Ischemic heart disease causes 40% of AV blocks. Damage of the conduction system secondary to hereditary fibrosis or sclerosis of the cardiac skeleton are known as idiopathic progressive cardiac conduction disease. AV block may be due to increased vagal tone that may be elicited during sleep, athletic training, pain, or stimulation of the carotid sinus. Understanding Atrioventricular BlockĪV blocks are conduction delays or a complete block of impulses from the atria into the ventricles. ![]() ![]() 2 The Purkinje cells have an intrinsic back up rate of 20-40 BPM when no signal is received from the SA node or AV node. 2 The right bundle branch travels under the endocardium along the right side of the ventricular septum to the base of the anterior papillary muscle. 2 The anterior fascicle innervates the anterolateral wall of the left ventricle the anterior papillary muscle, and the posterior fascicle innervates the lateral and posterior ventricular wall and the posterior papillary muscle. 3 The left bundle branch extends outward under the endocardium and forms several fascicles, which innervate various parts of the left ventricle. The Purkinje network functions to distribute a stimulus throughout the entire ventricles, leading to a much faster total activation of the ventricles than could be achieved by the spread of excitation solely through the ventricular muscle. 2 When conduction slowing becomes exaggerated or heterogeneous within the AV node, abnormal rhythms ensue, such as pathological conduction block or reentrant tachycardias. 4 Impulse conduction is considerably slower as compared to any other region within the normal cardiac conduction system (0.05 m/sec) and this delayed speed allows for sufficient time for atrial depolarization and contraction prior to ventricular depolarization and contraction. 5 In delaying transmission of the cardiac impulse from the atria to the ventricles, the AV node serves a critical function in augmenting ventricular filling during diastole and limiting the ventricular response during atrial tachyarrhythmias. 2 Conduction through the AV node delays propagation of impulses from atria to ventricles and thus permits atrial systole to augment ventricular filling during late diastole, with an added 15-35% contribution to ventricular volume. The AV node is located beneath the endocardium on the right side of the atrial septum, anterior to the opening of the coronary sinus. 2 The anterior nodal tract (Bachmann bundle) extends into the left atrium and then travels downward through the atrial septum to the AV Node, 2 the middle internodal tract (Wenckebach tract) curves behind the superior vena cava before descending to the AV node, and the posterior internodal tract (Thorel’s pathway) continues along the terminal crest to enter the atrial septum and then passes to the AV node. Three major internodal tracts exist: the anterior, middle, and posterior tracts. ![]() The SA node and AV node have conduction pathways between the two that are the primary route of impulse transmission and are called internodal tracts. 1 The intrinsic rate of the SA node is 60-100 beats per minute (BPM) and the speed of conduction to adjacent cells within the SA node is 0.5 m/sec. 2 The blood supply is via the sinus node artery and is from the initial branch of the right coronary artery in approximately 60% of individuals and takes its origin from the circumflex artery in the other 40%, with a few instances of lateral origin from either the right or left arteries or dual origins from both arteries. The SA node is a small collection of specialized cells and collagenous tissue located along the epicardial surface at the junction of the superior vena cava and the right atrium. The specific areas are the sinoatrial (SA) node, internodal tracts, atrioventricular (AV) node, atrioventricular bundle, and Purkinje system. The myocardium contains sets of specialized cells that form the conduction system of the heart, and are responsible for automaticity and rhythm maintenance.
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