What Is Bradycardia?
The normal heart rate is determined by the automaticity of its own anatomic “pacemaker,” the sinoatrial (SA) node. It typically ranges from 60-100 beats per minute, and <60 bpm is referred to as bradycardia.
Bradycardia can be normal in that the sinus rate and rhythm of the heart is influenced by a complicated interaction among physical conditioning, response to exercise, ventilation, vagal tone, stress, medication, and other daily influences. When bradycardia is abnormal–a “bradyarrhythmia”–it can result in subjectively unpleasant symptoms or dangerous conductivity effects on the heart and cardiac output. If severe enough, it can cause hypotension and even shock.
Causes of Bradycardia
- Sinus bradycardia: adaptive responses, sleep, medication (parasympathetic inhibition or sympathetic blockers resulting in inhibition, opioids), sick sinus syndrome, obstructive sleep apnea, inhibition by increased vagal tone, infection, hypothyroidism, hyperkalemia, and hypothermia
- Atrioventricular heart block
- Wandering atrial ectopic pacemaker
- Junctional (atrioventricular node) escape rhythms during ineffective atrial contractions (flutter or fibrillation)
Sick Sinus Syndrome (SSS)
SSS is due to SA node dysfunction which lowers the rate (automaticity) of this anatomic pace making tissue. It is most likely an aging phenomenon in the SA node, but it can also occur from cell damage due to ischemia or myocardial infarction. The bradycardia it creates can result in fatigue, lightheadedness, palpitations, syncope, and even alternating episodes of tachycardia.
Atrioventricular Heart Block
The normal conduction pathway of the waves of electrical depolarizations that result in efficient chamber contractions begin at the SA node. From there, the impulse reaches the atrioventricular junction and its atrioventricular (AV) node; from there, it migrates down the Bundle of His and then distributes throughout the ventricles by way of the Purkinje fibers. At any point in this pathway, there can be a block that undermines the dependency of the ventricles on the atrial pace making. If there is a block, the ventricles partially or wholly are “on their own” to generate a rate and rhythm, often bradycardic (bradyarrhythmia). The lower the interruption in this conductive pathway, the more severe the bradycardia.
Wandering Atrial Pacemaker
All of the cells of the heart have automaticity, i.e., the ability to rhythmically generate an electrical pulse for propagation. If there is more than one pacemaker–other than the normal one in the SA node–these are referred to as ectopic pacemakers. Since all depolarized tissue (after contraction) needs to repolarize so as to be ready for the next depolarization, any dyssynchrony (asynchrony) resulting from multiple uncoordinated depolarizations will be counterproductive to a unified action. Electrical sequences have periods of silence (refractory periods), and multiple ectopic pacemakers will cause many areas of refractoriness that can block any direct paths of depolarization.
Reentry of electrical impulses from above or below the atrioventricular junctional area can, like ectopic pacemakers, interfere with normal conduction by engendering areas of refractoriness that result in ventricular rhythms as “escape” rhythms.
How Is Bradycardia Diagnosed?
Bradycardia, a heart rate <60, may be normal in athletes or during sleep. Abnormal bradycardias result in unpleasant symptoms subjectively and possible life-threatening risks objectively. In diagnosing whether a bradycardia is normal or abnormal, a history and physical and an electrocardiogram are key components in exploring a lower-than-normal heart rate.
The first step is to confirm that a bradycardia is anything other than an adaptive sinus bradycardia, such as is seen in athletes. Is not uncommon for a very conditioned athlete to have a resting pulse of <60 beats per minute. This is a normal type of sinus bradycardia and is fairly easy to conclude with a history.
- Elderly patients may have bradycardia as an early sign of senescent sick sinus syndrome (SSS)
- The elderly, who are more likely to be taking several medications, are more at risk for bradycardia as a side effect to any one of them or a combination
- A history of coronary artery disease puts the blood supply to the SA node at risk
- Those with neurological disorders may have increased intracranial pressure, which can cause bradycardia
There is no specific heart rate below which all patients complain of symptoms, but vital signs are often closely related to what they may be experiencing. Certainly, a pulse <60 meets the definition of bradycardia. The rhythm of the pulse is telling and can be diagnostic depending on whether it is regular, irregular with patterns (“regular” irregular), or irregular without patterns (“irregular” irregular).
Blood pressure that indicates hypotension or compensatory normotension can assign the severity of danger a patient with arrhythmia may have.
Auscultation of the chest can reveal corroborating findings such as abnormal heart sounds, irregularly spaced heart sounds, or sounds indicating turbulence. The lungs can be evaluated in the context of COPD or other ventilatory conditions that may impact the rate and rhythm of the heart.
If bradycardia is abnormal, nothing will prove this better than an ECG, and nothing is more diagnostic than when an arrhythmia is identified as the cause of the bradycardia. The ECG will serve to
- Confirm whether the bradycardia is a sinus bradycardia
- Determine whether there is only one or more than one pacemaker
- Identify atrioventricular block of the normal electrical conductive pathway and where that block is occurring
- Identify any evidence of myocardial infarction that impacts the SA or AV nodes or other tissue along the conductive pathways
- Echocardiography, to identify possible chamber size abnormalities, valvular problems, or other causes or results of pathology
- Electrophysiologic testing is more in-depth than an ECG and can identify subtleties when the ECG is not helpful
- Blood tests can screen for hypothyroidism, electrolyte abnormalities, and other reversible causes of bradycardia
How Can I Manage Bradycardia?
Once bradycardia has been determined to be abnormal, its management and treatment depend wholly on the type of bradycardia and what is causing it and any symptoms or dangers associated with the resulting ventricular rate.
Sick Sinus Syndrome (SSS)
If unstable, an SSS patient should undergo advanced life support protocols with transcutaneous pace making, atropine (anticholinergic), and/or dopamine, epinephrine, or isoproterenol for hypotension. Once stabilized, the treatment is the same as for any stable SSS patient:
- Identify any reversible causes (medication, electrolyte, or autonomic nervous system imbalance)
- Address any cardiac ischemia
- Implantation of a permanent pacemaker if symptomatic, with a consideration for anticoagulation due to the increased risk of atrial fibrillation and thromboembolism seen in pacemaker patients
- Pharmacologic therapy
Symptomatic Sinus Bradycardia
- If unstable, a patient with bradycardia should undergo pharmacologic therapy (atropine, anticholinergic) and application of a transcutaneous pacemaker
- If stable, look for and treat any reversible causes, such as hypothyroidism, infection, or replacement of any medication(s) suspected of causing the bradyarrhythmia
- Treat any heart blocks with a pacemaker
Other Heart Disease
Other heart disease that results in bradycardia, such as previous infarction, ischemia, coronary artery disease, or congenital causes are treated primarily via supportive measures, with a pacemaker if symptoms warrant and it is not otherwise contraindicated.
Prevention of Bradycardia
Prevention of continued bradycardia relies upon an accurate diagnosis, whether a patient is stable or unstable, and whether he or she is symptomatic or asymptomatic. In those who are unstable with bradycardia, advanced life support (ACLS) protocols from the American Heart Association and those espoused by vascular experts are designed to prevent cardiac complications of such arrhythmias.
Prevention of bradycardia progressing to instability is by determining the pharmacologic efficacy of medications prescribed; the status of the bradycardia treatment can be followed by symptom appraisal and serial electrocardiography.
Thromboembolism can be prevented by echocardiography and, if indicated, anticoagulation. Heart blocks can be managed with artificial pacemakers.
Additionally, those with comorbidities should, where applicable:
- Stop smoking
- Maintain a target glycated hemoglobin A1c
- Look for equally effective medications when bradycardia is an untoward side effect of a replaceable medicine
- Attend to weight management and metabolic syndrome with the help of a dietitian/nutritionist
- Keep all follow-up appointments and report any new symptoms or changes in symptoms immediately