What increases intracellular calcium

[Dark tar]

I was watching khanacademymedicine's video on MAT (multifocal atrial tachicardia) and the association woth COPD ().
She explained the multiple automaticity foci with increased intracellular calcium. And wrote the reasons why intracellular calcium would increase, of which were hypokalemia, hypomagenesemia, and hypoxia.
I am interested right now with the hypokalemia part. Any one knows how hypokalemia would result in increased intracellular calcium?

Also, on the topic of calcium-potassium relashionship? What is the rationale behind giving calcium gluconate to a hyperkalemic patient?

I know I might be asking for too much but this would be the icing on the cake for my studies.
Many many thanks.

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[Jabbed]

I was watching khanacademymedicine's video on MAT (multifocal atrial tachicardia) and the association woth COPD ().
She explained the multiple automaticity foci with increased intracellular calcium. And wrote the reasons why intracellular calcium would increase, of which were hypokalemia, hypomagenesemia, and hypoxia.
I am interested right now with the hypokalemia part. Any one knows how hypokalemia would result in increased intracellular calcium?

Also, on the topic of calcium-potassium relashionship? What is the rationale behind giving calcium gluconate to a hyperkalemic patient?

I know I might be asking for too much but this would be the icing on the cake for my studies.
Many many thanks.

Hyperkalemia partially depolarizes the resting membrane potential, narrowing the gap between resting and threshold. Calcium stabilizes the electrical membrane by depolarizing the threshold potential.

 

[pd1112]

Hypokalemia paradoxically inhibits/decreases the conductance of potassium through Ikr channels during phases 2 & 3 of the AP, which prolongs APD & leaves other areas susceptible to EADs due to the heterogeneity of the potassium concentrations within the myocardium. Likewise, prolongation of phase 2 allows calcium channels in this phase to stay open for a longer duration, thus increasing intracellular Ca concentration, leaving areas susceptible to DADs.

 

[Dark tar]

Hypokalemia paradoxically inhibits/decreases the conductance of potassium through Ikr channels during phases 2 & 3 of the AP, which prolongs APD & leaves other areas susceptible to DADs due to the heterogeneity of the potassium concentrations within the myocardium. Likewise, prolongation of phase 2 allows calcium channels in this phase to stay open for a longer duration, thus increasing intracellular Ca concentration.

Thanks for answering. I have two more questions though, what do you mean by the "heterogeneity" of the potassium concentrations? The other question is, by what mechanism does the intracellular calcium increase automaticity? Help please

 

[pd1112]

Short answer: it's really complicated, I don't fully understand it and it's certainly beyond the scope of step 1.

Long answer that might confuse you: hypokalemia prolongs the APD throughout the heart as I said, but the potassium currents in phases 2-3 are heterogenous at different sites within the heart, such that it causes certain areas of the ventricles (mainly RV) to have prolonged refractory periods, while other areas (mainly LV) have shortened refractory periods. This results in increased susceptibility for unidirectional conduction blocks and re-entry EADs due to heterogenous increased/decreased automaticity in the ventricles. The increased intracellukar calcium causes spontaneous cycles of influx/efflux due reversal of Na-Ca exchange and the actions of SERCA, leading to EADs, DADs & aftercontractions. I don't fully understand either concept (honestly I doubt most cards fellows have a good grasp of this) but these articles will help if you have the time and are interested:

http://www.ncbi.nlm.nih.gov/pubmed/20584206
http://www.ncbi.nlm.nih.gov/pubmed/25772299
http://www.ncbi.nlm.nih.gov/pubmed/19151074

 

[Jabbed]

If you really want a deep understanding of this it's really worth spending time with a good text like Lilly's to understand the different mechanisms of arrhythmia. The questions that you're asking really boil down to "what is the mechanism of delayed after-depolarization triggered activity?"

 

[Dark tar]

I thank you both pd1112 and Jabbed. I know this is well beyond the scope of the step1 exam. I'm from a third world country with a third world-level university. I was not satisfied with the teaching in that university especially when I got a hold of the kaplan videos. Now I have this urge to understand everything rather than learning by heart, accepting and moving on. I have accepted so much crap my doctors threw at me without any explaination that I'm done with this way of learning. again I than you all very very much.

 

[Dark tar]

If you really want a deep understanding of this it's really worth spending time with a good text like Lilly's to understand the different mechanisms of arrhythmia. The questions that you're asking really boil down to "what is the mechanism of delayed after-depolarization triggered activity?"

Could you please give me an amazon link. I'd appreciate that.

 

[pd1112]

When are you taking the test?

 

[Jabbed]

Could you please give me an amazon link. I'd appreciate that.

Amazon product

 

[Dark tar]

When are you taking the test?

I have stopped my step1 prep for now. I'm graduating in approximately 3 months and I have a big national exam in my country that is required for me to earn my degree, so I'm studying for that. However, I've fininshed most of the kaplan vids and notes during the past year and so in order to understand the material. And I still come back to them once in awhile. I'm starting my first aid review right after I pass that exam. I'll take the step1 when I'm done with first aid and the usual qbanks. Approximately 5-7 months from now. I suppose step2 will be a walk in the park after all this. Any advise?

 

[Dark tar]

Amazon product

Thank you

 

[pd1112]

I don't know much about step 2. I would consider the PASS program if you really want to understand the material, but it's pretty expensive.