After cath with reperfusion dysrhythmias- WHY at the cellular level?

geekgolightly, BSN, RN · Nov 1, 2009

I want to know this, too. Good question!

Editorial Team / Admin · Nov 1, 2009

Found one article with some info:

http://circres.ahajournals.org/cgi/content/full/89/9/741

Apparently there are still many unanswered questions about the exact cellular mechanism during the reperfusion phase.

I agree, good question! :up:

fiveofpeep · Nov 1, 2009

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role is ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhytmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations.

Source: http://www.ncbi.nlm.nih.gov/pubmed/9919746

this is from 1998 though, yeck!

buddiage · Nov 2, 2009

I thank you for your responses. I got something now (which is better than nothing). Seriously, 1990's info? Man, doesn't any university want to know? I had a difficult time finding anything on the itnernet that described WHY as opposed to that it actually occurs. I'll bring it up at the floor rounds. If I get anything better, I'll post it so we can all be edified.

in2bate71, BSN, RN · Nov 2, 2009

I get the cardiac cells are "irritable." I don't understand why oxygenated blood would cause dysrhythmias when the heart muscle needs the oxygen. What is going on here? Is there something happening with the electrolytes? Is there lactic acid buildup and then too quick of a shift with oxygenated blood? Someone help me out, please.

I think it has to do with the washout that occurs after reperfusion...sends lactic acid, Ca++, etc downstream which angers the myocytes. Good question, I'm going to have to look it up.

buddiage · Nov 3, 2009

Sounds plausible. If you find out, let me know. :0)

allnurses Guide · Nov 3, 2009

The problem would be how to study it - at least in humans. Couldn't really induce reperfusion arryhthmias to study at cellular level. Looks like most of the research is in rats.

in2bate71, BSN, RN · Nov 3, 2009

the problem would be how to study it - at least in humans. couldn't really induce reperfusion arryhthmias to study at cellular level. looks like most of the research is in rats.

i agree, most of the articles i found describe rat studies. the only thing i found:

http://books.google.com/books?id=avsue7nh7bmc&lpg=pa67&ots=kdyuiekfoc&dq=lethal%20reperfusion%20injury&pg=pa66#v=onepage&q=lethal%20reperfusion%20injury&f=false

starts on page 66.

some other articles...nothing profound but here they are anyway:

http://www.pathologyportal.org/97th/pdf/companion20h04.pdf

http://ajpheart.physiology.org/cgi/content/full/289/1/h2

buddiage · Nov 3, 2009

That (google one) was an excellent source! Thank you!

Zookeeper3 · Nov 10, 2009

the problem would be how to study it - at least in humans. couldn't really induce reperfusion arryhthmias to study at cellular level. looks like most of the research is in rats.

great thesis suggestion. this could simply be done in the cath lab and in the first two hours post plasty in the icu. i can't believe it's only studied in rats, yet probably because the treatment is so standard and won't make and more pharmacutical $$$$, we won't find more studies!

i love reprofusion arrythmias, we've merged all the icu staff and those bursts freak out the micu and sicu nurses, it gets the adrenaline moving!