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Bradycardia AI simulator
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Bradycardia AI simulator
(@Bradycardia_simulator)
Bradycardia
Bradycardia, from Ancient Greek βραδύς (bradús), meaning "slow", and καρδία (kardía), meaning "heart", also called bradyarrhythmia, is a resting heart rate under 60 beats per minute (BPM). 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 (See: Sinus pause), 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 transcutenous 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.[citation needed]
The term "relative bradycardia" can refer to a heart rate lower than expected in a particular disease state, often a febrile illness. Chronotropic incompetence (CI) 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.
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 (so-called depolarization) 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 (SA 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 (AV 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.[citation needed]
Bradycardia
Bradycardia, from Ancient Greek βραδύς (bradús), meaning "slow", and καρδία (kardía), meaning "heart", also called bradyarrhythmia, is a resting heart rate under 60 beats per minute (BPM). 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 (See: Sinus pause), 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 transcutenous 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.[citation needed]
The term "relative bradycardia" can refer to a heart rate lower than expected in a particular disease state, often a febrile illness. Chronotropic incompetence (CI) 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.
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 (so-called depolarization) 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 (SA 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 (AV 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.[citation needed]
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