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Figure 6 A schematic illustration of the proposed arrhythmia mechanism is shown. Membrane voltage (Vm) is shown in black, and the calcium transient (Ca-T) is shown in orange. The Ca-T transient outlasts Vm even under control conditions. The difference between the Vm and the Ca-T is increased with action potential duration (APD) shortening observed after acetylcholine (ACH). The early afterdepolarization (EAD) formation is not observed because the Ca-T is also reduced in amplitude. With addition of norepinephrine (NE), the Ca-T is enhanced in amplitude while the APD remains abbreviated. The disparity between Vm and the Ca-T is increased, with inward sodium-calcium exchange (NCX) current producing an EAD. If even further enhancement of the Ca-T is observed after a tachycardia-pause interval, a second action potential is initiated. The Ca-T initiated by the first ectopic beat initiates the second ectopic beat, and so on, producing a repetitive rhythm.
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