TOC | Cardiology    The Evaluation and Management of Bradycardia

[NEJM -- March 9, 2000:342, No. 10 - J. Michael Mangrum, John P. DiMarco ]

clinical presentation |  Diff-Dx  | evaluation  |  treatment

Clinical Presentation

Differential Diagnosis of Bradycardia:       

I.  Sinus Node Dysfunction (Sick Sinus Syndrome)

It is a common cause of bradycardia. The prevalence of sinus-node dysfunction has been estimated to be as high as 1 in 600 patients over the age of 65 years, and the syndrome accounts for approximately 50 percent of pacemaker implantations in the United States. It may be manifested as sinus bradycardia, sinus pauses or arrest, sinus tachycardia, sinus brady-tachycardia synd, atrial fibrillation or flutter.

  1. Intrinsic cause: pathologic sinus node, or
  2. Extrinsic causes: include the use of pharmacologic agents (e.g., (beta)-adrenergic blockers, calcium-channel blockers, digoxin, some antihypertensive agents, and antiarrhythmic drugs), electrolyte imbalance, hypothermia, hypothyroidism, increased intracranial pressure, and excessive vagal tone.

II.  Atrioventricular-Conduction Disturbances

Unlike the sinus node, however, the atrioventricular node and bundle of His provide a discrete connection between the atria and ventricles, so focal injury from infarction, infection, or catheter-related trauma is a common cause of problems.

  1. First-degree atrioventricular block (PR Interval values over 0.2 second with a retained 1:1 atrioventricular relation constitute first-degree atrioventricular block)
  2. Second-degree atrioventricular block occurs when an organized atrial rhythm fails to conduct to the ventricle in a 1:1 ratio but some atrial-ventricular relation is maintained.
  3. Third-degree atrioventricular block is often referred to as "complete heart block." In such cases, atrial activity and ventricular activity are independent of each other. The location of the block is implied by the escape rhythm. A narrow QRS complex, typically with a rate between 40 and 60 beats per minute, implies the presence of atrioventricular nodal block. Wide QRS escape rhythms at slower rates imply that the block is located in the His-Purkinje system.


History and physical examination, esp. medication history, precipitating factors and associated symptoms or signs. Severe nocturnal bradycardia should raise a strong suspicion of obstructive sleep apnea. The diagnosis of neurocardiogenic syncope, also commonly called vasovagal syncope, can usually be made on clinical grounds. If the diagnosis is uncertain, testing while the patient is lying in a head-up position on a tilt table may be used to provoke an episode of syncope and confirm changes in heart rate and blood pressure during such episodes.

Laboratory studies:


The management of bradycardia is determined by the severity of symptoms, the degree of correlation between symptoms and confirmed bradycardia, and the presence of potentially reversible causes.  When bradycardia, even if extreme, is present only during sleep, pacing is usually not indicated.

Temporary Rx for Bradycardic cardiac arrest or symptomatic bradycardia:

There are few indications for intervention in patients with bradycardia who are truly asymptomatic. The American College of Cardiology and American Heart Association guidelines for the implantation of pacemakers (15) list only the following as universally accepted (class I) indications

In asymptomatic patients:

  1. Third-degree atrioventricular block with documented asystole lasting three or more seconds (in sinus rhythm) or escape rates below 40 beats per minute in patients while awake;
  2. Third-degree atrioventricular block or second-degree atrioventricular Mobitz type II block in patients with chronic bifascicular and trifascicular block; and
  3. Congenital third-degree atrioventricular block with a wide QRS escape rhythm,
  4. Ventricular dysfunction, or bradycardia markedly inappropriate for age.
  5. Potential (class II) indications for pacing in asymptomatic patients include

For symptomatic patients:
the correlation between symptoms and confirmed bradycardia and the potential reversibility of causative factors are the keys to appropriate decision making.

  1. Symptoms definitely related to simultaneous, confirmed bradycardia that is caused by intrinsic sinus-node dysfunction or atrioventricular block should be treated with permanent pacing.
  2. The sinus bradycardia or atrioventricular nodal block in the settings of myocardial infarctio or infection rarely requires permanent pacing.
  3. Permanent damage occurs more readily to the bundle of His than to the sinus and atrioventricular nodes, and even transient complete atrioventricular block in the His-Purkinje system due to infarction or infection justifies the insertion of a pacemaker.
  4. In cases in which only nonspecific symptoms, such as fatigue, dizziness, or heart failure, are present and the associated bradycardia is not extreme, pacing is rarely indicated. Among patients with recurrent unconfirmed syncope and chronic bifascicular or trifascicular block, pacing is indicated if other likely causes (e.g., ventricular tachycardia) have been ruled out.
  5. When symptomatic bradycardia is due to extrinsic causes, clinical judgment is required. Although a change in therapy should be considered if drug-induced bradycardia is suspected, pacing may be an acceptable approach if no agent with equivalent efficacy is available. Occasionally, use of pindolol, a (beta)-adrenergic blocker with intrinsic sympathomimetic activity, may prevent bradycardia while the patient is at rest.
  6. Pacing is also appropriate in patients with the bradycardia-tachycardia syndrome if the agents required for control of the ventricular rate during atrial arrhythmias cause bradycardia during sinus rhythm. Atrium-based pacing is preferred in patients with sinus-node dysfunction because it reduces the incidence of atrial fibrillation, pacemaker syndrome, and thromboembolism. (45) Dual-chamber pacing is needed if atrioventricular block is also present. When bradycardia occurs only in specific situations, patient education and prevention strategies should be tried first.
  7. The role of pacing in patients with neurocardiac syncope and confirmed bradycardia is controversial. Many of these patients also have a prominent vasodepressor component to their syndrome, and standard pacing techniques may not completely relieve symptoms. New algorithms that include short periods of high-rate pacing when bradycardia is detected may be more effective. (46) Patient education and pharmacologic trials are indicated before pacing in most patients with neurocardiac syncope.


Bradycardia is a common clinical finding. The clinician must determine the relation between bradycardia and symptoms and differentiate between physiologic and pathologic conditions. In cases in which bradycardia is symptomatic and irreversible, pacemaker therapy is highly effective for the relief of symptoms.


Heart Rate in Normal Subjects

Spodick and others estimated that the "normal" range of heart rates in the afternoon was 46 to 93 beats per minute for men and 51 to 95 beats per minute for women.  Nocturnal rates are slower, decreasing during sleep by an average of 24 beats per minute in young adults and by 14 beats per minute in those over 80 years of age. Ambulatory electrocardiography in healthy, asymptomatic persons has shown that transient bradyarrhythmias are common during sleep. Heart rates between 30 and 35 beats per minute, sinus pauses of 2.5 seconds or less, sinoatrial block, junctional rhythms, and first-degree and second-degree atrioventricular nodal block are common enough during sleep to be considered normal variants. Trained athletes are particularly prone to bradycardia, with heart rates below 40 beats per minute common at rest . In one series, sinus pauses lasting between two and three seconds were found in 37 percent of athletes during sleep.  In view of these findings, the current guidelines of the American College of Cardiology and the American Heart Association for pacemaker implantation suggest that asymptomatic episodes of sinus bradycardia (with the heart rate as low as 30 beats per minute), sinus pauses of up to three seconds, and atrioventricular nodal Wenckebach block should be considered to be within the normal range. (15) Even if more pronounced bradycardia is documented, reversible causes may be responsible. For example, profound bradycardia often develops in patients with obstructive sleep apnea and hypoxia but may be eliminated if the sleep apnea is appropriately treated. (16,17)

Pitcher et al. reviewed Holter-monitor tracings from 66 asymptomatic patients with chronic atrial fibrillation and found that two thirds of them had pauses longer than two seconds and 20 percent had pauses longer than three seconds. Therefore, they concluded that daytime pauses of up to 2.8 seconds and nighttime pauses of up to 4.0 seconds during atrial fibrillation should be considered to be within expected limits. On the basis of these data, it is wise to interpret isolated, asymptomatic pauses during atrial fibrillation conservatively.