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Therefore, when K+ diffuses out of a cell, it creates an electrical potential across the membrane that tends to attract it back into the cell. There exists one membrane potential called the potassium equilibrium potential at which the electrical forces tending to pull K+ into the cell exactly balance the concentration forces tending to drive K+ out. When the membrane potential has this value, there is no net movement of K+ across the membrane. 5 mY = z Iog [ X' ] inside 10 [ X' ] outside 26 I CHAPTER TWO and rapidly (essentially instantaneously) develop the potassium equilibrium poten­ tial.

Precise timing of the status of ion channels accounts for the characteristic membrane potential changes that occur when cardiac cells are activated. Figure 2-1 shows how ion concentration differences can generate an electri­ cal potential across the cell membrane. Consider first, as shown at the top of 1 "Channels" can be thought of as passive ion-specific holes in the membrane through which a particular ion will move according to the electrochemical forces acting on it. "Exchangers" are passive devices that couple the movement of two or more specific ions across the membrane according to the collective net electrochemical forces acting on all the ions involved.

Both cells have similarly shaped fast response-type action potentials, but their temporal displacement reflects the fact that it takes some time for the impulse to spread over the atria. As shown in Figure 2-5, action potential conduction is greatly slowed as it passes through the AV node. This is because of the small size of the AV nodal cells and the slow rate of rise of their action potentials. Since the AV node delays the transfer of the cardiac excitation from the atria to the ventricles, atrial contraction can contribute to ventricular filling before the ventricles begin to contract.