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.
Laboratory studies may be helpful if the cause of the bradycardia is thought to be related to electrolytes, drug, or toxins. In cases of sick sinus syndrome, routine laboratory studies are rarely of specific value.
Reasonable screening studies, especially if the patient is symptomatic and this is the initial presentation, include the following:
Routine imaging studies are rarely of value in the absence of specific indications.
12-lead ECG may be performed to confirm the diagnosis.
Intravenous access, supplemental oxygen, and cardiac monitoring should be initiated in the field.
In symptomatic patients, intravenous atropine may be used.
In rare cases, transcutaneous pacing may need to be initiated in the field.
Care in the ED should first rapidly ensure the stability of the patient's condition. This is followed by an investigation into the underlying cause of the bradycardia.
Patients in unstable condition may require immediate endotracheal intubation and transcutaneous or transvenous pacing.
Patients should have continuous cardiac monitoring and intravenous access.
In hemodynamically stable patients, attention should be directed at the underlying cause of the bradycardia.
In sick sinus syndrome, drug therapy approaches have been relatively disappointing. While atropine has aided some patients transiently, most patients ultimately require placement of a pacemaker. Guidelines on permanent pacing are available from the American College of Cardiology, American Heart Association, and Heart Rhythm Society.
In patients with sinus bradycardia secondary to therapeutic use of digitalis, beta-blockers, or calcium channel blockers, simple discontinuation of the drug, along with monitored observation, are often all that is necessary. Occasionally, intravenous atropine and temporary pacing are required.
Treatment of postinfectious bradycardia usually requires permanent pacing.
In patients with hypothermia who have confirmed sinus bradycardia with a pulse, atropine and pacing are usually not recommended because of myocardial irritability. Rewarming and supportive measures are the mainstays of therapy.
Sinus bradycardia may be seen in patients undergoing therapeutic hypothermia. These patients are likely to develop sinus bradycardia sometime during their course that will require close monitoring of perfusion status. If they show signs of adequate perfusion, no treatment is necessary. Treatment of inadequate perfusion would include pressors, atropine, and pacing.
Sleep apnea is usually treated with weight loss, nasal bilevel positive airway pressure (BiPAP) and, occasionally, surgery.
Drug treatment of sinus bradycardia is usually not indicated for asymptomatic patients. In symptomatic patients, underlying electrolyte or acid-base disorders or hypoxia should be corrected. Intravenous atropine may provide temporary improvement in symptomatic patients, although its use should be balanced by an appreciation of the increase in myocardial oxygen demand this agent causes.
Although in the past, isoproterenol was used quite commonly in patients with bradycardia, further appreciation of its substantial risks has diminished its role. Temporary pacing is recommended in symptomatic patients who are unresponsive or only temporarily responsive to atropine, or in whom atropine therapy is contraindicated. Transcutaneous pacing, where available, is the initial procedure of choice.
Clinical Context: Used to increase heart rate through vagolytic effects, causing increase in cardiac output.
These agents are indicated when symptoms of hypoperfusion exist. They are thought to work centrally by suppressing conduction in the vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.