Second degree AV block

• Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Mohammed Salih, M.D. Cafer Zorkun, M.D., Ph.D. [3] Syed Musadiq Ali M.B.B.S.[4]

Second-degree AV block is a disease of the electrical conduction system of the heart. It refers to a conduction block between the atria and ventricles. The presence of second-degree AV block is diagnosed when one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction. Second-degree AV block was first described as a progressive delay between the atrial and ventricular contraction by Dr. Wenckebach in 1899. Dr. Mobitz then divided the second-degree AV block into two subtypes. In 1905, Dr. Hay figured out the pause following a wave was due to the failure of ventricular muscles to respond to a stimulus. There are 4 distinct types of second degree AV block. The distinction is made between them because type 1 second-degree heart block is considered a more benign entity than the other types. In mobitz type 1 second degree AV block there is evidence of gradually PR prolongation and dropped beat and grouped beating pattern. In mobitz type 2 AV block there is suddenly dopped beats without evidence of preceding PR prolongation. In atrioventricular block with the pattern of 2:1, there is every other beat without conducting down to the ventricle. In a high-grade AV block, there are two or more consecutive P waves without conducting down to the ventricle. It is important to determine the anatomic site of AV block. In Mobitz type 1 AV block, the site is usually within the AV node, but in Mobitz type II AV block the site is almost always below the AV node. In the presence of wide QRS complex and 2:1 AV conduction it is more likely that the site of AV block is intranodal or infranodal. In some cases, second-degree atrioventricular block must be differentiated from other causes of pauses such as non-conducted premature atrial contractions or atrial tachycardia with block.In Mobitz type I (Wenckebach) there is a progressive prolongation of the PR interval (AV conduction) until eventually an atrial impulse is completely blocked. When an atrial impulse is completely blocked there will be a P wave without a QRS complex. This pattern is often referred to as a “dropped beat.” Mobitz type I occurs because each depolarization results in the prolongation of the refractory period of the atrioventricular (AV) node. When an atrial impulse comes through the AV node during the relative refractory period, the impulse will be conducted more slowly, resulting in a prolongation of the PR interval. Eventually, an impulse comes when the AV node is in its absolute refractory period and will not be conducted. This will manifest on the ECG as a P wave that is not followed by a QRS complex. This non-conducted impulse allows time for the AV node to reset, and the cycle continues. This phenomenon leads to a grouped beating. In Mobitz type II there is a constant PR interval across the rhythm strip both before and after the non-conducted atrial beat. Each P wave is associated with a QRS complex until there is one atrial conduction or P wave that is not followed by a QRS. Mobitz type II is often a problem in the infra-nodal conduction system, and therefore, is associated with a widened QRS complex, bundle-branch block, or a fascicular block. When more than one P wave is not conducted this is no longer a Mobitz type II and is considered a high degree AV block.Common causes of second degree AV block include acute myocardial infarction, acute rheumatic fever, myocarditis, and severe hypothermia, endocarditis, digoxin toxicity, dilated cardiomyopathy, betablockers, calcium channel blockers and calcific aortic stenosis.Second degree AV block must be differentiated from different abnormal and irregular cardiac rhythms as atrial fibrillation with slow ventricular response, atrial flutter, atrial tachycardia with block.There have not been large population-based studies on the prevalence of Mobitz type I or II atrioventricular blocks. In the United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individuals. Men and women are affected equally by second-degree AV block. There is no racial predilection for second- degree AV block.Common risk factors associated with progression of 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 no established screening method for atrioventricular block.Second-degree AV nodal block commonly is seen in acute clinical settings including acute inferior wall myocardial infarction, digitalis intoxication, myocarditis, rheumatic fever), after cardiac surgery. Chronic AV nodal block is seen in the setting of ischemic heart disease, mesothelioma of the AV node, atrial septal defect, aortic valvular disease, amyloidosis, Reiter’s syndrome, mitral valve prolapse, in healthy populations, and in trained athletes. Mobitz II second degree Av block due to block inferior to the AV node (infra-Hisian structures) may progresses to complete heart block.Common complications associated with mobitz type 2 second degree AV block include progression to Complete heart block, syncope, dizziness, chest pain, and death.Prognosis is generally good in patients with chronic second-degree AV nodal block without organic heart disease.However, in patients with heart disease prognosis is poor and dependent on the severity of underlying heart disease. Electrocardiography (ECG) is employed to determine the type of second-degree atrioventricular (AV) block present. Follow-up ECGs and cardiac monitoring are appropriate.Common symptoms in patients with second degree atrioventricular block include light-headedness, dizziness, fainting, fatigue, heart failure symptoms , pre-syncope, and syncope. Mobitz type 1 second degree AV block (Wenckebach) is often asymptomatic and can be seen in active, healthy patients without known heart disease. It may occur during exercise causing exertional intolerance or dizziness, or syncope. In patients with intermittent atrioventricular block leading syncope, initial evaluation including resting ECG, physical exam, echocardiography may be normal and intermittent episodes of the atrioventricular block can be found with long-term monitoring. Symptoms in patients with an atrioventricular block that conducts in a 2:1 pattern include fatigue and dizziness particularly if it persists during exertion.Patients with second degree AV block are usually asymptomatic. However, patients with previous chronic cardiac condition may appear in a distress. In symptomatic patients, common physical examination findings include bradycardia, hypotension, and syncope. Physical examination in patients with heart failure may include lung crackles, jugular venous distension, and peripheral edema.Laboratory tests in patients with second degree AV block include checking the levels of serum electrolytes as calcium, magnesium and potassium. Myocarditis related lab tests as lyme titres, HIV tests, PCR for enteroviruses, and Chagas titres should be done also.There are no x-ray findings associated with second degree AV block.Echocardiography is useful for finding the underlying structural heart disease including left ventricular systolic dysfunction in patients with atrioventricular block, especially in the presence of LBBB pattern on resting ECG. Transesophageal echocardiography, computed tomography, cardiac magnetic resonance imaging (MRI), or nuclear imaging are other advanced imagings that can be used in suspicion of structural heart disease in patients presented with bradycardia or bundle branch block.Electrocardiographic monitoring can be used to identify the changes in QRS morphology such as alternating bundle branch block in the presence of atrioventricular conduction abnormalities. Treadmill exercise stress testing may be diagnostic to differentiate that 2:1 atrioventricular block is Mobitz type I or II in some cases or identify the presence of infranodal disease. EPS may be helpful to determine the anatomic site of block in mobitz type 2 atrioventricular block including atrioventricular node, intra-His, or infra-His. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. However, improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventricular block.Treatment for a Mobitz type I second-degree AV block (Wenckebach) is often not necessary. Occasionally Mobitz type 1 second degree AV blocks may result in bradycardia leading to hypotension and responds well to medications. If unresponsive to atropine or beta-adrenergic agonists, pacing (transcutaneous or transvenous) should be initiated for stabilization. If the patient is on any beta-blockers, calcium channel blockers or digoxin, the medications should be discontinued. All patients with Mobitz 1 block should be admitted and monitored. Treatment for a Mobitz type II involves initiating pacing as soon as this rhythm is identified. Mobitz type II second-degree AV blocks may imply structural damage to the AV conduction system. This rhythm often deteriorates into a complete heart block. These patients require transvenous pacing until a permanent pacemaker is placed. Unlike Mobitz type I second degree AV block (Wenckebach), Mobitz type II AV block often do not respond to atropine or beta-adrenergic agonists.Unlike asymptomatic patients with Mobitz type I second degree AV block who do not require any specific therapy, patients with Mobitz type II second degree AV block have a high likelihood of progressing to symptomatic Mobitz type II second degree AV block or complete heart block and should be considered candidates for pacemaker insertion on initial presentation. So, patients should be continuously monitored with transcutaneous pacing pads in place in the event of clinical deterioration. While stable patients are being monitored, reversible causes of Mobitz type II second degree AV block such as myocardial ischemia, increased vagal tone, hypothyroidism, hyperkalemia, and drugs that depress conduction, should be excluded in patients prior to implantation of a permanent pacemaker. If no reversible causes are present, definitive treatment of Mobitz type II second degree AV block involves permanent pacemaker placement in most patients. There is no benefit of implantation of permanent pacacemaker in patients with long-standing asymptomatic persistent or permanent atrial fibrillation with a low heart rate and appropriate chronotropic response.Effective measures for primary prevention of atrioventricular block include treatment of hypertension and maintenance of normal blood glucose levels. Atrioventricular (AV) block is a common reason for pacemaker implantation, and the number of pacemaker implantations is increasing. Atrioventricular block most commonly occurs in the absence of significant cardiac disease and is generally attributed to idiopathic fibrosis of the conduction system. By definition, the cause of that fibrosis remains unknown without primary prevention strategy.Secondary prevention of atrioventricular block may include correction of electrolytes disturbance, ischemia, and treating decompensated heart failure.

Second degree AV block was first described as a progressive delay between the atrial and ventricular contraction by Dr. Wenckebach in 1899. Dr. Mobitz then divided the second degree AV block into two subtypes. In 1905, Dr. Hay figured out the pause following a wave was due to the failure of ventricular muscles to respond to a stimulus.

There are 4 distinct types of second degree AV block. The distinction is made between them because type 1 second-degree heart block is considered a more benign entity than the other types. In mobitz type 1 second degree AV block there is evidence of gradually PR prolongation and dropped beat and grouped beating pattern. In mobitz type 2 AV block there is suddenly dopped beats without evidence of preceding PR prolongation. In atrioventricular block with the pattern of 2:1, there is every other beat without conducting down to the ventricle. In a high-grade AV block, there are two or more consecutive P waves without conducting down to the ventricle. It is important to determine the anatomic site of AV block. In Mobitz type 1 AV block, the site is usually within the AV node, but in Mobitz type II AV block the site is almost always below the AV node. In the presence of wide QRS complex and 2:1 AV conduction it is more likely that the site of AV block is intranodal or infranodal. In some cases, second-degree atrioventricular block must be differentiated from other causes of pauses such as non-conducted premature atrial contractions or atrial tachycardia with block.

In Mobitz type I (Wenckebach) there is a progressive prolongation of the PR interval (AV conduction) until eventually an atrial impulse is completely blocked. When an atrial impulse is completely blocked there will be a P wave without a QRS complex. This pattern is often referred to as a “dropped beat.” Mobitz type I occurs because each depolarization results in the prolongation of the refractory period of the atrioventricular (AV) node. When an atrial impulse comes through the AV node during the relative refractory period, the impulse will be conducted more slowly, resulting in a prolongation of the PR interval. Eventually, an impulse comes when the AV node is in its absolute refractory period and will not be conducted. This will manifest on the ECG as a P wave that is not followed by a QRS complex. This non-conducted impulse allows time for the AV node to reset, and the cycle continues. This phenomenon leads to a grouped beating. In Mobitz type II there is a constant PR interval across the rhythm strip both before and after the non-conducted atrial beat. Each P wave is associated with a QRS complex until there is one atrial conduction or P wave that is not followed by a QRS. Mobitz type II is often a problem in the infra-nodal conduction system, and therefore, is associated with a widened QRS complex, bundle-branch block, or a fascicular block. When more than one P wave is not conducted this is no longer a Mobitz type II and is considered a high degree AV block.

Common causes of second degree AV block include acute myocardial ischemia or infarction, infiltrative diseases, collagen vascular disease, surgical trauma, endocrine abnormalities, autonomic effects, neuromuscular disorders, and medications.

Second degree AV block must be differentiated from different abnormal and irregular cardiac rhythms as atrial fibrillation with slow ventricular response, atrial flutter, atrial tachycardia with block.

There have not been large population-based studies on the prevalence of Mobitz type I or II atrioventricular blocks. In the United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individuals. Men and women are affected equally by second-degree AV block. There is no racial predilection for second- degree AV block.

Common risk factors associated with progression of 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 no established screening method for atrioventricular block.

Second-degree AV nodal block commonly is seen in acute clinical settings including acute inferior wall myocardial infarction, digitalis intoxication, myocarditis, rheumatic fever, after cardiac surgery. Chronic AV nodal block is seen in the setting of ischemic heart disease, mesothelioma of the AV node, atrial septal defect, aortic valvular disease, amyloidosis, Reiter’s syndrome, mitral valve prolapse, in healthy populations, and in trained athletes. Mobitz II second degree Av block due to block inferior to the AV node (infra-Hisian structures) may progresses to complete heart block. Common complications associated with mobitz type 2 second degree AV block include progression to Complete heart block, syncope, dizziness, chest pain, and death. Prognosis is generally good in patients with chronic second-degree AV nodal block without organic heart disease.However, in patients with heart disease prognosis is poor and dependent on the severity of underlying heart disease.

Electrocardiography (ECG) is employed to determine the type of second-degree atrioventricular (AV) block present. Follow-up ECGs and cardiac monitoring are appropriate.

Common symptoms in patients with second degree atrioventricular block include light-headedness, dizziness, fainting, fatigue, heart failure symptoms , pre-syncope, and syncope. Mobitz type 1 second degree AV block (Wenckebach) is often asymptomatic and can be seen in active, healthy patients without known heart disease. It may occur during exercise causing exertional intolerance or dizziness, or syncope. In patients with intermittent atrioventricular block leading syncope, initial evaluation including resting ECG, physical exam, echocardiography may be normal and intermittent episodes of the atrioventricular block can be found with long-term monitoring. Symptoms in patients with an atrioventricular block that conducts in a 2:1 pattern include fatigue and dizziness particularly if it persists during exertion.

Patients with second degree AV block are usually asymptomatic. However, patients with previous chronic cardiac condition may appear in a distress. In symptomatic patients, common physical examination findings include bradycardia, hypotension, and syncope. Physical examination in patients with heart failure may include lung crackles, jugular venous distension, and peripheral edema.

Laboratory tests in patients with second degree AV block include checking the levels of serum electrolytes as calcium, magnesium and potassium. Myocarditis related lab tests as lyme titres, HIV tests, PCR for enteroviruses, and Chagas titres should be done also.

On ECG, Type I Second degree AV block is characterized by progressive prolongation of the PR interval and progressive shortening of RR interval until a P wave is blocked. The RR interval containing the blocked P wave is shorter than the sum of 2 PP intervals. The increase in the PR interval is longest in the second conducted beat after the pause. Type II second-degree AV block is characterized by a constant PR interval. Most patients with type II second-degree AV block have associated bundle branch block.

There are no x-ray findings associated with second degree AV block.

Echocardiography is useful for finding the underlying structural heart disease including left ventricular systolic dysfunction in patients with atrioventricular block, especially in the presence of LBBB pattern on resting ECG.

Transesophageal echocardiography, computed tomography, cardiac magnetic resonance imaging (MRI), or nuclear imaging are other advanced imagings that can be used in suspicion of structural heart disease in patients presented with bradycardia or bundle branch block.

Electrocardiographic monitoring can be used to identify the changes in QRS morphology such as alternating bundle branch block in the presence of atrioventricular conduction abnormalities. Treadmill exercise stress testing may be diagnostic to differentiate that 2:1 atrioventricular block is Mobitz type I or II in some cases or identify the presence of infranodal disease. EPS may be helpful to determine the anatomic site of block in mobitz type 2 atrioventricular block including atrioventricular node, intra-His, or infra-His. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. However, improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventricular block.

Treatment for a Mobitz type I second-degree AV block (Wenckebach) is often not necessary. Occasionally Mobitz type 1 second degree AV blocks may result in bradycardia leading to hypotension and responds well to medications. If unresponsive to atropine or beta-adrenergic agonists, pacing (transcutaneous or transvenous) should be initiated for stabilization. If the patient is on any beta-blockers, calcium channel blockers or digoxin, the medications should be discontinued. All patients with Mobitz 1 block should be admitted and monitored. Treatment for a Mobitz type II involves initiating pacing as soon as this rhythm is identified. Mobitz type II second-degree AV blocks may imply structural damage to the AV conduction system. This rhythm often deteriorates into a complete heart block. These patients require transvenous pacing until a permanent pacemaker is placed. Unlike Mobitz type I second degree AV block (Wenckebach), Mobitz type II AV block often do not respond to atropine or beta-adrenergic agonists.

Unlike asymptomatic patients with Mobitz type I second degree AV block who do not require any specific therapy, patients with Mobitz type II second degree AV block have a high likelihood of progressing to symptomatic Mobitz type II second degree AV block or complete heart block and should be considered candidates for pacemaker insertion on initial presentation. So, patients should be continuously monitored with transcutaneous pacing pads in place in the event of clinical deterioration. While stable patients are being monitored, reversible causes of Mobitz type II second degree AV block such as myocardial ischemia, increased vagal tone, hypothyroidism, hyperkalemia, and drugs that depress conduction, should be excluded in patients prior to implantation of a permanent pacemaker. If no reversible causes are present, definitive treatment of Mobitz type II second degree AV block involves permanent pacemaker placement in most patients. There is no benefit of implantation of permanent pacacemaker in patients with long-standing asymptomatic persistent or permanent atrial fibrillation with a low heart rate and appropriate chronotropic response.

Effective measures for primary prevention of atrioventricular block include treatment of hypertension and maintenance of normal blood glucose levels. Atrioventricular (AV) block is a common reason for pacemaker implantation, and the number of pacemaker implantations is increasing. Atrioventricular block most commonly occurs in the absence of significant cardiac disease and is generally attributed to idiopathic fibrosis of the conduction system. By definition, the cause of that fibrosis remains unknown without primary prevention strategy.

Secondary prevention of atrioventricular block may include correction of electrolytes disturbance, ischemia, and treating decompensated heart failure.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Second-degree AV block was first described as a progressive delay between the atrial and ventricular contraction by Dr. Wenckebach in 1899. Dr. Mobitz then divided the second-degree AV block into two subtypes. In 1905, Dr. Hay figured out the pause following a wave was due to the failure of ventricular muscles to respond to a stimulus.

• In 1899, Dr. Wenckebach described progressive delay between atrial and ventricular contraction and the eventual failure of a P wave to reach the ventricles.
• Dr. Mobitz then divided the second-degree AV block into two subtypes.
• In 1905, Dr. John Hay discovered the second degree of AV block.^[1]
• Dr. Hay was examining a patient who complains of slow pulse and dyspnea on exertion for more than 2 years. Dr. Hay noticed the heart rate dropping from 80 beats to 40 beats per minute.
• Dr. Hay noted the a waves and the arterial pulse to remain stable in the beginning. However, recording pulsation several times resulted in “a” waves that were not followed by c wave. The a-c jugular wave interval was used as a measurement of AV conduction.
• Dr. Hay figured out that the pause following a wave was due to the failure of ventricular muscles to respond to a stimulus.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Mohammed Salih, M.D., Cafer Zorkun, M.D., Ph.D. [3], Raviteja Guddeti, M.B.B.S. [4]

There are 4 distinct types of second degree AV block. The distinction is made between them because type 1 second-degree heart block is considered a more benign entity than the other types. In mobitz type 1 second degree AV block there is evidence of gradually PR prolongation and dropped beat and grouped beating pattern. In mobitz type 2 AV block there is suddenly dopped beats without evidence of preceding PR prolongation. In atrioventricular block with the pattern of 2:1, there is every other beat without conducting down to the ventricle. In a high-grade AV block, there are two or more consecutive P waves without conducting down to the ventricle. It is important to determine the anatomic site of AV block. In Mobitz type 1 AV block, the site is usually within the AV node, but in Mobitz type II AV block the site is almost always below the AV node. In the presence of wide QRS complex and 2:1 AV conduction it is more likely that the site of AV block is intranodal or infranodal. In some cases, second-degree atrioventricular block must be differentiated from other causes of pauses such as non-conducted premature atrial contractions or atrial tachycardia with block.

^[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

• Type 1 second degree AV block, also known as Mobitz I or Wenckebach periodicity which is a disease of the AV node^[2][3].

• Mobitz I heart block is characterized by progressive prolongation of the PR interval on the electrocardiogram (EKG) on consecutive beats followed by a blocked P wave (i.e. a ‘dropped’ QRS complex).
• After the dropped QRS complex, the PR interval resets and the cycle repeats.
• One of the baseline assumptions when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be regular.
• If the atrial rhythm is not regular, there could be alternative explanations as to why certain P waves do not conduct to the ventricles.
• This is a benign condition for which no specific treatment is needed.

• Type 2 second degree AV block, also known as Mobitz II is almost always a disease of the distal conduction system (His-Purkinje System).

• Although the terms intranodal block or infrahisian block are often applied to this disorder, they are not synonymous with it.

• Infranodal block and infra-Hisian block are terms that refer to the anatomic location of the block, whereas,
• Mobitz II refers to an electrocardiographic pattern associated with block at these levels^[4].

• Mobitz II heart block is characterized on a surface ECG by intermittently non-conducted P waves not preceded by PR prolongation and not followed by PR shortening.
• The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge.
• In this case, the person may experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death.
• The definitive treatment for this form of AV Block is an implanted pacemaker^[5][6].

Likely EKG findings that help differentiate Mobitz type I from type II in the presence of a 2:1 conduction ratio include:

• Very long PR interval (> 300 msec) or narrow QRS complex – indicates the block is at the level of AV node
• Administration of atropine enhances AV nodal conduction resulting in less frequent non conducted beats – this confirms the type I Mobitz
• Mobitz I is worsened by carotid sinus massage which slows AV nodal conduction, unlike Mobitz II.
• Carotid sinus massage paradoxically eliminates infranodal block by slowing the sinus rate^[7].

• Another type of classification used to classify second-degree AV block is 2:1 AV block and high-grade AV block.
• In 2:1 AV block every other atrial impulse is conducted down the ventricle.
• Higher grade AV blocks (eg., 3:1) unlike third degree AV block conduct few beats down the ventricle.

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

In Mobitz type I (Wenckebach) there is a progressive prolongation of the PR interval (AV conduction) until eventually an atrial impulse is completely blocked. When an atrial impulse is completely blocked there will be a P wave without a QRS complex. This pattern is often referred to as a “dropped beat.” Mobitz type I occurs because each depolarization results in the prolongation of the refractory period of the atrioventricular (AV) node. When an atrial impulse comes through the AV node during the relative refractory period, the impulse will be conducted more slowly, resulting in a prolongation of the PR interval. Eventually, an impulse comes when the AV node is in its absolute refractory period and will not be conducted. This will manifest on the ECG as a P wave that is not followed by a QRS complex. This non-conducted impulse allows time for the AV node to reset, and the cycle continues. This phenomenon leads to a grouped beating. In Mobitz type II there is a constant PR interval across the rhythm strip both before and after the non-conducted atrial beat. Each P wave is associated with a QRS complex until there is one atrial conduction or P wave that is not followed by a QRS. Mobitz type II is often a problem in the infra-nodal conduction system, and therefore, is associated with a widened QRS complex, bundle-branch block, or a fascicular block. When more than one P wave is not conducted this is no longer a Mobitz type II and is considered a high degree AV block.

• The classic site of block in Mobitz type I second degree block is the AV node (70%-75%).
• In the remaining 25%-30% of the cases the site is infra-nodal (His bundle,bundle branches or fascicles).
• Mobitz type I is again composed of two variations which show Wenckebach periodicity: classic and atypical.^[1][2][3][4]

• Classic variety usually occurs within the AV node.
• It can be observed in antegrade AV conduction and also in retrograde VA conduction across the AV node.
• There is a gradually increasing PR interval and eventually a dropped beat.
• There is also usually a gradually decreasing R-R interval.
• The PR interval is usually shortest in the initial beat and gradually increases ending in a dropped beat and the cycle repeats.
• If the interval between the last conducted beat and the first beat of the next cycle is very long, the first beat may be a junctional escape rhythm rather than a conducted beat. This classic Wenckebach phenomenon occurs usually with ratios of 3:2, 4:3 or 5:4. This results in grouped beating^[5][6].

• This variant of Wenckebach pattern is defined as long Wenckebach and is also called pseudo-Mobitz type II pattern as it simulates Mobitz type II block.
• In this pattern the conduction ratios usually exceed 6:5 or 7:6 and the last few beats of the cycle, before a dropped beat, show a relatively constant PR interval (maximum variation of 0.02 sec among them).
• The beats after the dropped beat again show gradually prolonging PR intervals.^[7][8]

• Conduction delay in Mobitz type II second degree block is almost always infra-nodal (His bundle [20%], bundle branches or fascicles).
• Usually the morphology of the QRS complex is wide, except when the site of block is the His bundle.
• In this variant of second-degree heart block the PR interval is constant with occasional dropped beats as compared to the gradually prolonging PR interval in Mobitz type I.
• Bifascicular or trifascicular block is seen in two thirds of the patients with Mobitz type II.^[9][10]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Mahmoud Sakr, M.D. [3]

Common causes of second degree AV block include acute myocardial ischemia or infarction, infiltrative diseases, collagen vascular disease, surgical trauma, endocrine abnormalities, autonomic effects, neuromuscular disorders, and medications.

Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated^[1].

• Acute myocardial infarction^[2][3]
• Acute rheumatic fever
• Bacterial endocarditis
• Myocarditis
• Severe hypothermia

• Acute rheumatic fever
• Bacterial endocarditis^[4]
• Calcific aortic stenosis
• Digoxin
• Dilated cardiomyopathy
• Diltiazem
• Enhanced vagal tone
• HCM
• Hypertension
• Iatrogenic after surgical correction of VSD, tetralogy of Fallot, and endocardial cushion defect
• Inferior ST elevation MI
• Massive calcification of the mitral annulus
• Myocarditis
• Normal variants^[5]
• Penetrating and non-penetrating trauma of the chest
• Sclerodegenerative disease of the electrical conduction system
• Verapamil
• β blockers

Cardiovascular	Acute myocardial infarction, acute rheumatic fever, ASD, dilated cardiomyopathy, Ebstein’s anomaly, hypersensitive carotid sinus syndrome, hypertension, hypertrophic cardiomyopathy, Lev’s disease, myocardial bridging, myocarditis, normal variants, post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement, tetralogy of Fallot, endocardial cushion defect, transposition of the great vessels, valvular heart disease, VSD
Chemical / poisoning	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Amiodarone, beta-blockers, digitalis, calcium channel blockers, cholinesterase inhibitors, disopyramide, dofetilide, dolasetron, donepezil, eslicarbazepine acetate, fesoterodine, fingolimod, flecainide, ibutilide, lacosamide, magnesium, paliperidone, pramipexole, procainamide, propafenone, propoxyphene, quinidine, sotalol, terodiline
Ear Nose Throat	No underlying causes
Endocrine	Hyperthyroidism, myxedema, thyrotoxic periodic paralysis
Environmental	Hypothermia
Gastroenterologic	Hemochromatosis
Genetic	Emery-Dreifuss muscular dystrophy, Fabry disease, glycogenosis type 2b, hereditary neuromuscular disease, Kearns-Sayre syndrome
Hematologic	Multiple myeloma Lymphoma[6]
Iatrogenic	Post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement
Infectious Disease	Acute rheumatic fever, Chagas disease, diphtheria, Lyme disease, myocarditis, neonatal lupus erythematosus, protozoal infection, sarcoidosis, SLE, tuberculosis
Musculoskeletal / Ortho	Ankylosing spondylitis, hereditary neuromuscular disease, Kearns-Sayre syndrome, mitochondrial genome inherited conditions, muscular dystrophy
Neurologic	Enhanced vagal tone
Nutritional / Metabolic	Fabry disease, glycogenosis type 2b
Obstetric/Gynecologic	No underlying causes
Oncologic	Multiple myeloma
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	Sarcoidosis
Renal / Electrolyte	Hyperkalemia, hypokalemia
Rheum / Immune / Allergy	Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, SLE
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	Amyloidosis, degenerative diseases

Second degree AV block (except in patients with a functioning artificial pacemaker)^[7][8] is considered an absolute contraindication to the use of the following medications:

• Adenosine
• Atenolol
• Betaxolol
• Bisoprolol
• Brimonidine tartrate and Timolol maleate
• Carteolol
• Diltiazem
• Disopyramide
• Dronedarone
• Flecainide
• Metoprolol
• Mexiletine
• Nadolol
• Nebivolol
• Penbutolol
• Pindolol
• Propranolol
• Sotalol
• Timolol
• Labetalol^[9]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Second degree AV block must be differentiated from different abnormal and irregular cardiac rhythms as atrial fibrillation with slow ventricular response, atrial flutter, atrial tachycardia with block.

• Second degree AV Block may be simulated by blocked PACs. Must be very careful to assure that the P to P intervals are constant.
• 2:1 conduction may simulate sinus bradycardia as the blocked P waves may fall on the preceding T waves.

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

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

In the United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individuals. Men and women are affected equally by second-degree AV block. There is no racial predilection for second degree AV block.

• In the United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individual.^[1]
• Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block.

• Men and women are affected equally by second-degree AV block.

There is no racial predilection for second-degree atrioventricular block.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Ahmed Elsaiey, MBBCH [3]

Common risk factors associated with progression of 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 progression of 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

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Raviteja Guddeti, M.B.B.S. [3]

Second-degree AV nodal block commonly is seen in acute clinical settings including acute inferior wall myocardial infarction, digitalis intoxication, myocarditis, rheumatic fever, after cardiac surgery. Chronic AV nodal block is seen in the setting of ischemic heart disease, mesothelioma of the AV node, atrial septal defect, aortic valvular disease, amyloidosis, Reiter’s syndrome, mitral valve prolapse, in healthy populations, and in trained athletes. Mobitz II second degree Av block due to block inferior to the AV node (infra-Hisian structures) may progresses to complete heart block. Common complications associated with mobitz type 2 second degree AV block include progression to complete heart block, syncope, dizziness, chest pain, and death. Prognosis is generally good in patients with chronic second-degree AV nodal block without organic heart disease.However, in patients with heart disease prognosis is poor and dependent on the severity of underlying heart disease.

• Second-degree AV nodal block commonly is seen in acute clinical settings including acute inferior wall myocardial infarction, digitalis intoxication, myocarditis, rheumatic fever, or after cardiac surgery.
• Chronic AV nodal block is seen in the setting of ischemic heart disease, mesothelioma of the AV node, atrial septal defect, aortic valvular disease, amyloidosis, Reiter’s syndrome, mitral valve prolapse, in healthy populations , and in trained athletes.^[1].
• Mobitz II second degree Av block due to block inferior to the AV node (infra-Hisian structures) may progresses to complete heart block.^[2].

• Common complications associated with second degree AV block include:

• Complete heart block^[3]
• Stokes-Adams syndrome
• Syncope^[4]
• Dizziness
• Chest pain
• Death

• Common complications associated with pacemaker implantation can involve:

• Pneumothorax
• Cardiac tamponade
• Death^[5].

  After implantation, patients require generator changes, which carry a particularly high risk of infection and resultant endocarditis.^[6].

Prognosis is generally good in patients with chronic second-degree AV nodal block without organic heart disease. However, in patients with organic heart disease prognosis is poor and dependent on the severity of underlying heart disease.^[7]

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