Why is lidocaine preferred in patients with arrhythmias following myocardial infarction?
Hypoxic tissue is depolarized.
Na+ - K+ ATPase doesn't work.
Na+ has accumulated in the cell and no one pumps it out.
All the sodium channels are in the inactivated state.
These inactivated channels slow the conduction of electrical activity in ischemic tissue.
This is how arrhythmia arises.
It causes disparity in the way action potentials are propagated in the heart muscle cells.
The normal fibres wanting to go fast and the hypoxic tissues slowly firing in between :|
That's why you use class Ib antiarrhythmic, lidocaine, in patients with arrhythmias following myocardial infarction.
They block inactivated sodium channels.
Blocking inactivated sodium channels doesn't change any flux of sodium into the cells.
But if you are keeping it inactive, you are preventing it's return back to the resting state.
So you are keeping those cells in hypoxic tissue refractory, keeping them from going back to resting and preventing them in firing new action potentials on their own.
Lidocaine also decreases action potential duration by blocking slow sodium window channels.
In any other healthy cell, this would be proarrhythmic.
But in hypoxic tissue over here, which is already slow in conduction, you'd help it recover faster and help it go back with the healthy tissue for electrical speed.
Or simply by decreasing APD, you'll have more time in disatole for filling.
Either way, you are improving the cardiac output of the ischemic heart :)
Since digoxin is also going to depolarize the heart by blocking sodium channels, lidocaine is also used in digitalis toxicity.
Cool fact:
Lidocaine is also a local anesthetic.
However, preparations for cardiac use contain no preservatives.
Local anaesthetic preparartions should not be used for cardiac purposes.
It is used i.v. due to high first pass metabolism.
Another cool fact:
Mexiletine and Tocainide are lidocaine like drugs and are available in oral formulations.
That's all for today!
Have a happy healthy Saturday <3
-IkaN
Hypoxic tissue is depolarized.
Na+ - K+ ATPase doesn't work.
Na+ has accumulated in the cell and no one pumps it out.
All the sodium channels are in the inactivated state.
These inactivated channels slow the conduction of electrical activity in ischemic tissue.
This is how arrhythmia arises.
It causes disparity in the way action potentials are propagated in the heart muscle cells.
The normal fibres wanting to go fast and the hypoxic tissues slowly firing in between :|
That's why you use class Ib antiarrhythmic, lidocaine, in patients with arrhythmias following myocardial infarction.
They block inactivated sodium channels.
Blocking inactivated sodium channels doesn't change any flux of sodium into the cells.
But if you are keeping it inactive, you are preventing it's return back to the resting state.
So you are keeping those cells in hypoxic tissue refractory, keeping them from going back to resting and preventing them in firing new action potentials on their own.
Lidocaine also decreases action potential duration by blocking slow sodium window channels.
In any other healthy cell, this would be proarrhythmic.
But in hypoxic tissue over here, which is already slow in conduction, you'd help it recover faster and help it go back with the healthy tissue for electrical speed.
Or simply by decreasing APD, you'll have more time in disatole for filling.
Either way, you are improving the cardiac output of the ischemic heart :)
Since digoxin is also going to depolarize the heart by blocking sodium channels, lidocaine is also used in digitalis toxicity.
Cool fact:
Lidocaine is also a local anesthetic.
However, preparations for cardiac use contain no preservatives.
Local anaesthetic preparartions should not be used for cardiac purposes.
It is used i.v. due to high first pass metabolism.
Another cool fact:
Mexiletine and Tocainide are lidocaine like drugs and are available in oral formulations.
That's all for today!
Have a happy healthy Saturday <3
-IkaN
Nice explanation
ReplyDeleteThanks
ReplyDelete