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- ↵*Address for reprints: Leonard S. Dreifus, MD, Lankenau Hospital, Lancaster and City Line Avenues, Philadelphia, Pennsylvania 19151.
Clinicians have long recognized the potentially serious manifestations of extreme bradycardia. However, even marked bradycardia can often be physiologic, and in the presence of impaired ventricular function may offer important compensatory hemodynamic effects. Disorders of the sinoatrial node producing bradycardia include failure of impulse formation, sinoatrial conduction block, concealed sinus-perinodal reentry, carotid sinus hypersensitivity and the constellation of brady- and tachyarrhythmias that compose the "sick sinus syndrome." Bradycardia can also result from intraatrial block, atrioventricular nodal block or infranodal block. In addition, paroxysmal supraventricular tachyarrhythmias may produce concealment into the atrioventricular junction and simultaneous suppression of sinus node rhythmicity, resulting in long pauses. Pseudobradycardias manifesting as slow peripheral pulse rates can result from frequent, nonconducted early atrial premature beats, from ventricular bigeminy or runs of ventricular extrasystoles or from mechanical alternans.
Cardiac pacemakers play an important role in the management of patients with severe symptoms attributable to bradyarrhythmias. However, excessive use of pacemakers and the inappropriate selection of physiologically unfavorable pacemaker systems should be avoided. Frequently, patients who are only mildly symptomatic with bradycardia should not receive a cardiac pacemaker because the prognosis is favorable. Patients with the tachy-bradycardia syndrome often require both pharmacologic and pacemaker therapy. In selected patients electrophysiologic testing may be helpful, but the majority of patients are best managed by careful attention to the history, electrocardiogram and ambulatory electrocardiographic recordings.
- American College of Cardiology Foundation