Electrophysiology of Hypokalemia and Hyperkalemia

摘要: Basic Science for the Clinical Electrophysiologist Electrophysiology of Hypokalemia and Hyperkalemia James N. Weiss, MD; Zhilin Qu, PhD; Kalyanam Shivkumar, MD, PhD P Downloaded from http://circep.ahajournals.org/ by guest on March 18, 2017 otassium (K + ) was first isolated as an element in 1807 Sir Humphrey Davy when he electrolyzed potash (plant ashes soaked pots water), which its name is derived. Despite organic origin isolation, however, role K biology not elucidated until 20th century. In this article, we discuss basic science underlying effects both hypo- hyperkalemia cardiac excitability arrhythmias. As major intracellular cation, con- centrated 30- to 40-fold over extracellular concentration activity Na -K ATPase plasma membrane, hydrolyzes ATP pump 3 ions out cell exchange 2 into cell, generating outward current process. Because most cells express time-independent ion channels their high selective permeability other gener- ates a negative resting membrane potential (E m approaching equilibrium determined Nernst equation (−95 mV [K ] 4.0 140 mmol/L, respectively). excitable tissues such heart, E stabilizes working atrial ventricular myocytes during diastole, preventing spontaneous action potentials (APs) causing premature extrasystoles. For reason, serum closely regulated physiologi- cally, with normal values ranging 3.5 5.0 mmol/L. Outside range, lower higher have electrophysiological that commonly promote car- diac arrhythmias, solely because direct , but also cellular balances Ca 2+ are interlinked through -Ca (Figure 1A). Thus, directly impact balances. how these relationships First, review hypokalemia only reduces repolarization reserve suppressing conductances, significantly inhibits activity, accumulation. Increased loading acti- vates -calmodulin kinase (CaMK) signaling further reduce inducing late currents. This positive feedback loop promotes early afterde- polarization (EAD)–mediated especially channel-blocking drugs present, delayed (DAD)–mediated arrhythmias automaticity. We then turn hyperkalemia, systemic interstitial. depolarization conduction block reentry may phase reentry. Finally, describe inter- stitial prominent feature acute myocardial ischemia, contributes injury currents electrocar- diographic ST-segment elevation TQ-segment depres- sion including similar Brugada syndromes. Differences between responses system myocardium changes extracel- lular noted. encountered clinically complication diuretic therapy used treat hypertension, heart failure, renal disease, conditions. Its include hyper- polarization, inhibition, suppression channel conductances resulting AP duration (APD) pro- longation, reduced reserve, EAD, DADs, Arrhythmia Mechanisms Reduced predisposes EADs 1B) EAD-mediated includ- ing Torsades de pointes polymorphic tachy- cardia (VT), can degenerate fibrillation (VF) sudden death 2). 1 Reductions prolong APD heterogeneous manner, expression hetero- geneous throughout atria ventricles intrinsically chaotic, occurring irregularly instead reliably every beat. 4 gap junction coupling tissue prevents adjacent exhibiting markedly different APD, chaotic behav- ior causes some regions exhibit synchronously, whereas nearby do not. dynamical cess has been termed regional chaos synchronization generates marked dispersion areas long due juxtaposed next much shorter without 4,5 3). 6 Moreover, if His-Purkinje fibers or reach threshold triggered extra- systoles propagate recovered propagating Received December 19, 2016; accepted February 6, 2017. From UCLA Cardiovascular Research Laboratory Cardiac Center, Departments Medicine (Cardiology) (J.N.W., Z.Q., K.S.), Physiology (J.N.W.), Radiological Sciences (K.S.), David Geffen School at UCLA, Los Angeles, CA. Correspondence Laboratory, MRL 3645, 675 Charles E, Young Dr S, CA 90095. E-mail jweiss@mednet.ucla.edu (Circ Arrhythm Electrophysiol. 2017;10:e004667. DOI: 10.1161/CIRCEP.116.004667.) © American Heart Association, Inc. Circ Electrophysiol available http://circep.ahajournals.org 10.1161/CIRCEP.116.004667