# Calcium channel blockers



## rhan101277 (Dec 23, 2009)

I have a question about these, mainly cardizem.  I understand this drug works on voltage gated calcium channels in the cardiac muscle, but skeletal muscle also has voltage potential changes for muscle contraction.  I am trying to remember if calcium works by passive transport in skeletal muscle. Is this drug just sythensized somehow to just target cardiac cells?

Also apparently it doesn't block every channel or else I don't see how the heart could beat at all.  I want to learn as much as I can, but I don't won't to over complicate matters when it comes to giving a drug.  I need to be smart and know what it does, instead of just reading what the drug book says.


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## rhan101277 (Dec 24, 2009)

No input?


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## skivail (Dec 24, 2009)

The Ca++ is pumped back into the SR during rest and contained by the Calsequestrin.  They then diffuse when the Ca++ channel opens.  

As far as the action of the drugs, I cant help you.


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## 18G (Dec 24, 2009)

Diltiazem works on the slow calcium channels. It inhibits the influx of calcium going into the cell which keeps the level of calcium at a sub-threshold level. At a sub-threshold level, the cells are not going to be excited. This is where the main mechanism of action is. 

Diltizem works on the coronary and small arterioles which is why it is also used as an anti-hypertensive and anti-anginal. It works to dialiate coronary vessels improving blood flow to the myocardium and lowers blood pressure by reducing overall systemic vascular resistance by dilating the arterioles. 

And of course, as for its main use in rate control for atrial fibrillation/flutter, it decreases SA and AV node automaticity and conduction. It has no effect on ventricular conduction.  

One thing to keep in mind with all this is the drug Procardia which is sometimes used in EMS systems... even though it is a calcium channel blocker it does not work the same way as diltiazem. It will not work for rate control. Its mainly used to lower blood pressure. 

A calcium channel blocker does not completely inhibit calcium from entering the cells at therapeutic doses... it just limits the amount. In overdose, yes, more calcium is blocker which is why you may have substantial bradycardia and hypotension.

Hope this helps a bit.


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## rhan101277 (Dec 24, 2009)

Thanks it does help, it made me think it blocked all calcium channels.  Start pharmacology in January so I am sure it will clear up.


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## redcrossemt (Dec 25, 2009)

Some CCBs are more selective for vascular v. myocardial calcium channels than others. They all work on L-type calcium channels.

Dihydropyridines are the most specific for smooth muscle. These are drugs like nifedipine and felodipine. These cause mostly systemic vasodilation, and can cause reflex tachycardia - so they aren't typically used for angina.

Of the non-dihydropryridines, there are two classes. Diltiazem is an intermediate with some selectively for both vascular and myocardial CCs, and is sometimes used for angina. Verapamil is a commonly used drug of the phenylalkylamine class and is relatively selective for myocardium - making it a better choice for treatment of dysrythmias.


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## rhan101277 (Dec 25, 2009)

redcrossemt said:


> Some CCBs are more selective for vascular v. myocardial calcium channels than others. They all work on L-type calcium channels.
> 
> Dihydropyridines are the most specific for smooth muscle. These are drugs like nifedipine and felodipine. These cause mostly systemic vasodilation, and can cause reflex tachycardia - so they aren't typically used for angina.
> 
> Of the non-dihydropryridines, there are two classes. Diltiazem is an intermediate with some selectively for both vascular and myocardial CCs, and is sometimes used for angina. Verapamil is a commonly used drug of the phenylalkylamine class and is relatively selective for myocardium - making it a better choice for treatment of dysrythmias.



Did you learn all of that in pharmacology?  Do you have any tips for the class?


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## redcrossemt (Dec 25, 2009)

rhan101277 said:


> Did you learn all of that in pharmacology?  Do you have any tips for the class?



Learned much of that in the UMBC CCEMTP class because the instructor really liked pharmacology, but I had to look a couple things up to present it here accurately.

You probably won't get more than a sentence or at most a short paragraph about CCBs in the EMT-P class.


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## silver (Dec 26, 2009)

Something that many people don't normally understand is the vast diversity in our bodies. As stated earlier, there are multiple types, and the one found in vascular tissues and myocardial tissue is L type. This is also found in other tissues like I think in some neurons is one, which explains why diltiazem reduces migraines. However these different calcium channels have different subunits, and the most important one is a1(which should be alpha) to define different classes/types.

So the diltiazem is a benzothiazepine which is like verapamil, a phenylalkylamine (targets mostly myocardium), and dihydropyridines (vascular only), like amlodipine, crossed. All of them are ligands and attach to a stereoselective and specific receptor. The dihydropyridines' specific receptor is on the Alpha 1S subunit of L-type channels which is the specific gene and is called a dihydropyridine receptor. It acts as antagonist and closes the gate on the channel, which keeps intracellular calcium low. So these drugs must have natural relatives that are used for homeostasis for them to fit in a receptor. 

Hope that explains a bit.


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## rmellish (Dec 26, 2009)

So I guess my followup question is, why has verapamil fallen so far out of style?

Obviously dilatizem has it's uses for rate control.


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## fma08 (Dec 26, 2009)

rhan101277 said:


> Did you learn all of that in pharmacology?  Do you have any tips for the class?



Study your cell physiology in your A&P book... Or if you had an A&P book like mine, have google at your fingertips. As you come across a drug or drug class, pay attention to the mechanism of action. If you aren't getting something, look at what it's supposed to be affecting and read up on how that tissue works in your A&P book (or google). Membrane transport is a concept you'll want to have down along with all the other principals in pharmacology like bio-availability, half life, etc.


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## FLEMTP (Jan 2, 2010)

rmellish said:


> So I guess my followup question is, why has verapamil fallen so far out of style?
> 
> Obviously dilatizem has it's uses for rate control.




Cardizem is a much safer medication for EMS use. Too many medics would give verapamil like it was adenosine, and it would literally stop the heart. They dont call it verapakill for nothing!


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## redcrossemt (Jan 4, 2010)

rmellish said:


> So I guess my followup question is, why has verapamil fallen so far out of style?
> 
> Obviously dilatizem has it's uses for rate control.



What would you use verapamil for pre-hospitally? 

The only thing I can think of is an atrial tachycardia (whichever kind you choose) that could be safely and effectively treated with dilatizem...


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## FLEMTP (Jan 4, 2010)

it was used for a fib with RVR and SVT's refractory to adenosine...


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## redcrossemt (Jan 4, 2010)

FLEMTP said:


> it was used for a fib with RVR and SVT's refractory to adenosine...



Right... atrial tachycardias that dilatizem can be used for.


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