Introduction
Background
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.
Pathophysiology
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
United States
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.
Mortality/Morbidity
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.
Clinical
History
- Sinus bradycardia is most often asymptomatic. However, symptoms may include the following:
- Syncope
- Dizziness
- Lightheadedness
- Chest pain
- Shortness of breath
- Exercise intolerance
- Pertinent elements of the history include the following:
- Previous cardiac history (eg, myocardial infarction, congestive heart failure, valvular failure)
- Medications
- Toxic exposures
- Prior illnesses
Physical
- Cardiac auscultation and palpation of peripheral pulses reveal a slow, regular heart rate.
- The physical examination is generally nonspecific, although it may reveal the following signs:
- Decreased level of consciousness
- Cyanosis
- Peripheral edema
- Pulmonary vascular congestion
- Dyspnea
- Poor perfusion
- Syncope
Causes
- One of the most common pathologic causes of symptomatic sinus bradycardia is the sick sinus syndrome.
- The most common medications responsible include therapeutic and supratherapeutic doses of digitalis glycosides, beta-blockers, and calcium channel-blocking agents.
- Other cardiac drugs less commonly implicated include class I antiarrhythmic agents and amiodarone.
- A broad variety of other drugs and toxins have been reported to cause bradycardia, including lithium, paclitaxel, toluene, dimethyl sulfoxide (DMSO), topical ophthalmic acetylcholine, fentanyl, alfentanil, sufentanil, reserpine, and clonidine.
- Sinus bradycardia may be seen in hypothermia, hypoglycemia, and sleep apnea.
- Less commonly, the sinus node may be affected as a result of diphtheria, rheumatic fever, or viral myocarditis.
More on Sinus Bradycardia |
 Overview: Sinus Bradycardia |
| Differential Diagnoses & Workup: Sinus Bradycardia |
| Treatment & Medication: Sinus Bradycardia |
| Follow-up: Sinus Bradycardia |
| References |
| Next Page » |
References
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Sasaki Y, Shimotori M, Akahane K, Yonekura H, Hirano K, Endoh R, et al. Long-term follow-up of patients with sick sinus syndrome: a comparison of clinical aspects among unpaced, ventricular inhibited paced, and physiologically paced groups. Pacing Clin Electrophysiol. Nov 1988;11(11 Pt 1):1575-83. [Medline].
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Further Reading
Keywords
sinus bradycardia, vagal tone, bradycardia, inferior wall myocardial infarction, electrolyte disorders, tachycardia, sinus arrest, first-degree block, second-degree block, third-degree block, complete SA block, hypothermia, hypoglycemia, sleep apnea, diphtheria, rheumatic fever, viral myocarditis, digitalis glycosides, beta-blockers, calcium channel-blocking agents, class I antiarrhythmic agents, amiodarone, increased vagal tone, infection, hypothyroidism, increased intracranial pressure, sick sinus syndrome, cerebral hypoperfusion, sinoatrial block, SA block, carotid hypersensitivity, syncope, dizziness, shortness of breath, lightheadedness, chest pain, myocardial infarction, congestive heart failure, valvular failure
