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.