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[[Potassium]] is an [[electrolyte]], 98% of which is intracellular. The 2% remaining outside the cell has great implications for cells that generate action potentials. Doctors prescribe potassium for patients when potassium levels in the blood are insufficient, called [[hypokalemia]]. The potassium can be given orally, which is the safest route; or it can be given intravenously, in which case strict rules and hospital protocols govern the rate at which it is given.
The usual intravenous dose of 10–20 mEq per hour is given slowly since it takes time for the electrolyte to equilibrate into the cells. When used in state-sanctioned lethal injection, bolus potassium injection affects the electrical conduction of heart muscle and ultimately leads to cardiac arrest. The potassium bolus delivered for lethal injection causes a rapid onset of elevated extracellular potassium, also known as [[hyperkalemia]], causing [[depolarization]] of the resting membrane potential of the heart muscle cells, particularly impacting the heart's pacemaker cells. However, potassium's effect on membrane potential is concentration dependent and ultimately occurs in two phases. Given the reference range for serum potassium is 3.5-5.5 mEq/L, concentrations up to 8 mEq/L shorten action potential duration and the refractory period due to an allosteric effect of potassium ions on potassium channels, leading to increased conduction velocity and subsequently quicker potassium efflux which contributes to quicker repolarization and the mentioned shortening of the refractory period.<ref name=":6">{{Cite journal |last=Weiss |first=James N. |last2=Qu |first2=Xhilin |last3=Shivkumar |first3=Kalyanam |date=2017 March |title=The Electrophysiology of Hypo- and Hyperkalemia |url=https://www.ahajournals.org/doi/10.1161/CIRCEP.116.004667 |journal=Circulation: Arrhythmia and Electrophysiology |volume=10 |issue=3 |doi=10.1161/CIRCEP.116.004667 |via=PubMed}}</ref><ref>{{Citation |last=Rastegar |first=Asghar |title=Serum Potassium |date=1990 |work=Clinical Methods: The History, Physical, and Laboratory Examinations |editor-last=Walker |editor-first=H. Kenneth |url=https://www.ncbi.nlm.nih.gov/books/NBK307/ |access-date=2024-08-16 |edition=3rd |place=Boston |publisher=Butterworths |isbn=978-0-409-90077-4 |pmid=21250149 |editor2-last=Hall |editor2-first=W. Dallas |editor3-last=Hurst |editor3-first=J. Willis}}</ref> At approximately 8 mEq/L and beyond, the shortened refractory period and increased resting membrane potential diminishes the quantity of voltage-gated sodium channels ready to contribute to rapid phase 0 depolarization due to the inactivation gate requiring further repolarization to open back up.<ref name=":6" /> At potassium concentrations beyond 14mEq/L, enough sodium channels remain inactivated to no longer generate an action potential, ultimately leading to no heart beat.<ref name=":6" /> Heart potassium levels after lethal injection can reach 160.0 mEq/L.<ref>{{Cite journal |last=Bertol |first=Elisabetta |last2=Politi |first2=Lucia |last3=Mari |first3=Francesco |date=2012-01 |title=Death by potassium chloride intravenous injection: evaluation of analytical detectability |url=https://pubmed.ncbi.nlm.nih.gov/21923800/ |journal=Journal of Forensic Sciences |volume=57 |issue=1 |pages=273–275 |doi=10.1111/j.1556-4029.2011.01907.x |issn=1556-4029 |pmid=21923800}}</ref>
Depolarizing the muscle cell inhibits its ability to fire by reducing the available number of sodium channels (they are placed in an inactivated state). [[ECG]] changes
====Sodium thiopental====
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