Electrophysiology of Hypokalemia and Hyperkalemia
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Potassium (K+) was first isolated as an element in 1807 by Sir Humphrey Davy when he electrolyzed potash (plant ashes soaked in pots of water), from which its name is derived. Despite the organic origin of its isolation, however, the role of K+ in biology was not elucidated until the 20th century. In this article, we discuss the basic science underlying the effects of both hypo- and hyperkalemia on cardiac excitability and arrhythmias. As the major intracellular cation, K+ is concentrated 30- to 40-fold over its extracellular concentration by the activity of Na+-K+ ATPase in the plasma membrane, which hydrolyzes ATP to pump 3 Na+ ions out of the cell in exchange for 2 extracellular K+ ions into the cell, generating an outward current in the process. Because most cells express time-independent K+ ion channels in their plasma membrane, the high selective permeability to K+ over other ions generates a negative resting membrane potential (Em) approaching the K+ equilibrium potential (EK) as determined by the Nernst equation (−95 mV for extracellular and intracellular [K+] of 4.0 and 140 mmol/L, respectively). In excitable tissues such as the heart, the negative resting Em stabilizes working atrial and ventricular myocytes during diastole, preventing spontaneous action potentials (APs) from causing premature extrasystoles. For this reason, serum [K+] is closely regulated physiologically, with normal values ranging from 3.5 to 5.0 mmol/L. Outside of this range, lower and higher values of serum [K+] have electrophysiological effects that commonly promote cardiac arrhythmias, not solely because of direct effects of K+, but also because the cellular balances of K+, Na+, and Ca2+ are interlinked through Na+-K+ ATPase and …