3 important concepts:

1) Some Na Channels will begin opening while the RMP is below "threshold potential".
Threshold voltage of a cell is not a fixed magical voltage level where all of the sodium channels suddenly turn on.
Sodium channels are voltage-gated and turn on probabilistically. The more positive the membrane voltage, the higher the
probability a sodium channel opens. So even at very negative voltages, most sodium channels stay closed. Occasionally
a sodium channel may open briefly. These brief openings conduct such a small current that they have very little effect on
the RMP. At these very negative RMP values, the only channels that are open significantly are "leak" K channels and
thus the RMP (which is kind of a weighted average of the reversal potentials of all the conducting ions) remains close to
the K reversal potential. Now the (maybe to some) surprising part: if the membrane voltage depolarizes a little bit but is
still significantly below (more negative to) normal "threshold potential" of a cell, some Na channels will start opening
(although most stay closed). Again this is because Na channels are probabilistic and voltage dependent with no sharp
cutoff in their voltage dependence right at "threshold". Since you membrane voltage has depolarized some, the
probability of Na channels opening is no longer close to 0 and some of them will start opening (even though you are
below "threshold").
2) Threshold voltage is kind of a moving target that depends on the size of Na and K currents relative to each other.
At subthreshold depolarizations of membrane voltage, the opening of some Na channels does pull the membrage
voltage higher (depolarizes) but as long as there is significant K current pulling the membrage voltage towards
hyperpolarization, the Na current is sufficiently offset by the K current and the membrane voltage remains "subthreshold".
The "threshold" phenomenon occurs when membrane voltage is elevated enough that a large enough number of Na
channels open to overcome the K channels. The membrane voltage is like a weighted average so as Na channels open,
voltage is pulled towards the Na reversal potential (positive) from its resting state close to the K reversal potential
(negative). If enough Na channels open to overcome the hyperpolarizing influence of the K channels, the effect becomes
a positive feedback loop: as Na channels open, the membrane voltage becomes more positive and as it becomes more
positive, more Na channels open. This Na channel positive feedback causes the rapid phase 0 depolarization of the
action potential. It would run away unchecked if not for the fast inactivation of Na channels and a second set of K
channels the voltage gated K channels (as opposed to the leak K channels). These K channels' voltage dependence is
shifted more positive compared to the voltage gated Na channels and so they turn on later at more positive voltages,
helping to drive membrage potential back to ward the negative reversal potential of K.
3) Sodium channels inactivate after opening.
In activation is a process that makes Na channels non-conducting after being open. We talked about fast inactivation of
Na channels (ball and chain mechanism). There is also a slow inactivation (due to more overall conformational change of
the Na channel protein). Hyperpolarization relieves inactivation and resets the Na channels making them ready to fire. At
depolarized voltages, Na channels can open and some can go on to become inactivated. This effect is key to the
physiological effects of hyper/hypo kalemia.

Hyperkalemia:
Reversal potential of K is shifted positive. Driving force for K to leave the cell is decreased so there is less "leak" K
current and the RMP is depolarized compared to normal. The more positive RMP means more Na channels will randomly
open and more of them will become inactivated. This means fewer Na channels are available to respond by opening
when depolarization occurs. This effectively ALSO RAISES THE THRESHOLD POTENTIAL. Because there are fewer
Na channels available to conduct current, you need a greater voltage to get enough Na current to overcome the effect of
the K channels. Thus the "threshold" voltage, the voltage where Na wins over K, is now higher. Early in mild
hyperkalemia, the effect on K currents and RMP is more important than the effect on Na channels and Threshold
potential, so overall there is a small increase in excitability as the RMP is slightly closer to threshold potential. Soon
however, the hyperkalemia's effect on the Na channel inactivation dominates and you get an overall DECREASE in
excitability due to decreased availability of Na channels for phase 0. This results in a slow phase 0 depolarization and a
slow or widened QRS complex.
Hypokalemia:

Essentially reverse of above. Low serum K = shift negative in reversal potential of K = incr K driving force = more leak K
current and hyperpolarized RMP. This causes increased availability of Na channels for firing due to relief of inactivation
and actually shifts threshold potential towards the negative. Thus there is NOT as increase in the "distance" of the RMP
from threshold. Increased Na channels = faster depolarization and lower threshold voltage = INCREASED excitability.

T-waves:
The flat/peaked T-waves are a little more complex: the voltage dependent K channel proteins like to have a potassium
ion sitting in the pore near the extracellular end of the channel. This helps keep them conducting and prevents them from
collapsing shut. In hypokalemia, there is decreased extracellular K, so more of the voltage gated K channelsare
collapsed shut. In hyperkalemia, very few of these voltage gated K channels are collapsed and many more of them are
ready to fire when the cell depolarizes sufficiently. Thus in hyperkalemia, more K current after depolarization (ie after
phase 0, so during phase 2 and 3) means, phase 2 is shortened and phase 3 is faster. This results in shortened QT and
peaked T wave. Opposite in hypokalemia - collapsed K channels = less K current in phase 2 and 3 = long phase 2 and
slow phase 3 = long QT and flat T wave.
SA node:
HR changes are not a typically discussed as part of the cardiac syndrome caused by hyper/hypo kalemia. Take fhe
following with a grain of salt. This is what makes sense but really it is much more complex than our discussion.
I did want to mention regarding phase 4 depolarization that although a Sodium current is involved and K currents also
become important in phase 4 (in response to Acetylcholine) the channels involved are different in terms of both the Na
and K channels than those mentioned earlier so do not confuse them. Phase 4 is a balance of Na and K currents where
there is normally enough Na current to slowly overcome the K current and depolarize to threshold. These SA node phase
4 Na channels open at much lower voltages and have a very different voltage dependence than the myocardium phase 0
Na channels. Here the K concentration effects are more intuitive. Hypokalemia means a large difference in K across the
membrane = large K efflux = hyperpolarizes RMP, making it closer to reversal potential of K (negative) and farther from
threshold. Also the increased K efflux means the slope of phase 4 depolarization is flattened as the Na current must fight
against a larger K current. The Na channels in the SA node DO NOT INACTIVATE with slow inactivation at subthreshold
voltages and thus we don't have to worry about them the way we did before. Farther from threshold with slower rise in
voltage = slower HR = sinus bradycardia associated with Hypokalemia. Hyperkalemia would do the opposite depolarizes RMP and steepens phase 4 depolarization and thus increases HR.

Weakness:
In terms of weakness, some hand waving is necessary. Decreased excitability will obviously present as weakness but
increased excitablity can also cause weakness through "fatigue"-type effects. Furthermore, the K changes will have
myriad changes on other ion transporters directly and indirectly by changing other ionic gradients. Both hyper and hypo
kalemia cause problems in conduction. You need correct amount of K for conduction, not excessive nor too little (that is
why they both cause pathological ECG changes). The discussion above is for myocardium and EKG findings. Behavior

may be somewhat different for nerve and skeletal muscle.