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. The presence of sinus bradycardia in itself does not cause a change in the QRS complex and T wave.
The 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.
The pathophysiology of sinus bradycardia is dependent on the underlying cause.[1] Commonly, sinus bradycardia is an incidental finding in otherwise healthy individuals, particularly in young adults, athletes or sleeping patients.[2] 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,[3] 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.
Causes of sinus bradycardia include the following:
Mortality/morbidity
Sequelae of sinus bradycardia are related to its underlying etiology, including the following:
Patients with sick sinus syndrome may convert to atrial fibrillation, a rhythm that is amenable to medical therapy and may eliminate the need for pacemaker placement.
Sinus bradycardia after bariatric surgery
Approximately 121,000 bariatric surgical procedures are performed annually. There are anecdotal reports of unexplained sinus bradycardia (SB) after significant weight loss, but no systematic studies have been conducted. Malik et al investigated the frequency of incident SB; its timing; and its association with weight loss, clinical characteristics, and predictors by evaluating the clinical characteristics of 151 consecutive patients who underwent bariatric surgery.[4] Twenty-five of 137 patients (18%) experienced postoperative SB. Patients with SB had significantly greater reduction in body mass index (BMI) than in those without bradycardia. Heart rate reserve (HRR) was significantly greater in patients with SB than in those without bradycardia. Multiple logistic regression analysis revealed that the odds of developing SB were 1.96 and 1.91 and associated with the percent decrease in BMI or increase in HRR, respectively.[4]
Sinus bradycardia is most often asymptomatic. However, symptoms may include the following when severe:
Pertinent elements of the history include the following:
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:
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.
A 12-lead ECG may be performed to confirm the diagnosis.
In a study that evaluated normative ECG characteristics and the prevalence of abnormal ECG findings among competitive rowers, Wasfy et al reported that in 94% of the rowers, training-related 12-lead ECG findings included sinus arrhthmia in 55%, sinus bradycardia in 51%, and incomplete right bundle branch block in 42%.[5] Significant sex differences included isolated voltage criteria for left ventricular hypertropher and early repolarization pattern occurring more in men than women. The investigators noted that depending on the ECG criteria used (eg, 2010 European Society of Cardiology [ESC], 2013 "Seattle criteria"), the classification and diagnostic accuracy of an abnormal ECG may be affected.[5]
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/Heart Rhythm Society,[6] as well as from the European Society of Cardiology (ESC), in association with the European Heart Rhythm Association.[7]
The ESC guidelines state that in adults with acquired persistent bradycardia, pacing is indicated if a patient displays symptoms that are clearly caused by sinus bradycardia; moreover, pacing may be indicated in the presence of symptoms that, despite inconclusive evidence, are probably the result of sinus bradycardia. If sinus bradycardia is asymptomatic or produced by a reversible cause, according to the guidelines, pacing is not indicated.[7]
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.[8] 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.[9]
Sleep apnea is usually treated with weight loss, nasal bilevel positive airway pressure (BiPAP) and, occasionally, surgery.
Once the patient's condition is stabilized, inpatient care must be tailored to the inciting cause of the dysrhythmia.
Outpatient follow-up care is dependent on the underlying cause of the bradycardia.
Most patients should be able to follow up with their primary care provider or obtain a referral for a follow-up visit.
Some patients may require specialized referral to a cardiologist. Arrange prompt follow-up care in patients with symptomatic sinus bradycardia.
Regular follow-up care is necessary for patients in whom a permanent pacemaker is placed.
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.[10]
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.