Bradyarrhythmias—Conduction System Abnormalities

Atrioventricular conduction abnormalities

Atrioventricular (AV) block occurs when an atrial impulse either is not conducted to the ventricle or is conducted with delay. This assumes that the impulse occurs at a time that conduction would be expected to occur based on normal conduction and refractory period properties. Conduction block assumes that the rate of the atrial rhythm is in the normal physiological range and is regular. For example, a premature atrial impulse that is not conducted (“blocked”) is not considered to be AV block (AVB). AVB is classified on the basis of severity into three types. First-degree AVB is characterized by conduction of all sinus impulses but with a prolonged PR interval more than 0.20 seconds. In second-degree AVB, intermittent block of AV conduction occurs, manifesting as some nonconducted or blocked P waves, but with evidence of AV conduction on other beats. Second-degree AVB can be further categorized into Mobitz types I and II, 2:1, or high-degree (advanced) AVB. In third-degree AVB, there is complete absence of AV conduction when it would be expected.

First-Degree Block


First-degree AVB ( Fig. 2.1 ) represents delay in conduction from the atria to the ventricles and manifests as a prolonged PR interval of more than 0.20 seconds, but all impulses are conducted. The PR interval represents the time from the onset of atrial depolarization due to sinus node activation to the onset of ventricular repolarization (i.e., conduction time from the atrium → AV node [AVN] → His bundle → Purkinje system → ventricles). However, it does not reflect conduction from the sinus node to the atrial tissue. The conduction delay may occur in the atria, AVN, His bundle, and His-Purkinje system. If the QRS complex is narrow and normal appearing, the greatest AV delay usually occurs in the AVN. If the QRS is wide, the conduction delay or block is more likely to occur in the His-Purkinje system than it would be if the QRS were narrow. However, block in the AVN can manifest as a prolonged PR and wide QRS if preexisting bundle branch block (BBB) or rate-dependent aberrancy is present. Diagnosis is usually easy, based on the surface electrocardiogram (ECG) showing a prolonged PR interval. On the ECG during first-degree AVB, the P wave may be buried in the previous QRS complex (especially during sinus rhythm) or the previous T wave and can be difficult to distinguish from a junctional rhythm. If block is in the His-Purkinje system, first-degree AVB is usually associated with BBB.

Figure 2.1

Sinus rhythm with first-degree atrioventricular block.

In this lead V 1 and II rhythm strip, the P and T waves begin to merge, but close examination of the preceding T waves shows the superimposed P waves and first-degree AV block.

Associated Conditions

Spontaneous causes of first-degree AVB include intrinsic disease of the AVN and/or His-Purkinje system), high vagal tone, or dual AV nodal pathways (in which two separate populations of PR intervals may be seen). Other causes include drugs that slow AVN conduction, such as calcium channel blockers, β-adrenergic blockers, or digoxin. Isolated first-degree AVB can occur with anterior or inferior myocardial infarctions (MIs). First-degree AVB is generally self-limited and not associated with progression to complete heart block (CHB), but it may be associated with poorer prognosis in those with heart disease. Exceptions include rheumatic fever (for which it is a sign of acute carditis) and endocarditis (for which it may suggest the presence of a valve ring abscess, especially involving the aortic valve), in which first-degree AVB may presage the development of higher levels of block.

Clinical Symptoms and Presentation

First-degree AVB does not usually cause symptoms; however, if the PR interval is markedly prolonged (more than 300 to 600 ms), a loss of optimal AV synchrony may reduce the atrial contribution to ventricular filling, therefore decreasing cardiac output, especially in patients with diastolic dysfunction, and lead to symptoms of heart failure. Rarely the PR interval may be sufficiently long to cause nearly simultaneous contraction of the atria and ventricles, resulting in pacemaker syndrome–like symptoms (fatigue, shortness of breath, near syncope, neck fullness, chest pain).

Approach to Management

There is no specific therapy for first-degree AVB, unless the PR interval is so prolonged as to lead to symptoms. If permanent pacing is considered for symptomatic, very prolonged first-degree AVB, a dual-chamber pacemaker programmed to DDD mode of function but with or without rate response, is the recommended pacing system. His bundle pacing is an option if the level of block is at the AVN. Right ventricular pacing should be minimized because it can cause left ventricular (LV) dyssynchrony; however, His bundle pacing may not be achievable in some patients because it is technically more difficult to achieve than right ventricular apical or outflow tract pacing and is not available in all centers. If the level of block is infra-Hisian, His bundle pacing is not indicated. Another option, not well tested for isolated first-degree AVB, is cardiac resynchronization therapy (CRT) pacing, in which both right and left ventricles are paced. This approach is preferable especially if there is a longstanding need for ventricular pacing for hemodynamic purposes and there is ventricular dysfunction ( Table 2.1 , Algorithm 2.1 ).

Table 2.1

First-degree atrioventricular block management

Setting Therapy

  • Usually benign and requires no therapy.

  • If due to drugs, no need to discontinue.

Symptomatic, PR very long (300-400 ms)

  • Because such symptoms as lightheadedness and dizziness are nonspecific and common, especially in older persons, it is essential to exclude other causes before ascribing symptoms to first-degree AVB.

  • A rare indication for a DDD pacemaker. Shortening the PR interval to 150-200 ms may improve weakness, fatigue, and shortness of breath by restoring optimal AV synchrony. Consider His bundle pacing if the conduction prolongation is at the level of the AVN.

  • If patient is hospitalized and with refractory low cardiac output, consider temporary AV sequential pacing to improve hemodynamics and symptoms and to determine the benefit of permanent pacing.


  • No therapy usually required (possible exception if the PR is very long).

  • May be due to drugs to treat MI (e.g., β-adrenergic blockers, calcium channel blockers, digoxin). If asymptomatic, no medication changes are usually required. If symptomatic or PR very long, consider reducing dosage.

  • Consider atrial infarction or elevated atrial pressures as the cause and treat appropriately.


  • No specific therapy.

  • No need for temporary prophylactic pacing as it does not presage higher degrees of AVB.

  • If due to a drug, decrease the dose or stop using the drug if it is not essential.


  • If PR is markedly prolonged (300-400 ms) and hemodynamic compromise is suspected, dual-chamber pacing (at PV or AV interval of 150-200 ms) may improve hemodynamics.

  • This may be instituted if temporary pacing wires are present after cardiac surgery.

  • If first-degree AVB appears for the first time after aortic valve surgery, it may indicate damage to the His-Purkinje system (usually associated with left bundle branch block in these cases).

  • Prolonged PR intervals can cause hemodynamic problems after cardiac surgery since the timing of the “atrial kick” may be more important during this time in which diastolic dysfunction is possible.


  • Carefully evaluate for the presence of aortic insufficiency, consider TEE.

  • Acute development of first-degree AVB, especially if it occurs with a new bundle branch block (transient or persistent), is highly suspicious for the presence of a valve ring abscess.

  • Requires surgical treatment.

  • Consider TEE.

  • Transfer patient to a unit with cardiac telemetry (if not already there), as progression to higher levels of AVB can occur.

Rheumatic fever

  • First-degree AVB is a sign of rheumatic carditis and may presage the development of higher levels of AVB, including complete heart block.

  • May be an indication for steroids.

Infiltrative and restrictive cardiomyopathies

  • If PR is markedly prolonged (> 300 ms), dual-chamber pacing (at PV or AV interval of 150-200 ms) may improve hemodynamics and symptoms.

  • Ventricles with severe diastolic dysfunction are especially dependent on atrial kick to maximize cardiac output.

  • If prolongation is at the level of the AV node, consider His bundle pacing.

AV , Atrioventricular; AVB , atrioventricular block; AVN, atrioventricular node, MI, myocardial infarction; TEE , transesophageal echocardiography.

Algorithm 2.1

First-degree AVB. AVB, Atrioventricular block; AVR, aortic valve replacement; MI, myocardial infarction; PM, pacemaker.

Second-Degree Atrioventricular Block—Mobitz Type I


Periodic failure of conduction from the atria to ventricles (with regular atrial activation) characterizes second-degree AVB. In typical Mobitz type I second-degree AVB (Wenckebach AVB), there is progressive lengthening of the PR interval followed by one nonconducted P wave (P wave not followed by a QRS complex). Mobitz type I second-degree AVB often is associated with group beating with a constant P-P interval and changing (usually—and classically—shortening) R-R intervals with the cycle ending with a P wave not followed by a QRS complex. The R-R interval enclosing the nonconducted P wave is classically less than twice the preceding R-R interval. The more classic periodicity of Mobitz type I second-degree AVB is most common with shorter AV conduction ratios (e.g., 4:3 and 3:2) and can be atypical with longer AV conduction ratios (e.g., 9:8 and 10:9). Wenckebach AVB can occur at resting rates or with faster sinus rates. All AVNs demonstrate this normal physiologic behavior at fast enough rates (usually around 180 to 200 bpm). Mobitz type I second-degree AVB almost always occurs in the AVN. Only rarely is this rhythm due to AVB in the His bundle or His-Purkinje system. Infra-Hisian Wenckebach block may be present if AV Wenckebach occurs with a widened QRS complex (over 120 ms) ( Fig. 2.2 ). Infra-Hisian block is associated with a higher risk of progression to CHB, but typical Mobitz type I second-degree AVB with a narrow QRS ( Fig. 2.3 ) rarely progresses to advanced or CHB. Carotid sinus massage can help to distinguish block occurring in the AVN from infra-Hisian block: carotid massage will enhance the Wenckebach conduction in the AVN but have an opposite effect if the block is below the His bundle. In contrast, increasing the sinus rate by increasing sympathetic tone or decreasing vagal tone (e.g., with walking, exercise, or intravenous atropine) is expected to enhance AVN conduction but may worsen infra-Hisian block.

Figure 2.2

Mobitz type I second-degree atrioventricular block with wide QRS.

This ECG shows sinus rhythm (rate: 76 bpm) with grouped beating, gradual prolongation of the PR interval (resulting in a nonconducted P wave), and a wide QRS complex due to underlying right bundle branch block and left anterior fascicular block. The conduction ratio is 4:3 (four P waves for every three QRS complexes). Mobitz type I most commonly involves block at the level of the AVN but in the presence of BBB the level of block may be infranodal (intra- or infra-His block).

Figure 2.3

Mobitz type I second-degree atrioventricular block with narrow QRS.

Lead V 1 and II rhythm strip of second-degree AV block Mobitz I with narrow QRS. This is from a patient after cardiac surgery. There is ST elevation in lead II, consistent with pericarditis.

Associated Conditions

Intermittent Mobitz type I second-degree AVB occurs in up to 6% of healthy individuals. Atrial pacing to rates of 180 to 200 bpm will cause AV Wenckebach in 90% of individuals. Mobitz type I second-degree AVB is more common in the older population, in which it may be an isolated finding. “Vagotonic” AVB can mimic Mobitz type I second-degree AVB but is not a true Wenckebach phenomenon because the sinus rate in these cases is not regular and often slows prior to the nonconducted P wave. Vagotonic AVB is common in athletes and during sleep in healthy people. Long episodes with substantial slowing of ventricular rate may occur during sleep; there is no need for therapy. This rhythm is also not uncommon in sleep apnea patients, especially if they are obese. Pathologic causes include intrinsic disease in the AV conducting system (almost always in the AVN), drugs that block conduction or lengthen refractoriness in the AVN (digoxin, not necessarily at toxic levels, β-adrenergic blockers, calcium channel blockers), Lyme disease, the Bezold-Jarisch reflex (caused by inferior MI and the effect of increased vagal tone on the AVN), myocarditis, and rarely after radiofrequency ablation of the AV junction in an attempt to terminate AV nodal reentry.

Clinical Symptoms and Presentation

Symptoms are usually absent during this rhythm; however, especially if the AV conduction ratio is low (e.g., 3:2), it may occasionally cause severe symptoms at rest, including syncope, fatigue, weakness, lightheadedness, or palpitations, symptoms similar to that of pacemaker syndrome.

Approach to Management

Asymptomatic Mobitz type I second-degree AVB due to block in the AVN does not generally require any treatment, and permanent pacemaker implantation is not indicated because progression to advanced or complete AVB or asystole is rare. However, if Mobitz type I second-degree AVB is associated with a wide QRS complex, the level of the block may be in the His-Purkinje system and culminate into CHB. Symptomatic Mobitz type I second-degree AVB may require treatment, which is generally limited to stopping any offending drug or awaiting the effects of ischemia, infarction, or other injury to resolve. Permanent pacing is indicated if symptoms or hemodynamic compromise can be directly attributed to this rhythm ( Table 2.2 ).

Table 2.2

Mobitz type I second-degree atrioventricular block management

Setting Therapy

  • Treadmill testing will help assess chronotropic competence (if this rhythm is not related to myocardial ischemia), as well as enhance AVN conduction, thereby reducing the degree of Wenckebach block (e.g., from 5:4 to 8:7 or producing first-degree AVB only).

  • Holter monitoring can assess the degree and level of AVB and the persistence of the problem during activities of daily living and any diurnal variation.

  • If the QRS duration is wide and Holter monitoring or stress testing suggests infranodal block, an electrophysiology study may help to confirm the level of AVB.

    • If block is demonstrated to be intra- or infra-Hisian, permanent pacemaker implantation is reasonable, even in an asymptomatic patient.

    • On occasion, intra-Hisian block can be demonstrated in a patient with a narrow, normal-appearing QRS complex by the production of higher degrees of AV block during treadmill testing with the increase in sinus rate.

  • No therapy.

    • If not due to reversible cause (e.g., drugs or transient damage to the AV node from Lyme disease) and the QRS duration is normal, as more advanced or complete heart block rarely develops.

    • There may be increased risk of syncope and symptoms in the future.


  • Some AV nodal blocking drugs (digoxin, β-adrenergic blockers, calcium blockers) may be the cause and should be reduced or stopped if possible, and then only if severe symptomatic bradycardia occurs.

  • If older or at high risk for structural heart disease, consider an echocardiogram to assess LV function (even if no physical findings are present).

  • If due to a correctable cause such as AV nodal blocking drugs, stop the drug if possible.

  • If there is a wide QRS or bundle branch block, it is possible that Wenckebach can be due to block below the AV node (in the His-Purkinje system).

    • In this case, permanent pacemaker implantation is indicated.

  • Acutely, intravenous atropine or oral theophylline usually increases conduction through the AV node.

    • These may paradoxically decrease ventricular rate and increase the degree of block if the block is below the bundle of His.

  • Permanent pacemaker implantation is indicated if symptomatic second-degree AVB is not otherwise correctable.


  • Is often reversed during thrombolysis or angioplasty.

    • May also appear for the first time concomitantly with these procedures.

    • Transient in nature.

  • Temporary DDD pacing for the following:

    • Persistent low heart rate (< 40 bpm)

    • Low cardiac output

    • Ischemia

    • Refractory hypotension

    • Symptoms of lightheadedness and dizziness

  • Atropine or theophylline may reverse the block but can cause unwanted tachycardia during drug administration.

    • These drugs are only rarely indicated except at the time of presentation of the patient.

  • Atypical AV block is more common in inferior-posterior MIs due to the Bezold-Jarisch reflex and the effect of increased vagal tone on the AV node.

    • This is usually transient, and unless there is hemodynamic collapse, there is no need for a temporary pacemaker.

    • Rarely is there a need for a permanent pacemaker—this is true even if transient third-degree (complete) AV block occurs, as high degrees of block tend to resolve over 5-7 days.

  • If the AV block does not resolve but the ventricular rate is > 40 bpm, no therapy is required if patient is asymptomatic.

  • If the block does not resolve after 7 days and/or ventricular rate < 40 or if patient is symptomatic, a permanent pacemaker is indicated.


  • Assess drugs given and their need; stop offending drugs that enhance vagal tone, if possible.

  • If no symptoms, no therapy.

  • If symptomatic and no reversible causes, provide temporary pacing before surgery.

    • Need for permanent pacing can be accomplished in the postoperative setting.

  • Atropine or isoproterenol may be given to increase AV node conduction if symptomatic or hemodynamically significant.


  • Rare after CABG but, if it occurs, consider an offending drug or transient ischemia to the AV node.

    • No therapy is generally needed.

  • If associated with wide QRS complex, consider block below the His.

    • If it persists, consider an EP study to assess the level of the block.

  • If patient is asymptomatic and block is above His, no need for permanent pacemaker.

  • If patient is symptomatic or block is below the His, permanent pacemaker is indicated.

  • If the block is associated with valve (especially aortic) surgery, consider direct damage to the AV node.

    • If persistent, a pacemaker is indicated for symptoms or persistent slow rate (< 40 bpm or no increase in rate with exercise).

AV , Atrioventricular; AVB , atrioventricular block; CABG , coronary artery bypass graft; EP , electrophysiology; LV , left ventricular; MI, myocardial infarction.

Second-Degree Atrioventricular Block—Mobitz Type II


Mobitz type II second-degree AVB is characterized by single nonconducted (“blocked”) P waves with constant P-P and PR intervals (no change in the PR > 0.025 seconds) before and after the nonconducted P waves. This is generally due to block below the AV junction infranodal and in the His bundle (intra-His block) or lower in the His-Purkinje system (infra-His block) but not the AVN. Because the block is usually infra-Hisian, Mobitz type II second-degree AVB is associated with a high rate of progression to advanced or CHB. The QRS complex is typically wide ( Fig. 2.4 ) or demonstrates BBB, although rarely a narrow QRS complex is observed. In patients with 2:1 AVB, or intermittent “dropped” P waves, when the QRS complex is narrow, a Wenckebach pattern, gradually prolonging the PR interval before the nonconducted P wave (i.e., Mobitz type I second-degree AVB), should be sought in recorded rhythm strips or ECGs because the block may be in the AVN and have a much more benign prognosis. In contrast to Mobitz type I second-degree AVB, in Mobitz type II second-degree AVB, carotid sinus massage may have a paradoxical effect of improving 1:1 AV conduction due to slowing of the sinus rate; however, increasing the sinus rate (e.g., with walking, exercise, or intravenous atropine) may worsen Mobitz type II infra-Hisian block or elicit 2:1 AVB due to the early arrival of atrial impulses at the infranodal conduction system while it is still refractory.

Figure 2.4

Mobitz type II second-degree atrioventricular block with a wide QRS.

This lead V 1 , II, and V 5 rhythm strip shows sinus rhythm with Mobitz type II second-degree AVB with 3:2 conduction (three P waves for every two QRS complexes). There is no progressive PR interval lengthening prior to the nonconducted P wave. Block is likely to be infranodal.

Associated Conditions

Causes include intrinsic degenerative disease in the His-Purkinje system, drugs that slow or block conduction in the His-Purkinje system (e.g., propafenone, flecainide, procainamide, quinidine, disopyramide), coronary artery disease (CAD) including MI, myocarditis, infiltrative disease such as amyloid, sarcoidosis, Lyme disease, neuromuscular diseases, and ablation of the AV junction. It can be exacerbated by exercise and by drugs that increase AV nodal conduction and the sinus rate, such as atropine. When occurring in the setting of acute MI, Mobitz type II second-degree AVB is usually due to anterior MI due in turn to left anterior descending coronary artery obstruction with its distribution involving the septal perforator branch.

Clinical Symptoms and Presentation

Symptoms include lightheadedness, near syncope, and syncope, although many patients are asymptomatic, depending on the AV conduction ratio. Nevertheless, Mobitz type II second-degree AVB is associated with a high rate (> 50%) of progression to CHB, which may be sudden and unpredictable in onset.

Approach to Management

It is important to exclude vagotonic block and Mobitz type I second-degree AVB in the AVN. Extensive review of rhythm strips and ECGs is particularly important if the QRS complex is narrow because attribution of the level of block to the AVN in an asymptomatic patient requires no therapy, whereas diagnosis of block in the His-Purkinje system indicates a need for permanent pacemaker implantation. A wide QRS complex or BBB supports the level of block being in the His-Purkinje system. Carotid sinus massage or exercise can help to confirm the diagnosis; an electrophysiology (EP) study can be performed when there remains significant doubt as to the localization of the site of block. Because of the high risk of progression to CHB, Mobitz type II second-degree AVB is an indication for permanent pacemaker implantation ( Table 2.3 , Algorithm 2.2 ).

Table 2.3

Mobitz type II second-degree atrioventricular block management

Setting Therapy

  • Risk for complete heart block and death is significant (approximately 50%).

    • A dual-chamber permanent pacemaker is recommended as the pacing system of choice.

  • Admit the patient for a permanent pacemaker and place on a cardiac monitor.

    • In the absence of symptoms or progressive (higher-degree AVB), there is no need for a temporary pacemaker before permanent pacemaker implantation.

  • Avoid atropine.

  • Evaluate for the presence of underlying cardiac disease, such as infiltrative processes (e.g., amyloid), or MI.


  • Dual-chamber permanent pacemaker implantation is indicated.

  • Admit the patient and place on a cardiac monitor.

  • If symptomatic or hemodynamically detrimental ventricular bradycardia is present, a temporary pacemaker is indicated if a permanent system cannot be placed expeditiously.

  • Do not give atropine because this may worsen the AVB and produce a slower ventricular rate.

    • Exercise, sinus tachycardia, and catecholamines also can worsen the degree of block by enhancing AV nodal conduction and impinging on the refractory period of the His-Purkinje system.


  • Place temporary pacemaker.

    • Mobitz type II second-degree AVB is associated with a high rate of heart failure in this setting.

    • A permanent pacemaker is indicated if the AVB is persistent because the risk of complete heart block is > 50%.

    • Long-term prognosis may not be improved.

  • Avoid the use of antiarrhythmic drugs (including lidocaine) in the absence of a pacemaker, unless there is sustained ventricular tachyarrhythmia, as these drugs may worsen the degree of AVB.

  • Do not give atropine.

  • Mobitz type II second-degree AVB has a lower (albeit not known with certainty) incidence in the current early revascularization era but if present or of new onset may improve with time, but this is rare. After being present and persistent, a pacemaker will likely be needed.


  • Place permanent pacemaker.

    • If urgent or emergent surgery, place a temporary pacemaker with the plan for a permanent pacemaker after surgery.

  • If CABG, epicardial atrial and ventricular wires can be placed, with temporary pacing as standby, until a permanent transvenous pacemaker can be placed.

  • It is best to place the permanent pacemaker after CABG or other cardiac surgery as leads otherwise tend to dislodge.

  • If endocarditis, temporary pacemaker until infection resolves and after cardiac surgery.

    • Avoid antiarrhythmic drugs and atropine.


  • If bradycardia, temporary pacing (via epicardial wires, if present, after cardiac surgery).

  • Temporary Mobitz type II AV block may resolve after cardiac surgery.

    • It may be due to trauma near the His-Purkinje system (e.g., with aortic valve surgery, where left bundle branch block is a not infrequent accompaniment).

  • Persistent (e.g., more than 3-5 days) Mobitz type II block will require permanent pacing.

  • No antiarrhythmic drugs should be given unless an adequate backup ventricular pacing is available.

  • Endocarditis with abscess near the septum can destroy the His-Purkinje system.

    • Despite surgical repair, permanent pacing will likely be required.

  • For patients having tricuspid valve replacement, an endocardial lead can occasionally be placed across a porcine bioprosthesis without producing tricuspid regurgitation but should be avoided if there is a mechanical valve.

    • Tricuspid valve repair (e.g., annuloplasty) should not pose a problem in positioning a right ventricular lead.

AV , Atrioventricular; AVB , atrioventricular block; CABG , coronary artery bypass graft; MI, myocardial infarction.

Algorithm 2.2

Mobitz type II second-degree or advanced (high-degree) AVB. AVB, Atrioventricular block; EPS, electrophysiology study; MI, myocardial infarction; PM, pacemaker; SHD, structural heart disease (no overt evidence of myocardial, valvular, congenital or coronary heart disease).

Second-Degree Atrioventricular Block—2:1 Atrioventricular Block


2:1 second-degree AVB occurs when every other P wave is conducted to the ventricles but alternate P waves are not. AVB may be occurring at the level of the AVN, within the His bundle, or in the His-Purkinje system. If the QRS is narrow ( Fig. 2.5 ) and normal appearing, the level of the block is most likely in the AVN (which is more benign). If the QRS is wide ( Fig. 2.6 ) because of BBB or other nonspecific, intraventricular (IV) conduction delay, block in the AVN is still often more common, but block in the His-Purkinje system (infra-AV nodal) is more frequent than when the QRS complex is narrow. To help to define the level of the block, observation of a long monitored strip can be helpful because 2:1 AVB frequently does not persist. If and when the AV conduction ratio changes, the other forms of AVB (Mobitz type I or II) should then become apparent. Rhythm monitoring while the patient does some form of exertion (e.g., arm exercise, standing, and walking) may also help to demonstrate the level of block. Block at the level of the AVN should improve with the decrease in vagal tone and increase in adrenergic tone, but block below the AVN in the His-Purkinje system may worsen, with consequent slowing of ventricular rate, as AV nodal conduction improves and increases the frequency of inputs to the His-Purkinje system. Likewise, atropine and isoproterenol may improve AV conduction through the AVN but worsen infranodal block. Carotid massage may also help to distinguish the two by worsening AV nodal block but improving block in the His-Purkinje system by slowing the sinus and AV nodal inputs to the His-Purkinje system, allowing the His-Purkinje system to recover from its refractory state between inputs.

Figure 2.5

2:1 Atrioventricular block, narrow QRS.

This rhythm strip of leads V 1 and II shows sinus rhythm (rate: 84 bpm) with 2:1 AVB (ventricular rate: 42 bpm) that could represent either Mobitz type I or type II second-degree AVB. The narrow QRS complexes suggest that block is most likely to be in the AVN and that the nature of the 2:1 AVB is most likely to be Mobitz type I second-degree AVB. In general, a narrow QRS and 2:1 AV conduction is likely to be Mobitz type I second-degree AVB, whereas a wide QRS in 2:1 AV conduction is more likely to be infra-AV nodal block (Mobitz type II). Changing the AV conduction ratio (e.g., atropine) will help to define the site of block. Another way to help distinguish the level of the block is to exercise the individual and/or do continuous or long-term monitoring to determine if the 2:1 AV block is associated with other types of AV block (e.g., Mobitz type I or II second-degree AV block).

Figure 2.6

2:1 Atrioventricular block, wide QRS.

This lead V 1 and II rhythm strip shows sinus rhythm with 2:1 AV block. While the (> 0.12 sec) QRS complexes, consistent with right bundle branch block, suggest that Mobitz type II second-degree AV block is likely, this rhythm is simply called 2:1 AV block.

Associated Conditions

2:1 AVB occurs in the same conditions as those associated with Mobitz type I (Wenckebach) or type II second-degree AVB.

Clinical Symptoms and Presentation

Symptoms include lightheadedness, near syncope, and syncope, although some patients may be asymptomatic, depending on the sinus rate and consequent ventricular rate.

Approach to Management

Atropine and isoproterenol improve AV conduction if the level of block is in the AVN but may make it worse if the block is at the level of the His-Purkinje system. Therefore atropine is not recommended for suspected block in the His-Purkinje system. Depending on the level of block, approach to management follows recommendations and guidelines for Mobitz types I or II second-degree AVB. In the setting of acute MI with AVB, isoproterenol should be avoided because of the adverse effects of sinus tachycardia and ventricular ectopy ( Table 2.4 ).

Table 2.4

2:1 Atrioventricular block management

Setting Therapy
AV nodal site of block suspected (usually narrow, normal-appearing QRS complex)

  • If asymptomatic, evaluate (Holter monitor and exercise test for ventricular rates and diurnal variation) but no therapy.

  • Exercise testing may be required to help to elicit the site of block: if AV nodal, the AV conduction ratio will increase from 2:1 to 3:2 or higher.

  • If the AVB is intra-His or infra-Hisian, a higher degree of AV block will occur.

  • As AV nodal block may be due to a drug (e.g., digitalis, β-adrenergic blockers, calcium channel blockers, amiodarone), these drugs should be discontinued, if possible.

  • EP study with His bundle recording can help to determine the level of block, although this is rarely necessary in patients with AV nodal block.

  • In most cases, if observed over a period of time, 2:1 AV block will change to Mobitz type I or II second-degree AVB, allowing the site of block to be further characterized.

  • Atropine or isoproterenol can improve AV nodal conduction and may be useful as diagnostic maneuvers.

  • Block in the AV node is usually benign, but if it leads to asystole more than 3 seconds or complete heart block with escape rates of < 40 per minute with symptoms in awake patients, permanent pacing is indicated.

  • Hemodynamic instability or symptomatic bradycardia with 2:1 AVB that is not reversible is an indication for permanent cardiac pacing.

Infranodal site of block suspected (usually wide QRS complex)

  • If hemodynamically unstable, temporary pacing.

  • Infranodal block is suspected if bundle branch block is present, but even then the block can be in the AV node. May need EP study with His bundle recordings to clarify.

  • Observe long rhythm strips, including Holter monitoring, if feasible.

  • Attempt carotid massage and/or assess the effects of atropine or exercise to help determine level of block.

  • On rare occasions, it may be prudent to apply transcutaneous pacing electrodes.

  • If block is in the His-Purkinje system, a dual-chamber permanent pacemaker is indicated.

Inability to distinguish site of block by ECG or provocative maneuvers

  • Electrophysiology study to evaluate the level of the block, although this rarely needs to be performed.

  • If block is intra-His or below, a permanent pacemaker is indicated.


  • If anterior infarction is evident, block is likely in the His-Purkinje system.

  • Temporary pacing should be performed; this is often accomplished at the time of percutaneous revascularization procedures.

    • Because more than 90% of patients recover with 1:1 AV conduction, generally within a few days, permanent pacing should be considered only if the block is persistent.

  • If inferior infarction is evident, the block is likely in the AVN.

    • Temporary pacing should be performed only if the patient is symptomatic or hemodynamically compromised and can be accomplished expeditiously, without delaying revascularization procedures.

    • Otherwise, intravenous atropine, together with rapid revascularization, is expected to resolve the block.

    • There is usually no need for a permanent pacemaker because the block almost always resolves.


  • Perform provocative maneuvers or prolonged observation to define the site of the AVB.

  • If block is in the AVN, consider discontinuing drugs that may be initiating or maintaining the problem.

    • An exception might be the patient with coronary artery disease in whom perioperative β-blockade has morbidity and mortality advantages.

  • For cardiac surgery, epicardial pacing wires provide an opportunity for temporary AV sequential pacing if HR < 40 bpm or if there is:

    • Hemodynamic instability due to low heart rate

    • AV dyssynchrony

    • Symptoms

  • For noncardiac surgery and level of the block in the His-Purkinje system, temporary (if surgery emergent) or permanent (if surgery urgent or elective) pacing.


  • Level of block needs to be determined.

    • Even if in the His-Purkinje system, in the first few days after cardiac surgery (e.g., CABG or valve surgery), it may resolve post-op.

    • AV block is often due to trauma to AV node or His bundle, and reversibility generally occurs; recovery, however, may not be robust if the block is in the His-Purkinje system.

  • If related to endocarditis or aortic valve surgery and block is in the His-Purkinje system, resolution is unlikely and permanent pacing will usually be required.

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Jan 30, 2019 | Posted by in CARDIOLOGY | Comments Off on Bradyarrhythmias—Conduction System Abnormalities

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