hypokalemia and long qt

[cage92]

i need someone to explain how hypokalemia cause long qt interval and how long qt predispose to torsade

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[Psai]

What is a qt interval? What channels are involved? How does hypokalemia affect those channels?

 

[cage92]

can you explain it more?

 

[tantacles]

can you explain it more?

S/he's trying to help you answer the question yourself. So start answering the questions.

1. What is a QT interval?

 

[cage92]

qt interval is mechanical ventricular contraction as first aid said

 

[cage92]

it means ventricular depolarization and repolarization and i think hypokalemia will lead to hyperpolarization this mean will increase the threshold? plz explain more

 

[thehundredthone]

You need to think about QT interval as an electrophysiological process first. What you quoted from First Aid is simply the electromechanical association which is temporal, i.e. it just means "this is what the heart is actually doing when the ECG wave shows this". There is a delay between what happens on the ECG and in the heart muscle.

So, going back to what the other posters have asked, try to answer them based on what's happening with the ion channels, etc.

 

[nidusiamnot]

Lolz QT is interval for vent dep and rep. Depol occurs due to Na+ but the K+ outflow is responsible for the repol, so if there is hypokalemia isn't the gradient f*cked due to repol delay? as for torsade, what is it? an irregular twisting around a wire ie. polymorphic, now why does that happen? because depol happens within the rrp. hmm if i'm stupid, help me out here too!

 

[Psai]

ok depolarization is basically Na+ inflow. repolarization is k+ outflow with an early plateau because of ca flowing in.

k+ is high in cell. it's pumped in by a whole bunch of powered channels and k+ diffuses out passively.

k+ repolarizes the cell membranes back to the resting state by being pumped in by different pumps including na/k pump. if you have low k+ extracellularly (or if you use drugs that decrease k+ pump action like class 1a, class iii), cell becomes negative because more k+ will diffuse out to help balance the lower k+ outside the cell more causing hyperpolarization. remember that there's a balance between electrical charge and concentration of various ions in the cells. na is high outside, k is high inside. so na leaks in easily, k leaks out easily. the concentrations are maintained by different channels, most importantly the na/k pump. if your cell is hyperpolarized then it's far from threshold, takes longer for enough na influx to reach threshold so you have a long qt (longer time for depolarization and repolarization)

prolonged qt leads to increased chance for early afterdepolarizations (secondary depolarization that occurs before a real full depolarization which happens because there's enough time for recovery of inactivated calcium channels that reopen early and add inward positive current to depolarize). if the myocardium reaches threshold from an early afterdepolarization, there's a premature ventricular beat which can lead to complex reentrant circuits resulting in polymorphic ventricular tacyhcardia. we see this on the ekg as a changing qrs axis pattern called torsades


something like that. you don't need someone to explain things to you. you need to sit down and figure things out for yourself. there are stupid doctors out there that don't know what they're doing because they don't think about things. i'm probably one of these people but i strive to learn why things happen. don't wait for people to explain things to you, try to figure it out

 

[aspiringmd1015]

google the **** out of it, and then post. Thats what i do at least, even though i have pretty basic and dumb questions all the time.

 

[thehundredthone]

if you have low k+ extracellularly (or if you use drugs that decrease k+ pump action like class 1a, class iii), cell becomes negative because more k+ will diffuse out to help balance the lower k+ outside the cell more causing hyperpolarization.

While you're right about this in terms of the effect on resting membrane potential, it's effect on action potential is different. Hyperkalemia causes the resting membrane potential to become less negative, i.e. from -90 to -80 mV. Alongside this the threshold potential also decreases but not by as much initially. However, cardiac myocyte Ikr current channel conductance actually increases with increased serum K for unknown reasons. In hyperkalemia this increased Ikr current increases the slope of phase 2 and 3, i.e repolarisation, and that's thought to be responsible for the shortened QT and peaked T waves in hyperkalemia. See here.

Conversely, in hypokalemia, the resting membrane and threshold potential both become more negative due to the increased gradient. Myocyte automaticity is also enhanced, leading to increased risk of ectopic rhythm generation. Opposite to the mehanism of hyperkalemia, conductivity is decreased with hypokalemia, leading to a predisposition to reentrant arrhythmias. On the ECG, this delayed repolarisation flattens the T wave. See here.

In hypokalemia, there is a phenomenon called TU fusion which leads to an apparent QT prolongation because the QU is mistaken for QT. Whether or not there is actual QT prolongation in hypokalemia is not completely clear. See here and here

prolonged qt leads to increased chance for early afterdepolarizations (secondary depolarization that occurs before a real full depolarization which happens because there's enough time for recovery of inactivated calcium channels that reopen early and add inward positive current to depolarize). if the myocardium reaches threshold from an early afterdepolarization, there's a premature ventricular beat which can lead to complex reentrant circuits resulting in polymorphic ventricular tacyhcardia. we see this on the ekg as a changing qrs axis pattern called torsades

This is true. But I wonder whether the decreased Ikr may predispose to the same thing in hypokalemia, rather than through QT prolongation.

Here's an old discussion on SDN