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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology. 2017;10:e004667, originally published March 17, 2017
https://doi.org/10.1161/CIRCEP.116.004667

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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 1.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

A, Interconnectedness of K⁺, Na⁺, and Ca²⁺ balances in the...
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A, Interconnectedness of K⁺, Na⁺, and Ca²⁺ balances in the cardiac myocyte. Outward K⁺ loss through K⁺ channels (left) is recovered by the Na⁺-K⁺ ATPase removing 3 Na⁺ ions in exchange for 2 K⁺ ions. Some Na⁺ ions enter the cell via Na⁺ channels, but most via Na⁺-Ca²⁺ exchange (NCX) during diastole, which exchanges 1 Ca²⁺ ion for 3 Na⁺ ions. In the steady state, the Ca²⁺ removed by NCX balances the Ca²⁺ entering the cell via Ca²⁺ channels. Most Ca²⁺ in the cell recycles between the sarcoplasmic reticulum (SR) and cytoplasm, with uptake by sarcoendoplasmic reticulum Ca²⁺ ATPase (SERCA) and release through ryanodine receptors (RyR). Cytoplasmic free Ca²⁺ activates Ca²⁺-calmodulin kinase (CaMK), which regulates the properties of Na⁺, Ca²⁺, and K⁺ channels, and RyR in the SR (dotted arrows). B, Effects of hypokalemia on the action potential (AP). Superimposed AP recordings from an isolated rabbit ventricular myocyte with [K⁺]_o=5.4 mmol/L (black trace) vs [K⁺]_o=2.7 mmol/L (red trace), showing hyperpolarized E_m and early afterdepolarizations (EADs), the latter suppressed by the CaMK blocker KN-93 (green trace), but not by inactive KN-92 (blue trace). Adapted from Pezhouman et al¹ with permission of the publisher. Copyright © 2015, American Heart Association. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 2.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

[K⁺]_o dependence of hypokalemia-induced ventricular tachycardia (VT)/ventricular fibri...
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[K⁺]_o dependence of hypokalemia-induced ventricular tachycardia (VT)/ventricular fibrillation (VF) in isolated rabbit hearts, without or with dofetilide. When [K⁺]_o was lowered, the incidence of VT/VF within 90 min progressively increased to 100% at 2.0 and 1.0 mmol/L (black circles). Dofetilide (1 μmol/L) shifted the dose–response curve to the right. Reprinted from Pezhouman et al¹ with permission of the publisher. Copyright © 2015, American Heart Association.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 3.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Regional chaos synchronization of early afterdepolarizations (EADs) in tissue. In simulated paced homogeneou...
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Regional chaos synchronization of early afterdepolarizations (EADs) in tissue. In simulated paced homogeneous cardiac tissue, electrotonic coupling causes regional chaos synchronization to generate EAD islands (red regions), separated by regions without EADs (blue), whose position and size vary from beat to beat. Beat No. 1 illustrates a scenario in which a triggered premature ventricular contraction (★) arising from an EAD island blocks superiorly (dashed line) but conducts inferiorly (solid line), subsequently reentering the blocked region to induce reentry. Beat No. 2 illustrates a scenario in which the triggered premature ventricular contraction arising from an EAD island encounters another EAD island, resulting in conduction block (dashed line) and reentry (solid lines). Adapted from Weiss et al⁶ with permission of the publisher. Copyright © 2015, Elsevier. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 4.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Hypokalemia-induced positive feedback loops (red and blue arrows) promoting intracellular Na⁺ and...
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Hypokalemia-induced positive feedback loops (red and blue arrows) promoting intracellular Na⁺ and Ca overload, Ca²⁺-calmodulin kinase (CaMK) activation and early afterdepolarizations (EADs) during hypokalemia. The potentiation of the blue positive feedback loop by class III antiarrhythmic (AA) drugs is also shown. I_NaK=Na⁺-K⁺ ATPase outward current. APD indicates action potential duration. Reprinted from Pezhouman et al¹ with permission of the publisher. Copyright © 2015, American Heart Association.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 5.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Phase 2 reentry during simulated ischemia in canine epicardium. Traces show action potential (AP) recordings...
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Phase 2 reentry during simulated ischemia in canine epicardium. Traces show action potential (AP) recordings from 4 sites (Epi 1–4) in a canine epicardial sheet exposed to simulated ischemia ([K⁺]_o=6 mmol/L, hypoxia, pH=6.8). Sites 1 and 2 exhibit normal APs with accentuated AP domes, whereas sites 3 and 4 show early repolarization. Arrows show reexcitation of site 3 by the AP dome at site 2, inducing phase 2 reentry that self-terminates after 4 beats. Adapted from Lukas and Antzelevitch⁴² with permission of the publisher. Copyright © 1996, Oxford University Press. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 6.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

A, Schematic illustrating how action potential duration (APD) shortening because of ATP-sen...
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A, Schematic illustrating how action potential duration (APD) shortening because of ATP-sensitive K⁺ current (I_KATP) activation offsets net cellular K⁺ loss by decreasing the average driving force E_m−E_K for K⁺ efflux over the cardiac cycle. B, ADP shortening, conduction time (CT) delay, tension development, and interstitial [K⁺]_o accumulation vs time during acute global ischemia in rabbit ventricle. Reprinted from Weiss and Shine.⁴⁸ Copyright © 1982, the American Physiological Society.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 7.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Ventricular arrhythmias after injection of KCl (2.8 mg/kg) into the left anterior descending coronary artery...
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Ventricular arrhythmias after injection of KCl (2.8 mg/kg) into the left anterior descending coronary artery of a dog at the times indicated in A–E. Reprinted from Harris et al⁵⁰ with permission of the publisher. Copyright © 1954, the American Association for the Advancement of Science.
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Electrophysiology of Hypokalemia and Hyperkalemia
James N. Weiss, Zhilin Qu, Kalyanam Shivkumar

Circulation: Arrhythmia and Electrophysiology March 2017, 10 (3) e004667; DOI: https://doi.org/10.1161/CIRCEP.116.004667

Figure 8.
By James N. Weiss, Zhilin Qu and Kalyanam Shivkumar

Initiation of reentry during acute ischemia. A, Injury current across the border zone (BZ)...
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Initiation of reentry during acute ischemia. A, Injury current across the border zone (BZ) excites adjacent repolarized tissue in the nonischemic zone (NIZ) to trigger a premature ventricular contraction (★) which propagates through the NIZ and reenters the ischemic zone (IZ) to initiate reentry. B, In ischemic subepicardial tissue, regions of all-or-none early repolarization with very short action potential duration (APD; blue) are juxtaposed to adjacent regions with normal APD and accentuated action potential (AP) domes (red). The AP dome propagates into the repolarized region to trigger a closely coupled premature ventricular contraction (★) that propagates laterally until the normal AP region repolarizes and then reenters this region to initiate phase 2 reentry.
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Repolarization Reserve Evolves Dynamically During the Cardiac Action PotentialEffects of Transient Outward Currents on Early Afterdepolarizations
Thao P. Nguyen, Neha Singh, Yuanfang Xie, Zhilin Qu and James N. Weiss

Circulation: Arrhythmia and Electrophysiology. 2015;8:694-702, originally published March 14, 2015
https://doi.org/10.1161/CIRCEP.114.002451

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