I have watched many lectures special about this topic almost 15 video but they couldn't make me understand. I am very pleased with ur lecture mam.all my doubts has been cleared .Thanks a lot from bottom of my heart.
Thank you soooooo much.😊😊😊......No teacher might not present arrthymias in this beautiful way.... One doubt out of context ma'am 😅.....How ischemia leads to calcium overload in the cardiac muscle cell
Put the values of potassium in the Nernst equation. You will notice that when extra cellular potassium increases, RMP becomes less negative...I.e depolarisation occurs...for underlying concepts will make a video
wrong concept between tachyarrythmia and tachycardia. when heart is more than 100, it is specifically tachycardia not tachyarrythmia. A-fib is a tachyarrythmia but is not tachycardia. A-fib become tachycardia when associated with pre excitation.
At 5:58 you mention the channels will open as the membrane potential is above the threshold, but earlier you mentioned that calcium channels do not need voltage to open but time. Does this mean that calcium channels can open after a period of relaxation, but only if the membrane potential is above threshold?
Hello ma'am you said the calcium channel unlike sodium channel open with time. If that so can you explain how or when or which potential sodium channel opens after the inactive state. Thank you.
All sodium channels don’t open exactly at same potential. It’s a probability opening. So some convert from inactivated to closed state as well at less potential
Please check my video on Current of Injury...in the end I have spoken about wall infarction...but you need to see the video for understanding the end part
Generally +15mv is the threshold. But we don’t draw in the action potential because it recieves the signal electrically from nearby cells (syncytium) and potential change is very fast, hence a straight line from RMP
@@PhysiologyOpen I've understood it. +15 mV is the uppermost limit of Cardiac action potential or it's the threshold ? And one more doubt. Suppose action potential duration has got lengthened due to any reason. By now, L-type calcium channels have closed off. Now , due to reopening of the Calcium channels, won't a second pleatue appear as Calcium entry will nullity Potassium exit electrically? Why is the Calcium entry higher than potassium exit which results in an EAD unlike what happens in pleatue phase where both are equal in amplitude but opposite in polarity and hence the voltage inside the membrane doesn't change at all ? Kindly exolain, madam.
@@PhysiologyOpen Kindly make a video on potassium channels and their types. I m still in an ocean of doubts regarding what inward rectifier, delayed rectifier potassium channels are. These appear like an enigma to me.
