Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
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 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.
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.
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).
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 ).
Setting | Therapy |
---|---|
Asymptomatic |
|
Symptomatic, PR very long (300-400 ms) |
|
MI |
|
Preoperative |
|
Postoperative |
|
Endocarditis |
|
Rheumatic fever |
|
Infiltrative and restrictive cardiomyopathies |
|
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.
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.
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.
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 ).
Setting | Therapy |
---|---|
Outpatient—Asymptomatic |
|
Outpatient—Symptomatic |
|
MI |
|
|
|
Preoperative |
|
Postoperative |
|
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.
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.
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.
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 ).
Setting | Therapy |
---|---|
Outpatient—Asymptomatic |
|
Outpatient—Symptomatic |
|
MI |
|
Preoperative |
|
|
|
Postoperative |
|
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.
2:1 AVB occurs in the same conditions as those associated with Mobitz type I (Wenckebach) or type II second-degree AVB.
Symptoms include lightheadedness, near syncope, and syncope, although some patients may be asymptomatic, depending on the sinus rate and consequent ventricular rate.
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 ).
Setting | Therapy |
---|---|
AV nodal site of block suspected (usually narrow, normal-appearing QRS complex) |
|
Infranodal site of block suspected (usually wide QRS complex) |
|
Inability to distinguish site of block by ECG or provocative maneuvers |
|
MI |
|
Preoperative |
|
Postoperative |
|
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here