What's Incomplete atrioventricular heart block (AV)?

What's Incomplete atrioventricular heart block (AV)?

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This is unclear for me and I can not understand differences between complete and incomplete atrioventricular heart block.also I want an electrocardiograph of incomplete atrioventricular heart block.

What's Incomplete atrioventricular heart block (AV)? - Biology

Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. This activity describes the causes, pathophysiology, and diagnosis of atrioventricular block and highlights the role of the interprofessional team in the management of these patients.

  • Recall the causes of AV block.
  • Summarize the ECG features of atrioventricular block.
  • List the treatment and management options available for atrioventicular block.
  • Explain the interprofessional team strategies for improving care coordination and communication regarding the diagnosis and management of patients with atrioventricular block.


Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart&rsquos conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. In general, there are three degrees of AV nodal blocks: first degree, second degree (Mobitz type 1 or 2), and third-degree.[1][2][3]


Higher degrees of AV block than those seen from increased vagal tone often suggest some underlying pathology. This is known as a pathophysiologic AV block. About half of such cases are a result of chronic idiopathic fibrosis and sclerosis of the conduction system as seen in Lenegre&rsquos disease[4] and Lev's disease [5]

Another common source is ischemic heart disease which is responsible for around 40 percent of cases of AV block [6]. 

AV block is also associated with cardiomyopathies, including hypertrophic obstructive cardiomyopathy and infiltrative conditions such as sarcoidosis and amyloidosis. Infectious causes such as Lyme disease, rheumatic fever, endocarditis, viruses as well as autoimmune disease such as systemic lupus erythematosus should also be explored [7][8][9][10].

Other potential triggers include cardiac surgery, medications, and inherited conditions [11].


There have not been large population-based studies on the prevalence of AV blocks. One study suggested that First-degree AVblock was more prevalent in African-American patients compared with Caucasian patients in all age groups except in the eighth decade of life[12]. However, at this time, there is no well-characterized large study about the correlation between different types of AV block with age, racial, or gender. AV block is sometimes seen in athletes and in patients with congenital heart disorders.


First degree AV block can originate from various locations within the conduction system. The levels of conduction delay include the atrium, AV node (most common in first-degree heart block), Bundle of His, bundle branches, fascicles, Purkinje system. Mobitz type I second degree AV block usually occurs within the AV block while Mobitz type II second degree AV block mainly originates from conduction system disease below the level of the AV node (in the bundle of His and in the bundle branches). In third-degree AV block, no atrial impulses could reach the ventricle- it can occur in the AV node or in the infranodal specialized conduction system. [13] 


 The following medications can affect different levels of conduction delay: 

1) Increased parasympathetic tone, digoxin (which upgrades vagotonic action), calcium channel blockers (which obstructs the inward calcium current responsible for depolarization) and beta-blockers can affect the AV node 

2) Medications such as procainamide, quinidine, and disopyramide can block sodium channels and delay conduction in the bundle of His

3) Similarly though rarely, medications such as procainamide, quinidine, and disopyramide can also delay infra-Hisian conduction system 

History and Physical

History taking for patients with concerns for AV block should include: 

  • History of heart disease, both congenital and acquired
  • Full list of medications and dosing. Particular drugs of interest include beta-blockers, calcium channel blockers, antiarrhythmic drugs, digoxin
  • Recent cardiac procedure 
  • Signs and symptoms associated with other systemic diseases associated with heart block (amyloidosis, sarcoidosis) 
  • Baseline exercise capacity 
  • Potential expose to tick bites

 The following symptoms should raise concerns: 

  • Dyspnea
  • Fatigue
  • Chest pain
  • Presyncope or syncope
  • Sudden cardiac arrest 


First degree. In first-degree AV block, the P waves always precede the QRS complexes, but there is a prolongation of the PR interval. That is, the PR interval will be greater than 200 milliseconds in duration without any dropped beats. There is a delay, without interruption, in conduction from the atrium to the ventricle. In other words, while the impulse is slowed, it is still able to get through to the ventricles. All atrial activation is eventually transmitted to the ventricles. The delay is typically due to a minor AV conduction defect occurring at or below the AV node. If the PR interval is more than 300 milliseconds, it is considered &ldquomarked&rdquo first-degree AV block and the P waves may be buried in the preceding T wave.

  • Causes. There are multiple causes of first-degree AV block, including simply being a normal variant. Other causes include inferior myocardial infarction (MI), increased vagal tone (e.g., athletes), status post-cardiac surgery, myocarditis, hyperkalemia, or even medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
  • Clinical significance. This is a benign entity that does not result in any hemodynamic instability. No specific treatment is required.

Second degree (incomplete). Second-degree or incomplete AV block occurs when there is intermittent atrial to ventricle conduction. That is, the P waves are sometimes related to the QRS complexes. It often occurs in a regular P:QRS pattern with ratios of 2:1. 3:2, 4:3, 5:4, and so forth. Second-degree AV blocks can be further classified into Mobitz type 1 (Wenckebach) or Mobitz type 2, which can be distinguished by examining the PR interval.

Second degree, Mobitz type 1 (Wenckebach). In second-degree Mobitz type 1 AV block, there is a progressive prolongation of the PR interval, which eventually culminates in a non-conducted P wave. It is often evident by clustering of QRS complexes in groups that are separated by non-conducted P waves. The greatest increase in PR interval prolongation is often between the first two beats of the cycle. While the PR interval continues to prolong with each beat of the cycle, the subsequent PR lengthening is progressively shorter. Even though the PR interval is progressively increasing in duration, the PP interval remains relatively unchanged. One way to confirm the presence of this is by noticing that the PR interval after the dropped beat is shorter than the PR interval that came before the dropped beat. In other words, the PR interval before the dropped beat is the longest of the cycle, and the PR interval after the dropped beat is the shortest as the cycle starts over.

  • Mechanism. This is usually a result of a reversible conduction block at the level of the AV node. In fact, studies have shown that the site of block is likely at the crest of the AV node, where the atrium and AV node meet. There is typically a functional suppression of AV conduction. The AV nodal cells seem to progressively fatigue until they fail to conduct an impulse to the ventricles and a dropped beat occurs.
  • Causes. There are multiple causes of second-degree Mobitz type 1 (Wenckebach) AV block, including reversible ischemia, myocarditis, increased vagal tone, status post-cardiac surgery, or even medications that slow AV nodal conduction (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
  • Clinical significance. Differentiating between second-degree Mobitz type 1 (Wenckebach) and Mobitz type 2 AV blocks is important as the management and treatment is different. Mobitz type 1 is often a benign rhythm. Most patients are asymptomatic, and there is tends to be minimal hemodynamic disturbance. The risk of Mobitz type 1 (Wenckebach) progressing to third-degree (complete) heart block is much lower than Mobitz type 2. Patients that are asymptomatic do not require treatment and can be monitored on an outpatient basis. Patients that are symptomatic typically respond to atropine and rarely require permanent cardiac pacing. Medication-induced impairment of AV conduction is often reversible after stopping the offending agent.

Second degree, Mobitz type 2. In second-degree Mobitz type 2 AV block, there are intermittent non-conducted P waves without warning. Unlike Mobitz type 1 (Wenckebach), there is no progressive prolongation of the PR interval instead, the PR interval remains constant, and the P waves occur at a constant rate with unchanged P-P intervals. Because the P waves continue to occur at normal intervals, the R-R interval surrounding the dropped beat is simply a multiple of the preceding R-R interval and remains unchanged.

  • Mechanism. Whereas in Mobitz type 1 there was a reversible block at the level of the AV node, in Mobitz type 2 the block occurs further along the electrical conduction system below the AV node. It can occur at the level of the His Bundle, both bundles branches, or the three fascicles (i.e., the left anterior fascicle, left posterior fascicle, and right bundle branch).
  • In this case, the cells don&rsquot progressively fatigue, but rather abruptly and unpredictably fail to conduct a supraventricular impulse. This is often the result of structural damage to the conduction system, such as from MI, fibrosis, or necrosis. Many patients have a pre-existing left bundle branch or bifascicular block, and the remaining fascicle intermittently fails to conduct causing the second degree AV block.
  • Because the defect occurs below the AV node and often times distal to the His Bundle, it produces wide, bizarre-appearing QRS complexes. In the remaining cases, the defect is located within the Bundle of His, resulting in the normal, narrow QRS complexes. There can be a fixed P:QRS relationship (e.g., 2:1, 3:1) or no pattern at all.
  • Causes. Common causes of second-degree Mobitz type 2 AV block include anterior MI, causing septal infarction with necrosis of the bundle branches. Other causes include idiopathic fibrosis of the conducting system, autoimmune (e.g., systemic sclerosis or systemic lupus erythematosus) or inflammatory (e.g., myocarditis, Lyme disease, or rheumatic fever) conditions, infiltrative myocardial disease (hemochromatosis, sarcoidosis, or amyloidosis), electrolyte imbalance (e.g., hyperkalemia), medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blockers, digitalis, adenosine, or amiodarone), or status post-cardiac surgery (e.g., mitral valve repair).
  • Clinical significance. Mobitz type 2 AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole. Because the onset of dropped beats can occur abruptly and unexpectedly, hemodynamic instability and the consequential syncope and potential sudden cardiac death can occur at any moment. Thus, patients require a permanent pacemaker. While Mobitz type 1 can improve with atropine, giving atropine in the setting of Mobitz type 2 can worsen the block and increase the risk of complete heart block or asystole.

Note in cases in which every other QRS complex is dropped, there are never two consecutive PR intervals. Therefore, there is not enough information to evaluate the PR interval to further classify it as either second-degree Mobitz type 1 (Wenckebach) or Mobitz type 2 AV block. The site of block is also indeterminate.

Second degree, high-grade. High-grade AV block is a form of second-degree (incomplete) heart block that can commonly be confused with third-degree (complete) heart block. It occurs when there are two or more consecutively blocked P waves. This conduction disturbance can be particularly dangerous as it can progress to complete heart block. The anatomic region involved is almost always below the AV node as in Mobitz type 2. The P:QRS is 3:1 or higher and the ventricular rate is typically very slow. What differentiates high-grade AV block from the third-degree (complete) heart block is that there remains some relationship between the P waves and QRS complexes. In other words, there is still some AV conduction taking place.

Third-degree (complete). In third-degree, or complete, heart block there is an absence of AV nodal conduction, and the P waves are never related to the QRS complexes. In other words, the supraventricular impulses generated do not conduct to the ventricles. Instead, if ventricular conduction occurs, it is maintained by a junctional or ventricular escape rhythm. There is a complete dissociation between the atria and ventricles. The atria and ventricles conduct independent of each other. The P waves (atrial activity) are said to &ldquomarch through&rdquo the QRS complexes at their regular, faster rate. The QRS complexes (ventricular activity) also occur at a regular, but slower rate. There are two independent rhythms occurring simultaneously. 

  • Mechanism. Third-degree heart block is the end result of progressively worsening second-degree AV block. It can be from Mobitz type 1 if the AV nodal cells fatigue to a point in which they no longer conduct impulses through to the ventricles or from Mobitz type 2, where there can be an abrupt and complete conduction failure throughout the His-Purkinje system. Because third-degree heart block can occur above or below the AV node, two different rhythms can take over. If it occurs above or at the crest of the AV node, a junctional rhythm will take over and drive the ventricles. The resulting QRS complexes will be narrow and occur at the intrinsic rate of the AV node (40 to 55 beats/minute). Whereas if the block occurs below the AV node, a ventricular pacemaker must take over. In such cases, the QRS complexes will be wide and at the intrinsic rate of the ventricular pacemaker (20 to 40 beats/minute).
  • Causes. Complete heart block is often the result of the same causes as Mobitz type 1 and Mobitz type 2. Other causes include inferior MI, degeneration of the conduction system, and AV-nodal blocking agents such as beta-blockers, non-dihydropyridine calcium channel blockers, adenosine, digitalis, and amiodarone.
  • Clinical significance. Patients with complete heart block are at great risk of developing asystole, ventricular tachycardia, and sudden cardiac death. Insertion of a permanent pacemaker is required.

AV dissociation. AV dissociation occurs when there is no relationship between the P waves and QRS complexes however, the QRS complexes occur at a faster rate than the P rate. Unlike AV block, in which failure of an intrinsically more rapid atrial rhythm to conduct antegrade and supersede a slower ventricular rhythm is abnormal, failure of a rapid ventricular rhythm to conduct retrograde and supersede a slower atrial rhythm does not necessarily imply damage to the conducting system. In fact, AV dissociation with more rapid ventricular rates is typically due to unusual ventricular irritability.

Treatment / Management

In general, patients that present with first-degree or second-degree Mobitz type 1 AV block do not require treatment. Any provoking medications can be removed, and patients can be monitored on an outpatient basis. However, patients with higher degrees of AV block (Mobitz type 2 AV block, 3rd degree) tend to have severe damage to the conduction system. They are at a much greater risk of progressing into asystole, ventricular tachycardia, or sudden cardiac death. Hence, they require urgent admission for cardiac monitoring, backup temporary cardiac pacing, and insertion of a permanent pacemaker.[14][15][16][17]

Differential Diagnosis

Once diagnosed, underlying causes should be evaluated that include ischemic workup, autoimmune diseases in young patients that can cause fibrosis of the conducting system, offending medications and electrolyte disturbances such as hyperkalemia. 


Prognosis depends on the various factors that include age and other chronic medical conditions such as diabetes mellitus, chronic kidney disease, underlying heart disease, and underlying types of AV block.  


Pacemaker infection is common in the elderly, especially with underlying medical conditions. Also, sometimes it can be challenging for pacemaker patients who need other studies like MRI for diagnosing other medical conditions such as stroke.

Deterrence and Patient Education

Patients with first-degree and asymptomatic Mobitz type 1 AV block usually can continue their usual activities but should be advised to avoid medications that can prolong PR interval Patients with Mobitz type 2 and third-degree AV block should discuss with their cardiologists about the need for pacemakers. All patients should be educated on alarming symptoms of hypoperfusion such as fatigue, lightheadedness, syncope, presyncope, or angina and seek timely medical treatment 

Enhancing Healthcare Team Outcomes

The management of heart block is best done with an interprofessional team because if the diagnosis is missed (esp higher degrees of heart block), the condition can have significant morbidity and mortality.

Patients with heart block may be encountered by the nurse practitioner, primary care provider, internist or the emergency department physician. Except for a first-degree heart block, the rest of the patients should be referred to a cardiologist for more definitive workup. Some of these patients may require a pacemaker which can be life-saving. Following treatment, the cardiology nurse should follow up on the patients to ensure that the heart rate has normalized and the patients have no symptoms.[18]

Anytime patients with a pacemaker undergo surgery, the cardiologist should be consulted first. In some cases, the pacemaker may have to be deactivated with a magnet to prevent interference from electrocautery. After surgery, the pacemaker has to be reprogrammed. Today, most centers have a pacemaker nurse who monitors these patients for complications. Only through a combined team approach can the morbidity of heart block be decreased.

What is heart block?

Heart block, AV bundle, or bundle branch block affects the electrical system of the heart. It is different from coronary artery disease, which affects the heart’s blood vessels.

In heart block, the heart beats irregularly and more slowly than usual, potentially stopping for up to 20 seconds at a time.

This is due to a delay, obstruction, or disruption along the pathway that electrical impulses travel through to make the heart beat. It can result from injury or damage to the heart muscle or heart valves.

Heart block itself does not usually need direct treatment, but related underlying health conditions do.

Share on Pinterest Heart block disrupts the electrical impulses in the heart.

A healthy human heart beats at about 60 to 100 times a minute. A heartbeat is one contraction of the heart muscles, which pushes blood around the body.

Normally, every heart muscle contraction is controlled by electrical signals that travel from the atria, or the upper chambers of the heart, to the ventricles, or the lower chambers.

A partial heart block happens when the electrical impulses are delayed or stopped, preventing the heart from beating regularly.

A complete heart block is when the electrical signals stop completely. The heartbeat will drop to about 40 times per minute.

Even changes to impulses that last only a fraction of a second can cause heart block.

Sometimes, a heart block makes it difficult for the heart to pump blood properly through the circulatory system, so the muscles and organs, including the brain, do not get enough oxygen to function properly.

Heart block typically causes lightheadedness, fainting, and palpitations. Depending on the severity of the heart block, this can be dangerous. For example, a third-degree heart block can worsen pre-existing conditions, such as heart failure. It can cause loss of consciousness and even sudden cardiac arrest. There can also be chest pain.

Coronary heart disease, on the other hand, occurs when a waxy substance, called plaque, builds up in the coronary arteries. It can cause chest pain, known as angina, or heart attack, also called myocardial infarction (MI).

There are three types of heart block.

First-degree heart block involves minor heartbeat disruptions, such as skipped beats. It is the least serious type of heart block, and it does not generally require treatment.

Second-degree heart block occurs when some electrical signals never reach the heart, causing dropped or skipped beats. The patient may feel dizzy, and they may need a pacemaker. The ventricle may not contract, as the atrial impulse did not reach the ventricles.

Third-degree or complete heart block is when electrical signals do not travel between the upper and lower chambers of the heart. It is more common in patients with heart disease. Without a pacemaker, there is a serious risk of heart attack.

In a healthy heart, electrical impulses that travel inside a heart muscle instruct it to contract, or beat. The impulses move along a pathway, from the upper heart chambers, through the atrioventricular (AV) node, to the lower chambers.

Along this pathway is a cluster of cardiac fibers. These are called the bundle of His, the “bundle branch block” or the “AV bundle.” This bundle divides into two branches, the right and left bundles. The bundles conduct the electrical impulses to the heart ventricles. Each ventricle has a branch.

Damage to one of the branch bundles can cause uncoordinated ventricular contractions, and an abnormal heart beat can result.

A blocked signal on the right side of the heart is not usually serious, but a block on the left side can indicate a higher risk of coronary artery disease, or some other heart problem.

If a person has a heart block, they may experience:

  • slow or irregular heartbeats, or palpitations
  • shortness of breath
  • lightheadedness and fainting
  • pain or discomfort in the chest
  • difficulty in doing exercise, due to the lack of blood being pumped around the body

People with a heart block may appear healthy, but they may have an underlying heart problem.

The most common cause of heart block is scarring of the heart tissue as people get older. Some people are born with heart block, but older people with a history of heart disease or smoking are most at risk.

The following conditions increase the risk:

  • cardiomyopathy
  • coronary thrombosis
  • myocarditis, or inflammation of the heart muscle , or inflammation of the heart valves
  • scar tissue in the heart, following surgery or a heart attack.

Acute, or sudden, heart block may also occur after a heart attack or a heart operation. It can also occur as a complication of Lyme disease.

A physician will discuss symptoms with the patient and listen to their heart. Depending on age and medical history, the doctor may suspect heart disease, and will refer the patient to a cardiologist, or a heart specialist.

There are a number of diagnostic tests for heart block.

An electrocardiogram (ECG) is the most common test. It records heart activity. Probes placed on the skin of the chest show the electric impulses through the heart as wave patterns.

Wave abnormalities may indicate heart block. An ECG can also reveal whether the left or right branch is affected.

Holter tape is a portable device which records all the patient’s heartbeats. The patient wears it under their clothing, and it records information about the electrical activity of the heart while the person carries out their normal activities for 1 to 2 days.

When symptoms occur, the patient presses a button. This creates a record of the heart rhythms that are present at that moment.

An echocardiogram is an ultrasound scan that allows the doctor to see the heart muscles and valves.

An electrophysiology test uses tiny electrical shocks to determine the cause of the abnormal rhythm, and where in the heart it is.

In a tilt-table test, the patient lies on a bed that changes position. This can provoke arrhythmia, or abnormal heartbeats.

There is no heart-block-specific treatment. Most people with bundle branch block have no symptoms, and they do not require treatment. However, any underlying causes, such as hypertension, will need treatment.

If a person with left bundle branch block has a heart attack, reperfusion therapy may be given to restore blood flow through blocked arteries.

This can be done by using an anti-clotting agent, such as streptokinase, to dissolve blood clots and increase blood flow to the heart. However, anti-clotting drugs increase the risk of bleeding.

An artificial pacemaker, a small, battery-operated device, may be implanted under the skin in a patient with a history of fainting. It is placed near the collarbone during a surgical procedure lasting 1 to 2 hours, under a local anesthetic.

Many pacemakers can be set to produce an electrical impulse only when needed. Some can sense if the heart stops beating, and produce an electrical impulse to restart it. The battery can last many years.

Pacemakers are not affected by cell phones, personal stereos, or household appliances, but a person with a pacemaker should not undergo a magnetic resonance imaging (MRI) scan.

People with a left side bundle branch block have a higher risk of complications than those with a right side block.

Possible complications include:

  • arrhythmia, or irregular heart beat
  • bradycardia, or low heart rate
  • insufficient contraction
  • cardiac arrest and circulatory failure
  • sudden cardiac death, which can be fatal within one hour of symptoms starting

Heart block is not always avoidable, but the risk of heart disease can be reduced by consuming a healthy diet, exercising regularly, minimizing alcohol consumption, and avoiding tobacco.

Facts about Atrioventricular Septal Defect (AVSD)

An atrioventricular septal defect (pronounced EY-tree-oh-ven-TRIC-u-lar SEP-tal DEE-fekt) or AVSD is a heart defect affecting the valves between the heart&rsquos upper and lower chambers and the walls between the chambers.

What is Atrioventricular Septal Defect?

An atrioventricular septal defect (AVSD) is a heart defect in which there are holes between the chambers of the right and left sides of the heart, and the valves that control the flow of blood between these chambers may not be formed correctly. This condition is also called atrioventricular canal (AV canal) defect or endocardial cushion defect. In AVSD, blood flows where it normally should not go. The blood may also have a lower than normal amount of oxygen, and extra blood can flow to the lungs. This extra blood being pumped into the lungs forces the heart and lungs to work hard and may lead to congestive heart failure.

There are two general types of AVSD that can occur, depending on which structures are not formed correctly:

  1. Complete AVSD
    A complete AVSD occurs when there is a large hole in the center of the heart which allows blood to flow between all four chambers of the heart. This hole occurs where the septa (walls) separating the two top chambers (atria) and two bottom chambers (ventricles) normally meet. There is also one common atrioventricular valve in the center of the heart instead of two separate valves &ndash the tricuspid valve on the right side of the heart and the mitral valve on the left side of the heart. This common valve often has leaflets (flaps) that may not be formed correctly or do not close tightly. A complete AVSD arises during pregnancy when the common valve fails to separate into the two distinct valves (tricuspid and mitral valves) and when the septa (walls) that split the upper and lower chambers of the heart do not grow all the way to meet in the center of the heart.
  2. Partial or Incomplete AVSD
    A partial or incomplete AVSD occurs when the heart has some, but not all of the defects of a complete AVSD. There is usually a hole in the atrial wall or in the ventricular wall near the center of the heart. A partial AVSD usually has both mitral and tricuspid valves, but one of the valves (usually mitral) may not close completely, allowing blood to leak backward from the left ventricle into the left atrium.


The Centers for Disease Control and Prevention (CDC) estimates that about 2,118 babies (1 in 1,859 babies) are born with AVSD every year in the United States. 1

Causes and Risk Factors

The causes of congenital heart defects, such as AVSD, among most babies are unknown. Some babies have heart defects because of changes in their genes or chromosomes. In particular, AVSD is common in babies with Down syndrome, a genetic condition that involves an extra chromosome 21 (also called trisomy 21). Congenital heart defects are also thought to be caused by the combination of genes and other risk factors, such as things the mother comes in contact with in her environment, what she eats or drinks, or certain medications she uses during pregnancy.


AVSD may be diagnosed during pregnancy or soon after the baby is born.

During Pregnancy

During pregnancy, there are screening tests (also called prenatal tests) to check for birth defects and other conditions. AVSD may be diagnosed during pregnancy with an ultrasound test (which creates pictures of the baby using sound waves), but whether or not the defect can be seen with the ultrasound test depends on the size or type (partial or complete) of the AVSD. The healthcare provider can request a fetal echocardiogram to confirm the diagnosis if AVSD is suspected. A fetal echocardiogram is an ultrasound of the baby&rsquos heart which shows more detail than the routine prenatal ultrasound test. The fetal echocardiogram can show problems with the structure of the heart and how well the heart is working.

After the Baby is Born

During a physical exam of an infant, a complete AVSD may be suspected. Using a stethoscope, a doctor will often hear a heart murmur (an abnormal &ldquowhooshing&rdquo sound caused by blood flowing through the abnormal hole). However, not all heart murmurs are present at birth. Babies with a complete AVSD usually do show signs of problems within the first few weeks after birth. When symptoms do occur, they may include

  • Breathing problems
  • Pounding heart
  • Weak pulse
  • Ashen or bluish skin color
  • Poor feeding, slow weight gain
  • Tiring easily
  • Swelling of the legs or belly

For partial AVSDs, if the holes between the chambers of the heart are not large, the signs and symptoms may not occur in the newborn or infancy periods. In these cases, people with a partial AVSD might not be diagnosed for years.

Symptoms which might indicate that a child&rsquos complete AVSD or partial AVSD is getting worse include

  • Arrhythmia, an abnormal heart rhythm. An arrhythmia can cause the heart to beat too fast, too slow, or erratically. When the heart does not beat properly, it can&rsquot pump blood effectively.
  • Congestive heart failure, when the heart cannot pump enough blood and oxygen to meet the needs of the body.
  • Pulmonary hypertension, a type of high blood pressure that affects the arteries in the lungs and the right side of the heart.

The healthcare provider can request one or more tests to confirm the diagnosis of AVSD. The most common test is an echocardiogram. This is an ultrasound of the heart that can show problems with the structure of the heart, like holes between the chambers of the right and left side of the heart, and any irregular blood flow. An electrocardiogram (EKG), which measures the electrical activity of the heart, chest x-rays, and other medical tests may also be used to make the diagnosis. Because many babies with Down syndrome have an AVSD, all infants with Down syndrome should have an echocardiogram to look for an AVSD or other heart defects.


All AVSDs, both partial and complete types, usually require surgery. During surgery, any holes in the chambers are closed using patches. If the mitral valve does not close completely, it is repaired or replaced. For a complete AVSD, the common valve is separated into two distinct valves &ndash one on the right side and one on the left side.

The age at which surgery is done depends on the child&rsquos health and the specific structure of the AVSD. If possible, surgery should be done before there is permanent damage to the lungs from too much blood being pumped to the lungs. Medication may be used to treat congestive heart failure, but it is only a short term measure until the infant is strong enough for surgery.

Infants who have surgical repairs for AVSD are not cured they might have lifelong complications. The most common of these complications is a leaky mitral valve. This is when the mitral valve does not close all the way so that it allows blood to flow backwards through the valve. A leaky mitral valve can cause the heart to work harder to get enough blood to the rest of the body a leaky mitral valve might have to be surgically repaired. A child or adult with an AVSD will need regular follow-up visits with a cardiologist (a heart doctor) to monitor his or her progress, avoid complications, and check for other health conditions that might develop as the child gets older. With proper treatment, most babies with AVSD grow up to lead healthy, productive lives.


  1. Mai CT, Isenburg JL, Canfield MA, et al. for the National Birth Defects Prevention Network. National population-based estimates for major birth defects, 2010-2014. Birth Defects Res 2019 1&ndash 16.
Atrioventricular Septal Defect (AVSD)

The images are in the public domain and thus free of any copyright restrictions. As a matter of courtesy we request that the content provider (Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities) be credited and notified in any public or private usage of this image.

Atrioventricular Septal Defect (AVSD)

The images are in the public domain and thus free of any copyright restrictions. As a matter of courtesy we request that the content provider (Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities) be credited and notified in any public or private usage of this image.

Evaluation and Treatment of AV Block and Intraventricular Conduction Disturbances

AV block, or atrioventricular block, is a major cause of significant bradyarrhythmias. To diagnose and manage AV block, it is important to have a basic understanding of the anatomy of the conduction system of the heart.

The AV node lies at the AV junctional area. At the distal end of the AV node, the penetrating portion is known as the His-bundle, which lies on the left side of the interventricular septum in most cases. The conduction fibers then continue in the left septum, and divide into the left bundle branch and right bundle branch.

Clinically, we think of the left bundle branch dividing into bifascicular subdivisions of anterosuperior and posteroinferior branches. However, anatomically there is much individual variability. The bundle branches end in the Purkinje fibers, which form a network over the surface of the endocardium of the ventricles.

Slowed conduction, or blocked conduction, can occur anywhere along the path of conduction fibers, and can generally be identified by EKG analysis. Infra-Hisian block is the most important to identify, since it is the cause of most cases of symptomatic complete heart block.

Acquired AV block is most commonly caused by idiopathic fibrosis, acute myocardial infarction, or drug effects. AV block can also be congenital. If AV block is symptomatic, and determined to be permanent, pacing is the only effective long-term therapy.

Type I second-degree AV block = Mobitz I block = Wenckebach block

Type II second-degree AV block = Mobitz II block

Third-degree AV block = complete heart block

Left anterior fascicular block = left anterior hemiblock

Left posterior fascicular block = left posterior hemiblock

II. Diagnostic Confirmation: Are you sure your patient has AV Block?

Clinical criteria for confirming significant AV clock

Complete heart block or advanced AV block seen on an EKG or ambulatory monitoring in the presence of symptoms.

Block below the His-bundle or an HV internal >100 ms found during an invasive electrophysiology study in a patient with intermittent symptoms.

Causes of temporary or reversible AV block have been ruled out.

A. History Part I: Pattern Recognition:

Hemodynamically important signs of AV block

New or worsening heart failure

Ventricular tachycardia (due to long Q–T)

Fatigue, or decrease in exercise tolerance

Patients with acquired complete heart block or high-grade AV block with two or more nonconducted P waves in a row, are usually symptomatic. Children with congenital complete heart block are generally asymptomatic, but tend to develop symptoms as adults. Concomitant structural heart disease, a wide QRS complex, or long Q–T interval increases the risk of symptoms in the congenital group.

Flectrocardiogram (EKG) shows a constant P–nckebach) block, bundle branch blocks or fascicular blocks rarely produce symptoms.

B. History Part 2: Prevalence:

First-degree AV block, with a P–R interval greater than 200 ms, is rarely found in young, healthy adults during activity. However, a longer P–R interval, and even Mobitz I (Wenckebach) block can be seen in young, well-conditioned individuals at rest and during sleep. The P–R interval decreases and the Wenckebach block disappears with increased activity, and is considered normal vagal influence on the AV node.

Acquired complete heart block is rarely seen in young adults without heart disease. The highest incidence of complete heart block is seen in the seventh decade, with a 60% male predominance. Congenital complete heart block has an incidence of one in 15,000 to 25,000 live births, with a 60% female predominance.

Left anterior fascicular block, or hemiblock, is the most commonly seen conduction abnormality of the intraventricular system with up to a 6% prevalence in the normal population. After left anterior hemiblock, the next most common abnormality of the intraventricular conduction system is right bundle branch block, followed by left bundle branch block and left posterior fascicular block, or hemiblock.

Causes of AV block

Antiarrhythmic drug effects

Idiopathic fibrosis of the conduction system

Valvular calcification or endocarditis

Trauma to the conduction system

Collagen vascular diseases

Infectious or inflammatory diseases

Tumors that infiltrate the heart

There are many causes of AV block. Acute myocardial infarction (MI) is associated with varying degrees of AV block, and is the most common cause of acquired AV block.

The blood supply to the AV node is from the AV nodal artery, a branch of the right coronary artery in 90% of hearts, with the remaining 10% arising from the left circumflex coronary artery. The His-bundle has a dual blood supply from branches of the anterior and posterior descending coronary arteries. The bundle branches also have a dual blood supply from the left and right coronary arteries.

Complete heart block can occur with either an anterior or inferior acute MI. The site of block in an inferior wall MI is usually at the level of the AV node, resulting in a junctional escape rhythm with a ventricular rate of 50 to 60 bpm and a narrow QRS complex. By contrast, complete heart block in the setting of an acute anterior MI is usually due to infarction of the bundle branches. A ventricular escape rhythm of 30 to 40 bpm is seen with a wide QRS complex.

Antiarrhythmic drug effects are a common cause of acquired AV block. Calcium channel blockers and other antiarrhythmic drugs, such as amiodarone and dronedarone, slow conduction in the AV node.

Through their effect on the autonomic nervous system, digoxin and beta-blocking agents act indirectly on the AV node. Drugs that have significant sodium channel blocking effect, such as flecainide, slow conduction in the His-Purkinje system. This can result in infranodal block. When AV block occurs due to antiarrhythmic drug therapy, it is usually in patients with pre-existing conduction abnormalities.

The most common cause of acquired conduction system disease is idiopathic fibrosis. In the elderly population, Lev’s disease results in sclerosis of the left side of the cardiac skeleton, and affects the branching His bundle. Lenegre’s disease is thought to be a genetic hereditary disorder that can affect middle-aged people.

This degenerative process involves the more distal portions of the bundle branches. Both Lev’s and Lenegre’s diseases cause right bundle branch block and left anterior hemiblock in people without other cardiac abnormalities, and can eventually progress to complete heart block.

Mitral or aortic valve disease can cause AV block. In cases of valvular calcification, infective endocarditis, or valve replacement surgery, the frequency of AV block is greater with aortic than with mitral valve involvement.

Trauma to the conduction system can occur as a result of cardiac surgery. AV block is most frequently associated with aortic valve replacement, and is rarely seen post coronary artery bypass grafting, in the absence of concomitant MI or prolonged ischemia. Transcatheter aortic valve replacement (TAVR) carries a risk of producing AV block. The need for post procedural permanent pacemaker placement is higher (37.6%) with the self-expandable valve, compared to the balloon-expandable valve (17.3%).

Surgical repair of congenital heart defects in the region of the conduction system, such as endocardial cushion malformations, ventricular septal defects, and tricuspid valve abnormalities, can lead to transient or persistent AV block.

AV block is a complication in 1% to 2% of radiofrequency catheter ablations used to cure AV nodal reentrant tachycardia, or accessory pathways near the AV node.

Infiltrative cardiomyopathies and collagen-vascular diseases can also cause AV block. A variety of viral bacterial and parasitic etiologies of myocarditis can result in varying degrees of AV block. In the case of Lyme disease, transient complete heart block is commonly seen in patients with cardiac involvement.

Hyperkalemia and hypermagnesemia are reversible causes of AV block. Transient AV block can be seen with carotid sinus hypersensitivity and vasovagal syncope.

Other causes of acquired AV block include Addison’s disease and tumors that infiltrate the heart. Patients with neuromuscular diseases, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy, and peroneal muscle atrophy, can develop any degree of AV block which can unpredictably progress to complete heart block.

Congenital complete AV block can result from abnormal embryonic development of the AV node. The defect usually occurs proximal to the His-bundle, resulting in a narrow QRS complex.

In 50% of cases of congenital complete heart block, no other structural cardiac abnormalities are present. The other 50% have concurrent congenital heart disease, including corrected transposition of the great vessels, ventricular septal defects, ostium primum atrial septal defects, and Ebstein’s anomaly of the tricuspid valve. Congenital complete heart block can also be a result of maternal systemic lupus erythematosis.

C. History Part 3: Competing diagnoses that can mimic AV Block.

Mobitz II, or Type II, second degree AV block, can be confused with a nonconducted premature atrial complex. In Mobitz II block, the electrocardiogram (EKG) shows a constant P–R interval, followed by a sudden failure of a P wave to be conducted to the ventricles.

The P to P intervals remain constant and the pause, including the blocked P wave, equals two P to P intervals. In the case of a nonconducted premature atrial complex, the nonconducted P wave will be premature.

Mobitz II can be difficult to differentiate from Mobitz I, or Wenckebach block, with only minimal P–R variation. Wenckebach block is usually due to block within the AV node, with a narrow QRS complex. On the other hand, Mobitz II is generally associated with a wide QRS complex, due to infranodal disease.

If the nonconducted P waves are obscured by the T wave of the preceding conducted beat, 2:1 AV block can go unrecognized (Figure 1).

Wenckebach block with a narrow QRS complex.

Fixed 2:1 AV block makes the diagnosis of Mobitz I (Wenckebach) versus Mobitz II block difficult to confirm by surface EKG alone. If a narrow QRS is present, and Wenckebach block has also been recently seen, block at the level of the AV node is probably present. On the other hand, if 2:1 AV block is seen with a wide QRS complex, infranodal block is the most likely diagnosis.

When complete heart block is seen, it is important to determine whether loss of conduction will be persistent, or whether the block is temporary. Reversible causes of complete heart block can be due to metabolic abnormalities, drug effects, Lyme disease, or vasovagal episodes. In these cases, the complete heart block resolves once the abnormality has been treated.

In true complete heart block, the sinus rate is faster than the ventricular rate. If AV dissociation is seen, but the ventricular rate is faster than the sinus rate, a competing AV junctional or idioventricular rhythm may be present. This is due to slowing or failure of the sinus node, allowing a faster subsidiary escape focus to take over from the AV junction or ventricle.

Left anterior or posterior fascicular blocks, or hemiblocks, can mimic or mask the EKG signs of a myocardial infarction, ischemia, or ventricular hypertrophy. It may be difficult to distinguish between left axis deviation caused by left anterior hemiblock, and left axis deviation due to other causes. Left anterior hemiblock can mimic left ventricular hypertrophy in leads I and AVL, while hiding signs of left ventricular hypertrophy in the left precordial leads.

The diagnosis of myocardial infarction is difficult in the setting of a bundle branch block. Left bundle branch block is especially problematic, including hemiblocks.

A left anterior hemiblock can produce an initial R wave in the inferior leads, concealing an inferior infarction. Likewise, a left anterior hemiblock can hide an anterior infarction by causing small R waves in the anterior precordial leads, if the heart is horizontal or the chest leads are positioned too low.

On the other hand, a left anterior hemiblock may show a small Q wave in the leads V2 and V3, leading to the assumption of a previous anterior myocardial infarction, or can produce Q waves in leads I and AVL, mimicking a lateral infarct. A left posterior hemiblock can hide the signs of an inferior myocardial infarction. This is particularly important since left posterior hemiblock can occur as a result of inferior wall ischemia.

D. Physical Examination Findings.

When AV block is present, the physical exam should focus on establishing the hemodynamic significance of the conduction abnormality. An evaluation of the patient’s mental status and level of consciousness is important.

The patient’s blood pressure, heart rate, respiratory rate, and overall appearance helps determine the urgency of treatment for the AV block. If the patient is febrile, this may suggest an infectious etiology of the conduction abnormality.

On the other hand, if the patient has an unrelated infection, this will need to be treated prior to implanting a permanent pacemaker. Physical signs of congestive heart failure should be evaluated, since their presence would prompt initiation of early therapy. One should listen for mitral or aortic regurgitant murmurs, since valvular disease can result in AV block. A target lesion resulting from a tick bite suggests Lyme disease as the cause of AV block.

E. What diagnostic tests should be performed?

EKG (interpretation)/Monitors/EPS

The surface EKG is our most important tool for the diagnosis of AV block and intraventricular conduction disturbances. First-degree AV block is seen as a P–R interval >200 ms and each P wave is followed by a QRS complex with a constant, prolonged interval (Figure 2).

Figure 2.

Mobitz II AV block with a narrow QRS complex in a patient with Lyme disease.

The conduction delay is usually within the AV node, but can be anywhere in the system. When first-degree AV block is associated with a narrow QRS complex, the delay is within the AV node a majority of the time. However, when bundle branch block is present, an intracardiac electrogram is needed to localize the site of the block.

Second-degree Mobitz I block is also known as Wenckebach block. The classic features on the surface EKG are progressive lengthening of the P–R interval until an atrial impulse fails to be conducted to the ventricles. The P–R interval immediately post block returns to its baseline interval, which is shorter than the last conducted P–R interval.

Wenckebach block is almost always within the AV node when a narrow QRS complex is present (Figure 3). In the setting of a bundle branch block, the Mobitz I block could be below the His-bundle, but is still more likely to be in the AV node. An intracardiac electrogram would be needed to accurately localize the level of block.

Figure 3.

Complete heart block with ventricular escape beats.

When Wenckebach block is in the AV node, progressive prolongation of the A-H interval is seen until an atrial deflection is not followed by a His-bundle or ventricular deflection. In the case of Wenckebach, due to block below the His-bundle, progressive prolongation of the H-V interval is followed by a His-bundle deflection without an associated ventricular depolarization.

Second-degree, or Mobitz II, AV block is seen on the surface EKG as constant P–R intervals, followed by a sudden failure of conduction of the P wave to the ventricles. The P–P intervals remain constant and the pause, including the blocked P wave, equals two P–P intervals.

Mobitz II block is usually associated with bundle branch block or bifascicular block. In most cases the block is within or below the His-bundle. It is rare to see Mobitz II with a narrow QRS interval (Figure 4). When present, the block is intra-Hisian.

Figure 4.

Bifascicular block with right-bundle branch block and left anterior fascicular block.

An intracardiac electrogram can help confirm the site of block as infranodal. The blocked cycle will show atrial and His-bundle deflections without a ventricular depolarization. The conducted beats usually show infranodal conduction system disease, with a prolonged H-V interval or a split His-bundle potential.

When fixed 2:1 AV block is seen on a surface EKG, it can represent either Mobitz I or Mobitz II block. If a narrow QRS complex is present, Mobitz I is suspected. If a wide QRS complex is seen, the block is likely infranodal. An intracardiac electrogram at the region of the His-bundle would be needed to make a definitive diagnosis.

High degree, or advanced AV block, is characterized by two or more nonconducted consecutive P waves on the surface EKG. When the QRS complexes of the adjacent conducted beats are narrow, the block is usually at the AV node.

When the block is at this level, atropine can improve the block and produce 1:1 AV conduction. If the adjacent beats are conducted with a bundle branch block, and no improvement in the advanced AV block is seen with atropine, this points toward a block in the His-Purkinje system.

When third-degree AV block, or complete AV block is seen on the surface EKG, the P waves are completely dissociated from the QRS complexes. The atrial rate is faster than the ventricular rate, and the atrial impulse is never conducted to the ventricles.

Different levels of block are possible with complete heart block, and the level of the block determines the QRS morphology along with the rate of the escape rhythm. When the block is within the AV node, the QRS complex is narrow with an escape rate of 40 to 60 bpm.

In the intracardiac tracings, the His-bundle potential consistently precedes each ventricular electrogram. The atrial electrograms are completely dissociated from the H-V complexes.

Block in the His-Purkinje system results in a wide QRS complex and a ventricular escape rate between 20 and 40 bpm (Figure 5). The corresponding intracardiac electrogram shows a His-bundle deflection after each atrial signal, but the ventricular electrogram is completely dissociated from these.

Figure 5.

Complete heart block with ventricular escape beats.

When conduction abnormalities are intermittent, they may require more prolonged monitoring to document the rhythm present with symptoms. Holter monitors or loop recorders may then be useful. When syncopal episodes are months apart, and conduction abnormalities are considered a possible etiology, an implantable loop recorder may help in the diagnosis.

Determining the site of AV block is important, since prognosis and treatment depends on whether AV block is at the level of the AV node or His-Purkinje system. As described above, the EKG is a valuable tool. However, other noninvasive diagnostic techniques can also be helpful, such as vagal maneuvers, exercise, or administration of atropine.

These methods take advantage of the differences in autonomic innervation of the AV node versus the His-Purkinje system. The AV node is well innervated by both the sympathetic and parasympathetic nervous systems, but the His-Purkinje system is minimally influenced by the autonomic nervous system.

Carotid sinus massage increases vagal tone, which worsens the block at the AV node. In contrast, carotid sinus massage improves infranodal block due to slowing of atrial impulses conducted through the AV node.

Exercise or atropine improves AV nodal conduction due to sympathetic stimulation. On the other hand, these maneuvers worsen infranodal block by increasing the rate of atrial impulses conducted through the AV node.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Laboratory studies should be aimed at revealing possible reversible causes of AV block. Hyperkalemia, usually associated with acute renal failure, should not be overlooked.

Once the potassium level is corrected, the AV block should resolve. If the patient is taking an antiarrhythmic drug while being found to have AV block, a drug level can be obtained.

However, laboratory testing is not available for every drug, and when it is an option, there may be a delay of days before the results are known. A digoxin level can be obtained, and the results can be available on the same day.

It should be noted that digoxin can cause AV block even when the level is not in the toxic range. Levels of flecainide or amiodarone can take over a week to be processed. In a patient with AV block where Lyme disease is a possibility, Lyme titers can be obtained.

Preliminary results will be available in 3 to 4 days. If other infectious processes are suspected, the appropriate cultures should be obtained, as well as a white blood count with differential.

In all patients where temporary or permanent pacing is being considered, coagulation studies consisting of a platelet count, protime, and INR (international normalized ratio) should be evaluated. Additionally, a hemoglobin and hematocrit should be obtained to check for the presence of anemia. Significant abnormalities would need to be corrected prior to an invasive procedure being planned.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

When a patient presents with AV block, a chest radiograph can provide information regarding possible pulmonary or cardiac problems. Pneumonia or pulmonary edema can be seen, as well as evidence of cardiac chamber enlargement. Also, a baseline chest radiograph is recommended prior to proceeding with placement of a permanent pacemaker.

A cardiac echo is useful in patients with AV block to look for possible structural abnormalities and to evaluate heart function. Evidence of ischemic heart disease or valvular disease can be seen.

If a cardiomyopathy is present with a low ejection fraction, a patient needing a permanent pacemaker may need a device with defibrillation capability. In a patient with a congenital heart defect, the echo is essential to knowing whether transvenous pacing leads can be successfully placed.

III. Management.

Determine if the heart block is symptomatic. Once the diagnosis of the type of heart block is made, it is important to assess how symptomatic the patient is.

Symptoms are important in determining whether permanent pacing is needed. Many times patients are asymptomatic at rest, but have significant symptoms with exertion. The risk of syncope with trauma should be assessed. The patient with hemodynamic compromise requires more immediate urgent therapy.

Determine if the heart block is reversible. Before implanting a permanent pacemaker, it is important to look for potential reversible causes of heart block.AV nodal blocking agents and antiarrhythmic drugs should be stopped, if possible, to see if the block improves.

Electrolytes and renal function should be evaluated. Heart block can occur in the setting of acute renal failure with hyperkalemia. Once the electrolytes are corrected and the patient is dialyzed, the heart block resolves.

Lyme disease should be suspected, especially in a young person with sudden onset of complete heart block, who has been in an endemic area. In these patients, the heart block may be impressive, but always resolves within several days to 2 weeks.

Varying degrees of AV block occur in the majority of patients who develop myocarditis from Lyme disease. If Lyme disease is suspected, the placement of a permanent pacemaker should be delayed until the laboratory data is known, which takes several days.

A. Immediate management.

Once it has been determined that the patient has symptomatic AV block that is not reversible, pacing should be established as soon as possible. If a permanent pacemaker can be placed within a reasonable period of time, this is ideal.

If the patient is too hemodynamically unstable to wait for the permanent implant, a temporary pacing wire should be placed. At times drug therapy is needed if temporary pacing is delayed or cannot be accomplished.

There is no effective long-term medical therapy for symptomatic AV block. However, drug therapy is sometimes useful as a short-term emergency measure, until either temporary or permanent pacing can be initiated.

Atropine 1 mg IV can temporarily improve symptomatic AV block. However, when a wide QRS escape rhythm is present, infranodal block should be suspected.

Atropine will either not be effective in this setting or will worsen the block. As an alternative to atropine, dopamine infusion can be used. Epinephrine or isoproterenol infusions can also be used when there is not a potential for ischemia. When using any of these drugs, external pacing should be available in case the drug worsens the AV block or is ineffective.

In the presence of symptomatic second- or third-degree AV block, placement of a temporary pacing wire is usually required if infranodal block is present.

Indications for Temporary Pacing

Symptomatic complete heart block (congenital or acquired)

Symptomatic second-degree AV block

Acute MI (regardless of symptoms)

Alternating bundle branch block

New bundle branch block with transient complete heart block

Complete heart block with long Q–T and resulting ventricular tachycardia (VT)

In the case of symptomatic congenital or acquired complete heart block, permanent pacing should be instituted as soon as feasible. Some patients with newly acquired complete heart block will have a long Q–T interval and a resulting ventricular tachycardia. Temporary pacing at a rate above 85 bpm is then required to shorten the Q–T interval and prevent the ventricular tachycardia.

Temporary pacing should also be used in patients with symptomatic heart block that is expected to be temporary, as in drug toxicity, electrolyte abnormalities, or Lyme disease.

AV block can occur in the setting of an acute MI. Patients with complete heart block, alternating bundle branch block, or new bundle branch block with transient complete heart block should be temporarily paced, even if they are asymptomatic.

Heart block associated with an inferior wall MI is usually proximal to the His-bundle and transient, whereas AV block secondary to an anterior wall MI is more distal to the His-bundle and often persists. Many times when the patient presents with an acute MI, they are taken to the cardiac catheterization lab. If heart block is noted while in the lab, a temporary pacing wire can be placed at that time.

Heart block can be temporarily or persistently seen post valve surgery, especially aortic valve replacement. If the patient will be at risk for heart block postoperatively, the surgeon generally places temporary epicardial pacing wires.

Risks of Temporary Pacing

In patients with asymptomatic complete heart block, with the exception of those post-MI or postoperative complete heart block, the risks of a temporary wire can be greater than the benefit. The hemodynamic significance of the complete heart block should be fully assessed.

Not only is blood pressure an issue, but whether the patient shows signs of altered mental status, hypoxia, congestive heart failure, ischemia, or poor renal perfusion. If none of these signs are present, the patient can usually tolerate ventricular rates down to the 30s overnight until the permanent pacemaker can be placed the next day.

External transcutaneous pacing can be used as a backup for temporary pacing if the patient’s condition were to suddenly worsen. Although external pacing can be uncomfortable in a nonsedated patient, it can be used briefly until a transvenous pacing wire is placed. The safest approach is to briefly test the external pacing system on the patient to confirm capture, before pacing is needed.

There are risks associated with a temporary pacing wire. Dislodgement is the most common complication, since they are not active fixation leads. This can result in loss of capture and possible asystole. However, at our institution, we sometimes place an active fixation lead under fluoroscopy and use it as a temporary lead.

Perforation of the lead through the thin right ventricular wall is another potential complication. The risk increases with stiffer leads and decreases with balloon-tipped leads. Perforation can be suspected due to loss of pacing, diaphragmatic stimulation, or a right bundle branch block pacing pattern. Pericardial tamponade is the most serious consequence from perforation, and requires emergent pericardiocentesis.

When the access used is the subclavian or jugular vein, a pneumothorax can occur, which would require placement of a chest tube. Accidental access into the adjacent artery while trying to obtain venous access, can lead to bleeding complications, especially if the patient is on anticoagulants.

Bacteremia is another potential risk, and can lead to delay of the placement of a permanent pacing system. Even if a temporary wire is placed emergently, every effort must be made to maintain sterility. The risk of infection is significant if the wire is left in place for greater than a week. In the case of femoral access, the wire should be in place no longer than 2 to 3 days.

When it is determined that a temporary pacing lead is required, it is important to not use the access site that would be preferred for permanent pacing leads. In a right-handed patient, permanent leads are usually placed via the left subclavian or axillary vein.

The right internal jugular vein provides the most direct approach for placement of the temporary pacing lead. It is best to avoid the subclavian veins if there is uncertainty as to which side will be used for permanent pacing, or if there is a history of subclavian occlusion in the past.

Femoral vein access generally requires fluoroscopy for lead placement. This access may be used when the temporary lead is placed at the time of cardiac catheterization. The patient must be immobilized while a femoral lead is in place.

In general, permanent pacing is indicated for AV block if symptoms are present. In some disease states, prophylactic pacing is recommended in asymptomatic patients due to the high risk of progression to complete heart block. These include patients post-MI, those with congenital heart disease, or with certain neuromuscular diseases.

Indication for Pacing in AV Block

Class I (general agreement in need for pacing)

Symptomatic complete heart block (CHB)

Asystole >3 seconds, or escape rhythm <40 BPM in awake, asymptomatic patient with CHB

Symptomatic second-degree AV block (regardless of site of block)

CHB with neuromuscular disease (with or without symptoms)

Alternating bundle branch block

Bifascicular block with intermittent CHB

Bifascicular or trifascicular block with Mobitz II AV block

Persistent second-degree AV block with bilateral bundle branch block, or CHB that is infranodal, after acute MI

Transient advanced infranodal AV block with bundle branch block

Congenital CHB with wide QRS, and complex ventricular ectopy or ventricular dysfunction

Advanced AV block with symptoms, ventricular dysfunction or low cardiac output in patients with congenital heart disease

Device & Mode Selection for AV Block

Dual chamber pacing (DDD) is recommended for patients predominantly in sinus rhythm. Single chamber ventricular pacing (VVI) is used in patients with persistent atrial fibrillation. A single lead dual chamber VDD device is an option for a young patient with congenital AV block, who has normal sinus nodal function. Patients with chronotropic incompetence should also have the rate responsive feature programmed on.

B. Physical Examination Tips to Guide Management.

Once pacing is instituted, symptoms of AV block should resolve quickly. Refer to Section II. A. for hemodynamically important signs of AV block, and section II. D. for physical exam findings. Refer to section III. E. for possible complications of therapy.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Immediately postpacemaker placement an EKG should be performed, with and without magnet application. This documents proper sensing and capture of the pacing leads. A chest radiograph should also be done to document proper position of the leads and generator. A pneumothorax or lead perforation through the myocardium can also be identified.

D. Long-term management.

Patients with permanent pacemakers require routine follow-up of their device (see schedule below). Most implanting centers see patients in the device clinic 2 weeks postimplant. This allows assessment of the wound for proper healing, signs of infection, or hematoma. The function of the leads is also evaluated for possible dislodgement or acute rise in pacing threshold.

At this visit, the patient can be given a transtelephonic monitoring unit, or arrangements can be made for remote monitoring. At the 3-month post-op visit, the pacing threshold should be at the chronic level. Many times the output can be reprogrammed at this time to a lower voltage to help prolong battery life.

Patients will then receive periodic monitoring at home, transtelephonically or via remote transmission, and be seen in device clinic only once or twice a year. Transtelephonic monitoring gives limited information regarding the function of the leads, and is mainly used to detect battery end of life by the magnet rate.

Remote monitoring units can give as much information as an interrogation at a clinic visit. Both remote and transtelephonic monitoring can also be used to check the rhythm of patients’ experiencing a sudden change in symptoms.

The frequency of monitoring increases when the battery life reaches the final 18-month period. The pacemaker may also need more frequent monitoring if the generator or one of the leads is under an advisory by the manufacturer or FDA, and could experience earlier than expected failure.

Follow-up care for heart block

Children with complete heart block will require lifelong care by a cardiologist. Those with the less severe forms of heart block should also continue to see a cardiologist regularly.

Children with pacemakers will need to visit an electrophysiologist, a doctor who specializes in problems with the electrical system of the heart, once or twice a year, and will also need routine monthly testing of their pacemaker by telephone. Children with pacemakers can lead physically active and healthy lives. However, some sports and activities may not be allowed.

As a group, children with complex congenital heart defects who have had open heart surgery as infants are at a higher risk for neurodevelopmental issues when compared to children without congenital heart defects. The Cardiac Center at CHOP created the Cardiac Kids Developmental Follow-up Program to provide evaluation, screening and clinical care for children with complex congenital heart disease who are at risk for neurodevelopmental problems.

In addition, our pediatric cardiologists follow patients until they are young adults. We will help with the transition to an adult cardiologist. The Philadelphia Adult Congenital Heart Center, a joint program of Children's Hospital of Philadelphia and the University of Pennsylvania, meets the unique needs of adults who were born with heart defects.

Complete AV block:
Atrioventricular dissociation, P waves (red arrows) are not followed by QRS complexes

  • PP and R-R intervals are regular.
  • P waves bear no constant relation to QRS complexes.
  • Atrial rate is greater than ventricular rate.
  • Variable PR intervals.
  • Morphology and rate of the ventricular rhythm depends on the origin of the escape pacemaker.

Escape Rhythm in Complete AV Block

Escape Rhythm, QRS morphology:

The escape pacemaker usually originates from a site just distal to the block.

If the AV block is within the AV junction, the escape rhythm has narrow QRS complexes unless bundle branch block coexists.

If the block is below the bifurcation of the His bundle, the QRS complexes are wide.

Therefore in the presence of complete AV block, narrow QRS complexes indicate an AV junctional location of the block, but wide QRS complexes may be the result of bilateral bundle branch block or AV junctional block with a bundle branch block 1 .

Escape Rhythm, Heart Rate:

The heart rate (ventricular rate) associated with third-degree AV Block usually depends on the origin of the escape pacemaker.

Complete AV block:
Atrioventricular dissociation. Escape rhythm with narrow QRS complexes and rate of 29 bpm.

The rate of AV junctional escape rhythm is usually 40 to 60 bpm. The rate of the ventricular pacemaker is usually less than 40 bpm 1 .

Healthcare providers will try to find the cause of your heart block. An EKG will be used to diagnose your heart block. An EKG is used to check the electrical activity in your heart. You may need to wear an EKG monitor for a few days while you do your daily activities. This monitor is also called a Holter monitor. You may need any of the following to find the cause of your heart block:

  • Blood tests may be done to check for infection, measure your electrolyte levels, or check for other causes of heart block.
  • A chest x-ray will show the size of your heart and check for fluid in your lungs.
  • A stress test helps healthcare providers see the changes that take place in your heart while it is under stress. Healthcare providers may place stress on your heart with exercise or medicine.

Second-degree heart block

In this condition, some signals from the atria don't reach the ventricles. This causes "dropped beats." On an electrocardiogram, the P wave isn't followed by the QRS wave, because the ventricles weren't activated. There are two types:

  • Type I second-degree heart block, or Molitz Type I, or Wenckebach's AV block. Electrical impulses are delayed more and more with each heartbeat until a beat is skipped. This condition is not too serious but sometimes causes dizziness and/or other symptoms.
  • Type II second-degree heart block, or Molitz Type II. This is less common than Type I but generally more serious. Because electrical impulses can't reach the ventricles, an abnormally slow heartbeat may result. In some cases a pacemaker is needed.

Mutations in the SCN5A and TRPM4 genes cause most cases of progressive familial heart block types IA and IB, respectively. The proteins produced from these genes are channels that allow positively charged atoms (cations) into and out of cells. Both channels are abundant in heart (cardiac) cells and play key roles in these cells' ability to generate and transmit electrical signals. These channels play a major role in signaling the start of each heartbeat, coordinating the contractions of the atria and ventricles, and maintaining a normal heart rhythm .

The SCN5A and TRPM4 gene mutations that cause progressive familial heart block alter the normal function of the channels. As a result of these channel alterations, cardiac cells have difficulty producing and transmitting the electrical signals that are necessary to coordinate normal heartbeats, leading to heart block. Death of these impaired cardiac cells over time can lead to fibrosis, worsening the heart block.

Mutations in other genes, some of which are unknown, account for the remaining cases of progressive familial heart block.

Learn more about the genes associated with Progressive familial heart block

Additional Information from NCBI Gene:

Watch the video: How to Interpret AV Heart Blocks Ekg Heart Rhythms. 1st degree, 2nd degree, 3rd degree difference (June 2022).