Chapter 275 - The Bradyarrhythmias: Disorders of the Atrioventricular Node

Question 1

Name the different characteristics between the tissue present in atrioventricular (AV) node from those of the adjacent cells.

Answer 1

“Cells located in the AV node sit at a relatively higher resting membrane potencial than surrounding atrial and ventricular myocytes, exhibit spontaneous depolarization during phase 4 of the action potential, and have slower phase 0 depolarization (mediated by calcium influx in nodal tissue) than that seen in ventricular tissue (mediated by sodium influx).”

Question 2

Which group of diseases might lead to bradycardia? Which symptoms might one find in those?

Answer 2

“Bradycardia may occur when conduction across the AV node is compromised, resulting in ineffective ventricular rates, with the possibility of attendant symptoms, including fatigue, syncope, and (if subsidiary pacemaker activity is insufficient) even death.”

Question 3

Sinoatrial conduction and atrial systole might occur at a normal or even accelerated rates if there is abnormal atrioventricular conduction.
True or False?

Answer 3

True.

Question 4

How frequent is atrioventricular (AV) block in the young adult? How do you explain the pathophysiology of this situation?

Answer 4

“Transient AV conduction block is common in the young and is most likely the result of high vagal tone found in up to 10% of young adults.”

Question 5

Acquired and persistent atrioventricular (AV) is a rare entity in healthy adult populations.
True or False?

Answer 5

True.
“Acquired and persistent failure of AV conduction is decidedly rare in healthy adult populations, with an estimated incidence of 200 per million population per year.”

Question 6

Which population might have a higher incidence of persistent atrioventricular (AV) block?

Answer 6

“In the setting of myocardial ischemia, aging and fibrosis, or cardiac infiltrative diseases, however, persistent AV block is much more common.”

Question 7

What is the main therapy for atrioventricular (AV) dysfunction? How frequently is this therapy used in the United States in comparison to Europe?

Answer 7

“As with symptomatic bradycardia arising from sinoatrial node dysfunction, permanent pacing is the only reliable therapy for symptoms arising from AV conduction block. Approximately 50% of the 150 000 permanent pacemakers implanted in the United States and 70-80% of those in Europe are implanted for disorders of AV conduction.”

Question 8

The atrioventricular (AV) node is a subendocardium structure as well as the sinoatrial (SA) node.
True or False?

Answer 8

True: the AV node is located in the subendocardium.
False: the SA node is epicardial in location

Question 9

Which bundles converge into the atrioventricular node (AV)?

Answer 9

“Superior, medial, and posterior transitional atrionodal bundles converge on the compact AV node.”

Question 10

What are the dimensions and location of the atrioventricular node (AV)?

Answer 10

“The compact AV node (~1 x 3 x 5 mm) is situated at the apex of the triangle of Koch, which is defined by the coronary sinus ostium posteriorly, the septal tricuspid valve annulus anteriorly, and the tendon of Todaro superiorly.”

Question 11

How does one explain the correlation between some valvular diseases and atrioventricular node (AV) dysfunction?

Answer 11

“The compact AV node continus as the penetrating AV bundle where it immediately transverses the central fibrous body and is in close proximity to the aortic, mitral, and tricuspid valve annuli; thus it is subject to injury in the setting of valvular heart disease or its surgical treatment.”

Question 12

What is the moderator band?

Answer 12

“The right bundle branch (RBB) emerges from the distal AV bundle in a band that transverses the right ventricle (moderator band).”

Question 13

How come the atrioventricular node (AV) has a double vascularization system, as well as the bundle branches?

Answer 13

“The blood supply to the penetrating AV bundle is from the AV nodal artery and first septal perforator of the left anterior descending coronary artery. The bundle branches also have a dual blood supply from the septal perforators of the left anterior descending coronary artery and branches of the posterior descending coronary artery.”

Question 14

Which of the following components is extensively innervated by the sympathetic or parassympathetic systems: AV node or bundle branches?

Answer 14

AV node.

Question 15

When does decremental conduction occur in the transitioning AV node zone?

Answer 15

“Atrionodal transitional connections may exhibit decremental conduction, defined as slowing of conduction with increasingly rapid rates of stimulation.”

Question 16

Fast and slow pathways are anatomically disctinct from the AV node complex.
True or False?

Answer 16

Unknown.
“ Fast and slow AV nodal pathways have been described, but it is controversial wheter these two types of pathway are anatomically disctint or represent functional heterogeneities in different regions of the AV nodal complex.”

Question 17

What is the normal behaviour of the myocites present in the AV node?

Answer 17

“Myocytes that constitute the compact node are depolarized (resting membrane potencial ~-60mV) and exhibit action potentials with low amplitudes, slow upstrokes of phase 0 (less than 10V/s), and phase 4 diastolic depolarization; high-input resistance; and relative insensitivity to external [K+].”

Question 18

Explain the channels present in the myocites of the AV node and their functionality.

Answer 18

“The action potencial phenotype is explained by the complement of ionic urents expressed. AV nodal cells lack a robust inward rectifier potassium current (IK1) and fast sodium current (INa); L-type calcium current (ICa-L) is responsible for phase 0; and phase 4 depolarization reflects the compoise activity of the depolarizing currents - funny current (If), ICa-L, T-type calcium current (ICa-T), and sodium calcium exchanger current (INCX) - and the repolarizing currents - delayed rectifier (IKr) and acetylcholine-gated (IKaAch) potassium currents. Electrical coupling between cells in the AV node is tenuous due to the relatively sparse expression of gap junction channels (predominantly connexin-40 and increased extracellular volume.”

Question 19

Which molecule is predominante in gap junctions?

Answer 19

Connexin-40.

Question 20

Name the causes for AV node dysfunction.

Answer 20

• Autonomic: carotid sinus hypersensitivity, vasovagal;
• Metabolic/Endocrine: hyperkalemia, hypermagnesemia, hypothyroidism, adrenal insufficiency;
• Drug-related: beta blockers, calcium channels blockers, digitalis, adenosine, antiarrhythmics (Class I and III), lithium;
• Infectious: endocarditis, Lyme disease, Chagas’ disease, Syphilis, Tuberculosis, Diphteria, Toxoplasmosis;
• Heritable/Congenital: congenital heart disease, maternal SLE, Kerans-Sayre syndrome, Myotonic dystrophy, fascioscapulohumeral MD, Emery-Dreifuss MD, progressive familiar heart block;
• Inflammatory: SLE, MCTD (Mixed connective tissue disease), Rheumatoid arthritis, escleroderma;
• Infiltrative: amyloidosis, sarcoidosis, hemochromatosis;
• Neoplastic/Traumatic: Lymphoma, Mesothelioma, Melanoma, Radiation, Catheter ablation;
• Degenerative: Lev’s disease, Lenègre’s disease
• Coronary Artery Disease: Acute Myocardial Infarction.

Question 21

There are different ways of classifying atrioventricular disease. Regarding functional and structural diseases, name the functional ones and the correlation of these to reversibility.

Answer 21

“Those that are functional (autonomic, metabolic/endocrine, and drug-related) tend to be reversible. Most other etiologies produce structural changes, typically fibrosis in segments of the AV conduction axis that are generally permanent. Most other etiologis produce structural changes, typically fibrosis, in segments of the AV conduction axis that are generally permanent.”

Question 22

What is the correlation between AV node dysfunction and vasovagal tone?

Answer 22

The increased vasovagal tone might lead to AV node block. This might occur during sleep, with carotid sinus hypersensitivy, vasovagal syncope, as well as during cough and micturition syncope.

Question 23

How frequent is the cardiac involvement and AV node block in Lyme disease? Considering the carditis as a structural disease, is this block reversible?

Answer 23

“Lyme disease may involve the heart in up to 50% of cases; 10% of patients with Lyme carditis develop AV conduction block, which is generally reversible but may require temporary pacing support.”

Question 24

Aging is usually associated with AV node dysfunction. How come?

Answer 24

“Idiopathic progressive fibrosis of the conduction system is one of the more common and degenerative causes of AV conduction block. Aging is associated with degenerative changes in the summit of the ventricular septum, central fibrous body, and aortic and mitral annuli and has been described as “sclerosis of the left cardiac skeleton.”

Question 25

Degenerative AV node disease is common in aging. Which causes might be responsible for accelerated causes?

Answer 25

Risk factors (atherosclerosis, hypertension and diabetes mellitus) and heritable/congenital causes (progressive familiar heart block).

Question 26

Name the mutations identified so far as cause of progressive familiar heart block.

Answer 26

SCN5A (cardiac sodium channel gene)

Other loci in chromosomes 1 and 19.

Question 27

Give examples of heritable neuromuscular disorders associated with AV node block.

Answer 27

“AV conduction block has been associated with heritable neuromuscular diseases, including the nucleotide repeat disease myotonic dystrophy, the mitochondrial myopathy Kearns-Sayre syndrome, and several of the monogenic muscular dystrophies.”

Question 28

Which congenital heart diseases might have an association with AV block?

Answer 28

“Congenital AV block may be observed in complex congenital cardiac anomalies, such as transposition of the great arteries, ostium primum atrial septa defects (ASDs), ventricular septal defects (VSDs), endocardial cushion defects, and some single-ventricle defects. Congenital AV block in the setting of a structurally normal heart has been seen in children born to mothers with SLE.”

Question 29

Which type of intervention has a greater risk of AV node block?

Answer 29

Surgical repair of transposition of the great vessels.

Question 30

The AV block produce by coronary artery disease is always irreversible.
True or False?

Answer 30

False.

Question 31

Which coronary is mostly involved as a cause of AV node block?

Answer 31

Right coronary artery or one of its branches.

Question 32

In the event of second- or third-degree AV block associated with acute myocardial infarction, which cardiac wall is usually involved in the process? Would you say that this pattern has a worse prognosis?

Answer 32

“Second-degree block and higher-grade AV block tends to occur more often in inferior than in anterior acute MI; however, the level of block in inferior MI tends to be in the AV node with more stable, narrow escape rythms.”

Question 33

How frequent is transient AV block in acute myocardial infarction?

Answer 33

10-25%

Question 34

Which degree of AV block would you expect to find in acute myocardial infarction?

Answer 34

Most commonly first- or second-degree AV block, altough complete block might also occur.

Question 35

Describe the electrical blockage that might occur in anterior myocardial infarction.

Answer 35

“In contrast [to inferior myocardial infarction], acute anterior MI is associated with block in the distal AV node complex, His bundle, or bundle branches and results in wide complex, unstable escape rhythms and a worse prognosis with high mortality rates.”

Question 36

Where would you expect to find the slowing of conduction in first-degree AV block?

Answer 36

“The site of delay is typically in the AV node but may be in the atria, bundle of His, or His-Purkinje system.”

Question 37

Is there any correlation betweem the QRS duration and the site of AV node block?

Answer 37

Yes.
“A wide QRS is suggestive of delay in the distal conduction system, whereas a narrow QRS suggests delay in the AV node proper or, less commonly, in the bundle of His.”

Question 38

How do you characterize a Mobitz type I blockage?

Answer 38

“In second-degree AV block there is an intermittent failure of electrical impulse conduction from atrium to ventricle. Second-degree AV block is subclassified as Mobitz type I (Wenckebach) or Mobitz type II. The periodic failure of conduction in Mobitz type I block is characterized by a progressively lenghtening PR interval, shortening of the RR interval, and a pause that is less than two times the immediately preceding RR interval on the electrocardiogram (ECG). The ECG complex after the pause exhibits a shorter Pr interval than that immediately preeceding the pause. This ECG pattern most often arises because of decremental conduction of electrical impulses in the AV node.”

Question 39

Besides the ECG findings, which other findings might be helpful in characterizing a second-degree block as Mobitz I or Mobitz II (and especially if the blockage is 2:1)?

Answer 39

“Type II second-degree AV block typically occurs in the distal or infra-His conduction system, is often associated with intraventricular conduction delays (e.g., bundle branch block), and is more likely to proceed to higher grades of AV block than is type I second-degree AV block. Second-degree AV block (particularly type II) may be associated with a series of nonconducted P waves, referred to as paroxysmal AV block, and implies significant conduction system disease and is an indication for permanent pacing”

Question 40

A patient suffers from high-grade AV block. Which electrocardiographic finding might help you determine the level of the block?

Answer 40

“the duration of the QRS complex can be helpful in determing the level of the block. In the absence of a preexisting bundle branch block, a wide QRS escape rhythm implies a block in the distal His or bundle branches; in contrast, a narrow QRs rhythm implies a block in the AV node or proximal His and an escape rhythm originating in the AV junction.”

Question 41

What is the difference in rhytm and stability regarding the rhythms originating below the AV node?

Answer 41

“Narrow QRS escape rhythms are typically faster and more stable than wide QRS escape rhythms and originate more proximally in the AV conduction system.”

Question 42

Name all the maneuvers that help one to distinguish the level of block regarding the possibility of AV node block. How should one interpret the potential findings in those maneuvers?

Answer 42

“Vagal maneuvers, carotid sinus massage, exercise, and administration of drugs such as atropine and isoproterenol may be diagnostically informative. Owing to the differences in the innervation of the AV node and infranodal conduction system, vagal stimulation and carotid sinus massage slow conduction in the AV node but have less of an effect on infranodal tissue and may even improve conduction due to a reduced rate of activation of distal conduction through the AV node and impair infranodal conduiction.”

Question 43

How do patients with congenital and acquired complete heart block (CHB) respond to exercise?

Answer 43

“In patients with congenital CHB and a narrow QRS complex, exercise typically increases heart rate; by contrast, those with acquired CHB, particularly with wide QRS, do not respond to exercise with an increase in heart rate.”

Question 44

In electrophysiologic testing, where should one put the chatheter in order to have information at all levels of the AV conduction axis?

Answer 44

Superior margin of the tricuspid valve annulus.

Question 45

During an electrophysiologic test, how does one assess conduction times regarding the AV node?

Answer 45

“A properly recorded His bundle electrogram reveals local atrial activity, the His electrogram, and local ventricular activation; when it is monitored simultaneously with recorded body surface electrocardiographic traces, intraatrial, AV nodal, and infranodal conduction times can be assessed.”

Question 46

What do the AH and HV interval represent?

Answer 46

“The time from the most rapid deflection of the atrial electrogram in the His bundle recording to the His electrogram (AH interval) represents conduction through the AV node and is normally

Question 47

Which drugs can be responsible for prolonged AH interval?

Answer 47

Beta blockers, calcium channel blockers and digitalis.

it can also occur due to increased vagal tone

Question 48

The finding of a His bundle electrogram after every atrial electrogram indicates that block is ocurring in the distal conduction system.
True or False?

Answer 48

True.

Question 49

The risk of progressing AV node block increases with the prolongation of HV interval.
True or False?

Answer 49

True.

Question 50

What is the anual risk for complete AV block if the HV interval is >100ms?

Answer 50

10%

Question 51

Electrophisiologic study is mandatory in acquired complete heart block for assessing the need for pacing.
True or False?

Answer 51

False.
“In patients with acquired CHB, even if intermittent, there is little role for electrophysiologic testing, and pacemaker implantation is almost always indicated.”

Question 52

If patients are stable immediately after pharmacological therapy, pacing won’t be necessary.
True or False?

Answer 52

False.
“Adjunctive pharmacologic treatment with atropine or isoproterenol may be useful if the block is in the AV node., Since most pharmacologic treatment may take some time to initiate and become effective, temporary pacing may be necessary.”

Question 53

What type of temporary pacing is mostly acutely used? How should it be placed?

Answer 53

“The most expeditious technique is the use of transcutaneous pacing, where pacing patches are placed anteriorly over the cardiac apex (cathode) and posteriorly between the spine and the scapula or above the right nipple (anode).”

Question 54

Is there any limitations to transcutaneous pacing?

Answer 54

“Acutely, transcutaneous pacing is higly effective, but its duration is limited by patient discomfort and longer-term failure to capture the ventricle owing to changes in lead impedance.”

Question 55

Besides transcutaneous pacing, is there any other to place a temporary pacemaker?

Answer 55

Transvenous temporary pacing.

Question 56

Should asymptomatic second-degree AV node block patients should be considered for pacing under any circumstances?

Answer 56

“Patients who have asymptomatic second-degree AV block of either type should be considered for pacing if the block is demonstrated to be intra- or infra-His or is associated with a wide QRS complex.”

Question 57

What are the indications for permanent pacing colocation?

Answer 57

“Pacemaker implantation should be performed in any patient with symptomatic bradycardia and irreversible second-or-third-degree AV block, regardless of the cause or level of block in the conducting system. (…) Pacing in patients with asymptomatic AV block should be individualized; situations in which pacing should be considered are patients with acquired complete heart block, particularly in the setting of cardiac enlargement; left ventricular dysfunction; and waking heart rates equal or less than 40beats/min. Patients who have asymptomatic second-degree AV block of either type should be considered for pacing if the block is demonstrated to be intra- or infra-His or is associated with a wide QRS complex. Pacing may be indicated in asymptomatic patients in special circumstances, in patients with profound first-degree AV block and left ventricular dysfunction in whom a shorter AV interval produces hemodynamic improvement, and in the setting of milder forms of AV conduction delay (first-degree AV block, intraventricular conduction delay) in patients with neuromuscular diseases that have a predilection for the conduction system, such as myotonic dystrophy and other muscular dystrophies, and Kearns-Sayre syndrome.”

Question 58

Which symptoms might occur due to AV node dysfunction?

Answer 58

“Symptoms may include those directly related to bradycardia and low cardiac output or to worsening heart failure, angina, or intolerance to an essential medication.”

Question 59

In the setting of acute myocardial infarction (MI), what are the indications for pacing?

Answer 59

“AV block in acute MI is often transient, particularly in inferior infarction. The circumstances in which pacing is indicated in acute MI are persistent, second-or-third-degree AV block associated with bundle branch block. Pacing is generally not indicated in the setting of transiet AV block in the absence of intraventricular conduction delays or in the presence of fascicular block or first-degree AV block that develops in the setting of preexisting bundle branch block. Fascicular blocks that develop in acute MI in the absence of other forms of AV block also do not require pacing.”

Question 60

In the setting of bifascicular and trifascuclar block, what are the indications for pacing?

Answer 60

“Distal forms of AV conduction block may require pacemaker implantation in certain clinical settings. Patients with bifascicular or trifascicular block and symptoms, particularly syncope that is not attributable to other causes, should undergo pacemaker implantation. Pacemaking is indicated in asymptomatic patients with bifascicular or trifascicular block who experience intermittent third-degree, type II second-degree AV block or alternating bundle branch block. In patients with fascicular block who are undergoing electrophysiologic study, a markedly prolonged HV interval or block below the His at long cycle lenghts also may constitue an indication for permanent pacing. Patients with fascicular block and the neuromuscular diseases previously described should also undergo pacemaker implantation.”

Question 61

Single-(VVI) chamber pacing mode is associated with less benefits than dual-(DDD) chamber pacing mode in all patients.
True or False?

Answer 61

Unknown.
“In general, a pacing mode that maintains AV synchrony reduces complication sof pacing such as pacemaker syndrome and pacemaker-mediated tachycardia. This is particularly true in younger patients; the importance of dual-chamber pacing in the elderly, however, is not well established. Several studies have failed to demonstrate a difference in mortality rate in older patients with AV block trated with a single-(VVI) compared with a dual-(DDD) chamber pacing mode. In some of the studies that randomized pacing mode, the risk of chronic atrial fibrillation and stroke risk decreased with physiologic pacing. In patients with sinus rhythm and AV block, the very modest increase in risk with dual-chamber pacemaker implantation apperas to be justified to avoid the possible complications of single-chamber pacing.”