Can anyone answer this about BIOCHEM???

[christian15213]

Ok, here is the deal... when I observe this Cardiothoracic surgeon he requires me to write something after every observation... The thing he gave me last time was about cardioplegia... and why Potasium is used as the solution. I did the reasearch and found out about the Na / K pump and all of that <I haven't had BioChem yet> but I never found anything that specifically said that rushing the outside of the cell with K+ will prevent K+ from entering into the cells of the heart thus paralyzing it. My thought is something with osmosis but does anyone else have a better explanation???

Again, with osmosis I was thinking something that the lower concentration of particles, in this case K+, will go to the higher concentration of K+ thus allowing water to move into the cell... I dunno just a thought...

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[jash0624]

Ok, here is the deal... when I observe this Cardiothoracic surgeon he requires me to write something after every observation... The thing he gave me last time was about cardioplegia... and why Potasium is used as the solution. I did the reasearch and found out about the Na / K pump and all of that <I haven't had BioChem yet> but I never found anything that specifically said that rushing the outside of the cell with K+ will prevent K+ from entering into the cells of the heart thus paralyzing it. My thought is something with osmosis but does anyone else have a better explanation???

Again, with osmosis I was thinking something that the lower concentration of particles, in this case K+, will go to the higher concentration of K+ thus allowing water to move into the cell... I dunno just a thought...

AHHH I HAVE A FINAL ON THIS IN 3 DAYS AND I HAVE NO CLUE

 

[DrZeke]

Ok, here is the deal... when I observe this Cardiothoracic surgeon he requires me to write something after every observation... The thing he gave me last time was about cardioplegia... and why Potasium is used as the solution. I did the reasearch and found out about the Na / K pump and all of that <I haven't had BioChem yet> but I never found anything that specifically said that rushing the outside of the cell with K+ will prevent K+ from entering into the cells of the heart thus paralyzing it. My thought is something with osmosis but does anyone else have a better explanation???

Again, with osmosis I was thinking something that the lower concentration of particles, in this case K+, will go to the higher concentration of K+ thus allowing water to move into the cell... I dunno just a thought...

EW... I think I know the answer, but I am so not doing your homework for you.

 

[christian15213]

AHHH I HAVE A FINAL ON THIS IN 3 DAYS AND I HAVE NO CLUE

Are you serious? what class... because I just wrote a little paper and found some great websites that speak of it and one inparticular that has great little clips of atp, kreb cycle, and the na / k pump...

let me know and I will post it...

 

[Raindrop423]

I googled it (apparently studying for finals isn't exactly holding my full attention) and here's what I found:

"The proposed mechanism for potassium cardioplegia is that an excess of extracellular potassium ions abolishes the transmembrane gradient of potassium and inhibits repolarization; the heart thus remains flaccid, with no electrical or mechanical activity. Essentially, it is arrested in diastole. This is reversed over time (~15 to 20 minutes) by normal metabolic mechanisms present within the cell."

http://www.uspharmacist.com/oldform...Feat/Cardioplegic.htm&pub_id=8&article_id=873

I haven't learned about the mechanism involved yet either, but... my guess would be that it's sort of like action potentials and the cells need to pump out the K+ so that they can be negatively charged on the inside, but they can't because there's too much K+ out there already. That's just a guess, though. My brain is a little squishy right now. Good luck, though!

 

[MonkeyNuts!]

"The proposed mechanism for potassium cardioplegia is that an excess of extracellular potassium ions abolishes the transmembrane gradient of potassium and inhibits repolarization; the heart thus remains flaccid, with no electrical or mechanical activity. Essentially, it is arrested in diastole. This is reversed over time (~15 to 20 minutes) by normal metabolic mechanisms present within the cell."

Contraction of the heart is done by action potentials - cardiac action potentials that start at the sinoatrial node I believe and then move to the atrioventricular node and then down the wall that separates the two halves of the heart. An action potential is caused by the depolarization of the membrane in a cell - after the voltage passes a certain threshold the voltage gated sodium channels shoot open and Na enters, causing the inside of membrane to become positively charged. At a peak voltage, the sodium channels shut, and then the repolarization phase begins. Voltage gated potassium channels shunt potassium out of the cell to make it negatively charged again.

If the gradient of potassium is set to oppose the voltage gated potassium channels, the cardiac cells will not repolarize, and the heart will not be able to contract because of lack of action potentials.

BOOYAH JHU BME COMES IN HANDY FOR ONCE

 

[MinnyGophers]

That reminds me of the action potential for neurons in the brain...

Sodium-potassium pump with higher concentration of sodium ions outside the axon and higher concentration of potassium ions inside the axon.
When action potential starts, sodium gates open and allow sodium to enter the axon, which drives the inside of the cell to a more positive charge -> action potential. Sodium ions overflow into the next axon and basically cause a chain like transport system.
Potassium gates then open to allow potassium ions to leave the axon which drives the inside of the axon back to original resting potential.
Eventually, the pump removes the invading sodium ions and recaptures the escaping potassium ions.

Im guessing potassium is chosen because of its +1 charge.

Or I could be totally off topic

 

[MinnyGophers]

"The proposed mechanism for potassium cardioplegia is that an excess of extracellular potassium ions abolishes the transmembrane gradient of potassium and inhibits repolarization; the heart thus remains flaccid, with no electrical or mechanical activity. Essentially, it is arrested in diastole. This is reversed over time (~15 to 20 minutes) by normal metabolic mechanisms present within the cell."

Contraction of the heart is done by action potentials - cardiac action potentials that start at the sinoatrial node I believe and then move to the atrioventricular node and then down the wall that separates the two halves of the heart. An action potential is caused by the depolarization of the membrane in a cell - after the voltage passes a certain threshold the voltage gated sodium channels shoot open and Na enters, causing the inside of membrane to become positively charged. At a peak voltage, the sodium channels shut, and then the repolarization phase begins. Voltage gated potassium channels shunt potassium out of the cell to make it negatively charged again.

If the gradient of potassium is set to oppose the voltage gated potassium channels, the cardiac cells will not repolarize, and the heart will not be able to contract because of lack of action potentials.

BOOYAH JHU BME COMES IN HANDY FOR ONCE

Drats, beat me by one minute....

 

[MonkeyNuts!]

Drats, beat me by one minute....

Wheres BSBN at he needs to see I'm good for soemthing.

YO BSBN WH#ERRE U AT

 

[christian15213]

"The proposed mechanism for potassium cardioplegia is that an excess of extracellular potassium ions abolishes the transmembrane gradient of potassium and inhibits repolarization; the heart thus remains flaccid, with no electrical or mechanical activity. Essentially, it is arrested in diastole. This is reversed over time (~15 to 20 minutes) by normal metabolic mechanisms present within the cell."

Contraction of the heart is done by action potentials - cardiac action potentials that start at the sinoatrial node I believe and then move to the atrioventricular node and then down the wall that separates the two halves of the heart. An action potential is caused by the depolarization of the membrane in a cell - after the voltage passes a certain threshold the voltage gated sodium channels shoot open and Na enters, causing the inside of membrane to become positively charged. At a peak voltage, the sodium channels shut, and then the repolarization phase begins. Voltage gated potassium channels shunt potassium out of the cell to make it negatively charged again.

If the gradient of potassium is set to oppose the voltage gated potassium channels, the cardiac cells will not repolarize, and the heart will not be able to contract because of lack of action potentials.

BOOYAH JHU BME COMES IN HANDY FOR ONCE

Thanks for the info... specifically to the last very last sentence where it says, "set to oppose" this would mean flooding it with a high concentration of potassium correct? furthermore, it doesn't really have anything to do with osmosis per se, but rather the charge is being set outside of the cell (action potential) instead of inside the cell... am I coming a bit closer to making sense now...

 

[BNSN]

"The proposed mechanism for potassium cardioplegia is that an excess of extracellular potassium ions abolishes the transmembrane gradient of potassium and inhibits repolarization; the heart thus remains flaccid, with no electrical or mechanical activity. Essentially, it is arrested in diastole. This is reversed over time (~15 to 20 minutes) by normal metabolic mechanisms present within the cell."

Contraction of the heart is done by action potentials - cardiac action potentials that start at the sinoatrial node I believe and then move to the atrioventricular node and then down the wall that separates the two halves of the heart. An action potential is caused by the depolarization of the membrane in a cell - after the voltage passes a certain threshold the voltage gated sodium channels shoot open and Na enters, causing the inside of membrane to become positively charged. At a peak voltage, the sodium channels shut, and then the repolarization phase begins. Voltage gated potassium channels shunt potassium out of the cell to make it negatively charged again.

If the gradient of potassium is set to oppose the voltage gated potassium channels, the cardiac cells will not repolarize, and the heart will not be able to contract because of lack of action potentials.

BOOYAH JHU BME COMES IN HANDY FOR ONCE

CARDIAC ELECTROPHYSIOLOGY -- WOOHOO

 

[braluk]

The Nernst Equation is important here

-2.3RT/zF log(10) [k+]inside cell/[k+]outside cell = E

The concentration of potassiun inside is high, outside is low (i.e. negative membrane potential). By increasing the concentration of potassium extracellularly, you abolish the negative membrane potential and raise it. Usually cells hyperpolarize, which increases the number of closed sodium channels in the heart. Closed sodium channels are ready to respond to depolarization. The more you increase the RMP (resting membrane potential) closer to a positive value to around -50, you decrease the number of closed sodium channels and increase the number of inactive sodium channels (the normal phase of depolarization and its accompanying channel movement is closed --> open --> inactive then slowly returning to closed again (the refractory period is usually a result of an accumulation of rate limiting inactive sodium channels). By increasing the RMP by increasing extracellular potassium, you increase the number of inactive channels, which destroys repolarization after SA node conduction pathway actiation. Thus, your heart stays in constant asystole or fibrillation until you remove the potassium drips. At least this is what I remember from my first medical physiology unit a few months ago so dont quote me.

In a nutshell: it screws up with your resting membrane potentials so your heart cannot continue to propagate the pacemaker potential of the SA node simply because it cannot repolarize/depolarize.

 

[crazy_cavalier]

Osmosis has nothing to do with this.

Here is the cardiac action potential:

Normal resting cardiac potential is determined by conductance to K+ and is usually around -90 mV (close to the equilibrium potential for K+). This is shown as Phase 4 in the diagram above. The cardiac myocyte normally experiences a sharp depolarization due to a transient increase in Na+ conductance; the inward flux of Na+ drives the potential upward (upstroke, Phase 0) thereby depolarizing the cell and triggering the action potential. This is because [Na+] outside the cell is HIGH, whereas inside the cell [Na+] is LOW... now you are causing an influx that changes the difference across the membrane, hence the depolarization.

Depolarization could also be achieved at this stage if you were to add K+ to the extracellular environment... normally the concentration of K+ outside the cell is around 4 mMol, whereas inside the cell it's something like 150 mMol. By increasing the extracellular [K+] you are in effect pushing the membrane potential from -90 mV to something positive, which depolarizes the resting cardiac myocyte potential. Now you've got cardiac myocytes that have depolarized, but they are unable to REPOLARIZE (Phase 3) because the resting potential is in effect reset from -90 mV to something +, so you can't get another depolarization... which means no more contractions.

Obviously this is not a permanent change.


Btw you might benefit from some reading at this site: http://www.answers.com/topic/cardiac-action-potential
I got the image from this site after a google search for a cardiac action potential

 

[christian15213]

Thanks this made total sense... I am sure glad I didn't mention osmosis... LOL.. but I did read on that pharma site or another something about osmoslarity or something like that... but it was about the actual solution not the mechanism you are describing.

 

[goodoldalky]

Looks like you came to the right place, the replies were correct.. All K+ will do is essentially remove resting potential. On a sidenote, though, Kevorkian used solutions of KCl to stop his " patients' " hearts with this mechanism.

 

[hp540]

thanks for the replies. I was actually cramming for my physiology final and this was actually relevant

 

[szhao]

[various correct explanations]

over all, OP this is exactly the reasoning you gave with charger rather than water, except in more complex terms and also a mechanism. when it comes down to it, charge stay in there damn it stay in there.

 

[melissainsd]

The Nernst Equation is important here

-2.3RT/zF log(10) [k+]inside cell/[k+]outside cell = E

I could have gone 8 months without seeing the nernst equation again...thanks a lot

 

[braluk]

I could have gone 8 months without seeing the nernst equation again...thanks a lot

Lol sorry to remind you, and I also apologize for breaking it to you, when you get into medical school you'll be seeing some of the equations that you memorized and forgot for the MCAT (Especially in Cardiac Phys and Membrane Potentials)

 

[Dr. Dukes]

Long story short, they use K Cl in executions...stops the heart!
Look up info about the heart's specific physiology, and you'll see why (or read what everyone else has posted...)

 

[jash0624]

Are you serious? what class... because I just wrote a little paper and found some great websites that speak of it and one inparticular that has great little clips of atp, kreb cycle, and the na / k pump...

let me know and I will post it...

Mathematical modeling in medicine. That would be great thanks!

 

[Senor Fish]

Just remember there are two potential graphs for the heart. Earlier they were talking about the autorhythmic cells (SA node, etc). That graph is NOT the potential for the autorhythmic cells- that is for the contractile cells.
I don't have a graph of the other handy, just realize there are two differnt mechanisms for the two types of cells.

SF

Osmosis has nothing to do with this.

Here is the cardiac action potential:

Normal resting cardiac potential is determined by conductance to K+ and is usually around -90 mV (close to the equilibrium potential for K+). This is shown as Phase 4 in the diagram above. The cardiac myocyte normally experiences a sharp depolarization due to a transient increase in Na+ conductance; the inward flux of Na+ drives the potential upward (upstroke, Phase 0) thereby depolarizing the cell and triggering the action potential. This is because [Na+] outside the cell is HIGH, whereas inside the cell [Na+] is LOW... now you are causing an influx that changes the difference across the membrane, hence the depolarization.

Depolarization could also be achieved at this stage if you were to add K+ to the extracellular environment... normally the concentration of K+ outside the cell is around 4 mMol, whereas inside the cell it's something like 150 mMol. By increasing the extracellular [K+] you are in effect pushing the membrane potential from -90 mV to something positive, which depolarizes the resting cardiac myocyte potential. Now you've got cardiac myocytes that have depolarized, but they are unable to REPOLARIZE (Phase 3) because the resting potential is in effect reset from -90 mV to something +, so you can't get another depolarization... which means no more contractions.

Obviously this is not a permanent change.


Btw you might benefit from some reading at this site: http://www.answers.com/topic/cardiac-action-potential
I got the image from this site after a google search for a cardiac action potential

 

[dln72183]

It might be good, if you are going to include the SA node/AV node, purkinje fibers etc. pathway, that you understand the action potential of one nueron and it's Na+/K+ gradient first needs to activate membrane channels to release nuerotransmitters in order to initiate the action potential of the nueron next in line. Remember it is the nuerotransmitters, at least in this case, that start the action potential of the nueronal signals for contraction. Within the muscle cells, it takes place in the sarcoplasmic reticulum, so there aren't nuerotransmitters there. In short, there needs to be a signal to open the floodgates.

Please somebody correct me if I'm wrong. I would hate to be walking around thinking I know somehting, but in fact just sound like a dink.