Pathophysiology

Bradycardia may result from sinus node dysfunction or AV block.³ Sinus node dysfunction can be a result of increased vagal tone, as seen in athletes or conditioned young people or in older adults as the result of underlying disease processes, medications, or toxicity.⁴ AV block is also associated with various disease processes, including myocardial infarction, coronary artery spasm, digitalis toxicity, cardiac mesotheliomas, and infectious processes. Medications, particularly beta blockers and calcium channel blockers, may induce either sinus node or AV dysfunction.

Clinical Presentation

Some symptoms may be nonspecific, but dizziness, fatigue, and syncope are complaints commonly identified with bradycardia.³ Nausea, vomiting, and confusion have also been correlated with bradycardia. Any bradyarrhythmia associated with chest pain, shortness of breath, exercise intolerance, decreased level of consciousness, hypotension, seizure, congestive heart failure, or myocardial infarction is considered a prearrest condition. A careful symptom analysis and review of the patient’s medical history, including allergies and prescribed and over-the-counter medications, is necessary to discern the cause of the bradycardia so that appropriate treatment can be initiated.

Physical Examination

Although associated symptoms will often guide the physical examination, a focused history and physical examination are necessary. The patient’s level of responsiveness and vital signs (including temperature, blood pressure, pulse, respiratory rate, and oxygen saturation) are significant and should be continually reassessed. Hypotension, ventricular arrhythmias, and pulmonary congestion are serious signs indicating the need to identify the cardiac rhythm and to institute rapid, appropriate treatment.

Diagnostics

An electrocardiogram (ECG) is necessary for rhythm analysis and appropriate management. Further diagnostics are guided by the history and physical examination but can include drug levels, electrolyte values, glucose concentration, blood urea nitrogen (BUN) level, creatinine concentration, complete blood count (CBC), creatine kinase muscle-brain (CK-MB) fraction, troponin T or troponin I level, thyroid studies, and chest x-ray studies.

Differential Diagnosis

Determination of the bradyarrhythmia and associated disease is essential for treatment. Herbals and medications can be a common cause of bradycardia, but infections, vasovagal syncope, myocardial infarction, digitalis toxicity, sick sinus syndrome, bradycardia-tachycardia syndrome, hypothyroidism, and other disease states are also possible reasons.³

For correct identification of the cardiac rhythm, a 12-lead ECG is necessary. Patients with suspected myocardial infarction should be treated for acute coronary syndrome according to the 2010-2015 American Heart Association guidelines (with oxygen, if indicated; aspirin [162 to 325 mg chewed, if not aspirin allergic]; nitroglycerin; morphine; and, if appropriate, reperfusion therapy).⁵

Symptomatic patients with worsening clinical symptoms or prearrest conditions related to the bradycardia may require urgent intervention before a definitive underlying condition is identified. For adult patients with symptomatic bradycardia, especially if the bradycardia is associated with Mobitz type II second-degree heart block or third-degree heart block, the American Heart Association recommends atropine, 0.5 mg intravenously every 3 to 5 minutes (up to a total dose 3 mg), until a transcutaneous or transvenous pacer (class I intervention) is available.⁵ However, atropine can induce cardiac ischemia, precipitate ventricular tachycardia (VT) or fibrillation, and be deleterious for patients with a history of cardiac transplantation.⁵ In the presence of Mobitz type II second-degree heart block or third-degree heart block associated with wide-complex ventricular escape beats, atropine should be avoided and treatment with a transcutaneous or transvenous pacer applied as soon as possible.⁵ Some defibrillator monitors may also have a transcutaneous pacer component.

If the bradycardia is drug induced (e.g., beta blocker or calcium channel blocker overdose), a pacer is not available, atropine is contraindicated, or the patient is unresponsive to atropine or pacing, intravenous epinephrine 2 to 10 µg/min can be used to treat critical bradycardia.⁵ A dopamine infusion of 2 to 10 µg/kg/min can also improve cardiac output and increase blood pressure and may be used alone or in conjunction with an epinephrine infusion.⁵

Disposition and Referral

Patients experiencing signs and symptoms related to bradyarrhythmias require constant reassessment and definitive management in an emergency department. Immediate transfer to an emergency center is required.

Prevention

Prevention, when possible, may avert complications or serious injury. Patients who complain of syncope, fatigue, or other symptoms that may be related to bradycardia require diag­nostic assessment. A permanent pacemaker may be indicated for bradycardia associated with sinus node dysfunction and certain heart blocks (e.g., fascicular block or acquired AV block).^3,5,6

Patient and Family Education

Patients should understand the importance of calling their health care provider if they experience syncope, lightheadedness, or a slow heart rate that hinders activities. In addition, patients and caregivers should know how to activate the emergency medical system (911) if these symptoms occur with chest discomfort or shortness of breath.

Careful explanation and supportive therapy will enhance patient and family understanding. These measures will also help allay the anxiety inherent in an emergent situation. Medication regimens, if associated with the bradyarrhythmias, should be reviewed to prevent misinterpretation.