Sodium Channel Blocker Question

[JCicco345]

Quick question I'm sitting here bored in my OB rotation waiting for someone to pop out a little alien and also studying for the mid-term that is approaching. I was studying cardiac meds, and came across a question about antidysrythmics. The Brady book says sodium channel blockers class 1A, slow conduction, decrease repolarization rate, the ECG effects of the medications are widened QRS and prolonged QT. Which makes sense they slow the rate down. The confusing thing is that class 1B says it increases the rate of repolarization, and reduces the automaticity in ventricular cells, the ECG effects are the same widened QRS and prolonged QT. Increasing the rate of repolarization would increase the rate, right ? So why does that show a widened QRS and prolonged QT. Plus if you are using lidocaine for ventricular arrythmias wouldn't you expect a narrower QRS.

The only thing I can think of is that the drugs effect the repolarization rate but not the actual heart rate, they just put the cells into the refractory period for longer times.

I was hoping one of the senior medics on here or even a fellow medic student can find another way to put this, it doesn't seem to be clicking right now.

Thanks in advance.

[Code 8 Paramedic]

hmmm yeah what you said... my understanding... for what its worth, is this in regards to lidocaine, by suppressing the sodium channels, conduction is slowed, as well as the possibility for irritable cells... you hope to slow down the conduction in V-tach so that the SA node can take over. and then further suppress irritable cells

[AZCEP]

I was studying cardiac meds, and came across a question about antidysrythmics.

Much better now than when you have to use your knowledge to manage a patient.

The Brady book says sodium channel blockers class 1A, slow conduction, decrease repolarization rate, the ECG effects of the medications are widened QRS and prolonged QT. Which makes sense they slow the rate down.

Vaughn-Williams class IA antidysrhythmics are the strong sodium channel blocking agents. Procainamide is the prototypical example. Because of the "strength" of the medication's influence, the heart rate is slowed. This is due to the influence on the inotropic actions of the myocardium. The mechanics are weakened, so the rate of depolarization is reduced as well.

The confusing thing is that class 1B says it increases the rate of repolarization

Because class IB are weak sodium channel blockers. Lidocaine, for instance. It has a greater effect on the electrical system than the mechanical. The rate of repolarization is governed by the amount of Ca++ that is moving into, and out of the cell. The weak influence on the sodium channels causes more Ca++ to move out before more Na+/K+ can move.

reduces the automaticity in ventricular cells

The automaticity is slowed by the narrowing of the action potential. Sorry for bringing that up, but look the picture up while reading the descriptions. It will help you to understand it. Now, as the action potential narrows, phase 4 lengthens. When this happens, the time between action potentials forming increases, and the cell doesn't generate as many impulses. Voila!! less automatic.

Increasing the rate of repolarization would increase the rate, right ?

The cells repolarize faster, and use more time to recover in between action potentials. Thus the rate slows.

So why does that show a widened QRS and prolonged QT. Plus if you are using lidocaine for ventricular arrythmias wouldn't you expect a narrower QRS.

The QRS can widen because of the slowing of the conduction through the ventricles. If the impulses are being generated above the ventricles, the lower conduction system will slow them down some, widening the QRS. The QT prolongs, because now it takes longer for the cells to prepare for the next impulse. Consider that the cell relies on the previous intervals to help "set" how long it is supposed to take to perform a given function. For the QT to remain constant, the cells need to have the same influences applied to them. When we add a conduction disturbing medication, the cells can be thrown off from what they have determined "normal" to be. The QT widening is a fairly common response to antidysrhythmics.

The only thing I can think of is that the drugs effect the repolarization rate but not the actual heart rate, they just put the cells into the refractory period for longer times.

That will depend on which class of medication you are dealing with. Check into the various Vaughn-Williams classes a bit more for a better understanding.

Thanks in advance.

Your welcome.

[JCicco345]

Thanks that makes a lot more sense now, great explaination.

[Rezq304]

As always AZCEP, spot on!

[AZCEP]

Thanks, but it's probably bad form to mention "spots" in a thread mentioning OB rotations. :shock:

[Rezq304]

Thanks, but it's probably bad form to mention "spots" in a thread mentioning OB rotations. :shock:

LOL....nah, it'll give the kid something to do.