The National Institutes of Health defines *bradycardia as a heart rate <60 bpm in adults other than well-trained athletes.9 The determination on whether or not treatment is necessary for bradycardic events is generally based on the presence of symptoms. The clinical manifestations of bradycardia can vary widely from insidious symptoms to episodes of frank syncope. 5
Common symptoms of bradycardia include:
Bradycardia can stem from either sinus node dysfunction (SND) or atrioventricular block (AVB).
SND, historically referred to as sick sinus syndrome, is most often related to age-dependent, progressive, degenerative fibrosis of the sinus nodal tissue and surrounding atrial myocardium.6 Abnormalities of the sinus node, atrial tissue, atrioventricular nodal tissue, and the specialized conduction system can all contribute to bradycardia, discordant timing of atrial and ventricular depolarization, and abnormal ventricular depolarization.5
The electrocardiographic findings in patients with SND are varied and the diagnosis may be considered in patients with sinus bradycardia or atrial depolarization from a subsidiary pacemaker other than the sinus node (i.e. ectopic atrial rhythm, junctional rhythm, or ventricular escape), intermittent sinus pauses, or a blunted heart rate response with exercise (chronotropic incompetence).3 Chronotropic incompetence represents failure to reach a target heart rate with exertion that is inadequate to meet metabolic demand.5
The clinical manifestations of atrioventricular block will also depend on whether the atrioventricular block is fixed or intermittent and the ventricular rate or duration of ventricular asystole associated with atrioventricular block.5
When a patient is evaluated for symptomatic bradycardia, an in-depth history and physical is important, along with identification of possible reversible causes. The following is a list of conditions associated with bradycardia and conduction disorders:11
Further testing of patients with bradycardia after initial history and physical should include a 12-lead ECG, which might suggest structural heart disease, conduction disturbance, or other cardiac conditions that may predispose patients to bradyarrhythmias.7
Can be considered to establish a diagnosis or make a symptom-rhythm correlation, with longer-term monitoring resulting in higher yield.2
Although not routinely recommended for assessment of ischemia, exercise testing can be considered in patients with symptoms temporally related to exercise, asymptomatic second-degree AV block, or for suspected chronotropic incompetence.11
Recommended to evaluate patients with new left bundle branch block, Mobitz type II AV block, high-grade AV block, or complete AV block.5
Patients who screen positive should be considered for polysomnography and/or specialty consultation. The prevalence of sinus bradycardia in patients with sleep apnea can be as high as 40%, with episodes of second- or third-degree AV block in up to 13% of patients.8
A bradycardic rhythm is most often treated only when symptoms are present. If reversible causes aren’t immediately identified and/or if reversing the cause is taking too long, pharmacologic interventions are the first-line approach. Atropine 0.5 mg intravenous (IV) is given up to a total of 3 mg.1Atropine sulfate acts by reversing the cholinergic-mediated decreases in the heart rate and AV node conduction.1
If atropine is ineffective, two treatment pathways are available. The patient’s heart can be paced either intravenously or transcutaneously (TCP), or more emergency medicine can be given. The two pharmacologic choices are dopamine 2 to 20 mcg/kg/min and/or epinephrine 2 to 10 mcg/min.1
If no response occurs after atropine boluses, epinephrine and/or dopamine infusions, pacing is initiated. Transcutaneous pacing should be limited to bridging to transvenous pacing in patients acutely or critically ill due to the painful nature of the therapy and difficulty establishing and ascertaining consistent myocardial capture.11 One of the most important steps when a patient is paced is to ensure there is electrical and mechanical capture.1 Without mechanical capture, the cardiac muscle is not electrically depolarized to threshold and no muscle contraction will occur. The safety of temporary transvenous pacing has improved with balloon-floatation catheters when placed by experienced operators.1
Permanent pacemaker implantation is the definitive treatment for a patient with chronic symptomatic sinus node dysfunction. This includes patients who are on heart rate lowering medications that are clinically necessary when there is no alternative therapy.11 In patients with Mobitz type II second-degree AV block, high-grade AV block (greater than 2:1), or complete AV block, there is some evidence of improved survival with placement of a permanent pacemaker.10Permanent pacing is also warranted in patients with AV conduction system disturbance in disease processes with a more rapidly progressive nature.11
*Bradycardia and symptomatic bradycardia are topics so in-depth that it is impossible to review the types, causes, and treatments exhaustively. For the purpose of this article, the “2018 ACC/AHA/HRS Guideline on the Management of Patients With Bradycardia and Cardiac Conduction Delay” is referenced, and readers are encouraged to review the complete guideline.
Dan Bunker DNAP, MSNA, CRNA—Dan has worked in the healthcare industry for nearly 30 years. He worked as a registered nurse in the coronary care ICU for 7 years and was a flight nurse with Intermountain’s Life Flight for nearly 10 years. He has been a certified registered nurse anesthetist (CRNA) for 11 years, working in the hospital setting as well as maintaining his own private practice. In addition, he is a professor in the nurse anesthesia program at Westminster College in Salt Lake City, Utah. He has served in various leadership roles within the Utah Association of Nurse Anesthetists (UANA) and is currently the president-elect.