Bradyarrhythmias are most commonly caused by failure of impulse formation (sinus node dysfunction) or by failure of impulse conduction over the atrioventricular (AV) node/His-Purkinje system. Bradyarrhythmias may be caused by disease processes that directly alter the structural and functional integrity of the sinus node, atria, AV node, and His-Purkinje system or by extrinsic factors (autonomic disturbances, drugs, etc) without causing structural abnormalities (Table 86–1).
TABLE 86–1.Classification of Bradyarrhythmias ||Download (.pdf) TABLE 86–1. Classification of Bradyarrhythmias
|Sinus node dysfunction |
|Sinus bradycardia |
|Sinus pauses, sinus arrest |
|Sinoatrial exit block |
|Tachycardia-bradycardia syndrome |
|Chronotropic incompetence |
|Atrioventricular (AV) conduction abnormalities |
|First-degree AV block |
|Second-degree AV block |
| Mobitz type I (Wenckebach) |
| Mobitz type II |
| 2:1 AV block |
|High-grade AV block |
|Third-degree (complete) AV block |
|Atrioventricular dissociation |
|Bundle branch block |
|Left bundle branch block |
|Right bundle branch block |
|Left anterior hemiblock |
|Left posterior hemiblock |
|Bifascicular block/trifascicular block |
|Nonspecific intraventricular conduction defect |
ANATOMY OF THE SINUS NODE AND CONDUCTION SYSTEM
Normal electrical activation of the heart arises from the principal pacemaker cells that spontaneously depolarize, located laterally in the epicardial groove of the sulcus terminalis,1 near the junction of the right atrium and the superior vena cava (Fig. 86–1). The sinus node in adults measures approximately 1 to 2 cm long and 0.5 mm wide. The central zone of the sinus node containing the principal central pacemaker cells is small and located within a fibrous tissue matrix. In the periphery of the node along the crista terminalis, transitional cells with pacemaker function are also present. In essence, the sinoatrial (SA) node has a complex three-dimensional tissue architecture with central and peripheral components made up of distinct ion channel and gap junction expression profiles. This heterogeneity is necessary to maintain normal automaticity and impulse conduction. The principal pacemaker site within this region may migrate, resulting in subtle alterations in P-wave morphology. Once the impulse exits the sinus node and the perinodal tissues, it traverses the atrium to the AV node. The conduction of impulses from right to left atrium has been postulated to occur preferentially via Bachmann’s bundle, and secondarily across the musculature of the coronary sinus.
Schematic representation of the cardiac conduction system. AV, atrioventricular; IVC, inferior vena cava; RA, right atrial; SA, sinoatrial; SVC, superior vena cava. Copyright 2016, Elsevier Inc. All rights reserved. www.netterimages.com.
Once the sinus node impulse activates the atrium, electrical activation continues through the AV node, with a conduction delay ensuring complete atrial contraction before initiation of ventricular conduction. The AV nodal complex is considered to have three related regions: (1) the transitional cell zone, (2) the compact AV node, and (3) the penetrating AV bundle.2...