Third degree AV block

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Soroush Seifirad, M.D.[3] Cafer Zorkun, M.D., Ph.D. [4]Qasim Khurshid, M.B.B.S.

Complete heart block is a disease of the cardiac electrical conduction system where there is complete dissociation of the atrial and ventricular activity because of the absence of conduction through the atrioventricular node (AVN) or His-Purkinje system. In 1894, Dr. Engelman was the first to describe in detail the phenomenon of AV interval lengthening. In 1899, Karel Frederik published a paper on irregular pulses describing the impairment of AV conduction and blockage.Complete heart block may be transient due to increased parasympathetic tone defining vagally mediated atrioventricular block or due to persistent infranodal block whether there is evidence of conduction block distal to the atrioventricular node. Normally SA node generates impulses that travel to the AV node and gets delayed there to assure that the contraction cycle in atria is complete before a contraction begins in the ventricles. From the AV node, the impulses pass through the His-Purkinje system to cause ventricular contraction. Pathological delay in the AV node is visualized on an electrocardiogram as a change in the P-R interval. These delays are known as an AV block. No impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable. The most common cause of a complete heart block is coronary ischemia, but there are many other etiologies. The progressive degeneration of the electrical conduction system of the heart due to aging can cause a third-degree heart block. Complete heart block can be preceded by first degree AV block, second degree AV block, or bifascicular block. Acute myocardial infarction may present as a third-degree heart block. Lupus in a pregnant mother can cause congenital heart block in newborns. Maternal antibodies can cross the placenta and lead to a complete heart block during gestation. Sometimes no cause can be identified. Third-degree heart block should not be confused with high-grade AV block which is a second-degree block with a very slow ventricular rate with occasional AV conduction, or AV Dissociation defining to indicate the occurrence of independent atrial and ventricular contractions caused by entities other than third-degree heart block.AV blocks are fairly common however, third-degree AV block is relatively rare. The incidence in the general population appears to be low, approximately 20 to 40 in 100,000 individuals in the United States. Given the etiology of the disease, the incidence among the apparently healthy and presumptively asymptomatic is even lower at approximately 1 in 100,000. Common risk factors associated atioventricular block include older age, male sex, history of myocardial infarction, history of congestive heart disease, high systolic blood pressure, increased fasting blood glucose level.Transthoracic echocardiography may be helpful in the diagnosis of the underlying diseases that tend to third-degree AV block. Echocardiography might show shreds of evidence in favor of cardiomyopathies or valvular heart diseases. In particular case scenarios, transesophageal echocardiography is warranted and may help to diagnose etiologies such as valvular ring abscess. Furthermore, the left ventricular function can be determined using an echo and provide pieces of evidence in favor of the placement of a pacemaker or defibrillator. . Common indications for echocardiography in suspicion of cardiac origin of bradycardia or conduction disorder may include syncope, lightheadedness/presyncope, symptoms related to aortic stenosis, hypertrophic cardiomyopathy, heart failure.There are no x-ray findings associated with third-degree AV block. However, a chest x-ray may be helpful in the diagnosis of complications of third degree AV block such as pulmonary edema. Additionally, a chest x-ray may be helpful in the diagnosis of the underlying disease tend to third degree AV block, or in the diagnosis of the other complications of that disorder which may include cardiomegaly and hilar adenopathy. CT scan may be helpful in the diagnosis of cardiac and chest abnormalities related to the underlying organic disease in those with third-degree AV block. Cardiac MRI may be helpful in selected patients to identify the underlying structural heart disease associated conduction disturbance such as sarcoidosis, hemochromatosis, and amyloidosis. Nuclear imaging techniques might rarely be used and may be helpful in the diagnosis of complications of third-degree AV block or provide shreds of evidence in favor of the underlying disease in those with complete heart block. Ambulatory monitoring is warranted in cases of possible transient heart block, or some other bradyarrhythmias that might be mistaken with third-degree AV block. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. Improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventric-ular block. The management of third-degree AV block depends on the severity of signs, symptoms, and the underlying cause. In symptomatic patients and with hemodynamic distress, pharmacological therapy should be initiated immediately to increase heart rate and cardiac output. Most of the patients who do not respond to pharmacologic therapy require a temporary pacemaker. After stabilizing the patients, assessment and treatment of potentially reversible causes should be done. Some patients without reversible cause or unidentified etiology require a permanent pacemaker. Cardiac pacemakers are effective treatments for a variety of cardiac conduction abnormalities and can reestablish adequate circulation by generating appropriate heart rate and cardiac response. Two main factors guide the majority of decisions regarding permanent pacemaker insertion. First is the association of symptoms with arrhythmia, and second is the potential for progression of the rhythm disturbance. Symptoms related to atrioventricular block are determining factor of placing permanent pacemaker, regardless of the level of atrioventricular block. Permanent pacemaker is warranted if the site of atrioventricular block is Infranodal, regardless of the presence or absence of symptoms. Temporary transvenous pacing is used to provide hemodynamic support or back-up pacing to prevent asystole. If atrioventricular block seems to be irreversible, it is better to proceed directly with permanent pacemaker implantation. Patients with renal insufficiency, potassium electrolyte disturbances, and dehydration are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy. These patients should be carefully monitored for heart blocks. There is no secondary prevention.

In 1894, Dr. Engelman was the first to describe the phenomenon of AV interval lengthening in detail. In 1899, Karel Frederik published a paper on irregular pulses describing AV conduction and blockage impairment. 1906 Einthiven was the first to present a presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Dr. Ashmar in 1925 studied and described in detail these blocked impulses and their impact on the conduction in the muscle of the heart. In 1952 Dr. Paul Zoll developed the first temporary transcutaneous pacing.

Complete heart block may be transient due to increased parasympathetic tone defining vagally mediated atrioventricular block or due to infranodal block whether there is evidence of conduction block distal to the atrioventricular node.

Normally SA node generates impulses that travel to the AV node and gets delayed there to assure that the contraction cycle in atria is complete before a contraction begins in the ventricles. From the AV node, the impulses pass through the His-Purkinje system to cause ventricular contraction. Pathological delay in the AV node is visualized on an electrocardiogram as a change in the P-R interval. These delays are known as an AV block. No impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable.

The most common cause of a complete heart block is coronary ischemia, but there are many other etiologies. The progressive degeneration of the electrical conduction system of the heart due to aging can cause a third-degree heart block. Complete heart block can be preceded by first degree AV block, second degree AV block, or bifascicular block. Acute myocardial infarction may present as a third-degree heart block. Lupus in a pregnant mother can cause congenital heart block in newborns. Maternal antibodies can cross the placenta and lead to a complete heart block during gestation. Sometimes no cause can be identified.

Third-degree heart block should not be confused with high-grade AV block which is a second-degree block with a very slow ventricular rate with occasional AV conduction, or AV Dissociation defining to indicate the occurrence of independent atrial and ventricular contractions caused by entities other than third-degree heart block.

AV blocks are fairly common however, third-degree AV block is relatively rare. The incidence in the general population appears to be low, approximately 20 to 40 in 100,000 individuals in the United States. Given the etiology of the disease, the incidence among the apparently healthy and presumptively asymptomatic is even lower at approximately 1 in 100,000.

Common risk factors associated atioventricular block include older age, male sex, history of myocardial infarction, history of congestive heart disease, high systolic blood pressure, increased fasting blood glucose level.

There is insufficient evidence to recommend routine screening for third degree AV block. However, screening for congenital AV block is recommended

Spontaneous recovery from third-degree heart block is not common. Untreated third-degree heart block is associated with high mortality, which appears to occur as a consequence of the complications of decreased perfusion as a consequence of bradycardia and decreased cardiac output. Common complications of third-degree AV block include syncope, musculoskeletal injuries due to falling, and sudden cardiac death. The prognosis of the third-degree heart block is most likely dependent on the patient‘s underlying disease burden and severity of the clinical presentation on arrival. Patients treated with permanent pacemaker have an good prognosis.

A 12-lead Electrocardiography (ECG) is the gold standard test for the diagnosis of third degree AV block.

Patients with third-degree AV block typically experience a low blood pressure, decreased heart rate, and poor circulation. Some patients with complete heart block may experience difficulties in doing exercise, as the heart cannot react quickly to sudden changes in demand or sustain the higher heart rates required for sustained physical activity. Complete heart block associated with a slower pacemaker can result in dizziness, presyncope andsyncope.

Initial triage of patients with complete heart block consists of determining symptoms, taking vital signs, and looking for evidence of hemodynamic instability. Patients with complete heart block may have serve bradycardia, S3 gallop, new murmurs, peripheral edema, and hepatomegaly. Patients may have signs of hypoperfusion, such as altered mental status, lethargy, and hypotension.

There is not any recommendation about routine laboratory tests in patients presented with bradycardia or conduction disorder. However, in suspicion of the underlying causes of bradycardia including sepsis, rheumatologic disorder, or thyroid disease specific tests are warranted.

Transthoracic echocardiography may be helpful in the diagnosis of the underlying diseases that tend to third-degree AV block. Echocardiography might show shreds of evidence in favor of cardiomyopathies or valvular heart diseases. In particular case scenarios, transesophageal echocardiography is warranted and may help to diagnose etiologies such as valvular ring abscess. Furthermore, the left ventricular function can be determined using an echo and provide pieces of evidence in favor of the placement of a pacemaker or defibrillator. . Common indications for echocardiography in suspicion of cardiac origin of bradycardia or conduction disorder may include syncope, lightheadedness/presyncope, symptoms related to aortic stenosis, hypertrophic cardiomyopathy, heart failure.

There are no x-ray findings associated with third-degree AV block. However, a chest x-ray may be helpful in the diagnosis of complications of third degree AV block such as pulmonary edema. Additionally, a chest x-ray may be helpful in the diagnosis of the underlying disease tend to third degree AV block, or in the diagnosis of the other complications of that disorder which may include cardiomegaly and hilar adenopathy.

CT scan may be helpful in the diagnosis of cardiac and chest abnormalities related to the underlying organic disease in those with third-degree AV block.

Cardiac MRI may be helpful in selected patients to identify the underlying structural heart disease associated conduction disturbance such as sarcoidosis, hemochromatosis, and amyloidosis.

Determination the underlying cardiac or non-cardiac cause of bradycardia or conduction disorder has prognostic value. When the structural heart disease can not be identified by echocardiography, advanced imaging including TEE, cardiac computed tomography, cardiac MRI may be helpful in selected patients.

Ambulatory monitoring is warranted in cases of possible transient heart block, or some other bradyarrhythmias that might be mistaken with third-degree AV block. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. Improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventric-ular block.

The management of third-degree AV block depends on the severity of signs, symptoms, and the underlying cause. In symptomatic patients and with hemodynamic distress, pharmacological therapy should be initiated immediately to increase heart rate and cardiac output. Most of the patients who do not respond to pharmacologic therapy require a temporary pacemaker. After stabilizing the patients, assessment and treatment of potentially reversible causes should be done. Some patients without reversible cause or unidentified etiology require a permanent pacemaker.

Cardiac pacemakers are effective treatments for a variety of cardiac conduction abnormalities and can reestablish adequate circulation by generating appropriate heart rate and cardiac response. Two main factors guide the majority of decisions regarding permanent pacemaker insertion. First is the association of symptoms with arrhythmia, and second is the potential for progression of the rhythm disturbance. Symptoms related to atrioventricular block are determining factor of placing permanent pacemaker, regardless of the level of atrioventricular block. Permanent pacemaker is warranted if the site of atrioventricular block is Infranodal, regardless of the presence or absence of symptoms. Temporary transvenous pacing is used to provide hemodynamic support or back-up pacing to prevent asystole. If atrioventricular block seems to be irreversible, it is better to proceed directly with permanent pacemaker implantation.

Patients with renal insufficiency, potassium electrolyte disturbances, and dehydration are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy. Patients on multiple nodal agents are susceptible for the development of third-degree atrioventricular (AV) block (complete heart block). These patients should be carefully monitored for heart blocks.

There is no secondary prevention.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Aditya Ganti M.B.B.S. [3] Qasim Khurshid, M.B.B.S [4]

In 1894, Dr. Engelman was the first to describe in detail the phenomenon of AV interval lengthening. In 1899, Karel Frederik published a paper on irregular pulses describing impairment of AV conduction and blockage. 1906 Einthiven was the first to present a presentation of normal and abnormal electrocardiograms recorded with string galvanometer. Dr. Ashmar in 1925 studied and described in detail this blocked impulses and their impact on the conduction in the muscle of the heart. In 1952 Dr. Paul Zoll developed first temporary transcutaneous pacing.

• In 1895, Willem Einthoven invented the first practical electrocardiogram.
• In 1894, Dr. Engelmann described a phenomenon of AV interval lengthening.
  • Dr. Engelmann described a stimulus that is applied to the atrium followed by elongation of the AV interval.^[1]
• In 1899, Karel Frederik Wenckebach published a paper “On the analysis of irregular pulses”
  • Described the impairment of AV conduction leading to progressive lengthening and blockage of AV conduction in frogs.
  • This was later called Wenckebach block (Mobitz type I) or Wenckebach phenomenon.
• In 1906, Einthoven was the first to organize a presentation of normal and abnormal electrocardiograms recorded with help of string galvanometer
• In 1925, Dr. Ashmar further studied this blocked impulses and their impact on the conduction in the muscle of the heart.
• In 1930, Sanders was the first to describe infarction of the right ventricle.
• In 1949, Norman Jeff Holter developed a first Holter monitor which was a 75 pound backpack that can record the ECG of the wearer and transmit the signal.

• Paul Zoll in 1952: invented temporary transcutaneous cardiac pacing.
• Seymour Furman in 1958: developed temporary endocardial approach
• Åke Senningm and Elmqvist in 1958: developed Implantable Pacemakers.^[2]

Template:WH Template:WS

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Soroush Seifirad, M.D.[3] Cafer Zorkun, M.D., Ph.D. [4] Qasim Khurshid, M.B.B.S [4]

Third-degree or complete atrioventricular block suggests no conduction at all from atria to ventricles and may be paroxysmal or persistent and is usually associated with either a junctional or ventricular escape rhythm. Complete atrioventricular block may be identified in the setting of atrial fibrillation when the ventricular response is slow (<50 bpm) and regular. However, junctional rhythm in the setting of atrioventricular block may be present.

^[1]

Term	Classification	Definition
Atrioventricular block	First-degree atrioventricular block	P waves associated with 1:1 atrioventricular conduction PR interval >200 ms atrioventricular delay because no P waves are blocked
	Second-degree AV block	P waves with a constant rate (<100 bpm) Atrioventricular conduction is present but not 1:1 Mobitz type I P waves with a constant rate (<100 bpm) Presence of periodic single non conducted P wave associated with P waves before and after the non conducted P wave with inconstant PR intervals Mobitz type II Presence of P waves with a constant rate (< 100 bpm) with a periodic single non conducted P wave associated with other P waves before and after the non conducted P wave with constant PR intervals (excluding 2:1 atrioventricular block) 2:1 atrioventricular block P waves with a constant rate (or near-constant rate because of ventriculophasic sinus arrhythmia) rate (<100 bpm), every other P wave conducts to the ventricles Advanced, high-grade or high-degree atrioventricular block ≥2 consecutive P waves at a constant physiologic rate that do not conduct to the ventricles with evidence for some atrioventricular conduction
	Third-degree AV block (complete heart block)	No evidence of atrioventricular conduction Vagally mediated atrioventricular block Any type of atrioventricular block due to increased parasympathetic tone Infranodal block Atrioventricular conduction block with evidence of conduction block distal to the atrioventricular node

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Raviteja Guddeti, M.B.B.S. [4] Qasim Khurshid, M.B.B.S[5]

Normally SA node generates impulses that travel to the AV node and gets delayed there to assure that the contraction cycle in atria is complete before a contraction begins in the ventricles. From the AV node, the impulses pass through the His-Purkinje system to cause ventricular contraction. Pathological delay in the AV node is visualized on an electrocardiogram as a change in the P-R interval. These delays are known as an AV block. No impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable.

The normal physiology of the electrical activity of the heart can be understood as follows:

• Normal impulse is generated in the sinoatrial node (SAN).
• Electrical pulse then travels through the atrium.
• P wave is recorded in the ECG
• Wave reaches the atrioventricular node (AVN).
• Atrioventricular node later conducts the impulse to the His bundle.
• The bundle of his again gets divided into the right and left bundles, ultimately conducting this impulse to the ventricles.
• PR segment is recorded (atrial, AVN, and His-Purkinje conduction)
• Complete heart block occurs when complete block of this conduction occurs.

• • In complete heart block, because the impulse is blocked, an accessory pacemaker below the level of the block will typically activate the ventricles; this is known as an escape rhythm.
  • When there is no electrical connection between atria and ventricles, two independent pacemakers will generate impulse independent of SA node. EKG will show two rhythms independent of each other
    • One independent pacemaker will activate the atria and create the P waves with typically with a regular P to P interval.
    • The second independent pacemaker in ventricles will activate the ventricles and produce the QRS complex with typically regular R to R interval.
    • The PR interval will be a variable that is a hallmark feature of complete heart block and with no apparent relationship between P waves and QRS complexes.
  • Morphology of the QRS complex helps in determining the location at which the escape rhythms are occurring.
  • If the site of complete heart block is at the level of the AV node, two-thirds of the escape rhythms have a narrow QRS complex.
  • If the site of block is the His bundle, typically a narrow QRS complex is seen.
  • Patients with trifascicular block have a wide QRS complex (seen in 80% of the cases).
  • In short, if escape rhythm has a narrow QRS complex, the level of the block can be either AV node or His bundle, and if the QRS duration is prolonged, the level of block is in the fascicles or bundle branches.
  • Block at the level of the AV node gives rise to an escape rhythm that generally arises from a junctional pacemaker with a heart rate of 45-60 beats per minute. Such patients are hemodynamically stable.
  • Escape rhythms arise from the His bundle or bundle branch Purkinje system at rates slower than 45 beats per minute when the block is below the AV node.
  • These patients are hemodynamically unstable, and their heart rate is unresponsive to exercise and atropine.

• Third degree AV block is the result of ischemia in majority of the patients.
• In certain disease like lyme disease also we might observe AV block.
• Nevertheless, there are some rare cases of idiopathic AV block

• In those cases, third degree AV block is transmitted in autosomal dominant pattern most of the time.

Genes involved in the pathogenesis of third degree AV block
AV CONDUCTION DISEASE AND CONGENITAL CARDIAC MALFORMATIONS	NKX2.5
AV CONDUCTION DISEASE, VENTRICULAR HYPERTROPHY, AND WOLFF-PARKINSON-WHITE SYNDROME	PRKAG2
AV CONDUCTION DISEASE : A CHANNELOPATHY	SCN5A KCNJ2 (type 1 Andersen-Tawil syndrome) [1]

Conditions associated with third degree AV block include:

• Ischemic heart disease (Major)
• Congenital cardiac malformations
• Ventricular hypertrophy
• WPW syndrome
• Chenlopatioes such as Andersen-Tawil syndrome

• AV dissociation

AV dissociation is defined as:

• Independent atrial and ventricular activation either due to complete heart block or as a result of physiologic refractoriness of conduction tissue.
• It also may develop when the atrial/sinus rate is slower than the ventricular rate (accelerated junctional tachycardia or VT).

• This is called isorhythmic AV dissociation.
• Acceleration of the atrial/sinus rate with either maneuvers or medications will result in restoration of normal conduction.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Raviteja Guddeti, M.B.B.S. [4]; Hilda Mahmoudi M.D., M.P.H.^[5]

Atrioventricular block can be due to congenital or acquired causes. The latter are much more common form and include infectious, inflammatory, degenerative, ischemic, and iatrogenic causes. The degenerative cause are associated with increased age, chronic hypertension, and diabetes mellitus. Infectious cause of atrioventricular block such as lyme carditis may be reversible with medical therapy. Another reversible cause of atrioventricular block including ischemic inferior wall MI due to vagotonic effect should be considered.

The causes of third degree heart block can be broadly divided into acquired and congenital. Many of the acquired causes are the result of Infiltration, fibrosis, or loss of connection in the heart conduction system that can tend to develop heart block.

• Usually occurs at AVN. Patients are intially asymptomatic but may symptomatic during exertion. Mostly associated with maternal antibodies to SS-A (Ro) and SS-B (La).

• Ischemia or infarction:

• AV node (AVN) block associated with inferior wall myocardial infarction (MI)
• His-Purkinje block associated with anterior wall MI

• Drugs:

• Most of the antiarrhythmics like quinidine, , disopyramide,procainamide flecainide, encainide, beta-blockers propafenone, , amiodarone, sotalol, dofetilide, ibutilide, calcium channel blockers, Digoxin and other cardiac glycosides.

• Infectious disease:

• Lyme borreliosis (mostly in endemic areas)
• Myocarditis
• Aspergillus myocarditis
• Chagas disease: Trypanosoma cruzi infection
• Varicella-zoster virus infection
• Valve ring abscess

• Degenerative diseases:

• Lenègre disease (sclerodegenerative process involving only the conduction system)
• Lev’s disease (calcification of the conduction system and valves)
• Noncompaction cardiomyopathy
• Nail-patella syndrome
• Mitochondrial myopathy

• Rheumatic diseases:

• Ankylosing spondylitis
• Reiter syndrome
• Relapsing polychondritis
• Rheumatoid arthritis
• Rheumatic fever
• Scleroderma

• Infiltrative pathologies:

• Amyloidosis
• Sarcoidosis
• Malignant or benign tumors
• Hodgkin lymphoma
• Multiple myeloma

• Neuromuscular disorders:

• Becker muscular dystrophy
• Myotonic dystrophy

• Metabolic abnormality:

• Hypoxia
• Hyperkalemia
• Hypothyroidism^[1]

• Toxins:

• Grayanotoxin:“Mad” honey
• Natural cardiac glycosides such as oleandrin

• Bradycardia-related block
• Iatrogenic heart block

• Aortic valve surgery
• Septal alcohol ablation
• Percutaneous coronary intervention (PCI) to the left anterior descending artery
• Ablation of the slow or fast pathway of the AVN
• Ablation of accessory pathways near AVN

Third degree heart block is a life-threatening condition and must be treated as such irrespective of the causes. Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.

• Acute rheumatic fever
• Coronary ischemia
• Myocardial infarction ^[2]
• Systemic lupus erythematosus
• Valvular heart disease

Medications that Can Induce/Exacerbate Bradycardia or Conduction Disorders^[3]

Anti-hypertensive	Anti-arrhythmic	Psychoactive	Other
• Beta-Adrenergic Receptor Blockers • Clonidine • Methyldopa • Non-dihydropyridine calcium channel blockers • Reserpine	• Adenosine . • Amiodarone • Dronedarone • Flecainide • Procainamide • Propafenone • Quinidine • Sotalol	• Donepezil • Lithium • Opioid analgesics • Phenothiazine antiemetics and antipsychotics • Phenytoin • Selective Serotonin Reuptake Inhibitors • Tricyclic Antidepressants	• Anesthetic Drugs (propofol) • Cannabis • Digoxin • Ivabradine • Muscle relaxants (e.g. succinylcholine)

Cardiovascular	Acute rheumatic fever, amyloidosis, aspergillosis myocarditis, atrial septal defect, bacterial endocarditis, congenital heart block,[4] coronary ischemia, dilated cardiomyopathy, Ebstein’s anomaly, endocardial cushion defect, hypertension,[5] hypertrophic cardiomyopathy, hypertrophic cardiomyopathy alcohol septal ablation,[6] idiopathic heart block,[7][4] idiopathic hypereosinophilic syndrome, mitochondrial myopathy, myocardial infarction,[2] myocarditis, noncompaction cardiomyopathy, tetralogy of fallot, transposition of the great vessels, valvular heart disease, ventricular septal defect
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Arsenic trioxide, Beta-blocker, calcium channel blocker,[8] cardiac glycosides, cholinesterase inhibitor, digitalis, procainamide, quinidine
Ear Nose Throat	No underlying causes
Endocrine	Amyloidosis, hyperthyroidism,[9]
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Erb’s dystrophy, Kearns-Sayre syndrome, nail-patella syndrome
Hematologic	Thalassemia major[10]
Iatrogenic	Cardiac surgery
Infectious Disease	Aspergillosis myocarditis, bacterial endocarditis, Chagas disease, diphtheria, lyme disease,[11][12][13] varicella zoster
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	Enhanced vagal tone, idiopathic hypereosinophilic syndrome
Nutritional/Metabolic	Amyloidosis, hemochromatosis
Obstetric/Gynecologic	No underlying causes
Oncologic	Hodgkin disease, multiple myeloma, tumor[14][15]
Ophthalmologic	No underlying causes
Overdose/Toxicity	Alcohol intoxication[16][17]
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	Hyperkalemia
Rheumatology/Immunology/Allergy	Amyloidosis, ankylosing spondylitis, Becker muscular dystrophy, Churg-Strauss syndrome,[18] degenerative diseases, dermatomyositis, Erb’s dystrophy, idiopathic hypereosinophilic syndrome, muscular dystrophy[19] myotonic muscular dystrophy, peroneal muscular atrophy, Reiter’s syndrome, relapsing polychondritis,sarcoidosis, scleroderma,[20] neonatal lupus erythematosus
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Trauma[21][22]

Third degree AV block causes developed by WikiDoc.org

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Qasim Khurshid, M.B.B.S [3]

Third degree AV block must be differentiated from Mobitz type II, Junctional rhythm, and sinus bradycardia.

Third-degree AV block must be differentiated from Mobitz type II, Junctional rhythm, and sinus bradycardia, Paroxysmal supraventricular tachycardia. The following table summarizes the differential diagnosis of third-degree AV block.

Arrhythmia		Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrioventricular block[1]	First degree [2][3]	Regular		Normal	Prolonged PR interval (>200 msec)	Less than 0.12 seconds, consistent, and normal in morphology.	No treatment required	Prevalence: 650 to 1600 per 100,000 individuals in the united states.	Heart failure Coronary heart disease Cardiomyopathy Sarcoidosis Lyme disease Defenerative muscle disorders as Lev’s disease and Lenegre’s disease. Overly active vagus nerve.
	Second degree[4][5]	Regular irregular		Normal	Mobtiz I: Progressive PR prolongation Mobitz II: Normal PR interval	QRS is normal but dropped as the following: Mobitz I: QRS complex is dropped after a progressive lengthening of PR Mobitz II: QRS complex is dropped after a normal PR	Can be reversed by using a pacemaker.	Prevalence: 3 per 100,000 individuals in the united states.
	Third degree[6][7]	Regular		Normal but no relationship between P wave and the QRS. More P waves than the QRS complexes.	Varies	Normal QRS	Can be reversed by using a pacemaker.	The prevalence: 20 per 100,000 individuals worldwide.
Atrial Fibrillation (AFib)[8][9]		Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	2.7–6.1 million people in the United States have AFib 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter[10]		Regular or Irregular	75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common	Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1	Varies depending upon the magnitude of the block, but is short	Less than 0.12 seconds, consistent, and normal in morphology	Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)[11][12][13][14]		Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R’ in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)	Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction QRS alternans may be present	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal Atrial Tachycardia[15][16]		Irregular	Atrial rate is > 100 beats per minute	Varying morphology from at least three different foci Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia		Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)[17][18]		Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s Phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome[19][20]		Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	Less than 0.12 seconds	A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 – 300 per 100,000	Ebstein’s anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)[21][22][23]		Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia[24][25]		Regular	> 100 bpm (150-200 bpm common)	Absent	Absent Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation	Wide complex, QRS duration > 120 milliseconds	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] ; Aditya Ganti M.B.B.S. [3]

AV blocks are fairly common however, third-degree AV block is relatively rare. The incidence in the general population appears to be low, approximately 20 to 40 in 100,000 individuals in the United States. Given the etiology of the disease, the incidence among the apparently healthy and presumptively asymptomatic is even lower at approximately 1 in 100,000.

• The incidence of third degree block in the general population appears to be low, approximately 20 per 100,000 in USA.^[1][2][3]

• The prevalence of third degree AV block is approximately 40 per 100,000 worldwide.

• Third degree AV block is more commonly associated with advancing age.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Soroush Seifirad, M.D.[3] Aditya Ganti M.B.B.S. [4]

Common risk factors associated atioventricular block include older age, male sex, history of myocardial infarction, history of congestive heart disease, high systolic blood pressure, increased fasting blood glucose level.

• Common risk factors associated with atioventricular block include:^[1]

• Older age
• Male sex
• History of myocardial infarction
• History of congestive heart disease
• High systolic blood pressure
• Increased fasting blood glucose level

• Common risk factors associated with atrioventricular block after cardiac surgery include:^[2]

• Older age
• Atrial fibrillation
• Prior surgery
• Preoperative renal failure
• Active endocarditis

• Common risk factor associated with intraoperative bradycardia and hypotension in patients undergoing non-cardiac surgery include:^[3]

• Age (>60-65 years of age)
• Comorbidities
• Lower heart rates (<60 bpm) or blood pressure (<110/60 mm Hg) at baseline
• Use of concomitant drugs such as beta-blockers, renin-angiotensin system blockers

• Common risk factors associated with PPM implantation after valve surgery include:^[4]

• Preoperative RBBB
• Multivalve surgery , especially tricuspid valve
• Preoperative LBBB
• Preoperative PR interval >200 ms
• Prior valve surgery
• Age >70 years
• Reoperations
• Longer times of cross-clamp
• Absence of preoperative sinus rhythm

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Soroush Seifirad, M.D.[3] Aditya Ganti M.B.B.S. [4]

Ambulatory electrocardiographic monitoring is useful for finding intermittent atrioventricular block, LBBB and bifascicular block in asymptomatic patients. In patients with symptomatic atrioventricular block or bradycardia during sleep, screening about sleep apnea is recommended.

• Ambulatory electrocardiographic monitoring is useful for finding intermittent atrioventricular block, LBBB and bifascicular block in asymptomatic patients.
• In patients with symptomatic atrioventricular block or bradycardia during sleep, screening about sleep apnea is recommended.^[1]
• Screening for congenital complete heart block is recommended in pregnant women with Ro/SSA antibodies.^[2]
• Women with history of neonatal lupus, fetal echos are recommended weekly or every other week from week 18 to 28.
• It is unclear how often first degree heart block progresses to complete heart block, some cases my revert to normal sinus rhythm or complete heart block.

Recommendations for screening sleep apnea in patients with bradycardia or conduction disorder

(Class I, Level of Evidence B):

❑ Screening about sleep apnea syndrome is recommended In patients with documented or suspected bradycardia or conduction disorder during sleep ❑ Continuous airway pressure and weight loss is recommended in patients with bradycardia or conduction disorder during sleep and documented obstructive sleep apnea

(Class IIa, Level of Evidence B):

❑ In patients with previously PPM implantation for bradycardia or conduction disorder, screening about sleep apnea syndrome is reasonable

The above table adopted from 2018 AHA/ACC/HRS Guideline[3]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Raviteja Guddeti, M.B.B.S. [3] ; Aditya Ganti M.B.B.S. [4]

The majority of the patients with complete heart block do not recover spontaneously. Untreated complete heart block is associated with high morbidity and mortality. Patients with complete heart blocks are prone to decreased perfusion related to symptomatic bradycardia and decreased cardiac output. Common Complications of third-degree AV block include sudden cardiac death due to asystole, syncope, and musculoskeletal injuries secondary to fall after syncope. The prognosis of the third-degree heart block is most likely dependent on the patient‘s underlying disease burden and severity of the clinical presentation on arrival. Patients treated with permanent pacemakers have an excellent prognosis.

• Spontaneous recovery from third-degree heart block is very rare.
• The estimated overall mortality of non-paced patients with isolated AV block is 8%–16% in infants and 4%–8% in children and adults.^[1][2]
• If left untreated, third-degree heart block is associated with high mortality which appears to occur as a consequence of the complications of prematurity and bradycardia owing to the delayed initiation of pacing therapy.

• Patients with complete heart block are susceptible to hypotension related to decreased cardiac output and bradycardia.^[3]
• Patients with hemodynamic instability may be unable to protect their airway due to altered mental status leading to an aspiration that has high morbidity and mortality.
• Complications related to pace maker implantation include malposition or dislodgement of a pacemaker leads and cardiac perforation.

• Common complications of third degree AV block include:
  • Sudden cardiac death due to asystole
  • Syncope
  • Musculoskeletal injuries secondary to fall after syncope.
  • Cardiovascular collapse
  • Hypotension
  • Stokes-Adams syndrome
  • Ventricular tachycardia^[4][5]
  • Ventricular fibrillation
  • Worsening of heart failure
  • Worsening of angina
  • Death

• The prognosis of third degree heart block is most likely dependent on the patient‘s underlying disease burden and severity of the clinical presentation on arrival.^[6]
• Complete heart block is sometimes reversible in settings such as acute MI by restoring coronary perfusion and in conditions such as Lymes disease by treatment with antibiotics.^[7]
• Patients treated with permanent pacemaker have an excellent prognosis.
• Patients with complete heart block due to acute myocardial infarction are at a greater risk for sudden cardiac death.

Template:WikiDoc Sources