Several members of my seminar asked me to try to explain the skeletal muscle weakness and heart

arrhythmias seen with high and low K.

Here goes...

First, remember the phases of the cardiac transmembrane potential...draw yourself an action potential...I can't
do it here nor paste it in...sorry:
0 = FAST Na entry into the cardiac fiber (elec and chem gradients favor Na entry)s
1 = transient outward K current...partial repolarization
2 = plateau phase due to net influx of Ca (balanced by efflux of K)
3 = repolarization during wich forces that favor K efflux predominate over K influx
4 = very small efflux > influx...back to resting state

How does LOW plasma K affect this cycle of potentials?

Initially, hypokalemia increases the ratio of Kin/Kout thereby hyperpolarizing the cell membrane (inside of the
cell MORE NEGATIVE).
You would predict that membrane excitability SHOULD be reduced since resting potential is farther away from
threshold before you can generate an action potential.
HOWEVER!!!!
The initial hyperpolarization (greater inside negative) REMOVES the normal state of inactivated Na channels.
Thus, the Na permeability INCREASES (phase 0 above) and muscle excitability (cardiac or skeletal)
INCREASES, as less of an exciting stimulus is needed to generate an action potential.

On top of this, remember that just before repolarization starts (end of plateau phase the inside of the cell is
now POSITIVE) so K efflux is favored. The rate of REPOLARIZATION depends on K permeability of the cell
which appears to depend on plasma K concentration....LOW plasma K concentration decreases K permeability
(mechanisms not clearly known) so there is a delay in repolarization by the cardiac muscleand skeletal does
this too.

SO BOTTOM LINE....LOW plasma K = increased depolarization (excitability) phases 0 and decreased

repolarization (phase 3).

Delayed repolarization leads to increased refractory period and predisposes to re entrant arrhythmias and
depending on where this happens (atria, sinus, purkinje, ventricle) will lead to atrial fib, PVCs, etc. and skeletal
muscle spasms.

So how does HIGH plasma K affect this cycle of potentials?

The earliest change seen with high plasma K is abnormally RAPID repolarization (due to increased membrane
permeability to K and faster K efflux out of the cell)...this gives the tall peaked T waves.

Even tho high plasma K makes the resting potential less negative (closer to threshold), high plasma K
inactivates membrane Na channels thereby SLOWING the rate of depolarization (phase 0).. this leads to the
later development of the longer PR interval, disappearance of the P wave, widening of the QRS...sinewave and
then flat line.skeletal muscle becomes weak or flaccideven paralyzed.

Hope this helps...sorry I could not make it shorter.