Question about hypo/hyperkalemia?

[Dr. Lector]

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What causes PVC and neuromuscular hyperexcitability hypo or hyperkalemia? What causes central nervous system depression, hypo or hyperkalemia? And how does the hypo and hperkalemias relate to acidosis and alkalosis? My lecture notes are just really confusing me.

 

[ItsGavinC]

You've got to understand the general cellular functions of each ion.

Metabolic acidosis is a common biochemical disturbance presented by patients with renal failure. Disturbances in potassium balance are serious sequelae of renal dysfunction since only a small plasma concentration is compatible with life. The usual serum K+ concentrations have a general range of 3.4-5.4 mEq/L (although many texts/professors will give you slightly different numbers here. I remember these because they are simple). Abnormal serum concentrations lead to cardiac dysrhythmias, Gl disorders, and muscle weakness.

As kidney function continues to deteriorate, hyperkalemia ensues. Fatal dysrythimias will occur when the K+ level reaches ~7 mEq/L. Therefore, acidosis results in hyperkalemia, while alkanosis results in hypokalemia.

Of course, many other factors can influence potassium levels, such as insulin, glucagon, beta-adrenergic activity, hydrogen ion concentration, and potassium intake.

Decreasing the plasma calcium level will cause increased neruomuscular activity and hyperexcitability.

 

[nuclearrabbit77]

Use the Nernst equation to see how hyper and hypokalemia affect the membrane potential.

for example: hyperkalemia:


the drive for a ion to move is dependent on the concentration difference. if the extracellular environment of potassium is higher than normal, (hyperkalemia), then the gradient for potassium to leave the cell during repolarization isn't as strong. the resting membrane potential will be less negative.

in this case, it would seem that if the cell were more depolarized, it would be easier to trigger an action potential and be more excitable. however, the inactivation gates on Na+ channels can be closed, and actually make it LESS excitable.

 

[Dr. Lector]

The nernest equation is my problem see E=60/z log Koutside/Kinside. I don't know for sure how acidosis and alkalosis affects the K concentration on the inside and outside. I do know that there is an inverse relationship between intracellular H and K but what about the outside? So if I used the nernest equation wouldn't acidosis cause k to go out and the potential to become more postive making it easier to excite cells cause they are closer to threshold? Isn't this what happens when lethal injections of KCL is given causing dysrythimias and PVC? But at the same time I'm looking at my HY bio chem book and it states acidosis causing central nervous system depression and alkalosis causing neuromuscular hypersensitivity.

 

[ItsGavinC]

Acidosis decreases K+ secretion. The blood contains excess H+; therefore, H+ enters the cell and K+ leaves the cell. As a result, the intracellular K+ concentration and the driving force for K+ secretion decrease.

The higher serum concentration of K+ as a result of this = hyperkalemia.

The converse would be true for hypokalemia.

 

[Dr. Lector]

I get the acidosis causing hyperkalemia, but what about the neuromuscular hyperexcitability, potential becoming more positive? The HY bio chem book is stating acidosis causing central nervous system depression, isn't this do to making the potential more negative?

Well rabbit, it seems your correct there is Na gate inactivation and that is what causes the nervous system depression, but what about PVC and arythimias how does that come about w/hyperkalemia and how does slowing of the hear come about w/hypokalemia?