Editing Defibrillation (section)

== Mechanism ==

Defibrillation halts chaotic cardiac activity by forcibly depolarizing heart cells, disrupting re-entrant circuits, and allowing for the heart's natural pacemaker to take over.<ref name=":0">{{Cite journal |last1=Dosdall |first1=Derek J. |last2=Fast |first2=Vladimir G. |last3=Ideker |first3=Raymond E. |date=July 2010 |title=Mechanisms of Defibrillation |journal=Annual Review of Biomedical Engineering |language=en |volume=12 |issue=1 |pages=233–258 |doi=10.1146/annurev-bioeng-070909-105305 |issn=1523-9829 |pmc=3984906 |pmid=20450352}}</ref><ref name=":1">{{Cite journal |last1=Jones |first1=J.L. |last2=Tovar |first2=O.H. |date=March 1996 |title=The mechanism of defibrillation and cardioversion |url=https://ieeexplore.ieee.org/document/486742 |journal=Proceedings of the IEEE |volume=84 |issue=3 |pages=392–403 |doi=10.1109/5.486742|url-access=subscription }}</ref>

Cardiac cells require a strong electrical stimulus to raise their transmembrane potential to the activation threshold.<ref name=":0" /><ref name=":1" /> Only a small amount of electrical current enters the cell due to high membrane impedance.<ref name=":0" />The intracellular voltage of the cell remains uniform, while the extracellular voltage rapidly increases or decreases depending on proximity to the electrodes.<ref name=":0" />This creates a voltage gradient that alters the transmembrane potential of cells, potentially resetting irregular electrical activity to restore normal cardiac rhythm.<ref name=":0" /><ref name=":1" />

Irregular rhythms often result from re-entrant circuits, where electrical impulses circle within the heart tissue due to areas of slow conduction or unidirectional block.<ref name=":2">{{Cite journal |last1=Gill |first1=Gurnoor S |last2=Blair |first2=Jacob |last3=Litinsky |first3=Steven |date=2024-11-16 |title=Evaluating the Performance of ChatGPT 3.5 and 4.0 on StatPearls Oculoplastic Surgery Text- and Image-Based Exam Questions |journal=Cureus |volume=16 |issue=11 |pages=e73812 |doi=10.7759/cureus.73812 |doi-access=free |pmid=39691123 |pmc=11650114 |issn=2168-8184}}</ref> The widespread depolarization from the shock interrupts these circuits, stopping the erratic propagation of electrical signals.<ref name=":0" /><ref name=":1" /><ref name=":2" />

After the cells depolarize, they enter a refractory period, during which they cannot be re-excited.<ref name=":3">{{Citation |last1=Wei |first1=Xingyu |title=Physiology, Cardiac Repolarization Dispersion and Reserve |date=2024 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK537194/ |access-date=2024-11-22 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30725879 |last2=Yohannan |first2=Sandesh |last3=Richards |first3=John R.}}</ref><ref name=":4">{{Cite journal |last1=Fraser |first1=James |last2=Huang |first2=Christopher L-H |date=2005-04-01 |title=The interdependence of cell volume and resting membrane potential |url=http://dx.doi.org/10.36866/pn.58.21 |journal=Physiology News |issue=Spring 2005 |pages=21–22 |doi=10.36866/pn.58.21}}</ref> This allows the heart's natural pacemaker, the sinoatrial node, to resume control of the rhythm. During this period, ion pumps actively restore the normal distribution of ions, re-establishing the resting membrane potential.<ref name=":3" /><ref name=":4" />