Bradyarrhythmias, Atrioventricular Block, Asystole, and Pulseless Electrical Activity
Santosh S. Oommen
I. INTRODUCTION.
Bradyarrhythmias and conduction blocks are common electrocardiographic findings. Many of these arrhythmias are asymptomatic and do not require specific therapy, whereas others can be life threatening, requiring rapid intervention. Myocardial ischemia is an important cause of acute and potentially dangerous bradyarrhythmia.
II. ANATOMY
A. Sinoatrial node.
The sinus beat originates in the sinoatrial (SA) node, a focus of automatic cells near the junction of the superior vena cava and right atrium.
1. The blood supply to the SA node is from the sinus node artery, which arises from the proximal right coronary artery in 55% of the population (Fig. 22.1) and from the circumflex artery in 35%. The SA node receives a dual supply of blood from both the right coronary artery and the circumflex artery in 10% of the population.
2. The automaticity of the SA node is affected by both the parasympathetic and sympathetic nervous systems. If the SA node fails to generate an impulse, other foci in the atrium, atrioventricular (AV) node, or ventricle can act as “backup” pacemaker sites.
B. AV node.
The AV node is located in the anteromedial portion of the right atrium just anterior to the coronary sinus.
1. The impulse generated by the SA node progresses through the atrium to the AV node. The AV node is also innervated by both the parasympathetic and sympathetic nervous systems.
2. The AV node receives its blood supply from the AV node artery, which arises from the posterior descending artery in 80% of the population (Fig. 22.1), from the circumflex artery in 10%, and from both arteries in 10%.
3. Collateral blood supply from the left anterior descending artery makes the AV node somewhat less prone to ischemic damage than the SA node.
C. His bundle and bundle branches
1. After a delay of < 200 milliseconds in the AV node, the electrical impulse is propagated down the His bundle to the right and left bundle branches. The left bundle branch splits further into anterior and posterior fascicles. The autonomic nervous system does not have a major effect on conduction below the AV node.
2. The His bundle and right bundle branch receive their blood supply from the AV nodal artery and from septal penetrating branches of the left anterior descending artery. The anterior fascicle of the left bundle branch receives blood from the septal perforating branches of the left anterior descending
artery. The posterior fascicle has a dual blood supply: from the septal perforating branches of the left anterior descending artery and branches of the posterior descending artery.
artery. The posterior fascicle has a dual blood supply: from the septal perforating branches of the left anterior descending artery and branches of the posterior descending artery.
 FIGURE 22.1 Diagrammatic representation of the conduction system and its blood supply. SAN, sinoatrial node; RCA, right coronary artery; AVN, atrioventricular node; PDA, patent ductus arteriosus; RBB, right bundle branch; LCx, left circumflex artery; LAD, left anterior descending; LLB, left lateral branch. |
III. SINUS NODE DYSFUNCTION.
Sinus node dysfunction encompasses any dysfunction of the sinus node and includes inappropriate sinus bradycardia, SA exit block, SA arrest, and tachycardia-bradycardia syndrome.
A. Clinical presentation.
There is a wide range of presentations, and some patients’ disease may be asymptomatic.
1. Syncope and presyncope are the most dramatic presenting symptoms. Fatigue, angina, and shortness of breath are more subtle consequences of sinus node dysfunction.
2. In the tachycardia-bradycardia syndrome, the primary complaint may be palpitation. Documentation of the arrhythmia may be difficult because of the sporadic and fleeting nature of the problem.
B. Etiology.
The intrinsic and extrinsic causes of sinus node dysfunction are listed in Table 22.1. Idiopathic degenerative disease is the most common cause of intrin sic sinus node dysfunction, and the incidence increases with age. Acute coronary syndromes are a common cause of bradyarrhythmias, occurring in 25% to 30% of patients with myocardial infarction (MI) (Table 22.2).
C. Electrocardiographic findings
1. Inappropriate sinus bradycardia, also known as “chronotropic incompetence,” is defined as a sinus rate of < 60 beats/min that does not increase appropriately
with exercise. Inappropriate sinus bradycardia must be differentiated from a low resting heart rate, which may be normal in athletes and sleeping individuals.
with exercise. Inappropriate sinus bradycardia must be differentiated from a low resting heart rate, which may be normal in athletes and sleeping individuals.
TABLE 22.1 Etiologies of Sinus Node Dysfunction | ||||||||||||||||||||||||||||||||||||||||||
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TABLE 22.2 Incidence of Bradyarrhythmia in the Setting of Acute Myocardial Infarction | ||||||||||||||||||||||||||
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2. Sinus arrest, or sinus pause, occurs when the sinus node fails to depolarize on time. Pauses of < 3 seconds may be seen on Holter monitoring in up to 11% of normal adults (especially athletes) and are not a cause for concern. However, pauses lasting longer than 3 seconds are generally considered abnormal and are suggestive of underlying pathology, especially if the patient is awake when they occur.
3. SA exit block, although similar to sinus arrest on the electrocardiographic tracing, may be distinguished by the fact that the duration of the pause is a multiple of the sinus PP interval. High-grade SA exit block cannot be differentiated from prolonged sinus arrest and is treated in the same manner.
4. Tachycardia—bradycardia syndrome, also referred to as “sick sinus syndrome,” is characterized by episodes of sinus or junctional bradycardia interspersed with an atrial tachycardia, usually paroxysmal atrial fibrillation.
D. Diagnostic testing.
Invasive testing is used when noninvasive methods have failed to yield a diagnosis and sinus node dysfunction is still strongly suspected.
1. Noninvasive testing
a. Electrocardiogram (ECG). In evaluating sinus node dysfunction, the initial workup should include a 12-lead ECG, followed by a 24-hour to 48-hour ambulatory ECG monitoring, if necessary. Use of a diary during the record ing period can help correlate symptoms with the cardiac rhythm. For less frequent events, a loop recorder or an event recorder may be used to assess symptoms over a 2-week to 4-week period. Stress testing can help document the severity of chronotropic incompetence.
b. Autonomic testing includes physical maneuvers, such as carotid sinus mas sage and tilt table testing, as well as pharmacologic interventions to test the autonomic reflexes.
(1) Carotid sinus massage distinguishes intrinsic sinus pause/sinus arrest from a pause due to carotid sinus hypersensitivity, which is a 3-second
or longer pause and/or a ≥ 50 mm Hg or greater drop in blood pressure that occurs with massage of the carotid sinus (firm pressure applied to one carotid sinus at a time for 5 seconds). Carotid sinus massage should not normally precipitate sinus pause/sinus arrest, although it will decrease the rate of depolarization of the SA node and slow conduction in the AV node.
or longer pause and/or a ≥ 50 mm Hg or greater drop in blood pressure that occurs with massage of the carotid sinus (firm pressure applied to one carotid sinus at a time for 5 seconds). Carotid sinus massage should not normally precipitate sinus pause/sinus arrest, although it will decrease the rate of depolarization of the SA node and slow conduction in the AV node.
(2) Tilt table testing may help differentiate between syncope caused by sinus node dysfunction and that due to autonomic dysfunction. Bradycardic episodes precipitated by tilt table testing are usually caused by autonomic dysfunction and not by sinus node dysfunction.
(3) Pharmacologic testing may be used to differentiate between sinus node dysfunction and autonomic dysfunction. Total autonomic blockade is achieved after administration of atropine 0.04 mg/kg and propranolol 0.2 mg/kg. The resulting intrinsic heart rate represents the sinus node rate, devoid of autonomic influences. Assuming that the normal intrinsic heart rate (in beats/min) is defined by the formula
then an intrinsic heart rate lower than predicted using this formula is consistent with sinus node dysfunction; an intrinsic heart rate close to the predicted rate in a patient with a clinical presentation of sinus node dysfunction is suggestive of an autonomic dysfunction as a cause of the bradyarrhythmia.
2. Invasive testing.
The two most common tests use indirect measurements of SA node function. Direct measurement of SA node function is laborious and rarely performed.
a. Sinus node recovery time (SNRT) is the time it takes the SA node to recover following paced overdrive suppression of the node.
(1) A delay of longer than 1,400 milliseconds is considered abnormal. This measurement may be corrected by subtracting the intrinsic sinus cycle length (in milliseconds) from the recovery time. A corrected SNRT > 550 milliseconds is suggestive of sinus node dysfunction.
(2)The limitations of this test are as follows:
(a) It is an indirect measurement of SA node function and reflects both sinoatrial node conduction time(SACT) and automaticity.
(b) It may be falsely shortened by an SA node entrance block during atrial pacing (due to failure of the paced impulse to reset the sinus node) or falsely prolonged by an SA node exit block (the sinus node is normal but the impulse cannot leave the node), which affects its specificity.
(c) The SNRT is not prolonged in all patients with sinus node dysfunction, which affects its sensitivity.
b. Sinoatrial node conduction time
(1) The steady-state atrial rate is determined (A1-A1 interval or the time between P waves). Then premature atrial extra stimuli (A2) are introduced by pacing high in the right atrium, starting in late diastole at progressively shorter intervals until atrial refractoriness is found (i.e., A2 does not result in a P wave). The duration before the next spontaneous atrial impulse (A3) is measured and the baseline rate is subtracted.
(2) The test assumes that SA node automaticity is not affected by pacing, that con duction time into the node is equal to conduction time out of the node, and that there is no shift in the principal pacemaker site.
E. Therapy.
Treatment for symptomatic sinus node dysfunction may be pharmacologic, pacing, or a combination of both.
1. Indications for pacing in sinus node dysfunction are determined by symptoms (e.g., correlation with a documented arrhythmia; Table 22.3). Another common indication is when drug therapy that causes sinus node dysfunction cannot be stopped or changed.
2. Medications that suppress sinus node automaticity should be stopped if possible. If this is not possible, it may be necessary to place a temporary or permanent pacemaker (Table 22.3).
3. For patients with tachycardia-bradycardia syndrome, a pacemaker is often placed for management of the bradyarrhythmia, and antiarrhythmic drugs are added for treatment of the tachycardia episodes.
4. Acute treatment for patients with symptomatic sinus node dysfunction includes the following:
(a) Atropine (0.04 mg/kg intravenous bolus)
(b) Temporary pacing for patients whose conditions fail to respond to drug therapy
(c) Isoproterenol (starting at 1 µg/min intravenously), which may be used as a bridge to pacemaker placement. Isoproterenol is not indicated in most patients with cardiac arrest
IV. AV CONDUCTION DISTURBANCES.
These disturbances are classified as first-degree, second-degree, or third-degree block, depending on the severity of the conduction abnormality.
A. Classification
1. First-degree AV block is characterized by the prolongation of the PR interval beyond 200 milliseconds. This finding may occur as a normal variant in 0.5% of asymptomatic young adults without overt heart disease. In older individuals, it is most often caused by idiopathic degenerative disease of the conducting system.
2. Second-degree AV block
a. Second-degree AV block is characterized by a failure of one or more, but not all, atrial impulses to conduct to the ventricles. The block may be at any level of the AV conduction system.
b. When more than one atrial impulse is present for each ventricular complex, the rhythm may be described as a ratio of the number of atrial impulses to the number of ventricular complexes (for three P waves preceding each QRS complex, 3:1 second-degree AV block is present).
(1) Lesser degrees of AV block (i.e., 4:3 or 3:2) with a prolonging PR interval prior to a nonconducted atrial impulse are described as Mobitz type I AV block (also known as Wenckebach block).
(a) The conducted impulse of a Mobitz type I block will generally be narrow, and the site of block is often in the AV node above the His bundle.
(b) A Mobitz type I block with a bundle branch block is still likely to be above the His bundle, but a His bundle ECG is needed to confirm the level of block.
(2) High-grade AV block (3:1, 4:1, or greater) is typically described as Mobitz type II AV block. The conducted impulses will generally be preceded by constant PR intervals and have a wide QRS morphology (right bundle branch block [RBBB] or left bundle branch block [LBBB] pattern). The site of block is often below the AV node. A Mobitz type II block is usually intra-Hisian or infra-Hisian and has a greater propensity for progressing to third-degree AV block.
(3) Pure 2:1 conduction patterns cannot be reliably classified as Mobitz type I or type II, and if diagnostic maneuvers (such as exercise) are not able to elucidate one type of second-degree block versus the other, an electrophysiology study may be warranted.
TABLE 22.3 Indications for Permanent Pacing | ||||||||||
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