Bradycardia or transient asystole can result from a wide variety of disorders of the sinus node and cardiac conduction system interacting with neural and humoral influences.1-2 Abnormalities may be discovered as incidental electrocardiographic (ECG) findings during screening or monitoring for other medical problems. Alternatively, they may be discovered after investigation for symptoms suggesting transient or persistent bradycardia. There is little difficulty when the abnormality is persistent and clearly related to presenting symptoms. Transient abnormalities, on the other hand, may be very difficult to demonstrate. A sudden and transient loss of consciousness or a feeling of impending unconsciousness (presyncope) are the major symptoms suggesting transient asystole. However, a wide variety of symptoms possibly reflecting chronic or intermittent hypoperfusion of the central nervous system or other organ systems may be caused by intermittent or chronic bradycardia, including dizzy or lightheaded spells, fatigue, cognitive disturbances, dyspnea, and so on. The diagnostic difficulties are compounded in the elderly, who frequently have multiple chronic medical disorders and conduction system abnormalities that may be difficult to relate to symptoms.
The asymptomatic patient with unexpected ECG abnormalities is discussed in more detail in Chapter 11. In general, intervention is rarely indicated, although a reasonable search for silent cardiac disease with follow-up is usually warranted. The assessment of the patient presenting with symptoms suggesting bradycardia or conduction disorders can be guided by 3 general principles. First, a broad approach is necessary to understand the problem in its clinical context. Symptoms suggesting bradycardia are frequently nonspecific, with a wide variety of potential causes. A “reflex” focus on the cardiac conduction system without clinical correlation is inappropriate. Secondly, transient symptoms are an exercise in monitoring. The goal is to acquire ECG information with direct correlation between these 2 variables—symptoms and data—the desired end point. If a clear precipitating factor is described, it can be useful to try to reproduce the situation observing the patient and monitoring the ECG. Thirdly, it may be impossible to obtain ECG data while the symptom is occurring. In such cases, inferences can be made using the presence of abnormalities detected even though they have not been associated with symptoms. For example, the detection of transient third-degree atrioventricular (AV) block suggests that the patient’s presenting light-headed spell was related to AV block, even though the episode recorded was not associated with symptoms. These inferences sometimes require considerable clinical judgment. In general, the more striking the abnormality, the more confident the clinician is in making the inference that it is causing the symptoms.
From a broad point of view, symptomatic bradycardia requires pacing regardless of the mechanism unless a primary reversible issue is recognized and treated. On the other hand, there should be a high burden of proof of future adverse effect to recommend permanent pacing in the asymptomatic patient.
History and Physical Examination