Bradycardia is defined as a heart rate less than 60 beats per minute. This traditional rate cutoff is arbitrary, and many asymptomatic people have heart rates below 60 beats per minute who have no cardiac abnormalities (see “sinus bradycardia”). Pathologic causes of bradycardia are diverse and can be divided into intrinsic and extrinsic etiologies: these are listed in Table 19.1. Intrinsic causes of bradycardia may be related to conduction abnormalities of the sinus or atrioventricular (AV) nodes, His-Purkinje system, and atrial or ventricular myocardium. Because the cardiac conduction system is composed of specialized cardiac myocytes, common myocardial diseases such as ischemia, infarction, hypertension, surgical trauma, age-related degeneration, and dilated cardiomyopathies can also result in bradycardia. Less common pathologic causes of bradycardia include infiltrative disorders, collagen vascular diseases, familial conduction-system diseases, and infections such as endocarditis or Lyme disease. Because a portion of the atrioventricular conduction system is a narrow electrical corridor without redundancy, small pathologic lesions can result in profound bradycardia. Occasionally, bradycardia is caused by idiopathic degeneration of the conduction tissue. Bradycardia can also be a result of intentional or unintentional catheter ablation of the sinus node or atrioventricular junction.

Congenital heart block tends to occur in children of women with autoimmune diseases and results from transplacental transfer of maternal anti-Ro or anti-La antibodies or both. Sinus bradycardia may be associated with congenital complete heart block (1).

Extrinsic causes of bradycardia include hypervagotonia, drugs, hypoxemia, central nervous system disease, thyroid disease, and electrolyte abnormalities. Sleep is normally accompanied by marked bradycardia, especially in young patients. Complex partial seizures have also been included among the long list of functional causes of bradycardia (2).

An abnormal increase in vagal tone is responsible for the bradycardia seen during vasodepressor syncope, carotid sinus hypersensitivity, and cough and micturition syncope, although adrenergic withdrawal can also be a factor. Careful identification of reversible causes can lead to prevention of unnecessary therapy. For example, tracheostomy can correct the bradycardia associated with sleep apnea (3).

Patients with bradycardia have a broad spectrum of signs and symptoms. Because symptoms are usually nonspecific, it is important to be as certain as possible that the symptoms are secondary to bradycardia. Patients with persistent bradycardia can have symptoms that progress gradually, such as fatigue, dizziness, or exercise intolerance, or can have symptoms that occur suddenly, such as syncope, congestive heart failure, or cardiac arrest. Patients with paroxysmal bradycardia usually are first seen with palpitations, dizzy spells, presyncope, syncope, or seizures, depending on the escape rhythm and the
degree of cerebral perfusion during the bradycardia. Many patients with bradycardia are asymptomatic.

Bradycardia is often accompanied by a bounding pulse and a large pulse pressure. When complete heart block is present, the physical examination can reveal signs of atrioventricular dissociation, such as cannon A waves in the neck veins and variable atrioventricular-valve closure sounds. In affected elderly patients, confusion is occasionally the sole manifestation of bradycardia.

Proper characterization of a bradycardia often helps identify the cause. For example, transient atrioventricular block that occurs at the same time as transient sinus slowing is diagnostic of a vagal cause and does not require further evaluation. However, when an intrinsic cause is suspected, further testing is usually warranted, to exclude underlying structural heart disease.

An electrocardiographic recording is necessary to establish a diagnosis of bradycardia. Simple palpation of the pulse can lead to an erroneous diagnosis of bradycardia in the setting of atrial or ventricular bigeminy. A 12-lead electrocardiogram should be obtained for all patients with symptoms suggestive of bradycardia.

For patients with daily symptoms suggestive of bradycardia, an ambulatory Holter monitor can be helpful for characterizing the rhythm. For patients with less-frequent symptoms, a continuous-loop recorder collects data better than does a Holter monitor. Continuous-loop recorders can be worn for several weeks and can be used to transmit a rhythm strip over the phone after a patient has symptoms (4). An implantable loop recorder is also available for patients who have infrequent symptoms but is usually reserved for patients with recurrent, unexplained syncope (5).

A formal exercise-treadmill test can be helpful in establishing a diagnosis of chronotropic incompetence. However, a simple recording of the cardiac rhythm before and immediately after a short walk or stair climbing is often sufficient and saves the expense of formal exercise testing.

Maneuvers or medications that increase the sinus rate, such as ambulation or atropine, are useful tests in the setting of second-degree atrioventricular block. If the atrioventricular block worsens when the sinus rate increases, the conduction block is usually pathologic and related to an intrinsic abnormality of the His-Purkinje system.

Electrophysiologic testing can be useful in the evaluation of patients with symptoms suggestive of bradycardia (6). Measurement of the sinus node recovery time—the time between cessation of rapid atrial pacing and the first spontaneous atrial depolarization from the sinus node—is a useful test of sinus node function. Intracardiac recordings are valuable in patients with atrioventricular block when the surface electrocardiogram is not sufficient to determine the level of block. Intracardiac His-bundle recordings can reveal whether atrioventricular block is at or below the level of the atrioventricular node. If the level of atrioventricular block is below the atrioventricular node, placement of a pacemaker is often indicated. Early studies suggested
that electrophysiologic testing should be performed in patients with bundle-branch block to determine whether the patient is at risk for developing higher-degree atrioventricular block (7). However, the predictive value in this setting is low. Therefore electrophysiologic testing is currently not indicated for the evaluation of asymptomatic patients with isolated bundle-branch block.

Patients with unexplained syncope and bundle-branch block should undergo electrophysiologic testing to exclude inducible ventricular tachycardia before paroxysmal bradycardia is assumed to be the cause of syncope, especially in the setting of left ventricular dysfunction (8).

Bradyarrhythmias can be categorized as those caused by dysfunction of the sinus node and those caused by dysfunction of the atrioventricular conduction system. The characteristics of each bradyarrhythmia are described in the following sections. Proper characterization of the bradyarrhythmia is important because it helps determine the cause, prognosis, and treatment.

Tissues that constitute the cardiac conduction system have the ability to depolarize spontaneously. The intrinsic spontaneous rate of depolarization usually decreases in the anatomic direction of normal impulse propagation. The dominant pacemaker normally arises from within the sinus node complex and suppresses spontaneous depolarization of the distal conduction tissue. During bradycardia, these latent pacemaker cells are unmasked and give rise to the dominant rhythm. Escape beats and rhythms are also described hereafter.