Diagrams of action potentials of cardiac tissue cause considerable consternation in student and physician alike. However, understanding a few simple concepts on the microscopic or cellular level facilitates arrhythmia evaluation and treatment.
Figure 27-31 is a schematic representation of the transmembrane action potentials of the fast, Na+ inward current cell and the slow, Ca++ inward current cell. In the left panel, Phase 4 represents the resting transmembrane potential and is -90 mV, with the intracellular area being negative. This membrane potential difference is maintained by a sodium/ potassium pump utilizing energy to maintain the difference. The membrane is permeable to potassium (K+) and impermeable to Na+ at rest. By expending energy, 3 Na+ ions are pumped out of the cell in exchange for 2 K+ ions into the cell. Positive K+ ions flow across their chemical gradients out of the cell, thus leaving the intracellular space electronegative.
Phase 0 is characterized by the rapid influx of Na+ ions into the cell, thus depolarizing the cell. Sodium influx is gated. When a sufficiently large depolarization occurs, ion channels are recruited and open, allowing for more influx of ions. Conductance declines as the channel is open and the equilibrium potential for the ion is reached. The channel closes, and Na+ is again impermeable to influx. Phase 1 represents a
rapid repolarization of the cell through transient K+ outward currents and beta-adrenergic, adenosine monophosphate (AMP), and histamine activated chloride (Cl-) inward current restoring the membrane potential toward 0 mV.
Phase 2 or the plateau phase is a long phase that may last several hundred milliseconds. Conductance to all ions falls dramatically. Continued Na+/K+ pump activity reduces the membrane potential slightly. An inward rectifying K+ current further depolarizes the cell along with continued Ca++ influx through the slow inward calcium channels. Phase 3 represents the final rapid repolarization of the cell membrane. This occurs from inactivation of the slow inward calcium current and from activation of an outward K+ current. The intracellular space becomes more negative, and potassium conductance increases in a regenerative manner.
Phase 4 resumes at the end of phase 3. In portions of the heart, however, a small depolarization current occurs and may result in threshold being reached and depolarization of the cell. This inward depolarizing current is noted in the SA node, distal AV node, and His-Purkinje fibers. This results in automaticity. The rate of depolarization is greater in the SA node than in other structures and thus results in the SA node as the dominant pacemaker. Adrenergic and cholinergic modulation further results in the SA node as the faster pacemaker, subordinating the automaticity of other pacemaker-like tissues. More frequent stimulation results in shortening of phases 2 and 3 of the action potential, resulting in unchanged or slightly increased conduction velocity.
In the right panel of Figure 27-31, the action potential of the slow inward current type of cells is shown. In these cells, C++ and K+ play a greater role in setting the resting membrane potential slightly less negative than in Purkinje or myocytes (phase 4). Phase 0 occurs through activation of slow Ca++ current. No phase 1 is noted, and the plateau phase is not as prolonged because of the relative importance of the Ca++ and K+ currents dominated by the slow activating and inactivating C++ current. More frequent stimulation leads to a decrease in the resting membrane potential, lower peak phase 0 velocity, slower phase 3 repolarization, and ultimately slower overall conduction velocity (Rosen and Schwartz, 1991).
Antiarrhythmic drugs have differential effects on the Na+, K+, and Ca++ channels or on receptors that mediated the channels. By slowing or enhancing cellular membrane pore activity, one observes changes in either conduction or repo-larization characteristics. This may be reflected in changes in the surface ECG as well.
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