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Talk:Cardiac action potential

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Untitled

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Can someone alter the table so that it is not as wide--as shown it is too wide and can cover the text depending on the size of the browser window. 70.237.47.94 00:36, 19 February 2007 (UTC)Reply

EKG

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Previously in the discussion of the AP Phases, there were connections drawn between the phases of the AP and the waves of the EKG. We removed those because we believed them to be incorrect, is this the case? Or is there a connection between AP phases and EKG waves?

I did not see the previous connections you are talking about, but based on your description I believe you are correct that there is no connection between the AP phases and EKG waves. The EKG waves demonstrate the net wave of depolarization as it moves through the myocardium. The AP phases describe what is happening in each individual cell. Wtkd (talk) 17:21, 23 July 2010 (UTC)Reply

The above statement is not correct. There is a connection between the stages of the action potential and the EKG. While the phases of the action potential explain what is happening in each myocyte, because the depolarization of a single cardiac muscle fiber depolarizes all cardiac muscle fibers, the cardiac AP can be related to the EKG waveform. Rapid depolarization of the action potential (Stage O of the action potential)is evident on the first half of the EKG P wave for the left atrium, the Q wave for the interventricular septum, and the R wave for the ventricles, respectively. This can be continued with the remaining stages. To maximize reader comprehension it may be preferable to limit the relation of the stages of the action potential to ventricular depolarization, contraction duration, and repolarization. More pragmatically, the page could be enhanced by relating the action potential stage to a relevant anti-arrhythmic and posting a EKG strip alongside showing the result of the pharmaceutical stimulation or antagonism of the stage, e.g. a Lead II strip showing Digoxin effects alongside action potential stage 2. Signed, a 2nd year Cdn RT student. — Preceding unsigned comment added by 68.147.40.99 (talk) 02:53, 30 October 2011 (UTC)Reply

Funny Current

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Added link to funny current. Not sure if "If" channels are exactly the same as the channels described in the automaticity section, though... Horus (talk) 21:54, 3 April 2008 (UTC)Reply

References

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General comment - well structured informative article but lacks references.

Expert/Updating

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This probably needs to be re-written in light of the fact that the pacemaking effects of the Inward-funny current aren't quite as describe given that blocking the If current with cesium, etc. doesn't abolish Sinoatrial nodal rhythm(If does seem important for AV node, however). Ryanodine receptors and calcium sparks are the proposed alternative method of rhythmic control. Atosecond (talk) 01:11, 23 August 2011 (UTC)Reply

Proposed merge with Autorhythmicity

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A small stub having same meaning as automaticity and much more often referred to as such. Iztwoz (talk) 09:54, 26 November 2014 (UTC)Reply

Suggesting a new section.

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This article explains the normal interaction of electrolytes and the process of depolarization and repolarization. But how is premature depolarization explained. That's happens to people who suffer from premature, or ectopic, heartbeats. The heart cells depolarize prematurely causing a contraction to happen before the next normal contraction. It is felt as a thump in the chest followed by what seems to be a skipped beat (actually the filling cycle resetting). In regard to the interaction of electrolytes, what is actually happening during premature depolarization? Is there a chemical reason for it?

2600:8801:B011:300:B09F:3FEF:E7EB:2AC5 (talk) 00:05, 26 February 2021 (UTC) Thanks, James.Reply

Redundancy

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In section Channels, Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as a gene.

I don't know if someone reading this article doesn't know that or needs to be reminded of this fact. Hah! Smlckz (talk) 02:52, 9 April 2021 (UTC)Reply

Possible Errors in Descriptions of Chloride Ion Movement Directions

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In the two diagrams of action potentials:

https://commons.wikimedia.org/wiki/File:Cardiac_action_potential.png

https://commons.wikimedia.org/wiki/File:Action_potential_ventr_myocyte.gif

I believe that the labelling for chloride ions (Cl-) is inaccurate, as it describes Cl- leaving/exiting the cell ("out"). The relevant current, ICl(Ca), also known as Ito2 ("to" meaning "transient outward"; see: https://pmc.ncbi.nlm.nih.gov/articles/PMC2290232/), is produced by the electrochemical gradient of migrating Cl- ions, mediated by chloride channels in the membrane; as calcium Ca2+ ions from the sarcoplasmic reticulum unbind and enter the cytoplasm in phase one, they activate these chloride channels. Since the extracellular concentration of Cl- is higher than the intracellular concentration, these channels would have Cl- enter the cell, travelling down their chemical concentration gradient. The electrical gradient, however, would still be outward, as negatively charged ions entering the cell would act as a repolarizing force across the membrane. Electrostatically, positive ions leaving the cell, and negative ions entering the cell, have the same repolarizing effect.

Further, while https://pmc.ncbi.nlm.nih.gov/articles/PMC2290232/ indicates that the ICl(Ca) current is most important in phase 1, it also states that it occurs in phase 2, supporting (and consistent with) the article's description of Cl- movement (described as "influx") in phase 2: "The movement of all these ions results in the membrane potential remaining relatively constant, with K+ outflux, Cl− influx as well as Na+/K+ pumps contributing to repolarisation and Ca2+ influx as well as Na+/Ca2+ exchangers contributing to depolarisation." Aspensmonster (talk) 09:50, 31 August 2026 (UTC)Reply