Sodium Channel blockers

[hammerpcp]

So, Lidocaine is a sodium channel blocker and an antiarrhythmic, right? And we give sodium bicarbonate to tricyclic antidepressant overdose to unblock the sodium channels, are you still with me? So TCA is a sodium channel blocker, yet it causes lethal arrhythmias and that is why it is so dangerous if an OD is taken. So like WTF? What am I missing here? Why does one Na+ channel blocker prevent dysrrhythmia (usually) and the other causes them?

[BushyFromOz]

I thought the TCA overdose caused excessive catecholamine buildup in the synapses because of its blockade of the amine pump and the arrhythmias start from the excessive adrenergic stimulation. The lignocaine is used to slow down and reduce the number of action potentials generated by blocking the sodium channels therfore stabilising the membrane, not by acting directly on the catecholamine levels in the synapse nor the adrenergic receptors????????????

Something about what i just wrote doesnot seem to be right, methinks i will have to do some reading.......... :?

[AZCEP]

Bushy, What you wrote was correct, but you seem to be thinking of them separately.

Lidocaine is a class 1b antidysrhythmic, meaning that it is a weak sodium channel blocker. It's primary effect is on phase 4 of the action potential, rather than phase 0-1. It will effectively lengthen the duration of phase 4, allowing for more time between impulse generation.

TCA's will block the sodium channels much more effectively than lidocaine, as a side effect of their primary actions. When this happens you will notice a widening of the QRS complex, along with an increased heart rate. The QRS width is caused by the sodium channel blockade, slowing the progression of phase 4-1-0 in the action potential. The increased rate is related to the sympathetic dysfunction that they cause. When you add the two together, the myocardial cell is both less able to generate a normal impulse, and it is being stimulated to create more of them. This leads to the tachydysrhythmias that are common with these agents. They also carry an anticholinergic action that will add to the situation.

[BushyFromOz]

im not sure i quite understand.....

TCA OD produces a wide QRS tachy that you slow down by blockading the sodium channels further in orde to dampen the effects of the adrenergic stimulation? So you end up with a wide QRS rhythm thats not so tachy?

[AZCEP]

Not quite.

Treating a wide complex tachycardia caused by sodium channel blockade with Lidocaine will have more effect on blunting the sympathetic stimulation, than it will block the sodium channels. Lidocaine is placed in this category due to it's actions, but they are not terribly strong, nor reliable. By steepening phase 3-->phase 4 transition, the lidocaine can, theoretically help to reduce the heart rate.

The better choice for treatment is sodium bicarbonate. This will narrow the QRS complexes, and alkalinize the urine to help draw the TCA out of solution. By helping to eliminate the offending agent, the bicarb will do more to mitigate the situation than other possibilities. Treat the underlying cause, instead of the presenting symptom.

[BushyFromOz]

ah ha!

makes sense now

[fiznat]

The better choice for treatment is sodium bicarbonate. This will narrow the QRS complexes, and alkalinize the urine to help draw the TCA out of solution. By helping to eliminate the offending agent, the bicarb will do more to mitigate the situation than other possibilities. Treat the underlying cause, instead of the presenting symptom.

Correct me if I'm wrong here (perhaps we are both right...), but I thought Bicarb was used in TCA OD in order to retard + prevent metabolism of the injested drug? This is the reason why Bicarb should only be given to TCA OD if the injestion was recent. Ingested TCA that has already been metabolised wont be affected by Bicarb, if I am remembering correctly?

[northernmedic]

There are also different classes of sodium channel blockers (weak, moderate and strong) otherwise known as Vaughn-Williams Classes Ia, Ib and Ic. Lidocaine is a weak sodium channel blocker which is used as was explained above. Use of lidocaine (or other sodium channel blockers) is still a little bit controversial. Just about everyone who used to have an MI got lidocaine. Now the focus is more on treating underlying ischemia or finding a treatable cause (as was previously mentioned). We could go crazy on uses and indications here but we'd have to get kevkei in here for some freaky in depth physiology and pharmacology :wink:

[AZCEP]

Correct me if I'm wrong here (perhaps we are both right...), but I thought Bicarb was used in TCA OD in order to retard + prevent metabolism of the injested drug? This is the reason why Bicarb should only be given to TCA OD if the injestion was recent. Ingested TCA that has already been metabolised wont be affected by Bicarb, if I am remembering correctly?

Sodium bicarbonate does work in the way you describe, but it is also used to provide a greater amount of Na+ to counter the sodium channel blockade that TCA's create. The alkalinizing properties cause the TCA to move more quickly into the urine and be eliminated, while the sodium counteracts the ionic movement limitations.

[OVeractiveBrain]

Correct me if I'm wrong here (perhaps we are both right...), but I thought Bicarb was used in TCA OD in order to retard + prevent metabolism of the injested drug? This is the reason why Bicarb should only be given to TCA OD if the injestion was recent. Ingested TCA that has already been metabolised wont be affected by Bicarb, if I am remembering correctly?