients with the mixed type may experience hypotension caused both by a drop in peripheral vascular resistance and by significant bradycardia. Only the first and third types of hypersensitive carotid sinus syndrome may effectively be managed with the implantation of a permanent pacemaker. A group of international experts suggested that the classification of hypersensitive carotid sinus syndrome into three types should be revised. They recommend that all patients with the syndrome should be classified as "mixed" between vasodepression and cardio-inhibition because isolated cardio-inhibition does not occur [39]. Aging is a major risk factor for the development of hypersensitive carotid sinus syndrome [19,20,21,22,38].

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.

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].

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.

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]:

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 determining that permanent pacemaker implantation is indicated, it should then be determined which type of pacemaker system will be the most effective. A number of factors should be considered in the decision, including patient factors, technical aspects, and procedural issues. Patient factors include [28,50]:

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].

After informed consent is obtained and the preoperative preparation is complete, the patient is taken to the operating room or cardiac catheterization lab. IV access is obtained, and continuous monitoring of ECG rhythm, oxygen saturation, and blood pressure is initiated. Depending on the implantation site and the physician's judgment, the patient will receive either moderate sedation or general anesthesia. Commonly used agents for sedation include midazolam and fentanyl. Once the patient is sedated, a small surgical incision is made, approximately 2–3 inches in length, beneath the patient's clavicle. Preferably, the patient's nondominant side is chosen for placement of the incision and pacemaker generator; use of the nondominant side lessens the risk that the pacemaker leads will be dislodged by repetitive arm and shoulder movements. The incision site is positioned to provide the physician with ready access to either the subclavian or cephalic vein for transvenous insertion. Depending on the type of pacemaker, one or two pacemaker leads are inserted transvenously and passed through the vessels into the heart. Fluoroscopy is used to monitor the passage of the pacing lead through the vessels. Generally, an atrial pacemaker lead will be positioned inside the right atrial appendage; a ventricular pacemaker lead is positioned in the apex of the right ventricle. Once it is determined that the lead is in the correct position, the lead tip is attached to the endocardial surface of the heart. When the leads are properly positioned, a small area is opened beneath the skin in the region of the original incision. This area, called a "pacemaker pocket," is designed to hold the pulse generator. In most people, the pacemaker pocket is created in the subcutaneous tissue located on top of the pectoralis muscle. For extremely thin individuals, the pacemaker pocket may be created beneath the pectoral muscle to provide adequate support and stability for the pacemaker generator. The connector end of the leads is firmly attached to the connector block on the outside of the pulse generator and the screw tightened to ensure good contact and stable position. The pacemaker generator is then inserted into the pacemaker pocket, and the skin is sutured shut. A dressing is applied. In some institutions, a pressure dressing may be applied. Antibiotics are frequently administered to reduce the risk of infection. The exact routine varies from institution to institution; some administer a single dose before or during the procedure, while others administer IV antibiotics for a 24-hour period following implantation. Extreme care is taken throughout placement of the generator and leads to avoid impairing the range of motion of the upper extremity on the affected side. Care is also taken to make sure that the generator and leads are well protected by body tissue to prevent the accidental erosion of either the leads or pacemaker generator through the skin. As previously noted, most pacemakers contain a small amount of steroid at the endocardial end of the lead to reduce the probability of inflammation causing abnormalities in function soon after implantation. Finally, the initial pacemaker settings are programmed, and pacemaker function is tested [3,4,18,19,20].

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].

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].

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:

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:

Discharge education begins prior to the implantation of a permanent pacemaker and continues through the patient's brief hospital stay, the initial follow-up appointment following discharge, and the long-term follow-up period. The major emphases of patient education during the patient's hospitalization include:

Failure to capture occurs when a correctly delivered pacing impulse fails to depolarize the heart. On ECG tracing, the pacemaker spike appears at the proper time, but it is not followed by the expected P wave or QRS complex. In the initial period following pacemaker implantation, failure to capture may be caused by dislodgment of the pacemaker leads or poor positioning of the electrodes on the lead tip. Later in the life of the pacemaker, failure to capture may be caused by [15]:

Failure to sense (i.e., undersensing) occurs when the pacemaker fires randomly at any point during the cardiac cycle instead of at the indicated or appropriate time. In failure to sense, the pacemaker fails to detect previous electrical activity and the pacemaker fires inappropriately. The ECG tracing shows random pacemaker spikes appearing throughout the ECG tracing. Failure to sense causes the pacemaker to compete with the heart's intrinsic rhythm. The presence of random atrial spikes does not usually present a major problem; these spikes may interfere with the optimal functioning of the pacemaker, but because they are low in voltage, they do not usually precipitate the development of a chaotic electrical rhythm in the heart. The presence of random ventricular spikes presents more of a problem. Under certain circumstances, such as in the presence of myocardial ischemia or acute MI, random pacemaker spikes falling at a vulnerable point in the cardiac cycle may trigger an erratic, ineffective rhythm. Failure to sense may be caused by multiple factors; some of these are not true malfunctions but are the result of pacemaker programming. For example, a paced beat is normally followed by a period in which the pacemaker is refractory and does not sense any intrinsic electrical activity. If a premature beat occurs during the pacemaker's refractory period, the pacemaker may not sense it and may appear to fire "early." The presence of multiple or frequent pacemaker spikes that occur randomly throughout a tracing are an indication of a true malfunction. Causes of failure to sense include poor electrode position or dislodged electrode, break in the pacemaker lead's insulation, battery failure, inappropriate programming of sensitivity of the pulse generator, a nondocumented change in programming to asynchronous mode, or MI. If failure to sense is caused by programming problems, noninvasive reprogramming of the pacemaker's settings may correct the problem. A failure to sense caused by problems with the generator, circuitry, or leads requires replacement of the broken component [21,23,64].

First identified in the 1970s, pacemaker syndrome is a complex of signs and symptoms that occurs when AV synchrony is lost during pacing and relieved when AV synchrony is restored. Once thought to occur solely with VVI pacing, pacemaker syndrome has also been shown to occur under certain circumstances with other types of pacemakers [65]. Pacemaker syndrome should be suspected any time the patient experiences a recurrence of preimplantation symptoms in the presence of a well-functioning pacemaker. The definition of pacemaker syndrome varies; some define it in terms of the presence of syncope, presyncope, or malaise. Others suggest that pacemaker syndrome may be present in a patient who fails to achieve his or her optimal functional status following pacemaker implantation. Pacemaker syndrome may be defined as a constellation of specific symptoms that occur in the setting of a temporary or permanent pacemaker and result from loss of physiologic timing of atrial and ventricular contractions [65]. The exact incidence of pacemaker syndrome is unclear; estimates range widely from 7% up to 83% depending on which definition of pacemaker syndrome is applied [19,65].

Symptoms associated with pacemaker syndrome are linked to either the drop in cardiac output or the elevation in atrial and pulmonic pressures. Common signs and symptoms include [19,20,21,65]:

Biventricular pacing has shown great promise as a therapy to restore coordinated contraction of the right and left ventricles [74]. With biventricular pacing, carefully timed pacing impulses are sent to both the right and left ventricles to stimulate coordinated contraction. In several large clinical trials, the use of biventricular pacing in select populations with NYHA class III and class IV heart failure has been shown to be effective in reducing symptoms, increasing activity tolerance, and improving quality of life (Table 7) [8,69,70,75,77,88]. According to a published analysis of clinical trial data, biventricular pacing is equally effective in the management of both men and women with heart failure who meet the criteria for implantation of a biventricular device [76].

Based on data from major clinical trials, a patient should meet the following criteria to be eligible for biventricular pacemaker implantation [7,8,71,81]: