Nahc03 for tca OD

[aspiringmd1015]

UW states that adding nahc03- will cause the TCA to become non-ionized, and have less access to the Na channel. If its non-ionized, wont it bind easier to the channel? or do you have to be polarized to be able to block channels, and if nonionized itll just diffuse into membranes or something

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[chillaxbro]

I assume it has to be +1 charged like Na

 

[soop]

UW states that adding nahc03- will cause the TCA to become non-ionized, and have less access to the Na channel. If its non-ionized, wont it bind easier to the channel? or do you have to be polarized to be able to block channels, and if nonionized itll just diffuse into membranes or something

The way I understood it was that the increased serum sodium competes with TCA's blockade of Na+ channels thus reducing the cardiotoxicity. The bicarb alkalinizes the urine, preventing tubular reabsorption thus facilitating urinary excretion.

 

[aspiringmd1015]

The way I understood it was that the increased serum sodium competes with TCA's blockade of Na+ channels thus reducing the cardiotoxicity. The bicarb alkalinizes the urine, preventing tubular reabsorption thus facilitating urinary excretion.

TCA is a weak base, it would decrease urniary excretion

 

[soop]

TCA is a weak base, it would decrease urniary excretion

Yep you're right. My mistake. Not sure where I heard it was a weak acid.

 

[dorster]

apparently the mechanism isn't well understood at least according to uptodate but it says that for some reason the sodiumbicarb allows for more sodium to enter the channels regardless of the TCA blockade so basically the sodium overrides the TCA blockade and it decreases the cardiotoxicity like was mentioned above, it doesn't have to do with increasing excretion of TCA