Editing Cardiac action potential (section)

==Overview==
{| class="wikitable"
|+ '''Figure 1: Intra- and extracellular [[ion]] concentrations ([[mole (unit)|mmol]]/[[Litre|L]])'''
|-----
! width="50" style="background:#efefef;" | Element
! width="25" style="background:#efefef;" | Ion
! width="50" style="background:#efefef;" | Extracellular
! width="50" style="background:#efefef;" | Intracellular
! width="50" style="background:#efefef;" | Ratio
|-----
| Sodium || Na<sup>+</sup> || 135 - 145 || 10  || 14:1
|-----
| Potassium || K<sup>+</sup> || 3.5 - 5.0 || 155 || 1:30
|-----
| Chloride || Cl<sup>−</sup> || 95 - 110 || 10 - 20 || 4:1
|-----
| Calcium
| Ca<sup>2+</sup>
| 2
| 10<sup>−4</sup>
| 2 x 10<sup>4</sup>:1
|-----
| style="border-bottom:3px solid grey;" colspan="5" align="center" | <span style="font-size:87%;">''Although intracellular Ca<sup>2+</sup> content is about 2 mM, most of this is bound or sequestered in intracellular organelles (mitochondria and sarcoplasmic reticulum).''<ref name="Lote2012p150">{{Cite book |last=Lote |first=C. |url=https://books.google.com/books?id=JwMxiaul2LkC&pg=PA150 |title=Principles of Renal Physiology |publisher=Springer |year=2012 |isbn=9781461437840 |edition=5th |page=150}}</ref></span>
|}
Similar to skeletal muscle, the [[resting membrane potential]] (voltage when the cell is not electrically excited) of [[ventricle (heart)|ventricular cells]] is around −90&nbsp;millivolts (mV; 1&nbsp;mV&nbsp;=&nbsp;0.001&nbsp;V), i.e. the inside of the membrane is more negative than the outside. The main ions found outside the cell at rest are sodium (Na<sup>+</sup>), and chloride (Cl<sup>−</sup>), whereas inside the cell it is mainly potassium (K<sup>+</sup>).<ref name="santana 496 901">{{Cite journal |last=Santana |first=Luis F. |last2=Cheng |first2=Edward P. |last3=Lederer |first3=W. Jonathan |date=2010-12-01 |title=How does the shape of the cardiac action potential control calcium signaling and contraction in the heart? |journal=Journal of Molecular and Cellular Cardiology |language=en |volume=49 |issue=6 |pages=901–903 |doi=10.1016/j.yjmcc.2010.09.005 |pmc=3623268 |pmid=20850450}}</ref>

The action potential begins with the voltage becoming more positive; this is known as [[depolarization]] and is mainly due to the opening of [[sodium channel]]s that allow [[sodium|Na<sup>+</sup>]] to flow into the cell. After a delay (known as the [[absolute refractory period]]), the action potential terminates as potassium channels open, allowing K<sup>+</sup> to leave the cell and causing the membrane potential to return to negative, this is known as [[repolarization]]. Another important ion is [[Calcium in biology|calcium (Ca<sup>2+</sup>)]], which can be found inside the cell in the [[sarcoplasmic reticulum]] (SR) where calcium is stored, and is also found outside of the cell. Release of Ca<sup>2+</sup> from the SR, via a process called [[calcium-induced calcium release]], is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in [[cardiac excitation-contraction coupling]].<ref>{{Cite journal |last=Koivumäki |first=Jussi T. |last2=Korhonen |first2=Topi |last3=Tavi |first3=Pasi |date=2011-01-01 |title=Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study |journal=PLOS Computational Biology |language=en |volume=7 |issue=1 |page=e1001067 |bibcode=2011PLSCB...7E1067K |doi=10.1371/journal.pcbi.1001067 |pmc=3029229 |pmid=21298076 |doi-access=free}}</ref>

There are important physiological differences between the [[pacemaker cells]] of the [[sinoatrial node]], that spontaneously generate the cardiac action potential and those non-pacemaker cells that simply conduct it, such as [[Ventricle (heart)|ventricular myocytes]]). The specific differences in the types of [[ion channels]] expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2.

=== Cardiac automaticity ===
'''Cardiac automaticity''' also known as '''autorhythmicity''', is the property of the specialized [[Electrical conduction system of the heart|conductive]] [[cardiomyocytes|muscle cells]] of the heart to generate spontaneous cardiac action potentials.<ref>{{Cite book |title=Clinical arrhythmology and electrophysiology: a companion to Braunwald's heart disease |vauthors=Issa ZF, Miller JM, Zipes DP |date=2019 |publisher=Elsevier |isbn=978-0-323-52356-1 |veditors=Issa ZF |edition=Third |location=Philadelphia, PA |pages=51–80 |chapter=Electrophysiological Mechanisms of Cardiac Arrhythmias: Abnormal Automaticity |doi=10.1016/B978-0-323-52356-1.00003-7}}</ref><ref>{{Cite journal |vauthors=Antzelevitch C, Burashnikov A |date=March 2011 |title=Overview of Basic Mechanisms of Cardiac Arrhythmia |journal=Cardiac Electrophysiology Clinics |volume=3 |issue=1 |pages=23–45 |doi=10.1016/j.ccep.2010.10.012 |pmc=3164530 |pmid=21892379}}</ref> Automaticity can be normal or abnormal, caused by temporary [[ion channel]] characteristic changes such as certain medication usage, or in the case of abnormal automaticity the changes are in [[Electrotonic potential|electrotonic environment]], caused, for example, by [[myocardial infarction]].<ref>{{Cite web |title=Cardiac Arrhythmias - Textbook of Cardiology |url=https://www.textbookofcardiology.org/wiki/Cardiac_Arrhythmias |access-date=2022-05-17 |website=www.textbookofcardiology.org |vauthors=Krul S}}</ref>