In a study to examine the basis of rate-related changes in the electrocardiographic P wave we found a multicentric rather than unifocal origin of the atrial depolarization wave in dogs. Three to five pacemakers, or origin points, were distributed over a 30- to 40-mm area compared to the 11-mm size of the sinus node. Two or three of the sites could excite simultaneously, or one specific site would dominate excitation. Each separate origin point dominated excitation within a specific range of heart rates, and on reaching either the upper or lower limits of this range, a new focus abruptly dominated and initiated the atrial wave front. We have obtained evidence to suggest that these findings may be explained by a widely distributed atrial pacemaker complex. The spatial distribution of this system exceeded the dimensions of the canine sinus node by a factor of three to four times. The pacemaker centers, although distributed, were consistently located at specific positions along the superior vena caval-right atrial junction. Also, each separate pacemaker site appeared functionally differentiated to generate a specific range of heart rates. We propose that in addition to the sinus node there are other specialized atrial pacemaker centers, and that this specialization, including the differentiated response and coordination, is conferred by focal receptor characteristics and their inputs.

In studies to ascertain the basis of dynamic changes in the P wave, bipolar epicardial potentials were recorded from multiple atrial electrodes in dogs. One hundred to 120 activation times were displayed by a digital computer and used to construct atrial isotemporal activation sequence maps. Changes in heart rate or beat-to-beat cycle length were induced by vagal stimulation or infusion of autonomic mediating drugs. Changes in cycle length were associated with dynamic changes in the atrial activation sequence and surface P-wave. A conspicuous finding was that epicardial atrial depolarization began at three widely separated locations. These three points were consistently present in all animals and were generally located at the 12, 3, and 6 o'clock positions of the superior vena cava-right atrial junction. The dynamic changes in P waves and atrial activation sequence which accompanied the changes in cycle length were due to sudden shifts in the point of earliest activity between the three early sites. Asymmetric atrial depolarization with more rapid conduction along the crista terminalis, superior interatrial band, and pectinate muscles was present in all dogs. Although the anisotropic atrial geometry played an important role in the asymmetric conduction, the widely distributed onset of activity contributed significantly to the uneven spread. The multiple points of origin of the atrial wavefront might be explained by either a trifocal, distributed pacemaker or the epicardial exits of three specialized pathways conducting an impulse emanating from a single focus. These data explain the dynamic variation in P-wave morphology in normal hearts and also imply a relationship between the altered origin of atrial depolarization, atypical P waves, brady- or tachyarrhythmias, and heart rate control.

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