# Beta Blockers, Potassium Ch. Blockers and other blockers



## xrsm002 (Jun 23, 2012)

I was wondering if anyone could "dumb" down the differences of Beta Blockers, Potassium Channel Blockers, and Sodium Channel Blockers.  I am having a hard time being able to tell the difference.  I understand if I am right they all have an effect on the cardiovascular system in some form.  Do they have other effects on other body systems?


----------



## DPM (Jun 23, 2012)

xrsm002 said:


> I was wondering if anyone could "dumb" down the differences of Beta Blockers, Potassium Channel Blockers, and Sodium Channel Blockers.  I am having a hard time being able to tell the difference.  I understand if I am right they all have an effect on the cardiovascular system in some form.  Do they have other effects on other body systems?



Beta Blockers are simply that. There's lots of different types, they tend to end in -olol and they block Beta adrenergic receptors that Epi and NorEpi act on. They basically inhibit your body's response to the adrenalin it produces, thus keep heart rate and Blood Pressure down.

Calcium channel blockers help to reduce cardiac contractillity and to relax the smooth muscle in blood vessels. This means that the blood vessels 'get bigger' and the heart doesn't beat as hard, keep blood pressure down again.


Sodium channel blockers work on reducing cardiac irritability (Lidocain is a good example.) and are used to treat things like V Fib / V Tach / SVT etc.

I hope this makes sense and isn't too watered down!


----------



## xrsm002 (Jun 23, 2012)

Nope not watered down at all I'm slowly starting to understand it


----------



## NYMedic828 (Jun 23, 2012)

You really can't make it any more watered down than that...

100 words is pretty watered down considering there are people on this forum are capable of writing you a 30 page essay for each one.


Sympathetic nervous stimulation of the heart increases heart rate and force of contraction. If we block beta receptors, we block this action. Slower heart rate, less forceful contraction. Ultimately, lower blood pressure.

Calcium causes muscle fibers in striated/cardiac muscle to pull towards one another, ultimately creating contraction. Less calcium, less contraction and less heart rate because the influx of calcium is slowed.

Sodium channel blockers come in a few forms but they usually reduce the automaticity or slow the conduction velocity of the heart, potentially stabilizing irritable pacemakers by hindering their ability to generate an impulse.

Potassium channel blockers slow re-polarization in phase 3 of the cardiac action potential, prolonging the refractory period.


----------



## Handsome Robb (Jun 24, 2012)

A good understanding of the physiology of the cardiac system will make understanding the medications and their uses much easier. 

I don't have a better explanation for you than what those two already put up so I'm not going to just keep repeating what's already been said since they did a pretty good job of it.

What I will add is that beta blockers can effect the respiratory system as well since you asked about other body systems. Either nonspecific or beta2 blockers can/will cause bronchochonstriction since the catecholamines (epi, nor-epi, dopamine) are being blocked at the B2 adrenergic receptor sites.


----------



## Veneficus (Jun 24, 2012)

http://www.amazon.com/High-Yield-He...d=1340512508&sr=8-1&keywords=high+yield+heart

problem solved.


----------



## DrankTheKoolaid (Jun 24, 2012)

I was always under the impression that CA blockers slowed rate by decreasing the firing rate through the CA dependent AV node


----------



## NYMedic828 (Jun 24, 2012)

Corky said:


> I was always under the impression that CA blockers slowed rate by decreasing the firing rate through the CA dependent AV node



CC blockers act to reduce cardiac contractility via a negative inotropic effect as well as decrease peripheral vascular resistance via vasodilation of smooth muscle fibers.

They also have potentional to prolong phase 2, the plateau, of the cardiac action potential where calcium flows back in to the cells just prior to the third phase where potassium becomes dominant inside the cells again.

I think the SA/AV node are pretty dependent on calcium channels so the action is the same. Slowing influx of calcium slows the action potential and decreases contractility.


----------



## VFlutter (Jun 24, 2012)

Veneficus said:


> http://www.amazon.com/High-Yield-He...d=1340512508&sr=8-1&keywords=high+yield+heart
> 
> problem solved.



+1 A good understanding of patho will be a huge help when learning about various drugs. Then you will not only understand the antagonists but you can also apply that knowledge and better understand how agonists (Dobutamine, Levophed) work. a solid knowledge of Adernergic Receptors goes a long way


----------



## MSDeltaFlt (Jun 25, 2012)

Corky said:


> I was always under the impression that CA blockers slowed rate by decreasing the firing rate through the CA dependent AV node



CC blockers do slow the contractility of the heart. The reason is that calcium is what is required to make muscles contract. Body builders will take a preworkout supplement that has a boat load of calcium in it for that reason.  So a calcium channel blocker will block some the calcium from getting in the calcium channels of certain muscles (kinda like a key hole) from "completing a circuit" as it were in order to decrease certain muscles (heart) from contracting so hard thus slowing the heart rate or lowering the blood pressure.


----------



## ZootownMedic (Jun 29, 2012)

Corky said:


> I was always under the impression that CA blockers slowed rate by decreasing the firing rate through the CA dependent AV node



I was taught the same and we are all right. Diltiazem is a prefect example and slows conduction time in both the SA and AV nodes which causes a negative dromotropic and then chronotropic effect. Since it also inhibits cardiac contractility it also has a negative inotropic effect as NVRob stated. Just different ways of explaining it I guess but absolutely effects the AV node.


----------



## Doczilla (Jun 30, 2012)

Here's how I explain it to my PA students, check it out: 

The atrium uses calcium to depolarize. So what would you use for A fib/flutter with RVR provided its not contraindicated?


The ventricles use sodium to depolarize. So what route do you go for ventricular arrythmias ,  including multifocal PVCs with more than 6 per minute?


----------



## Handsome Robb (Jul 1, 2012)

Doczilla said:


> Here's how I explain it to my PA students, check it out:
> 
> The atrium uses calcium to depolarize. So what would you use for A fib/flutter with RVR provided its not contraindicated?
> 
> ...



I like it. Good explanation provided the person you are explaining it to knows the answer to the question. 

I'll bite, while ventricles use sodium to depolarize why is it that resuscitation guidelines have moved towards a potassium channel blocker, being amiodarone, rather than still using a sodium channel blocker such as lidocaine for ventricular arrythmias? All the while keeping in mind that amiodarone acts on all the "classes" of antidysrhythmics but is technically classified as a potassium channel blocker.

I have no experience with lidocaine, only amiodarone. We carry lido but the only standing order we have for it is R-on-T PVCs or conscious IOs.


----------



## NYMedic828 (Jul 1, 2012)

Amiodarone is a sodium/potassium/beta blocker.

Not just potassium.


----------



## Handsome Robb (Jul 1, 2012)

NYMedic828 said:


> Amiodarone is a sodium/potassium/beta blocker.
> 
> Not just potassium.



Agreed, I thought I said that but I very well may not have. It's late/early and I worked all night, leave me alone 

It does have multiple blocking properties but is still classified as a Class III antidysrythmic.


----------

