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medstu2006

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I'm a first year med student and I was confused about the foll. question.
What happens to the membrane potential if the Na/K ATPase is blocked? Does it hyperpolarize or depolarize?

I thought that the membrane potential hyperpolarizes because K ions are leaking out of the cells through leak channels, thus the cell is becoming more neg. since pos. charges are leaving the cell. But the ans. is the cell membrane depolarizes. Can anyone explain this?
 

anon-y-mouse

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I'm a first year med student and I was confused about the foll. question.
What happens to the membrane potential if the Na/K ATPase is blocked? Does it hyperpolarize or depolarize?

I thought that the membrane potential hyperpolarizes because K ions are leaking out of the cells through leak channels, thus the cell is becoming more neg. since pos. charges are leaving the cell. But the ans. is the cell membrane depolarizes. Can anyone explain this?

Your assumption is that the Na/K ATP-ase exactly counterbalances the leak K channels. This is an incorrect assumption.

What happens when an action potential is fired? Na rushes into the cell, and so on, you know the rest. The purpose of the Na/K pump is to push 3 Na out (and 2 K in) to maintain the cell potential. What happens if you keep firing action potentials and don't have the Na/K pump to reset the Na levels to where they should be? Too much Na buildup inside the cell. Hence, the cell membrane is depolarized (becomes closer to a 0 V potential difference of charges inside and outside the cell).

I think this is right, someone can correct me if not.
 

braluk

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Im goin to take a shot at this, but Im probably off since the action potential block of med physiology was a long time ago in the fall but here goes:

potassium leaks out of the cell bringing the membrane to a hyperpolarized state
In a normal cell at rest that gets depolarized from an action potential:

Closed Na Channel--> Open Na Channel --> Inactive Na Channel ---------------> Closed Na Channel (takes long for Inactive--> closed state- which explains the absolute refractory period of an AP)

A hyperpolarized state will increase the number of closed Na channels relative to inactivated Na channels which makes it much easier to depolarize. (hyperpolaized membranes are easier to depolarize than partially depolarized membranes because Na channels inactivate at aorund -50mV while virtually all Na channels are in the closed, "ready to open" state when it is hyperpolarized around -90mV). Thus a cell easily depolarizes with an incoming action potential, but it stays depolarized because Na/K pump cannot function to bring the cell back to hyperpolarization.

Also, keep in mind it probably takes many many action potentials before the chemical concentrations significantly change.
 
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anon-y-mouse

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because Na/K pump cannot function to bring the cell back to hyperpolarization.

This is NOT what the pump does. It maintains the resting membrane potential (which is polarized, i.e. negative with respect to the outside). The definition of "hyperpolarization" is "even more polarized (i.e. more negative) than RMP"... thus an action potential is depolarization, repolarization, hyperpolarization, then after-hyperpolarization (as the K channels inactivate). I know what you're basically trying to say (which isn't what the original guy asked, I think), but you're using the wrong terminology... hyperpolarization (if you can even call that a state) is transient, the dip under the resting membrane potential after an action potential. Wow, too many parentheses.
 

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you got it right anon-y-mouse. in a normal working cell, the Na/K ATP-ase hyperpolizes the cell (albeit its contribution to the membrane resting potential is minimal), so by blocking the pump, the opposite will occur.

taking it one step further, what happens next (in the cardiac cell)? higher levels of Na in the cell reduces the effectivness of the Na/Ca exchanger, and thus keeps Ca in the cell longer. This leads to a positive inotropic effect, longer APs, and a slower heart rate.

A drug that does this is digitalis (remeber James Bond in Casino Royale, although they messed it up since digitalis poisoning causes brady and not tachycardia)


Your assumption is that the Na/K ATP-ase exactly counterbalances the leak K channels. This is an incorrect assumption.

What happens when an action potential is fired? Na rushes into the cell, and so on, you know the rest. The purpose of the Na/K pump is to push 3 Na out (and 2 K in) to maintain the cell potential. What happens if you keep firing action potentials and don't have the Na/K pump to reset the Na levels to where they should be? Too much Na buildup inside the cell. Hence, the cell membrane is depolarized (becomes closer to a 0 V potential difference of charges inside and outside the cell).

I think this is right, someone can correct me if not.
 

Miami_med

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you got it right anon-y-mouse. in a normal working cell, the Na/K ATP-ase hyperpolizes the cell (albeit its contribution to the membrane resting potential is minimal), so by blocking the pump, the opposite will occur.

taking it one step further, what happens next (in the cardiac cell)? higher levels of Na in the cell reduces the effectivness of the Na/Ca exchanger, and thus keeps Ca in the cell longer. This leads to a positive inotropic effect, longer APs, and a slower heart rate.

A drug that does this is digitalis (remeber James Bond in Casino Royale, although they messed it up since digitalis poisoning causes brady and not tachycardia)

Yeah, though in the cardiac cell, the change in Na/K function induced by say Digitalis is primarily a failure to repolarize the cell, due to the continuous activity of cardiac myocytes. The Na/K pump both maintains polarity AND helps to hyperpolarize the cell. In vitro, a cell with a poisoned Na/K ATPase will depolarize very slowly, as Na and K balance out (along w/ the charge) across a semi-permeable membrane. In a cell that recently depolarized however, the Na/K pump helps to bring it back to its resting potential (a polarized state), and blocking the pump prevents the cell from depolarizing as much.
 
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From an energy perspective (correct me if I'm wrong), the cell wants to be at the lowest energy state which is depolarized (at perfect equillibrium with the ECF). The main (only?) source of energy to create membrane polarization comes from the Na/K ATPase, which converts the bond energy of ATP into the membrane gradient. If you kill the Na/K ATPase, you remove the energy source that powers the membrane polarization, so the membrane will tend to go back to its equillibrium state.
 

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Your assumption is that the Na/K ATP-ase exactly counterbalances the leak K channels. This is an incorrect assumption.

What happens when an action potential is fired? Na rushes into the cell, and so on, you know the rest. The purpose of the Na/K pump is to push 3 Na out (and 2 K in) to maintain the cell potential. What happens if you keep firing action potentials and don't have the Na/K pump to reset the Na levels to where they should be? Too much Na buildup inside the cell. Hence, the cell membrane is depolarized (becomes closer to a 0 V potential difference of charges inside and outside the cell).

I think this is right, someone can correct me if not.
This is absolutely correct!

It's all about keeping it simple. The question is testing your understanding of only two points: 1) The number of ions, the charge, and the direction of flow when the pump is working. 2) Knowing that membrane potential is internally negative at rest (measured inside with respect to outside) and that the potential can change with the flux of ANY ion - not only as you learn conventionally via the action potential (where K+ efflux hyperpolarizes). It's got nothing to do with voltage-gated ion channels at this stage. 3Na+(out)/2K+(in) when it's working, so net +1 out (hyperpolarization)...and the opposite if you inhibit the pump.
 

sirus_virus

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I'm a first year med student and I was confused about the foll. question.
What happens to the membrane potential if the Na/K ATPase is blocked? Does it hyperpolarize or depolarize?

I thought that the membrane potential hyperpolarizes because K ions are leaking out of the cells through leak channels, thus the cell is becoming more neg. since pos. charges are leaving the cell. But the ans. is the cell membrane depolarizes. Can anyone explain this?

I think the focus of the answer should be simply on the Na/K ATpase, because if you are going to bring up K+ leaving the cell, then you might as well bring up other ways Na+ enters the cell(Na-glucose cotransport, Na-ca countertransport, Na-H exchange etc). But if you keep it simple, then you will see that Anonymouse is correct.
 

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the na/k pump is just a bilge pump for the na that leaks in and the potasium that leaks out.
 

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What happens to the membrane potential if the Na/K ATPase is blocked? Does it hyperpolarize or depolarize?

After the Na+ rushes into the cell during an A.P., the voltage gated Na+ channels close so Na+ is locked in the cell (The K+ ions that were pumped in earlier are still locked in the cell also). The result is a cell that is actually temporarily more positive than it's outside environment, AND the concentration of Na+/K+ is greater inside the cell at this point. This difference causes the V.G. K+ channels to open and the K+ travels down the gradient and into the environment outside the cell. (Keep in mind that the Na+ couldn't go anywhere b/c it's V.G. Na+ channels are still closed.)

Now we have a situation where Na+ is locked into the cell and after the V.G. K+ close, the K+ is locked out. This is where the Na/K pump kicks in to restore the RMP of -90mv. (3Na+ out and 2K+ in)

If Na/K ATPase is blocked, the sodium ions inside the cell after an A.P. will stay there since there is no pump to remove them. The K+ ions will be close to equilibrium, but not in the cell where they will be needed later to help w/ repolarization. The result will be K+ ions close to equilibrium inside/outside the cell and a charge more positive than the -90mv RMP due to the NA+ ions stuck inside the cell. Since the cell never becomes repolarized, it can't depolarize again in response to a neighboring cells neurotransmitters.

Somebody please correct me if I'm wrong or missed something.
 
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cfdavid

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I think that the logic goes as follows. First, recall that the resting membrane potential is determined MOSTLY by the ratio of K+ inside the cell relative to outside the cell. I say mostly, because the permeability of K+ far surpasses that of the other major ions.

Again, this is a concept that requires one to "look at it this way", because it can be reasoned in a few different ways that could lead someone down the wrong track. SO, think of how the K+ is NOT being pumped back into the cell anymore (due to inhibition (or damage, like MI) of the Na+/K+ pump).

Now, sure, what about those leak channels..... Wouldn't K+ just leak out (since it's way more permeable than those other ions)? And, wouldn't this suggest a hyperpolarization??? Yeah, but that's not the right LOGIC.

Always consider the Nerst potential. And think about this new ratio of an increased concentration of K+ outside of the cell relative to that inside the cell. This will make it less attractive for K+ to want to leave the cell (through those leaky channels), since there's now more K+ outside due to inhibition of the Na+/K+ ATPase. So, the new membrane potential is now LESS NEGATIVE (not more negative), and therefore slightly depolarized. Again, it's all in the Nerst equation.
 
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fakin' the funk

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I have a related question.

So, to my knowledge, hypokalemia hyperpolarizes the membrane, and hyperkalemia depolarizes the membrane.

Which causes INCREASED activity of excitable cells? I think the logical answer is hyperkalemia (moves RMP closer to 0), however, isn't there some hitch about how RMP depolarization closes the Na+ channels that are initially active in an action potential?

Thx
 
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sirus_virus

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I have a related question.

So, to my knowledge, hypokalemia hyperpolarizes the membrane, and hyperkalemia depolarizes the membrane.

Which causes INCREASED activity of excitable cells? I think the logical answer is hyperkalemia (moves RMP closer to 0), however, isn't there some hitch about how RMP depolarization closes the Na+ channels that are initially active in an action potential?

Thx

I think neither one of them do, because excitability depends on the ability to rapidly depolarize an repolarize. Both things lead to an ultimate increase in threshold, therefore reduced excitability.
 

sacallaco

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forget about the membrane potential, your cells will burst and youll be dead in a few seconds!
 

G0S2

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the na/k pump is just a bilge pump for the na that leaks in and the potasium that leaks out.

This is the best explanation so far, seriously. Na is high on the outside and K is high on the in. Block the pump and which way will things move? Down their concentration gradients. Once you understand how drugs work next year, like digitalis with regard to the Na/K-ATPase, it will clarify some physio and vice versa.
 

sacallaco

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you got it right anon-y-mouse. in a normal working cell, the Na/K ATP-ase hyperpolizes the cell (albeit its contribution to the membrane resting potential is minimal), so by blocking the pump, the opposite will occur.

taking it one step further, what happens next (in the cardiac cell)? higher levels of Na in the cell reduces the effectivness of the Na/Ca exchanger, and thus keeps Ca in the cell longer. This leads to a positive inotropic effect, longer APs, and a slower heart rate.

A drug that does this is digitalis (remeber James Bond in Casino Royale, although they messed it up since digitalis poisoning causes brady and not tachycardia)

dude what are you talking about? Digitalis is a cardiac stimulant and if overdosed or poisoned, the victim would at least have tachycardia, fibrillation and what not.

oh and for the OP, you would have extreme depolarization which technically couldnt occur because of what I said earlier.
 

G0S2

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dude what are you talking about? Digitalis is a cardiac stimulant and if overdosed or poisoned, the victim would at least have tachycardia, fibrillation and what not.

oh and for the OP, you would have extreme depolarization which technically couldnt occur because of what I said earlier.


Digitalis increases cardiac contractile stength (inotropic), not rate. It is used to Tx heart failure to increase the ejection fraction.
 

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I don't get how a bolus of digitalis leads to brachycardia....

I thought that digitalis is a Na/K/ATPase block (though a block for only alpha types 2 and 3 sodium pumps, which are located near the junctional complex.) This would lead to locally increased [Na] in the junctional complex. This increased [Na] would then cause the NCX to facilitate the movement of Na down its local concentration gradient (meaning out of the cell) in exchange for Ca into the cell. This local Ca would then bind to an RyR, releasing calcium stored in the SR, which then causes cardiac fiber contraction. Following this first contraction, all the calcium (including the new calcium brought in by the NCX) is sequestered into the SR. Since digitalis is still locally blocking the Na/K/ATPase, this cycle keeps repeating itself, but each time, more and more calcium is resequestered into the SR.

I would think this cycle would cause greater force contractility and a smaller time period between thresholds since the cell is becoming more and more depolarized over time. Wouldn't this then lead to increased HR followed by death due to eventual loss of the cell's ability to repolarize/relax?
 

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Digitalis increases cardiac contractile stength (inotropic), not rate. It is used to Tx heart failure to increase the ejection fraction.

I seem to remember learning that only a moderate/small amount of digoxin could be of benefit in heart failure, since its effect would then only be temporary (i.e., not last long enough to be detrimental and cause death.)
 

G0S2

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I seem to remember learning that only a moderate/small amount of digoxin could be of benefit in heart failure, since its effect would then only be temporary (i.e., not last long enough to be detrimental and cause death.)

You are correct in that it has a low therapeutic index, however, it is used in some patients that can be accurately titrated for the Tx of of left-ventricular failure after all else has been tried (ACEi's etc).
 

cfdavid

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I don't get how a bolus of digitalis leads to brachycardia....

I thought that digitalis is a Na/K/ATPase block (though a block for only alpha types 2 and 3 sodium pumps, which are located near the junctional complex.) This would lead to locally increased [Na] in the junctional complex. This increased [Na] would then cause the NCX to facilitate the movement of Na down its local concentration gradient (meaning out of the cell) in exchange for Ca into the cell. This local Ca would then bind to an RyR, releasing calcium stored in the SR, which then causes cardiac fiber contraction. Following this first contraction, all the calcium (including the new calcium brought in by the NCX) is sequestered into the SR. Since digitalis is still locally blocking the Na/K/ATPase, this cycle keeps repeating itself, but each time, more and more calcium is resequestered into the SR.

I would think this cycle would cause greater force contractility and a smaller time period between thresholds since the cell is becoming more and more depolarized over time. Wouldn't this then lead to increased HR followed by death due to eventual loss of the cell's ability to repolarize/relax?

That's pretty much what I learned. Only, I was thinking more along the lines of "knocking out" the Na+/K+ ATPase essentially decreases the gradient for Na+ driving into the cell. Thus, less Ca2+ is shuttled out of the cell and this increases the intracellular Ca2+ concentration. Therefore, this increases contractility (pos. inotropicity).

I'd imagine, like everything else in medicine, there would be side effects. In fact, I know that digitalis also has diuretic effects in that when it inhibits the Na+/K+ ATPase in renal tubular cells, this lessens the gradient for Na+ to be reabsorbed. Thus, you see more Na+ and H2O excreted in the urine.

I'd think that dosing is critical, as it would be for most drugs....
 

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Digitalis poisoning does not kill people because of bradycardia...digitalis in an overdose prolongs the QT interval and this can result in ventricular tachycardia and ventricular fibrillation (so it would in a poisoning situation actually cause tachycardia per se).
 

anon-y-mouse

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Digitalis poisoning does not kill people because of bradycardia...digitalis in an overdose prolongs the QT interval and this can result in ventricular tachycardia and ventricular fibrillation (so it would in a poisoning situation actually cause tachycardia per se).

Umm, don't you mean *shortens* the QT interval causing VF?

As for digitalis, it definitely prolongs the PR interval (tons of intracellular Na, meaning tons of intracellular Ca, b/c Na/Ca has nothing to work on... hence prolonged AP, positive inotropic effect... but in toxic quantities, this delays the AP so much that successive AP's happen during the refractory period). This is obviously under non-toxic circumstances hence the bradycardia, but under toxic circumstances, the huge conduction delay causes v tach / vfib i.e. through short QT.

Agh... someone please clarify if I'm incorrect.
 

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Some of you have really not grasped how the resting potential is generated. I apologize in advance for any possible errors in my handling of the English technical terms, as I am from, and am studying in, a non English speaking country.

The resting membarne potenital is generated by interaction of :

1. The conductances of the ions
2. The driving force for the ions

As there is a higher potassium concentration in the intracellular fluid compared to the extra cellular fluid, potassium tends to diffuse out of the ion channels in the membrane. This, however, creates an excess of postive charge on the outside of the cell. This gives rise to an electric force wanting to push potassium into the cell again. The energy arising from the concentration gradient can be calculated, the same goes for the energy created by the potential difference across the membrane. In steady state, these two driving forces are equal, hence one can put "Energy stored in the concentration gradient" = "Energy in the separation of electrical charge", and one gets the Nernst equation.

If the membrane is only permeable to potassium, then there will be no net movement of potassium over the membrane, as no current flows in the steady state. As current is proportional to the charge of the ion and the net movement of the ion, there can be no net movement of potassium, as that would give rise to a current that would change the membrane potential.

However, the leak channels of the neuron are permeable to both potassium and sodium. Hence the resting membrane potential is a compromise between the equilibrium potentials for sodium and potassium. The flow of these ions through the channels is determined by:

1. The conductance of the ion channels for the ion in question
2. The size of the force driving the ions through the channels

This gives rise to a current which is proportional to the conductance and the driving force. ( I = U/R Conductance = 1/R). As the permeability for potassium is greater, the membrane potential will have to be closer to the equilibrium potential for potassium to reach steady state. When the outward current carried by potassium is equal to the inward current carried by sodium, no net current flows across the membrane, and the resting potential has been reached. However, notice that although no net charge flows across the membrane, both sodium and potassium still flows down their concentration gradients!

This means that if the Na/K ATPase is blocked, sodium and potassium will flow down their concentrations gradients, which in the end results in that these gradients will disappear. This necessarily gives rise to a depolarisation, as the negative membrane potential is generated by the gradients in the first place. Of a bizarre reason, some peope in this thread seem to believe that the leak channels are impermeable to sodium, this is not the case. The Na/K ATPase do have an electrogenic effect (albeit very small), but it is NOT involved in the hyperpolarisation of a cell after it has fired an action potential. In fact, nor are voltage sensitive potassium channels necessary, which is illustrated by myelin sheated axons who lack these ions channels at the nodes of ranvier. (They are loacted in the internode) The hyperpolaraisation at a node of ranvier is caused by the closing of the voltage sensitive sodium channels. This returns the conductance of the membrane to normal. As the membrane potential at this point deviates from the resting membrane potential (decided by the concentrations of the ions), an outward current will flow out of the leak channels and return the membrane potential to its resting level.
 

anon-y-mouse

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Some of you have really not grasped how the resting potential is generated. I apologize in advance for any possible errors in my handling of the English technical terms, as I am from, and am studying in, a non English speaking country.

The resting membarne potenital is generated by interaction of :

1. The conductances of the ions
2. The driving force for the ions

As there is a higher potassium concentration in the intracellular fluid compared to the extra cellular fluid, potassium tends to diffuse out of the ion channels in the membrane. This, however, creates an excess of postive charge on the outside of the cell. This gives rise to an electric force wanting to push potassium into the cell again. The energy arising from the concentration gradient can be calculated, the same goes for the energy created by the potential difference across the membrane. In steady state, these two driving forces are equal, hence one can put "Energy stored in the concentration gradient" = "Energy in the separation of electrical charge", and one gets the Nernst equation.

If the membrane is only permeable to potassium, then there will be no net movement of potassium over the membrane, as no current flows in the steady state. As current is proportional to the charge of the ion and the net movement of the ion, there can be no net movement of potassium, as that would give rise to a current that would change the membrane potential.

However, the leak channels of the neuron are permeable to both potassium and sodium. Hence the resting membrane potential is a compromise between the equilibrium potentials for sodium and potassium. The flow of these ions through the channels is determined by:

1. The conductance of the ion channels for the ion in question
2. The size of the force driving the ions through the channels

This gives rise to a current which is proportional to the conductance and the driving force. ( I = U/R Conductance = 1/R). As the permeability for potassium is greater, the membrane potential will have to be closer to the equilibrium potential for potassium to reach steady state. When the outward current carried by potassium is equal to the inward current carried by sodium, no net current flows across the membrane, and the resting potential has been reached. However, notice that although no net charge flows across the membrane, both sodium and potassium still flows down their concentration gradients!

This means that if the Na/K ATPase is blocked, sodium and potassium will flow down their concentrations gradients, which in the end results in that these gradients will disappear. This necessarily gives rise to a depolarisation, as the negative membrane potential is generated by the gradients in the first place. Of a bizarre reason, some peope in this thread seem to believe that the leak channels are impermeable to sodium, this is not the case. The Na/K ATPase do have an electrogenic effect (albeit very small), but it is NOT involved in the hyperpolarisation of a cell after it has fired an action potential. In fact, nor are voltage sensitive potassium channels necessary, which is illustrated by myelin sheated axons who lack these ions channels at the nodes of ranvier. (They are loacted in the internode) The hyperpolaraisation at a node of ranvier is caused by the closing of the voltage sensitive sodium channels. This returns the conductance of the membrane to normal. As the membrane potential at this point deviates from the resting membrane potential (decided by the concentrations of the ions), an outward current will flow out of the leak channels and return the membrane potential to its resting level.

Wow :thumbup: :thumbup: It's clear why Sweden is so much more awesome than America...

ps, are there study abroad opportunities at your school? That is, if I (an American med student) wanted to do a rotation there, could I do it? I don't speak any Germanic languages let alone Swedish... would this be difficult?
 

Thievery Corp.

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Umm, don't you mean *shortens* the QT interval causing VF?

As for digitalis, it definitely prolongs the PR interval (tons of intracellular Na, meaning tons of intracellular Ca, b/c Na/Ca has nothing to work on... hence prolonged AP, positive inotropic effect... but in toxic quantities, this delays the AP so much that successive AP's happen during the refractory period). This is obviously under non-toxic circumstances hence the bradycardia, but under toxic circumstances, the huge conduction delay causes v tach / vfib i.e. through short QT.

Agh... someone please clarify if I'm incorrect.

I don't recall that toxicity of digitalis was related to the QT interval (short or long-Torsade de point), rather that it caused delayed after-depolarizations, because of the increased amounts of Ca++ hanging around, which was what would degenerate into VF/VT. I believe the toxicity of digitalis is also increased in hypokalemic, and hypomagnesimic (sp?) pts.
 

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Im goin to take a shot at this, but Im probably off since the action potential block of med physiology was a long time ago in the fall but here goes:

potassium leaks out of the cell bringing the membrane to a hyperpolarized state
In a normal cell at rest that gets depolarized from an action potential:

Closed Na Channel--> Open Na Channel --> Inactive Na Channel ---------------> Closed Na Channel (takes long for Inactive--> closed state- which explains the absolute refractory period of an AP)

A hyperpolarized state will increase the number of closed Na channels relative to inactivated Na channels which makes it much easier to depolarize. (hyperpolaized membranes are easier to depolarize than partially depolarized membranes because Na channels inactivate at aorund -50mV while virtually all Na channels are in the closed, "ready to open" state when it is hyperpolarized around -90mV). Thus a cell easily depolarizes with an incoming action potential, but it stays depolarized because Na/K pump cannot function to bring the cell back to hyperpolarization.

Also, keep in mind it probably takes many many action potentials before the chemical concentrations significantly change.
Above post has confusing explanation. Inaccurate role of the Na/K pump.
medstu2006, Take the post of anon-y-mouse. Simpler :thumbup:
JohanK's is OK too, but rather long for a short simple question :)
 
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Critical Mass

Whoa--it's like one of those "let's pimp each other threads" from the clinical rotations forums.

There is no reason to worry about potassium balance when you can just instruct your patient to decrease or increase banana consumption. I hope that they have that option on step 1.
 
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