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Calcium Chloride + Atropine

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I have been trying to learn and be familiar with some of the ALS drugs because I have 12 hours of down time when I work (security) and I figured I may as well read and learn ALS protocols instead of wasting time reading some other silly book.

I want to apologize in advance because my knowledge of these drugs is non-existent. I'm an (EMT) and these drugs are not in my scope. Maybe I shouldnt be trying to learn about things that are out of my scope, but eh...

So...I read that one of the indications for Calcium Chloride is: -used in hyper-kalemic cardiac arrest.

My question is how do you it is. Arent all of them hyper-kalemic because of the fact it is a cardiac arrest (no O2, acid balance changes)

Also read about Atropine that: it is used in pre-intubation (especially in children).

also sais it is used to reverse vecuronium.

If it used pre-intubation... Im confused. Its used before you tube someone but isnt vecuronium given to aid intuabtion? so why would you give it before hand?

I'm sorry for being ignorant, I am not familiar at all with those drugs. If anyone is willing to give it a shot and try to explain any of this it would make my day! If you guys know of a good web site that has information as to how those drugs work etc...

Thank you so much.

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You just might be making this more complicated than necessary.

Check rxlist.com for more specifics on the pharmacology.

Calcium chloride:

-Hyperkalemia is a pre-existing condition that leads to cardiac arrest. The hyperkalemia that presents following cardiac arrest is a result of the typical acidosis, so the lab value is elevated, but the actual amount is not increased.

Atropine:

-It will usually be used to reduce the vagal activity that comes with the process of intubation. When using it to reverse Norcuron(vecuronium), the idea is to allow the normal mechanisms of acetylcholine transmission return. If you are using atropine to reverse Norcuron, it is because you have discovered that you can't get the patient intubated, and don't want to provide BLS airway management for the 40+ minutes until the Norcuron wears off.

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They probably mean hyperkalemic induced arrests, which would normally be seen with dialysis patients. CaCl is used as a cardio-protective drug in these circumstances, I think having something to do with Phase 2 of the action potential. I don't remember specifically...

Atropine is used pre-intubation for kids (under 10 usually as I recall) because they have a common vagal response to laryngealscopy. Pretreatment of atropine aids in reducing this effect.

Ummm, perhaps you read it wrong, but I don't recall atropine as the reversal for vec, or any other NDNMB's. Vec (as I recall) blocks acetylcholine receptors with nicotinic and muscuric action and there for negates muscle contraction (mainly nicotinic) and causes paralysis. To counter this (reverse paralysis) you would want a drug that increases the concentration of acetylcholine at the pre-synaptic cleft, increases the concentration gradiatant on displacing the NDNMB. Drugs that do this are prostigmine and such...

Prostigmine is a acetylcholenesterase inhitibor which negates the break down of ACh at the post-synapic cleft, cause a buildup and so forth...

Spelling sucks and some of this may be a little off, I don't use any of the drugs listed for the purpose described and learned about this stuff like a year ago.

Close enough though.

EDIT - I did a quick search, it looks like atropine is used in conjuction with a -stigmine to facilitate recovery from RSI using NDNMB. I don't recall reading that in the Walls book though, and I'm not sure if that is standard practice.

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Atropine is also used to increase heart rate and dry up secretions in the nerve agent casualty. (organophosphates in the civilian world) Most nerve agents work by binding cholinesterase and prevent acetylcholine from being deactivated. This is the basic mechanism of nerve agent poisoning. If you do a little research, the physiological processes behind non depolarizing blockers are similar in some ways.

AZCEP & Vs-eh? are correct regarding CA++ CL-. CA++ CL- helps to normalize the gradient between the resting and threshold potential of cardiac cells. Hyperkalemia results in the a drastic elevation of this potential. Remember CA++ CL- is only a stop gap treatment that will buy you about an hour. It does not eliminate the K+.

Focus_911, I think you are also confusing hyperkalemia with other words.

Hyperkalemia = elevated potassium

Hypoxia = low oxygen

Hypoxemia = low blood oxygen

Hypercapnia = high carbon dioxide

I hope this helps.

Take care,

chbare.

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Very interesting topic and I agree with what vs has said I think you are right on the money from what I remember in class. We actually discussed in class the roll of atropine in being an antidote for succs overdoses. One of my classmates said that someone at his local hospital told him that it is in there algorithm on the crash cart to use atropine after a succs od. We couldn't really come to a conclussion or ever find out how this works anyone know???

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Ffmedic9588, atropine may be considered in the rare event of succ OD. (Repeated doses would be the most common cause) In most cases succ causes what is caused a phase I block. Or the typical depolarizing block we all know and love. Succ attaches at the neuromuscular junction in place of acetylcholine and causes the muscle to depolarize and stay in that state. Hence, the faciculations we all talk about with succ. In cases of succ OD this phase I block may take on superficial characteristics of a phase II block. Or a non depolarizing type block. Non depolarizers attach at the junction in place of AcH, but do not cause the muscle to depolarize. Rather, they prevent depolarization. So, in succ OD we may have a pseudo phase II block. In cases of this block, we may need to give an anticholinesterase medication such as neostigmine. If we give neostigmine, we need to anticipate anticholenesterase type side effects. So, we may need to give an anticholinergic such as atropine to combat these side effects. A WORD OF CAUTION!! Phase II block must be verified and confirmed because if we have a prolonged phase I block and we give neostigmine, we have just complicated our problems 10 fold. Verification of a phase II block requires peripheral nerve stimulation, and I would advise against following your protocol in the field.

I hope this helps.

Take care,

chbare.

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Succs is a different class of drug than the -croniums, as it is a DEPORALZIING NMB. It would make more sense (esp. for peds) to pre-treat with atropine (because of heightened vagal response period, regardless of laryngealscopy). I guess atropine could be the reversal (I don't remember) it kinda makes sense...

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Focus, I can't add any more on the meds that the others have already posted but as far as your statement about reading and researching over your level, LORD I wish my EMT partners would have that kind of ambition. Nothing wrong about learning more on Meds and treatment. Keep your education going, weather you stay an EMT or become a Paramedic.

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Thank you very much :lol:

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Treatment of hyperkalemia is calcium choride, sodium bicarb and regular insulin. Basically these cause the potassium to shift back into the cell where it belongs and corrects the acidosis. Rapid correction of hyperkalemia is risky and is not usually done unless the K is > 6. You can also use lasix to treat hyperkalemia but you will have to monitor volume status. I have given calcium and bicarb in dialysis patients suffering from cardiac arrest in the field on two occasions (we don't carry insulin on the truck). Both times I almost immediately got a perfusing rhythm with a blood pressure. Both patients died later on in the hospital. Could have been a coincidence but I don't know.

Atropine is given as a pretreament prior to succinylcholine in children to combat bradycardia because kids are one big vagal nerve. Atropine alone does not reverse suxs or any other neuromuscular blocking agent (NMB).

I'm not sure what a succinylcholine overdose is. If you are talking about a patient with atypical plasma cholinesterase then the treatment is sedation and put them on the ventilator until the suxs wears off sometime in the next few days. If you give vecuronium or some other NMB before the suxs has worn off you can get a Phase 2 blockade in which case the treatment is the same--put them on the ventilator. This type of blockade will probably wear off in a few hours.

Reversal of NMB's requires a few conditions. First the blockade has to be in the process of degrading. We place a nerve stimulator over either the facial or ulnar nerves and measure the train of four. The stimulator gives four impulses and we watch for the muscles to twitch. You must have 2 of 4 twitches before you can reverse the NMB. We give neostigmine and glycopyrrolate (robinul) to reverse the NMB. Neostigmine binds to the enzyme that degrades acetylcholine (ACH)(acetylcholinesterase) causing a rise in ACH and return to normal muscle function. Neostigmine given alone will cause profound bradycardia because of its muscarinic effects so we give the robinul along with it. Robinul is an anticholinergic like atropine but is a quaternary amine instead of a tertiary amine like atropine so it does not cross the blood brain barrier and make patients goofy as atropine can sometimes do.

We give neostigmine and robinul together because their onsets of action are similar. Atropine has a faster onset than robinul so we don't use it with neostigmine. It used to be used with edrophonium (same class as neostigmine) which also has a fast onset. I was just looking at edrophonium in my ePocrates drug program and is says edrophonium is no longer available in the USA. I haven't used edrophonium and atropine since I did my anesthesia training over ten years ago.

Hope this helps. Keep up the good work and education focus 911.

Live long and prosper.

Spock

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LOL.... "may the tube be with you"... sorry thats hilarious.

I have another question for you guys. It was reading about D50. It sais it is used for: Pt's with Altered LOC of unknown etiology. hmmmm....I dont get it. If you have someone who is altered you should be doing a full work up anyways(ECG, Vitals, BGL) and then you would know if the BGL might be the cause of the alteration depending on the numbers you get, and for head injuries you are supposed to give the first half, re-assess and then you decide from there if continue with the other half.

I dont get it how it can really be unknown because once you get the BGL you will know whether or not it is a D50 candidate wouldnt you? If you are in a position where taking a BGL is just not possible then its different but what am I missing? Are there conditions where it is still a treatment despite a good BGL? I dont get it :?

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Do you understand the term "relative hypoglycemia"?

There are a good many reasons for a blood sugar to be in the normal labratory range, and still be inadequate for the metabolic demand of the body. The most common is the diabetic that has an elevated normal glucose level, undergoes some type of stressor, the blood glucose level drops quickly and remains in the normal range, but their body can't compensate for the alteration from normal.

The problems that can happen following unneccessary administration of dextrose are much less severe to manage than the damage that is caused by an extended, possibly hypoglycemic episode.

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CaCl stabilizes the membrane of the cell wall to control the leakage of the K. You can also use albuterol in hyper K pts, does the same thing.

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Spock thanks for your response to the atropine for succs od very imformative. and thanks to everyone esle for a great discussion.

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We use CaCL2 in the prehospital field in Nova Scotia for :

.Resp depression if after MgSO infusion

.Hyperkalemia with cardiovascular toxicity

.Calcium Channel blocker OD

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