Bradycardia
Bradycardia, from Ancient Greek βραδύς, meaning "slow", and καρδία, meaning "heart", also called bradyarrhythmia, is a resting heart rate under 60 beats per minute. While bradycardia can result from various pathological processes, it is commonly a physiological response to cardiovascular conditioning or due to asymptomatic type 1 atrioventricular block.
Resting heart rates of less than 50 BPM are often normal during sleep in young and healthy adults and athletes. In large population studies of adults without underlying heart disease, resting heart rates of 45–50 BPM appear to be the lower limits of normal, dependent on age and sex. Bradycardia is most likely to be discovered in the elderly, as age and underlying cardiac disease progression contribute to its development.
Bradycardia may be associated with symptoms of fatigue, dyspnea, dizziness, confusion, and syncope due to reduced blood flow to the brain. The types of symptoms often depend on the etiology of the slow heart rate, classified by the anatomical location of a dysfunction within the cardiac conduction system. Generally, these classifications involve the broad categories of sinus node dysfunction, atrioventricular block, and other conduction tissue diseases. However, bradycardia can also result without dysfunction of the conduction system, arising secondarily to medications, including beta blockers, calcium channel blockers, antiarrythmics, and other cholinergic drugs. Excess vagus nerve activity or carotid sinus hypersensitivity are neurological causes of transient symptomatic bradycardia. Hypothyroidism and metabolic derangements are other common extrinsic causes of bradycardia.
The management of bradycardia is generally reserved for people with symptoms, regardless of minimum heart rate during sleep or the presence of concomitant heart rhythm abnormalities, which are common with this condition. Untreated sinus node dysfunction increases the risk of heart failure and syncope, sometimes warranting definitive treatment with an implanted pacemaker. In atrioventricular causes of bradycardia, permanent pacemaker implantation is often required when no reversible causes of disease are found. In both SND and atrioventricular blocks, there is little role for medical therapy unless a person is hemodynamically unstable, which may require the use of medications such as atropine and isoproterenol and interventions such as transcutaneous pacing until such time that an appropriate workup can be undertaken and long-term treatment selected. While asymptomatic bradycardias rarely require treatment, consultation with a physician is recommended, especially in the elderly.
The term "relative bradycardia" can refer to a heart rate lower than expected in a particular disease state, often a febrile illness. Chronotropic incompetence refers to an inadequate rise in heart rate during periods of increased demand, often due to exercise, and is an important sign of SND and an indication for pacemaker implantation.
Normal cardiac conduction
The heart is a specialized muscle containing repeating units of cardiomyocytes, or heart muscle cells. Like most cells, cardiomyocytes maintain a highly regulated negative voltage at rest and are capable of propagating action potentials, much like neurons. While at rest, the negative cellular voltage of a cardiomyocyte can be raised above a certain threshold by an incoming action potential, causing the myocyte to contract. When these contractions occur in a coordinated fashion, the atria and ventricles of the heart will pump, delivering blood to the rest of the body.Normally, the origination of the action potential causing cardiomyocyte contraction originates from the sinoatrial node. This collection of specialized conduction tissue is located in the right atrium, near the entrance of the superior vena cava. The SA node contains pacemaker cells that demonstrate "automaticity" and can generate impulses that travel through the heart and create a steady heartbeat.
At the beginning of the cardiac cycle, the SA node generates an electrical action potential that spreads across the right and left atria, causing the atrial contraction of the cardiac cycle. This electrical impulse carries on to the atrioventricular node, another specialized grouping of cells located in the base of the right atrium, which is the only anatomically normal electrical connection between the atria and ventricles. Impulses coursing through the AV node are slowed before carrying on to the ventricles, allowing for appropriate filling of the ventricles before contraction. The SA and AV nodes are both closely regulated by the autonomic nervous system's fibres, allowing for adjustment of cardiac output by the central nervous system in times of increased metabolic demand.
Following slowed conduction through the atrioventricular node, the action potential produced initially at the SA node now flows through the His-Purkinje system. The bundle of His originates in the AV node and rapidly splits into a left and right branch, each destined for a different ventricle. Finally, these bundle branches terminate in the small Purkinje fibers that innervate myocardial tissue. The His-Purkinje system conducts action potentials much faster than can be propagated between myocardial cells, allowing the entire ventricular myocardium to contract in less time, improving pump function.
Classification
Most pathological causes of bradycardia result from damage to this normal cardiac conduction system at various levels: the sinoatrial node, the atrioventricular node, or damage to conduction tissue between or after these nodes.Sinus node
Bradycardia caused by the alterations of sinus node activity is divided into three types.Sinus bradycardia
is a sinus rhythm of less than 50 BPM. Cardiac action potentials are generated from the SA node and propagated through an otherwise normal conduction system, but they occur at a slow rate. It is a common condition found in both healthy individuals and those considered well-conditioned athletes. Studies have found that 50–85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied. The heart muscle of athletes has a higher stroke volume, requiring fewer contractions to circulate the same volume of blood. Asymptomatic sinus bradycardia decreases in prevalence with age in middle aged adults, with an increase seen after 65.Sinus arrhythmia
Sinus arrhythmias are heart rhythm abnormalities characterized by variations in the cardiac cycle length over 120 milliseconds. These are the most common type of arrhythmia in the general population and usually have no significant consequences. They typically occur in the young, athletes or after administration of medications such as morphine. The types of sinus arrhythmia are separated into the respiratory and non-respiratory categories.Respiratory sinus arrhythmia
Respiratory sinus arrhythmia refers to the physiologically normal variation in heart rate due to breathing. During inspiration, vagus nerve activity decreases, reducing parasympathetic innervation of the sinoatrial node and causing an increase in heart rate. During expiration, heart rates fall due to the converse occurring.Non-respiratory sinus arrhythmia
Non-respiratory causes of sinus arrhythmia include sinus pause, sinus arrest, and sinoatrial exit block. Sinus pause and arrest involve slowing or arresting of automatic impulse generation from the sinus node. This can lead to asystole or cardiac arrest if ventricular escape rhythms do not create backup sources of cardiac action potentials.Sinoatrial exit block is a similar non-respiratory phenomenon of temporarily lost sinoatrial impulses. However, in contrast to a sinus pause, the action potential is still generated at the SA node but is either unable to leave or delayed from leaving the node, preventing or delaying atrial depolarization and subsequent ventricular systole. Therefore, the length of the pause in heartbeats is usually a multiple of the P-P interval, as seen on electrocardiography. Like a sinus pause, a sinoatrial exit block can be symptomatic, especially with prolonged pause length.
Sinus node dysfunction
A syndrome of intrinsic disease of the sinus node, referred to as sinus node dysfunction or sick sinus syndrome, covers conditions that include symptomatic sinus bradycardia or persistent chronotropic incompetence, sinoatrial block, sinus arrest, and tachycardia-bradycardia syndrome. These conditions can be caused by damage to the native sinus node itself and are frequently accompanied by damaged AV node conduction and reduced backup pacemaker activity. The condition can also be caused by dysfunction of the autonomic nervous system that regulates the node and is commonly exacerbated by medications.Atrioventricular node
Bradycardia can also result from the inhibition of the flow of action potentials through the atrioventricular node. While this can be normal in young people due to excessive vagus nerve tone, symptomatic bradycardia due to AV node dysfunction in older people is commonly due to structural heart disease, myocardial ischemia, or age-related fibrosis.Atrioventricular block
s are divided into three categories, ranked by severity. AV block is diagnosed via surface ECG, which is usually sufficient to locate the causal lesion of the block without the need for an invasive electrophysiology study.In 1st degree AV block, electrical impulses originating in the SA node are conducted with significant delay through the AV node. This condition is diagnosed via ECG, with PR intervals in excess of 200 milliseconds. The PR interval represents the length of time between the start of atrial depolarization and the start of ventricular depolarization, representing the flow of electrical impulses between the SA and AV nodes. Despite the term "block," no impulses are fully lost in this conduction but are merely delayed. The location of the causal lesion can be anywhere between the AV node and the His-Purkinje system but is most commonly found in the AV node itself. Generally, isolated PR prolongation in 1st degree AV block is not associated with increased mortality or hospitalization.
2nd degree AV block is characterized by intermittently lost conduction of impulses between the SA node and the ventricles. 2nd degree block is classified into two types. Mobitz type 1 block, otherwise known by the eponym Wenckebach, classically demonstrates grouped patterns of heartbeats on ECG. Throughout the group, the PR interval gradually lengthens until a dropped conduction occurs, resulting in no QRS complex seen on surface ECG following the last P wave. After a delay, the grouping repeats, with the PR interval shortening again to baseline. Type 1 2nd degree AV block due to disease in the AV node rarely needs intervention with pacemaker implantation.
2nd degree, Mobitz type 2 AV block is another phenomenon of intermittently dropped QRS complexes after characteristic groupings of beats seen on surface ECG. The PR and RR intervals are consistent in this condition, followed by a sudden AV block and dropped QRS complex. Because type 2 blocks are typically due to lesions below the AV node, the ability for ventricular escape rhythms to maintain cardiac output is compromised. Permanent pacemaker implantation is often required.