Transmembrane action potential of a Purkinje fiber as recorded with an intracellular microelec-trode. When the electrode tip penetrates the fiber, a resting membrane potential of -90 mV is recorded. The application of a subthreshold stimulus (#1) produces a depolarizing current that fails to result in excitation of the myocardial cell. The application of a threshold stimulus (#2) reaches the threshold potential (TP) and results in an inward current and an action potential. Major transmembrane currents carried by specific ions entering the cell through selective ion channels are depicted to the right. Antiarrhythmic agents alter the electrophysiologic properties of the cardiac cells by modulating one or more of the transmembrane currents, especially the fast inward sodium current and the transmembrane currents carried by the potassium ion (IK and IK-ATP). I na — fast inward sodium current; Ica — "L"-type calcium current; Ito — transient outward current; INa-Ca — sodium-calcium exchange current; IK-ATP — adenosine triphosphate-sensitive potassium current; IK — inward rectifying potassium current; IK — delayed rectifying potassium current.
sarcolemmal membrane. The membrane potential at which this occurs may be calculated using the Nernst equation:
In this equation, x is the ion in question, [x]i is the concentration inside the cell, and [x]o is the concentration outside the cell. For potassium, using a [K]i of 140 mM and a [K]o of 4 mM, the EK is equal to -94 mV, which is almost identical to the normal resting membrane potential of -90 mV. The contribution of other ionic species to the resting membrane potential is smaller because of the low transmembrane permeability at hyperpolarized resting membrane potentials.
An examination of the relationship of [K+]o] and [K+]i] in the Nernst equation shows that an increase in the [K+]o will result in a decrease in the membrane resting potential (less negative). Changes in the extracellular concentration of another ion (Na+, Ca++, Mg++, Cl-) may also modify the resting potential.
To produce membrane depolarization, a current stimulus of sufficient intensity to exceed the outward K+ current must be applied to the cell. If the depolarizing stimulus raises the membrane potential above a threshold value, sodium channels within the sarcolem-mal membrane change their conformation and open their ion-selective pore, allowing Na+ to enter the cell driven by the electrochemical gradient. The open sodium channels raise the membrane potential toward the equilibrium potential of sodium (+65 mV) and set into motion the intricate and precisely coordinated series of ion channel openings and closings leading to the characteristic action potential.
The action potential has been divided into five phases, rapid depolarization (phase 0), early repolarization (phase 1), plateau (phase 2), rapid repolarization (phase 3) and finally the resting phase in myocytes or slow diastolic depolarization (phase 4). The last is a property in cells with the potential for automaticity (defined later). A brief outline of each of these phases in the normal myocyte is given next.
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