Atrioventricular Block


Article Author:
Anthony Kashou
Amandeep Goyal
Tran Nguyen


Article Editor:
Lovely Chhabra


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
11/15/2019 6:41:11 PM

Introduction

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. 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]

Etiology

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’s 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].

Epidemiology

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.

Pathophysiology

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] 

Toxicokinetics

 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 

Evaluation

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 “marked” 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 2 (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’t 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 “march through” 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

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.  

Complications

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.


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Atrioventricular Block - Questions

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In a progressive AV block one would expect:



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A 17-year-old male presents to the emergency department after a syncopal event. He denies any current chest pain, palpitations, or shortness of breath. He recalls a camping trip about one month ago with friends during which he got multiple tick bites. Otherwise, the patient states that he is healthy and very active. Vitals are stable and the physical exam is unremarkable. Further testing revealed Lyme carditis as the cause of syncope and a temporary pacemaker was placed. He improved with medical therapy. Which of the following did the patient's initial electrocardiogram in the emergency department likely show?



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A 65-year-old male presents to the emergency department with chest discomfort. He describes a squeezing, chest tightness at the substernal region that does not radiate. Initial vital signs and exam are unremarkable. However, an atrioventricular (AV) conduction delay is noted on a 12-lead electrocardiogram. Which of the following represents an AV conduction delay associated with a pattern of progressively prolonged PR intervals followed by a dropped beat?



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A 65-year-old female with a history of coronary artery disease and an inferior myocardial infarct presents to the clinic for her yearly follow-up. She has been asymptomatic and compliant with her medications. She denies any exertional symptoms, chest pain, shortness of breath, or leg swelling. She states that she has stopped smoking and is actively involved with an exercise group. A repeat 12-lead electrocardiogram was performed prior to the appointment, which showed a rhythm originating from the sinus node with delayed conduction through the atrioventricular (AV) node without any dropped beats. Which of the following was most likely seen on the patient's recent electrocardiogram?



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A 65-year-old male presents to the emergency department with acute shortness of breath. He is unresponsive and hemodynamically unstable. A portable chest x-ray reveals bilateral pleural effusions. Bedside echocardiogram reveals a flailed mitral leaflet with a left ventricular ejection fraction of 25%. His last echocardiogram performed 6 months prior showed an ejection fraction of 52%. Despite optimal medical therapy, the patient continues to deteriorate and requires immediate mitral valve surgery. On postoperative day 2, the patient is recovering well until he becomes unresponsive again. Repeat imaging demonstrated a normal mitral valve with a normal ejection fraction. A 12-lead electrocardiogram reveals regular but dissociated atrial and ventricular rhythms and the likely source for his current unresponsive state. Which of the following is most likely demonstrated on the electrocardiogram?

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Atrioventricular Block - References

References

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Saadi M,Tagliari AP,Danzmann LC,Bartholomay E,Kochi AN,Saadi EK, Update in Heart Rhythm Abnormalities and Indications for Pacemaker After Transcatheter Aortic Valve Implantation. Brazilian journal of cardiovascular surgery. 2018 May-Jun;     [PubMed]
Ali H,Furlanello F,Lupo P,Foresti S,De Ambroggi G,Epicoco G,Semprini L,Fundaliotis A,Cappato R, Clinical and electrocardiographic features of complete heart block after blunt cardiac injury: A systematic review of the literature. Heart rhythm. 2017 Oct;     [PubMed]
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Epstein AE,Dimarco JP,Ellenbogen KA,Estes NA 3rd,Freedman RA,Gettes LS,Gillinov AM,Gregoratos G,Hammill SC,Hayes DL,Hlatky MA,Newby LK,Page RL,Schoenfeld MH,Silka MJ,Stevenson LW,Sweeney MO, ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary. Heart rhythm. 2008 Jun;     [PubMed]
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LENEGRE J, ETIOLOGY AND PATHOLOGY OF BILATERAL BUNDLE BRANCH BLOCK IN RELATION TO COMPLETE HEART BLOCK. Progress in cardiovascular diseases. 1964 Mar     [PubMed]
LEV M, ANATOMIC BASIS FOR ATRIOVENTRICULAR BLOCK. The American journal of medicine. 1964 Nov     [PubMed]
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