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Key Clinical Questions

  • image What is the epidemiology of bradycardia?

  • image What are the conduction abnormalities that lead to bradycardia?

  • image What external factors can cause bradycardia?

  • image When is treatment necessary for bradycardia?

  • image When is pharmacologic versus pacemaker therapy indicated?

Bradycardia is commonly encountered in clinical practice. It is usually defined as a heart rate of less than 60 beats/min, and its clinical significance varies depending upon the underlying etiology and the population being studied. For example, a low heart rate is an accepted signal of superior health in trained athletes and, in this population, has been associated with better long-term cardiovascular outcomes. In contrast, a resting heart rate below 62 beats/min in certain elderly populations is an independent risk marker of mortality when compared to age matched controls with higher resting heart rates. The appropriate approach to bradycardia requires an understanding not only of the underlying conduction system of the heart, but also of the patient in whom it is observed and the associated symptoms in order to determine its prognostic significance and the appropriate treatment.

Bradycardia can result from intrinsic disease of the conducting tissues of the heart or as a result of extrinsic and often reversible influences that may be metabolic, autonomic, iatrogenic, or toxic. Sinus node dysfunction, or sick sinus syndrome (SSS), is generally a disease of the elderly, occurring in 1 out of 600 cardiac patients older than 65, and accounts for approximately 50% of all pacemaker implantations in the United States. While it is associated with a high risk of syncope, the presence of SSS is not associated with an increased risk of mortality in population-based studies, independent of pacemaker therapy. Bradycardia resulting from high grade AV block (Mobitz type II or complete AV block) is rare in healthy population and generally associated with significant underlying heart disease and increased morbidity and mortality. Prognosis for bradycardia resulting from extrinsic influences on the heart largely depends upon the underlying diagnosis. For example, transient, asymptomatic asystole associated with obstructive sleep apnea is not associated with adverse outcomes compared to sleep apnea patients without bradycardia, and has been shown to resolve with effective CPAP treatment.


The electrical activation of the heart originates in the sinoatrial (SA or sinus) node, which is located in the right atrium and functions as the normal pacemaker of the heart. The sinus node is located in the subepicardial tissue on the lateral wall of the right atrium near the junction of the SVC and the right atrium. It is on average 10 to 20 mm in length. Its vascular supply is from the SA nodal artery, a branch of the right coronary artery (~60% of people) or the left circumflex artery (~40% of people). It contains the principal pacemaker cells that spontaneously depolarize, causing atrial depolarization. It has extensive input from both the parasympathetic ...

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