The myocardium contains sets of specialized cells that form the conduction system of the heart, and are responsible for automaticity and rhythm maintenance. The specific areas are the sinoatrial (SA) node, internodal tracts, atrioventricular (AV) node, atrioventricular bundle, and Purkinje system.
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.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.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.
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. Three major internodal tracts exist: the anterior, middle, and posterior tracts.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.
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 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.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.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.2 When conduction slowing becomes exaggerated or heterogeneous within the AV node, abnormal rhythms ensue, such as pathological conduction block or reentrant tachycardias.4
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.3 The left bundle branch extends outward under the endocardium and forms several fascicles, which innervate various parts of the left ventricle.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.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 Purkinje cells have an intrinsic back up rate of 20-40 BPM when no signal is received from the SA node or AV node.
AV blocks are conduction delays or a complete block of impulses from the atria into the ventricles. AV block may be due to increased vagal tone that may be elicited during sleep, athletic training, pain, or stimulation of the carotid sinus. Damage of the conduction system secondary to hereditary fibrosis or sclerosis of the cardiac skeleton are known as idiopathic progressive cardiac conduction disease. Ischemic heart disease causes 40% of AV blocks.6 AV blocks are also seen in cardiomyopathies, myocarditis, congenital heart diseases, and familial diseases. A plasma potassium concentration above 6.3 mEq/L may also cause AV block. They may be iatrogenic, from medications such as Verapamil, Diltiazem, Amiodarone, and Adenosine, or from cardiac surgeries and catheter ablations for arrhythmias.
AV blocks are further classified according to the degree of blockage and include first degree AV block, second degree AV block, and third-degree AV block.
The measurement of conduction time between the atria and ventricles is represented by the PR interval on electrocardiograms (ECG). This component includes the intra-atrial conduction, represented by the P wave, and the conduction from the AV node into the His-Purkinje system. Prolongation of the PR interval of more than 200 milliseconds is considered to be a first-degree AV block. These can be due to structural abnormalities within the AV node, an increase in vagal tone, and drugs that slow conduction such as digoxin, beta-blockers. and calcium channel inhibitors. It is important to note that in first degree AV block, no actual block occurs.
Second-degree AV blocks are occasional non-conducted P waves with prolonged RR intervals. There are two types under this classification. Mobitz type I (Wenckebach) occurs when there is an intermittent conduction block within the AV node that results in a failure to conduct an impulse from the atria into the ventricles. The impaired nodal conduction is progressive to the point that there is a total block. This causes an absent impulse into the ventricles, reflected by the disappearance of the QRS complex in the ECG. Mobitz type I is a benign condition that rarely causes hemodynamic instability; asymptomatic patients need no further treatment. Symptomatic patients will require a pacemaker.
The Mobitz type II AV block is secondary to a disease involving the His-Purkinje system, in which there is a failure to conduct impulses from the atria into the ventricles. A block occurs after the AV node within the bundle of His, or within both bundle branches. The His-Purkinje system is an all-or-none conduction system; therefore, in Mobitz type II, there are no changes in the PR interval, even after the non-conducted P wave. Because of this, Mobitz type II has a higher risk of complete heart block compared to Mobitz type I.
A complete failure of the AV node to conduct any impulses from the atria to the ventricles is the main feature of third-degree AV block. There is AV dissociation and escape rhythms that may be junctional or ventricular, which represent perfusing rhythms. This is due to AV nodal disease or a disease involving the His-Purkinje system caused by coronary artery disease, enhanced vagal tone, a congenital disorder, underlying structural heart disease such as myocardial infarction, hypertrophy, inflammation or infiltration, Lyme disease, post-cardiac surgery, cardiomyopathies, rheumatologic diseases, autoimmune diseases, amyloidosis, sarcoidosis, or muscular dystrophy. At any time, the patient may suffer ventricular standstill that may result in sudden cardiac death. Pacemaker insertion is necessary to provide needed perfusion.