Bradycardia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ibtisam Ashraf, M.B.B.S.[2]

Bradycardia is generally characterized as a heart rhythm of less than 60 beats per minute. It can be a significant problem if the heart doesn’t pumps enough oxygen-rich blood into the bloodstream. When symptomatic, fatigue, weakness, dizziness, nausea and fainting will result. Numerous factors influence it, differing in part with age and conditioning. Sinus arrhythmia, variation in sinus rate due to respiratory processes, also causes sinus bradycardia. It is graded by impulse origin i.e. atria, AV junction, ventricles, and infantile. There are numerous pathophysiological disorders that can contribute to bradycardia such as acute myocardial infarction, obstructive sleep apnea, elevated vagal activity, heightened intracranial pressure, and infectious diseases such as Lyme disease, rocky mountain spotted fever, Chagas disease, psittacosis, Q fever and typhoid fever but the most common are sinus node and AV node dysfunction.

Jan Evangelista Purkinje found a net of gelatinous fibers in the subendocardium of the heart in 1839. Later on, in the 1880s, Walter Gaskell found that the region where the cardiac impulse generated was near the sinus venosus. The conduction bundle which links the sinus node and AV node was found by Wilhelm His Jr in 1893. In 1906, Sunao tawara assumed that a tissue present at the proximal end of the his bundle was the beginning of an electrical conducting system, which proceeded from the AV node through the bundle of His, separated into the bundle branches, and ended up as the Purkinje fibers. In the same year, Flack and Keith made the first observation of the mammalian sinoatrial node (SAN).

Bradycardia is a decrease in the heart rate due to abnormalities in the atria, AV node or ventricles. Atrial is further divided into Respiratory Sinus Arrhythmia, Sinus Bradycardia, and Sick Sinus Syndrome. The atrioventricular nodal bradycardia or junctional escape rhythm is usually caused by the absence of the electrical impulse from the sinus node. Ventricular bradycardia, also known as ventricular escape rhythm or idioventricular rhythm, is a heart rate of less than 50 bpm. This is a safety mechanism when there is a lack of electrical impulses or stimuli from the atrium. For infants, bradycardia is defined as a heart rate of less than 100 bpm (normal is around 120-160). Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood.

The underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker. There are generally two types of problems that result in bradycardia: Sinus node dysfunction and AV node dysfunction. Sinus bradycardia can also be seen in Acute myocardial infarction, obstructive sleep apnea, exaggerated vagal activity, increased intracranial pressure and Infectious causes such as Lyme disease, Chagas disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever.

Pathologic bradycardias are caused by disorders of impulse generation (impaired automaticity at SA node), impulse conduction (heart block) or escape pacemakers and rhythms. Bradycardia can be underlain by several causes, which are best divided into cardiac and non-cardiac causes or based on the location of the abnormality. Many drugs causes bradycardia such as Calcium gluconate, Ceritinib,Cosyntropin, Crizotinib, Dolasetron mesylate, Fosphenytoin sodium, Fosaprepitant, Lanreotide and Lorcaserin. Some Life-threatening causes include conditions such as acute myocardial infarction, Acute renal failure, Respiratory failure, Acute respiratory failure, Acute rheumatic fever, Bacterial endocarditis, Beta blocker overdose, Carbamate poisoning, Cervical spine injury.

Bradycardia must be differentiated from Sinoatrial Block, Atrioventricular heart block or dissociation, Wandering atrial pacemaker, Junctional (AV nodal) escape rhythms and Ventricular escape (idioventricular) rhythms.

Incidence is One in 600 adults over the age of 65 has sinus node dysfunction. The frequency of sick sinus syndrome is unknown in the general population, while in cardiac patients it has been estimated to be 3 in 5000. Bradycardia is more common in older patients, over the age of 65 years. There is no racial predilection to bradycardia. Bradycardia affects men and women equally.

Common risk factors in the development of bradycardia include Congenital heart disease, Infection of the heart tissue, Heart surgery, Hypothyroidism or other metabolic condition, Damage caused by a heart attack or heart disease, electrolyte imbalance in the blood, Obstructive sleep apnea, Inflammatory diseases (rheumatic fever or lupus).

There is insufficient evidence to recommend routine screening for bradycardia.

Sinus bradycardia occurs as an adaptive response in healthy patients, particularly in well-conditioned individuals or while sleeping, but it may also occur as a pathological response in different circumstances. Sinus bradycardia does not cause symptoms directly, but a patient with comorbid conditions worsened by reduced cardiac output ( e.g. angina, heart failure) can intensify symptoms of comorbidity. Slower sinus rates are also well-tolerated. Asymptomatic bradycardia, particularly in professional athletes and young adults, are not chronic and may not need medication.

Common complications of bradycardia include Heart failure, Syncope, Angina pectoris, hypotension and hypertension.

The prognosis is good when the rhythm is quickly identified by the healthcare provider. Nevertheless, people with sick sinus syndrome who have bradycardia appear to have a poor 5-year survival prognosis of 45-70 percent.

Most patients with sinus bradycardia do not have symptoms. Individuals with symptoms can experience fatigue, exercise intolerance, lightheadedness, dizziness, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive delay.

Common physical examination findings of bradycardia include decreased level of consciousness, cyanosis, peripheral edema, pulmonary vascular congestion, dyspnea, poor perfusion and syncope.

Laboratory findings pointing towards the diagnosis of bradycardia include electrolyte levels, glucose level, calcium level, magnesium level, thyroid function tests, toxicologic screen and troponin.

An ECG may be helpful in the diagnosis of bradycardia. An upright P wave in leads I, II, and aVL, and a negative P wave in lead aVR, indicates a sinus origin of the bradycardia. It is vital to exclude other causes of bradyarrhythmias such as AV block.

There are no x-ray findings associated with bradycardia.

There are no echocardiography/ultrasound findings associated with bradycardia.

There are no CT scan findings associated with bradycardia.

There are no other imaging findings associated with bradycardia.

There are no other diagnostic studies associated with bradycardia.

Medical treatment is categorized into emergent and permanent. Usually, sinus bradycardia treatment is not recommended for asymptomatic patients. Correcting underlying electrolyte or acid-base deficiencies or hypoxia in symptomatic patients. Intravenous atropine can temporarily help symptomatic patients. Persistently severe bradycardia is considered an absolute contraindication to the use of the medications such as Acebutolol, Atenolol, Carvedilol, Metoprolol and Nebivolol.

Surgery is not the first-line treatment option for patients with bradycardia. However, temporary pacemaker followed by permanent pacemaker therapy may be required in some conditions.

There are no established measures for the primary prevention of bradycardia.

There are no established measures for the secondary prevention of bradycardia.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Jan Evangelista Purkinje found a net of gelatinous fibers in the subendocardium of the heart in 1839. Later on, in the 1880s, Walter Gaskell found that the region where the cardiac impulse generated was near the sinus venosus. The conduction bundle, which links the sinus node and AV node, was found by Wilhelm His Jr in 1893. In 1906, Sunao tawara assumed that a tissue present at the proximal end of his bundle was the beginning of an electrical conducting system, which proceeded from the AV node through the bundle of His, separated into the bundle branches, and ended up as the purkinje fibers. In the same year, Flack and Keith made the first observation of the mammalian sinoatrial node (SAN).

• Gelatinous fibers in the subendocardium was first discovered by Jan Evangelista Purkinje, in 1839.^[1]
• Later on, in the 1880s, Walter Gaskell found that the region where the cardiac impulse generated was near the sinus venosus.
• Conduction bundle which links the sinus node and AV node was found by Wilhelm His Jr in 1893.
• In 1906, Sunao tawara assumed that a tissue present at the proximal end of his bundle was the beginning of an electrical conducting system, which proceeded from the AV node through the bundle of His, separated into the bundle branches, and ended up as the purkinje fibers.^[2]
• In the same year Flack and Keith made the first observation of the mammalian sinoatrial node (SAN).^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Bradycardia is a decrease in the heart rate due to abnormalities in the atria, AV node or ventricles.

Bradyarrhythmia

The origin of the impulse: Atria

The origin of the impulse: AV junction

The origin of the impulse: Ventricles

Sinus node dysfunction: Respiratory sinus arrhythmia Sinus bradycardia Sinoatrial block Sinus arrest Sick sinus syndrome Normal variant: Respiratory sinus arrhythmia

Abnormality in the atria: Low atrial focus bradycardia Atrial bigeminy

AV node dysfunction: First degree AV block Second degree AV block Complete or third-degree AV block

Junctional escape rhythm Junctional bigeminy

Isorhythmic A-V dissociation Slow VT (idioventricular rhythm) Ventricular escape rhythm Escape capture bigeminy

• Respiratory sinus arrhythmia, is usually found in young and healthy adults.
• The heart rate increases during inhalation and decreases during exhalation.
• This is thought to be caused by changes in the vagal tone during respiration.^[1]
• If exhalation is associated with a drop in the heart rate below 60 bpm with each breath, this type of bradycardia is usually deemed benign and is considered a sign of good autonomic tone.

• Sinus bradycardia is a sinus rhythm of less than 60 bpm. It is a common condition found in both healthy individuals and those who are considered well-conditioned athletes.
• Studies have found 50-85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied.
• The heart muscle of athletes has become conditioned to have a higher stroke volume, so it requires fewer contractions to circulate the same volume of blood.^[1]

• Sick sinus syndrome covers conditions that include:
  • Severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia–tachycardia syndrome (atrial fibrillation, flutter, and paroxysmal supraventricular tachycardia).^[1]

• An atrioventricular nodal bradycardia or junctional escape rhythm is usually caused by the absence of the electrical impulse from the sinus node.^[2]
• This usually appears on an EKG with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.^[1]
• An AV junctional escape is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node.^[1]
• Dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block.^[3]
• This is a protective mechanism for the heart, to compensate for an SA node that is no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so.
• This would present with a longer PR interval. A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node. Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.^[1]

• Ventricular bradycardia, also known as ventricular escape rhythm or idioventricular rhythm, is a heart rate of less than 50 bpm.
• This is a safety mechanism when there is a lack of electrical impulse or stimuli from the atrium. Impulses originating from or below the His bundle, also known as ventricular, will produce a wide QRS complex with heart rates between 20 and 40 bpm.^[1]
• Those above the His bundle, also known as junctional, will typically range between 40 and 60 bpm with a narrow QRS complex.
• In a third degree heart block, approximately 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the His bundle.
• AV block may be ruled out with an EKG indicating “a 1:1 relationship between P waves and QRS complexes. Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block.”
• Treatment often consists of the administration of atropine and cardiac pacing.^[1]

• For infants, bradycardia is defined as a heart rate of less than 100 bpm (normal is around 120-160).^[4][5]
• Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood.
• Some researchers think the spells are related to centers inside the brain, that regulate breathing, which may not be fully developed.
• Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate.
• Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary.
• NICU standard practice is to electronically monitor the heart and lungs for this reason.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M.Umer Tariq [2] Ibtisam Ashraf, M.B.B.S.[3]

Bradycardia generally results from sinus node dysfunction and AV node dysfunction. However, other pathophysiologic conditions can also result in bradycardia such as acute Myocardial infarction, obstructive sleep apnea, exaggerated vagal activity, increased intracranial pressure, and infectious diseases such as Lyme disease, rocky mountain spotted fever, chagas disease, psittacosis, Q fever, and typhoid fever.

The underlying mechanism is not clinically relevant to the treatment.

There are generally two types of problems that result in bradycardia:

• Impaired automaticity – Sinus node dysfunction/sick sinus syndrome)^[1][2]

• Atrioventricular conduction disturbances result from impaired conduction in the AV node, or anywhere below it, such as in the bundle of HIS.

Sinus bradycardia can also be seen in these pathophysiologic settings:^[3][4]

• Patients with acute myocardial infarction, especially those with the right coronary artery, are affected by bradycardia as it supplies the SA node.^[5]

• Those with obstructive sleep apnea also have sinus bradycardia, which can be extreme (< 30 beats per minute) during apnea.^[6]

• Vasovagal responses may be associated with severe bradycardia due to elevated parasympathetic involvement and sympathetic suppression of the SA node. These stimuli include carotid sinus stimulation, vomiting, coughing, and Valsalva maneuver.

• Increased intracranial pressure should be excluded when sinus bradycardia arises in a patient with neurological dysfunction. Sinus bradycardia is often associated with damage to the cervical or thoracic spine, where the sympathetic denervation of the heart leaves an uncontested parasympathetic tone.^[7]

• Infectious agents associated with relative sinus bradycardia include Lyme disease, Chagas disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever. ^[8][9]

• On microscopic histopathological analysis, a few patients with sinus bradycardia may show no nodal histopathology, yet some microscopic findings are associated with the condition which includes the following:^[10][11]
  • Nodal cell reduction
  • Nodal cell and fibrosis
  • Amyloidosis in the nodal region
  • Sinus node hypoplasia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M.Umer Tariq [2]; Ogheneochuko Ajari, MB.BS, MS [3]

Pathologic bradycardias are caused by disorders of impulse generation (impaired automaticity at SA node), impulse conduction (heart block), or escape pacemakers and rhythms. Bradycardia can be underlain by several causes, which are best divided into cardiac and non-cardiac causes or based on the location of the abnormality.

• Drugs:

• Agalsidase beta
• Ambenonium
• Aprotinin
• Amobarbital sodium
• Beractant
• Bromocriptine
• Caspofungin acetate
• Calcium gluconate
• Ceritinib
• Cosyntropin
• Crizotinib
• Dolasetron mesylate
• Fosphenytoin sodium
• Fosaprepitant
• Lanreotide
• Lorcaserin
• Meropenem
• Metipranolol
• Nalmefene
• Pasireotide
• Pergolide
• Pilocarpine
• Poractant Alfa
• Prednisolone
• Secobarbital sodium
• Sodium aurothiomalate
• Trichophyton mentagrophytes and trichophyton rubrum
• vandetanib

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Cardiovascular	Acute coronary syndrome, Acute myocardial infarction, Acute rheumatic fever, Andersen cardiodysrhythmic periodic paralysis, Aspergillosis myocarditis, Atherosclerosis, Atrial septal defect, Atrioventricular block, Brugada syndrome, Calcific aortic stenosis, Cardiac arrhythmia, Cardiac catheterization, Cardiac glycosides, Cardiac transplantation, Cardiac tumor, Cardioinhibitory syncope, Cardiomyopathy, Cardioversion, Carotid sinus hypersensitivity, Complete heart block, Congenital heart block, Congenital heart disease, Congestive heart failure, Coronary artery bypass grafting, Coronary heart disease, Coronary ischemia, Coronary reperfusion therapy, Diabetes mellitus, Dilated cardiomyopathy, Ebstein’s anomaly, Electrophysiological studies, Endocardial cushion defect, Endocarditis, Enhanced vagal tone, Fontan procedure, High fitness level, Hypersensitive carotid sinus syndrome, Hypertension, Hypertensive heart disease, Hypertrophic cardiomyopathy alcohol septal ablation, Hypertrophic cardiomyopathy, Hypervagotonia, Idiopathic heart block, Idiopathic hypereosinophilic syndrome, Infraclavicular brachial plexus block, Ischemic heart disease, Isorhythmic a-v dissociation, Jervell and lange-nielsen syndrome, Junctional rhythms, Lateral medullary syndrome, Left ventricular noncompaction, Lenegre’s disease, Lev’s disease, Long qt syndrome, Lown-ganong-levine syndrome, Lqt type 4, Lqt4 mutation, Mahaim fiber tachycardia, Maze procedure, Micturition syncope, Mitral regurgitation, Mitral stenosis, Mitral valve prolapse, Myocardial bridging, Myocardial contusion, Myocardial infarction  , Myocardial ischaemia, Myocardial rupture, Myocarditis, Neurocardiogenic syncope, Noncompaction cardiomyopathy, Normal variants of pr prolongation, Normal variation in vagal tone, Nstemi, Pacemaker malfunction, Paroxysmal supraventricular tachycardia, Pericarditis, Permanent pacemaker, Peroneal muscular atrophy, Post aortic valve replacement, Post catheter ablation for arrhythmias, Post closure of a ventricular septal defect, Post mitral valve replacement, Preexcitation syndrome, Premature atrial beats, Pulmonary embolism, Pulmonary stenosis, Restrictive cardiomyopathy, Rheumatic mitral valve disease, Romano-ward syndrome, Sick sinus syndrome, Sinoatrial block, Sinus arrest, Sinus bradycardia, Sinus node disease, Sinus node fibrosis, Stemi, Subarachnoid hemorrhage, Sustained ventricular tachycardia, Tachycardia-bradycardia syndrome, Takotsubo cardiomyopathy, Tetralogy of fallot, Tilt testing, Timothy syndrome, Trained athletes, Transcatheter aortic valve implantation, Transposition of the great vessels, Vagal maneuvers, Vagal reaction, Valsalva maneuver, Valvular heart disease, Vasovagal syncope, Ventricular septal defect, Wolff-parkinson-white syndrome
Chemical/Poisoning	5-fluorouracil, Alcohol intoxication, All-trans retinoic acid, Carbamate poisoning, Carbamates, Crizotinib toxicity, Digitalis, Dimethyl sulfoxide, Disopyramide, Fentanyl, Heart block, Heart surgery, Heat exhaustion, Isoprenaline infusion, Lily of the valley poisoning, Magnesium, Organophosphate poisoning, Parathion poisoning, Poisonous spider bites, Pyrethroid poisoning, Scorpion toxin, Toluene sniffing
Dental	No underlying causes
Dermatologic	Dermatomyositis, Obstructive jaundice
Drug Side Effect	Acetylcholine, Alfentanil, Ambenonium, Amiodarone, Amlodipine, Amphetamines, Anidulafungin, Anthracyclines, Antiarrhythmic drugs, Atenolol, Atetylcholine, Barbiturate, Berberine, Beta-blockers, Bethanechol, Bortezomib, Bupivacaine, Calcium channel blocker, Cannabis, Carbamazepine, Celecoxib, Ceritinib, Certain medications, Cilobradine, Cimetidine, Citalopram, Clonidine, Cocaine, Dapoxetine, Daunorubicin, Deserpidine, Dexmedetomidine, Digoxin, Diltiazem, Diphenhydramine, Distigmine, Dobutamine, Dolasetron, Donepezil, Doxorubicin, Dronedarone, Drugs, Edrophonium, Ephedrine, Epirubicin, Eslicarbazepine acetate, Febuxostat, Fesoterodine, Fingolimod, Flecainide, Flumazenil, Fluoxetine, Fluvoxamine, Fosphenytoin, Granisetron, Grayanotoxin, Guanethidine, Guanfacine, H2 receptor antagonist, Halothane, Hyoscyamine, Ibutilide, Idarubicin, Isoproterenol, Ivabradine, Labetalol, Lacosamide, Lanatoside c, Lanreotide, Lidocaine, Lithium, Lofexidine, Medications, Mefloquine, Mepivacaine, Mesalamine, Methyldopa, Methylprednisolone, Mexiletine, Morphine, Muscarine, Nadolol, Nefazodone, Nelfinavir, Neostigmine, Nerve agent, Nicorandil, Paclitaxel, Paliperidone, Palonosetron, Phenothiazine, Phenylephrine, Phenytoin, Physostigmine, Procainamide, Propafenone, Propanolol, Propofol, Propoxyphene, Propranolol, Pyridostigmine, Quinidine, Rabeprazole, Regadenoson, Remifentanil, Rescinnamine, Reserpine, Rilmenidine, Ropivacaine, Salbutamol, Sedative, Somatostatin, Sotalol, Sufentanil, Suxamethonium, Sympathomimetic agents, Tacrine, Tacrolimus, Terodiline, Theophylline, Thiamylal, Thiazides, Timolol, Tolterodine, Topical cocaine, Tramadol, Tricyclic antidepressants, Urapidil, Vecuronium, Verapamil, Veratridine (false hellebore), Zaleplon, Zatebradine
Ear Nose Throat	Esophageal or nasopharyngeal stimulation, Sjogren’s syndrome
Endocrine	Cretinism, Cushing’s syndrome, Hashimoto’s thyroiditis, Hyperthyroidism, Hypothyroidism, Myxedema, Profound hypothyroidism, Thyrotoxic periodic paralysis, Thyrotoxicosis
Environmental	No underlying causes
Gastroenterologic	Nausea, Vomiting
Genetic	Becker muscular dystrophy, Fabry disease, Hcm, Hcn4 mutation, Hereditary neuromuscular disease, Jervell and lange-nielsen syndrome, Kearns-sayre syndrome, Mitochondrial genome inherited conditions, Nail-patella syndrome, Scn5a mutation, Timothy syndrome, X-linked inherited conditions
Hematologic	Anemia, Churg-strauss syndrome, Hemochromatosis, Hypercalcemia, Hypercapnia, Hyperkalemia, Hypermagnesemia, Hypocalcemia, Hypoglycemia, Hypokalemia, Hypomagnesemia, Hypoxia, Sepsis, Thalassemia major
Iatrogenic	No underlying causes
Infectious Disease	Aspergillosis myocarditis, Brucellosis, Chagas disease, Dengue fever, Diptheria, Legionellosis, Leptospirosis, Lyme disease, Malaria, Meningitis, Pneumonia, Protozoal infection, Q fever, Rabies, Rocky mountain spotted fever, Salmonellosis, Sepsis, Septic shock, Trichinosis, Tuberculosis, Typhoid fever, Typhus, Varicella zoster, Viral hemorrhagic fever, Yellow fever
Musculoskeletal/Orthopedic	Arnold-chiari malformation, Dermatomyositis, Duchenne’s muscular dystrophy, Emery-dreifuss muscular dystrophy, x-linked, Erb’s dystrophy, Hereditary neuromuscular disease, Limb-girdle muscular dystrophy type 1b (lgmd1b), Mitochondrial myopathy, Muscular dystrophy, Myotonic dystrophy, Myotonic muscular dystrophy
Neurologic	Bezold-jarisch reflex, Degenerative diseases, Diabetic neuropathy, Epilepsy, Friedreich ataxia, Increased intracranial pressure, Miller-dieker syndrome, Neurocardiogenic syncope, Raised intracranial pressure, Severe brain injury, Sleep apnea, Sleep, Timothy syndrome
Nutritional/Metabolic	Cerebral edema, Diabetes mellitus, Diabetic ketoacidosis, Diabetic neuropathy, Glycogen storage disease type ii, Glycogenosis type 2b, Hypoglycemia, Kwashiorkor, Malnutrition, Metabolic acidosis, Obesity, Pompe disease, Severe anorexia nervosa, Starvation, Very low birth weight infants
Obstetric/Gynecologic	Fetal distress, Pregnancy
Oncologic	Hodgkin disease, Hodgkin lymphoma, Multiple myeloma, Pheochromocytoma, Tumor lysis syndrome, Tumor
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	Anorexia nervosa, Severe anorexia nervosa
Pulmonary	Acute respiratory failure, Altitude sickness, Breath holding spells, Chronic obstructive pulmonary disease, Cough syncope, Decompression sickness, Drowning, Obstructive sleep apnea, Post lung transplantation, Pulmonary embolism, Pulmonary stenosis, Sarcoidosis, Sleep apnea, Tuberculosis
Renal/Electrolyte	Acute renal failure, Amyloidosis, Chronic renal failure, Electrolyte disturbances, Hyperkalemia, Hypokalemia, Renal failure
Rheumatology/Immunology/Allergy	Acute rheumatic fever, Ankylosing spondylitis, Churg-strauss syndrome, Neonatal lupus erythematosus, Reiter’s syndrome, Relapsing polychondritis, Rheumatic fever, Rheumatic mitral valve disease, Rheumatoid arthritis, Sarcoidosis, Scleroderma, Sinus node fibrosis, Sjogren’s syndrome, Systemic lupus erythematosus, Systemic sclerosis
Sexual	No underlying causes
Trauma	Cervical spine injury, Electric shock, Hypothermia, Pain, Septic shock, Severe brain injury, Spinal cord injury, acute, Starvation, Surgical trauma, Trauma
Urologic	No underlying causes
Miscellaneous	Aging, Defecation, Idiopathic

• Anidulafungin
• Atherosclerosis
• Congestive heart failure
• Digitalis
• Guanfacine
• Hypercapnia
• Morphine
• Myocardial infarction
• Normal variation in vagal tone

Amiodarone Amyloidosis Antiarrhythmics Atherosclerosis Atrial septal defect Beta blockers Calcium channel blockers Cardiac surgery in children Cardiomyopathies Carotid sinus hypersensitivity Chagas disease Cimetidine Clonidine Congenital heart disease Coronary artery disease Digitalis Diphtheria Disopyramide Ebstein anomaly Electrolyte imbalance Friedreich ataxia Grayanotoxin Guanethidine HCN4 mutation Hemochromatosis Hyperkalemia Hypertension Hypocalcemia Hypothermia Hypothyroidism

Hypoxia Idiopathic Ischemic heart disease Lanatoside C Lidocaine Lithium Lyme disease Methyldopa Muscular dystrophy Myocardial infarction Myocarditis Myotonic dystrophy Neoplasm Neurocardiogenic syncope Pericarditis Phenytoin Procainamide Propranolol Quinidine Reserpine Rheumatic fever Rhododendron sp Sarcoidosis Scleroderma Sepsis Sinus node fibrosis Sleep apnea Systemic lupus erythematosus Tachycardia-bradycardia syndrome Verapamil

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Bradycardia must be differentiated from sinoatrial block, atrioventricular block, wandering atrial pacemaker, junctional escape rhythms, and ventricular escape rhythms.

Bradycardia must be differentiated from sinoatrial block, atrioventricular block, wandering atrial pacemaker, junctional escape rhythms and ventricular escape rhythms.^[1]

Differential Diagnosis

Sinoatrial Block

Atrioventricular heart block or dissociation

Wandering atrial pacemaker

Junctional (AV nodal) escape rhythms

Ventricular escape (idioventricular) rhythms

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ibtisam Ashraf, M.B.B.S.[2]

Bradycardia is mostly the result of sinus node dysfunction found in one in 600 individuals over 65 years of age. There is no racial predilection for bradycardia and it affects all genders equally.

• The incidence of bradycardia is approximately 1 in 600 individuals worldwide.^[1]

• The prevalence of unexplained sinus bradycardia (SB) is approximately 400 per 100,000 individuals worldwide.^[2]
• The frequency of sick sinus syndrome is unknown in the general population, while in cardiac patients it has been estimated to be 3 in 5000.

• Bradycardia is more common in older patients, over the age of 65 years.

• There is no racial predilection to bradycardia.

• Bradycardia affects men and women equally.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Common risk factors in the development of bradycardia include congenital heart disease, infection of the heart tissue, heart surgery, hypothyroidism or other metabolic condition, damage caused by a heart attack or heart disease, electrolyte imbalance in the blood, obstructive sleep apnea, inflammatory diseases (rheumatic fever or lupus).

Common risk factors in the development of bradycardia include:^{[1][2][3][4][5][6][7]}

• Sinus node dysfunction
• Drugs that are used to manage atrial fibrillation (AF), which include drugs like amiodarone.
• Congenital heart disease
• Infection of the heart tissue
• Heart surgery
• Hypothyroidism or other metabolic condition
• Damage caused by a heart attack or heart disease
• Electrolyte imbalance in the blood
• Obstructive sleep apnea
• Inflammatory diseases (rheumatic fever or lupus)

Less common risk factors in the development of bradycardia include:

• High blood pressure (hypertension)
• Smoking
• Heavy alcohol use
• Use of recreational drugs
• Psychological stress or anxiety

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

There is insufficient evidence to recommend routine screening for bradycardia.

There is insufficient evidence to recommend routine screening for bradycardia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ibtisam Ashraf, M.B.B.S.[2]

Common complications of bradycardia include heart failure, syncope, angina pectoris, hypotension and hypertension. The prognosis is good when the rhythm is quickly identified by the healthcare provider. Nevertheless, people with sick sinus syndrome who have bradycardia appear to have a poor 5-year survival prognosis of 45-70 per cent.

• Sinus bradycardia occurs in healthy patients as an adaptive response, particularly in well-conditioned persons or while sleeping, but it can also occur as a pathologic response in a variety of conditions.^[1]
• Sinus bradycardia itself does not cause symptoms directly, although a patient with comorbid conditions that may be exacerbated by decreased cardiac output (e.g. angina, heart failure) may have worsening symptoms related to comorbidity.
• Slower sinus rates are often very well tolerated. Asymptomatic resting bradycardias, particularly in trained athletes and young individuals is not pathological and doesn’t require treatment.

• Common complications of bradycardia include:^[2]
  • Heart failure
  • Syncope
  • Angina pectoris
  • hypotension
  • hypertension

• The prognosis is good when the rhythm is quickly identified by the healthcare provider.^[3]
• Nevertheless, people with sick sinus syndrome who have bradycardia appear to have a poor 5-year survival prognosis of 45-70 per cent.^[4]

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