Hyperkalemic cardiac arrest

[ManUtdForever]

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Can anyone explain to me how kyperkalemia can cause cardiac arrest? I know hyperkalemia can increase excitability of the cells but i cant relate this to cardiac arrest. Thanks

 

[sirenomelia]

http://answers.yahoo.com/question/index?qid=20080930130706AAHuN4m

 

[ModerateMouse]

http://answers.yahoo.com/question/index?qid=20080930130706AAHuN4m

"Increased potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-controlled sodium channels, but not enough to generate an action potential."

But I've always been taught that action potentials are "all or nothing."

If some sodium channels are being opened, shouldn't they all be opened?

Or is there a normal distribution of voltage gated sodium channels with respect to the sensitivity (i.e., distribution of threshold voltages)?

In that case it's understandable how only a small proportion of all the channels would be triggered.

 

[SoundofSilver]

Resting membrane potential is pretty close to the equilibrium potential for potassium since it's the most permeable ion when the cell is at rest. When extracellular potassium increases, the equilibrium potential for potassium becomes more positive and therefore resting membrane potential is more depolarized.

Due to the resting potential being more depolarized than normal, the probability of a voltage gated sodium channel activation and therefore inactivation (remember depolarization triggers opening of the M gate and closure of the H gate [H gate is time delayed]) increases and a fraction of these channels actually activate and then inactivate. In essence, due to these sodium channels that have closed their inactivation gates (which would have never occurred at normal resting potential), you have reduced the effective number of voltage gated sodium channels that can respond to a stimulus. This will cause muscle weakness because it will be harder to generate an action potential for a given excitatory post synaptic potential, but the ability to generate an action potential remains possible. The same result (muscle weakness) also happens (by a different mechanism) if extracellular potassium is too low due to higher resting hyperpolarization which makes it harder for a given stimulus to bring the cell to threshold for an action potential.

Now if you increase extracellular potassium really high, you'll basically get paralysis (or cardiac arrest) due to the fact that the cell will depolarize and will be unable to repolarize. I believe this is due to the fact that the H gates (inactivation gates) on the sodium channel need the membrane to repolarize in order to be released. This can be thought of as a never-ending absolute refractory period.

In conclusion, high extracellular potassium can cause muscle weakness and if it's high enough it can cause paralysis.

 

[ModerateMouse]

Now if you increase extracellular potassium really high, you'll basically get paralysis (or cardiac arrest) due to the fact that the cell will depolarize and will be unable to repolarize. I believe this is due to the fact that the H gates (inactivation gates) on the sodium channel need the membrane to repolarize in order to be released. This can be thought of as a never-ending absolute refractory period.

Ok, the rest makes sense, but -- why do the inactivation gates on the sodium channel need to be released in order to repolarize the membrane?

The sodium channel is only important for establishing an action potential (as the sodium rushes inside the cell), not for repolarizing.

Isn't it more the Na+/K+ pumps that re-establish the gradients?

 

[SoundofSilver]

Ok, the rest makes sense, but -- why do the inactivation gates on the sodium channel need to be released in order to repolarize the membrane?

The sodium channel is only important for establishing an action potential (as the sodium rushes inside the cell), not for repolarizing.

Isn't it more the Na+/K+ pumps that re-establish the gradients?

You're right. I guess what I was trying to say there is that generation of another action potential will be impossible since the H gates are closed. But generation of action potential is going to be impossible anyway since the cell can't repolarize. And repolarization is what resets the sodium channels. The reason the cell doesn't repolarize is the same reason why it depolarized in the first place: high extracellular potassium. The driving force of potassium out of the cell is not sufficient to bring back the membrane potential to normal resting values once you have dramatically increased the extracellular concentration. Unlike in a normal cell where there is a huge driving force for potassium to leave the cell at the peak of the action potential which is mainly what repolarizes the cell and of course Na/K ATPase helps re-establish the proper gradients.

 

[ModerateMouse]

Unlike in a normal cell where there is a huge driving force for potassium to leave the cell at the peak of the action potential which is mainly what repolarizes the cell and of course Na/K ATPase helps re-establish the proper gradients.

Didn't know this. It sounds like you are right (I thought it was just the ATPase that re-established the membrane potential, but what you are saying makes sense).

During an action potential the intracellular membrane potential increases (more Na+), which makes potassium more likely to leave the cell.

So then here is my next question. How come they use K+ to stop people's hearts during open heart surgery?

If the heart muscle is in a constant state of depolarization, doesn't this mean that the muscles will always attempt to contract, expending energy?

 

[SoundofSilver]

Didn't know this. It sounds like you are right (I thought it was just the ATPase that re-established the membrane potential, but what you are saying makes sense).

During an action potential the intracellular membrane potential increases (more Na+), which makes potassium more likely to leave the cell.

So then here is my next question. How come they use K+ to stop people's hearts during open heart surgery?

If the heart muscle is in a constant state of depolarization, doesn't this mean that the muscles will always attempt to contract, expending energy?

I could be wrong here, but I think what happens with a depolarization arrest during cardiac surgery is that the heart contracts initially but once that initial intracellular calcium influx is cleared via the sodium/calcium exchanger, calcium atpase, SERCA, etc. the heart remains in a state of flaccid paralysis.

 

[VisionaryTics]

.

 

[Marcus Brody]

It precipitates into crystals that condense into a banana which occludes the aorta.

 

[CaptainSSO]

Yo I thought it was because the cell ccouldn't repolarize? Repolarization = potassium going out. XS extracellular potassium = potassium doesnt 'go out.

Occam's razor, rigth?

So I believe the heart remains contracted.

 

[Longshanks]

Yo I thought it was because the cell ccouldn't repolarize? Repolarization = potassium going out. XS extracellular potassium = potassium doesnt 'go out.

Occam's razor, rigth?

So I believe the heart remains contracted.

It won't remain contracted. The cardiomyocyte still has ATP to release the actin-myosin interaction. As SoundofSilver stated, there'll be a contraction due to the action potential, but since the cell can't repolarize (K+ unable to leave the cell) the cell is unable to undergo another action potential, so it is not getting any signal to contract. So you are right about being unable to repolarize, and SoundofSilver also points out the effect of Ca2+ being removed as well.

 

[ManUtdForever]

Sorry guys..so in the end hyperkalemia causes the opening of some voltage gated sodium channels and 'it's because of these voltage gated channels's refractoric period the threshold for the action potential generation is rised so it will be harder to generate excitation am I right?

So basically, first hyperkalemia causes increase excitability, but then after a while it decreases the excitability. Can I make this conclusion?

Regarding the surgery part.. never came across my mind though.. bt a good question.. anyone has a complete explanation?? cant seem to get an answer by the fragments of answers..=)

 

[aldolase]

Reviving an old thread but I have a question:

If extracellular potassium gets very high, can't it act like sodium and go do down the gradient through (leak channels or voltage gated) into the cell to create action potential?

 

[SpecterGT260]

But I've always been taught that action potentials are "all or nothing."

If some sodium channels are being opened, shouldn't they all be opened?

Or is there a normal distribution of voltage gated sodium channels with respect to the sensitivity (i.e., distribution of threshold voltages)?

In that case it's understandable how only a small proportion of all the channels would be triggered.

K flux is an important step in repolarization of cardiac muscle. Hyperkalemia = no/reduced k gradient

 

[SpecterGT260]

Reviving an old thread but I have a question:

If extracellular potassium gets very high, can't it act like sodium and go do down the gradient through (leak channels or voltage gated) into the cell to create action potential?

No. While there are generic ion channels around, they play no significant role in AP. Extracellular K will depolarise the cells by itself.

 

[aldolase]

No. While there are generic ion channels around, they play no significant role in AP. Extracellular K will depolarise the cells by itself.

Ok. I get how inc. extracellular K can alter the ratio of nerst equation and depolarize the cell. I was wondering though as to why K+ doesn't go into the cell down the gradient if extracellular K is high.

 

[ChE04]

Ok. I get how inc. extracellular K can alter the ratio of nerst equation and depolarize the cell. I was wondering though as to why K+ doesn't go into the cell down the gradient if extracellular K is high.

I don't know that you'd be alive if you had an extracellular K concentration that was high enough to completely reverse the gradient. Seems to me you would be seriously f'ed up before it got to that point (potassium concentration outside the cell is something like 30x less than the concentration inside).

 

[SpecterGT260]

Ok. I get how inc. extracellular K can alter the ratio of nerst equation and depolarize the cell. I was wondering though as to why K+ doesn't go into the cell down the gradient if extracellular K is high.

It might to a small extent but that doesn't play a significant role in the problem. Remember that EC K would depolarize so flowing back in would move towards repolarization. Depo isn't just flux of ions, it is flux of specific ions causing changes in specific ions gradients.