Nice lecture overall. Effects of K+ on Heart are really confusing.... I would like to add some points regarding hypokalemia :- Hypokalemia causes EAD and inc. excitability in Ventricular muscles by various mechanisms as follows :- 1. Hypokalemia inhibits Na+ -K+ atpase activity ( as you explained in the video). 2. Hypokalemia doesn't increase the activity of Sodium Calcium exchanger. You said in the video that due to hypokalemia , 3NA+ moves out the cell and 1 Ca+ is pumped in. If that was the case , inside the cell would have become "Negative" due to "3"positive charges(Na+) moving out and only 1 positive charge"Ca+" moving in and that would have prevented 'EAD". The role of sodium calcium exchanger in Normal physiological conditions is to pump 3 Na+ in the cell for every 1 Ca+ removed from the cell. In Hypokalemia, what happens is Due to Dec. Sodium potassium atpase activity, Sodium conc. starts increasing inside the cell. This increased sodium conc. inhibit the Sodium calcium exchanger( that in normal conditions Pump 3 Na+ "In" the cell and 1 Ca+ out the cell) that decreases calcium from going out the cell, thus inc. Ca+ levels inside cells. C. Hypokalemia directly inhibits potassium channel activity/permeability. So, Repolarization occurs slowly , Action potential duration and risk of EAD increases. Link:- www.ncbi.nlm.nih.gov/pmc/articles/PMC5399982/
@@medicinewithdrshamama.92 Mam, hyperpolarisation in SA node increases excitability because of activation of HCN channels(hyperpolarisation sensative cyclic nucletide gated sodium channel) Could it be this reason for hyperexcitibility in SA node?
I have a question, in my physiology book its says that hypokalemia at the begining leads to hyperpolarization and then by blockage of Na/K chanels to depolarisation, but it doesnt explain why the begining hyperpolarization. I think it may be due to icreased K outflow by K chanels before they shut down but I am not sure.
Because ions want to go towards where there is less of themselves. To start with, membrane hyperpolarization is caused by the potassium wanting to go outside the cell because there is less potassium outside... so the threshold is lowered to -110mV (more negative). But because of this, there is now a negative charge inside the cell, meaning the positive sodium ions are going to rush into the cell QUICKER, since negative attracts positive. That's why velocity is faster when the sodium leaks into the cell to cause the rapid depolarization.
Hi! So I didn't mention it previously, but these early/rapid depolarizations in heart cells can also lead to arrhythmias sometimes by SLOWED conduction (like you see in muscle/nerve cells) that end up triggering the automatic pacemaker cells to fire strangely, leading to reentrant tachycardia, for example. Also a little more complicated, fast heart rates are also caused by calcium levels inside the cell, which build up when there is less K+ around. So sadly it's a little more complicated than just 1 ion being the main depolarization. /// I get why you have your question about muscle cells and it made me have to think about it, but my understanding is that with too little potassium in your system, your muscle cells aren't going to spit out all of its potassium to meet the low concentration of your bloodstream (and if they do release their potassium because of diffusion, it's going to be reused by the cells immediately because your body's cells need that potassium to be metabolically active.) I would think of the problem as, since there are too few K+ to go around for every cell, there just isn't enough in your body to keep your muscles active... which is why hypokalemia leads to muscle paralysis. Your heart (and brain) is the body's number 1 priority, so the heart has a special ability to make sure it automatically depolarizes no matter what. And of course if left untreated, hypokalemia will eventually cause cardiac arrest too because there's not enough for correct conduction. I know that's a long explanation but I hope it made sense.
