The cardiac impulse begins in the sinoatrial node in the high lateral right atrium near the junction of the superior vena cava and the right atrium. Excitation leaves the sinoatrial node and spreads throughout the atrium. The myocytes (both atrial and ventricular) are long thin structures linked electrically via low-resistance pores known as gap junctions. The gap junctions are hetero-geneously dispersed throughout the sarcolemmal membrane, although they are mainly concentrated on the ends of the myocytes. This distribution leads to polarity of the myocyte, with end-to-end conduction occurring at a more rapid rate than side-to-side (anisotropic) conduction. The difference in conduction velocity is up to a factor of three and may be important in supporting certain types of arrhythmias.
After the excitatory wave has spread throughout the atrium, it enters the atrioventricular (A-V) node. Importantly, the atrium and ventricle are electrically isolated from one another by a fibrous ring encircling the atrioventricular groove with the only connection occurring through the A-V node. If additional connections exist between the atrium and ventricle (accessory pathway), the potential for arrhythmia is present (atrioven-tricular reciprocating tachycardia), such as occurs with the Wolff-Parkinson-White syndrome. Conduction velocity slows significantly as the electrical signal enters the AV-node, where cellular depolarization depends on ICa++ rather than INa. The delay in ventricular excitation allows the atria to contract and enhances the filling of the ventricle. After passing through the A-V node, the electrical signal is carried via the right and left bundle branches to the body of the right and left ventricles.
The principal determinant of conduction velocity within the myocardium is the maximum rate of depolarization (Vmax) of phase 0 of the action potential in individual myocytes. The number of sodium channels that are recruited to open by a depolarizing stimulus determines the Vmax in atrial and ventricular muscle. Changes in the configuration of the sodium channel in the sarcolemmal membrane at resting membrane potentials, which are more positive (depolarized) than -75mV, cause the channels to enter an inactivated state in which they cannot participate in an action potential. As a result, there is a reduction in the peak sodium current leading to a reduction in upstroke velocity, action potential amplitude, excitability, and conduction velocity. This has important ramifications for the genesis of arrhythmias. One common clinical cause of depolarization of myocardial tissue is ischemia resulting from coronary artery disease.
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