Effects of high extracellular K⁺ in atrium on pacemaker activity of sinoatrial node.

Sinoatrial node (SAN) plays a significant role in rhythmic firing in hearts. Little is known about the pacemaker activity of SAN when the extracellular K⁺ concentration [K⁺]o is accumulated in the atrium at the tissue level. In this paper, a gradient model of the intact SAN and its surrounding atrial muscle was developed by considering details of the SAN heterogeneous electrophysiology. The operator splitting method was used to solve the computer model. A factor k was introduced to [K⁺]o of the atrial cell to simulate the accumulation of [K⁺o. The results showed that with the elevation of [K⁺]o in the atrium, the maximum diastolic depolarization of the peripheral SANCs became less negative while their action potential amplitude became smaller than that of the control condition, but little effect was found on the central SANCs. The conduction block occurred in the atrium after [K⁺]o was elevated to greater than 2.5 times of its control condition. The larger the [K⁺]o was, the earlier the conduction block occurred. The elevation of [K⁺]o in the atrium shifted the leading pacemaker site from the center to the periphery, together with a slightly increased sinus rate. Coupling conductance within the SAN had effects on the excitation propagation in the high [K⁺]o setting. For a same [K⁺]o, the more the conductance was enhanced, the shorter the excitation propagated away from the center. In conclusion, the high [K⁺]o in the atrium was shown to modulate the pacemaker activity of SAN and impair its ability to pace and drive the atrium.