Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats per minute or less. However, few patients actually become symptomatic until their heart rate drops to less than 50 beats per minute. The action potential responsible for this rhythm arises from the sinus node and causes a P wave on the surface ECG that is normal in terms of both amplitude and vector. These P waves are typically followed by a normal QRS complex and T wave.
The pathophysiology of sinus bradycardia is dependent on the underlying cause. Commonly, sinus bradycardia is an incidental finding in otherwise healthy individuals, particularly in young adults or sleeping patients. Other causes of sinus bradycardia are related to increased vagal tone.
Physiologic causes of increased vagal tone include the bradycardia seen in athletes. Pathologic causes include, but are not limited to, inferior wall myocardial infarction, toxic or environmental exposure, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intracranial pressure.
Sinus bradycardia may also be caused by the sick sinus syndrome, which involves a dysfunction in the ability of the sinus node to generate or transmit an action potential to the atria. Sick sinus syndrome includes a variety of disorders and pathologic processes that are grouped within one loosely defined clinical syndrome. The syndrome includes signs and symptoms related to cerebral hypoperfusion in association with sinus bradycardia, sinus arrest, sinoatrial (SA) block, carotid hypersensitivity, or alternating episodes of bradycardia and tachycardia.
Sick sinus syndrome most commonly occurs in elderly patients with concomitant cardiovascular disease and follows an unpredictable course. Some studies have shown that these patients have a functional decrease in the number of nodal cells, while others have demonstrated the presence of antinodal antibodies. Although these and other developments are beginning to focus our understanding of this syndrome, most cases remain idiopathic.
SA block occurs when the SA node fails to excite the atria uniformly. SA block may be associated with abnormal intrinsic nodal function, a failure of the SA junction, or a failure of propagation in the surrounding tissue. The 3 forms of SA block are first-, second-, and third-degree block.
Both first- and third-degree SA blocks are essentially undiagnosable on the surface ECG. First-degree SA block is characterized by a delay in the propagation of the action potential from the SA node to the atria. Unlike first-degree atrioventricular (AV) block, this delay is not reflected in the surface ECG. In third-degree, or complete, SA block, the surface ECG is identical to that of sinus arrest, with absent P waves. Second-degree SA block is characterized by an occasional dropped P wave (analogous to the dropped QRS complex of second-degree AV block), reflecting the inability of the SA node to consistently transmit an action potential to the surrounding myocardium.
Frequency of sinus bradycardia is unknown, given that most cases represent normal variants. Although the frequency of sick sinus syndrome is unknown in the general population, in cardiac patients it has been estimated to be 3 in 5000.
Sequelae of sinus bradycardia are related to its underlying etiology.
In patients who present with toxic exposure, the prognosis is good once the offending agent has been removed.Patients with sick sinus syndrome have a relatively poor prognosis, with 5-year survival rates in the range of 47-69%. However, whether this mortality rate is due to factors intrinsic to the sinus node itself or the concomitant heart disease is unclear. PreviousProceed to Clinical PresentationÂ