If I gave you a whole list and said which of these statements is true about the mechanism of action of epinephrine and atropine, would you get it right? Let's find out. By the end of this video, you're gonna know it cold. Every medication or drug has three names. The chemical name, which we're never really going to see after the lab, but I put it here for you, the chemical name.
So in this example, we're using Tylenol. The generic name, we're going to see a lot what our patients on their med list. talking about medications, and also on the patient's pill bottles themselves. So generic name, acetaminophen.
The brand or trade name, that's Tylenol. So the patient may be familiar with generic or the brand when you speak with them. This right here is what a drug card looks like.
So when you're filling out your drug cards in paramedic school, this is what they look like. We start generic and brand name. The class.
The class means essentially like for example the drug was a anti-hypertensive medication or anti-pyretic medication or sympathomimetic. We're going to talk about all these things in a little bit. So what does the drug do basically is how it determines its class right. Mechanism of action is what the drug does when it enters the body. How does the drug have its effect?
The mechanism of action is so important to the MOA. Why it's so important? If I know what a drug does and I understand the mechanism of action and how it translates to what goes on in the body, I can fill out this whole drug card basically, all the indication and contraindications.
For example, if I know a drug is going to increase someone's heart rate, right? If the indication means when I give it. So...
If I know a drug increases the heart rate of a patient, if their heart rate's too low, I might want to give it. But what would I not give it if it's already too high? Right.
What might the adverse effects be? If I'm going to raise your heart rate up, you might get restless, you might get anxiety, you might get palpitations, right? Dose, that's a term on a drug.
And then what route? So what route am I going to give this drug? Is it going to be IV?
Is it IO? Is it PO? is oral. What is it? Is it intramuscular?
What is it? Every drug has some special considerations that you want to think about when giving the drug. So we have here the sympathetic and the parasympathetic nervous system. One is fight or flight.
One is rest and digest. So the thing about the sympathetic and the parasympathetic nervous system is they're always in balance with each other depending on what's going on, right? Remember this. Pupils, heart rate, blood pressure, respiratory rate, and digestion.
Those are the key factors of what they do. So, in sympathetic, if I'm in a fight or I'm fleeing because a giant lion is chasing me, right, what is my body going to do? Well, my pupils are going to dilate so I can see better. Also, my heart rate is going to increase. My blood pressure is going to increase.
My respiratory rate is going to increase. So, I'm able to move and perform better, right? And also, we're not going to worry about digesting that food I had two hours ago.
There's a lion chasing me. So we're going to reduce digestion. Now, with parasympathetic, it's rest and digest.
So now you're relaxed, you're back, you're hanging out, you're getting ready to go to bed, right? That's the way I think about it. So pupils start to get constricted, heart rate and blood pressure go down, respiratory rate goes down, and And digestion is going to be increased in the rest and digest phase.
Okay, so that's what we're looking at for sympathetic versus parasympathetic. Let's get a little more advanced now. Now we just learned about the sympathetic and parasympathetic. I have some key terms for you. Gotta know this.
Sympathomimetics. What that is. It's a drug that mimics the actions of the body's sympathetic nervous system. thus turning it on, right?
So these drugs are also called adrenergics because they're related to that receptor in the body, okay? So sympathomimetics could be also called adrenergics. You might hear that. I want to tell you about that. Now notice this.
Sympatholitics do the opposite effect. So we get a parasympathetic effect from a sympath... Parasympatholytic, we're shutting off the sympathetic side.
So, sympathomatics, turn on the sympathetic nervous system. Sympatholytics, shut it off. Agenergics, that goes with the sympathomatics.
Now, over here, parasympathomatics, that's going to turn on the parasympathetic system. A parasympatholytic, for example, like atropine. right epinephrine would be a sympathomimetic atropine would be a parasympatholytic because it's going to shut off this side and turn on this side right a cholinergic drug that turns on that receptor that has to go with Parasympathomimetic.
It's a mouthful I know, but you gotta know these words. They're gonna come up in class and on exam day. Now, real quick, the top part of this that we talked about, the bottom part, the top part is agonist versus antagonist.
So an agonist is any drug that turns on a receptor. And I'm gonna teach you right here in a second about the different receptors that we're gonna learn about. Now, An agonist turns the receptor on. So let's say a receptor, when we turn it on, caused vasoconstriction. That's an agonist.
Now, what if a drug enters the body and it's a blocker? Okay, it's an antagonist. Then that means it would go into that receptor and it would block the action, right? So let's go a little deeper on this topic. These are the main three receptors you need to know.
EMS. So let's talk about first when they're activated, what happens. So let's say the alpha 1 receptor is turned on, right?
There's an action being taken place. We get vasoconstriction, okay, of the blood vessels, vasoconstriction. Beta 1, we have one heart, so beta 1 has to do with the heart.
It's going to increase the heart rate of the patient. And this is a big word, contractility. There it is.
The contractility, how well the heart can contract. So it makes a stronger beating heart. That's going to increase the heart rate. Beta-2 receptors, we have two lungs. So we're going to dilate the patient's lung.
Now think about this for a minute. If your patient's having an asthma attack, Would it make sense to give a drug that's an agonist to the beta-2 receptor? We do that.
That's albuterol, right? That's epinephrine too, right? Someone had anaphylaxis. They're wheezing. We give epi and albuterol.
That acts in the beta-2 because we want bronchodilation. We want the bronchioles in the lungs to open up. Now you're getting it. What if...
someone's heart rate's too low. I might want to give an agonist of a beta-1 drug like epinephrine to raise their heart rate and increase the contractility of their heart because it's so slow and low. Right. What if someone's got low blood pressure? Would I want to give a vasoconstricting agent to raise their blood pressure in certain circumstances?
Yes. Epinephrine does that too. Right.
Now. We see here epinephrine, which is the main, really, really is the main drug of EMS, epinephrine. It's an emergency medication.
It's an agonist on alpha-1, beta-1, and beta-2. It's a sympathomimetic, and it does, it acts on all these receptors. Now, I'm going to throw a little curveball at you.
What if your patient takes a medication, it ends in O? L-O-L. That's a beta blocker.
Wait a second. I just learned about that. Yeah. Well, beta blockers are in the, could already be in your patient.
Meaning, the patient takes a beta blocker, it's the opposite effect. So, would it make sense if you were a doctor to prescribe somebody that actually has... asthma in their history, would it make sense to prescribe them a beta blocker when we can use something different?
That wouldn't make sense. Basically, we know right here, right? Because if we block the beta-2 receptor, we get the opposite effect, which would be bronchoconstriction.
Whoa, you see where I'm going? So that would be a special consideration. See how we're learning, right?
So again, if we block... The beta receptors, I'm going to give you one more pearl here. I got to give it to you.
Most beta blocker drugs that are an antagonist that block the beta receptors, the majority of them try to select which beta receptor they want to block, right? So some beta blockers, for example, why do we give beta blockers in the first place? Well, the patient would be prescribed a beta blocker because they want to lower their high blood pressure, right?
So, beta 1 could lower the heart rate, could lower the conductivity of the heart, could lower the patient's blood pressure, right? So, the thing is, if we give any beta drug... Even if it selects the beta-1, they're twins.
There's always a little crossover effect into the other one. So that's something to keep in mind. Now we learned how epinephrine is a sympathomimetic. It's going to go in the body and mimic our own sympathetic nervous system.
It's going to increase our heart rate, right? Now what about atropine? How does atropine increase the patient's heart rate? But it's not a sympathometic.
It's something different. So atropine is a parasympatholitic. So what this means, atropine goes in, it's going to, again, sympathetic and parasympathetic are always in balance. So it's going to lower the parasympathetic's ability to work. So by default, sympathetic goes up, right?
So we get a effect that looks like sympathetic is turned on, but really, Parasympathetic is just down, so we get an increased heart rate, meaning what actually happens? Our vagus nerve. Think about it being plugged in to the heart, right? So when patients have a really high heart rate in the ambulance, we can have them bear down, like they're passing a bowel movement, to actually lower their heart rate.
That turns on the vagus nerve and gives them a parasympathetic response. Pretty cool, right? Now...
What atropine does, atropine basically makes a roadblock, a block in that vagus nerve. Thus, parasympathetic can't act on the heart. So the heart goes, well, this nerve is down right now.
I'm going to go increase, right? So that's how atropine is able to increase the heart rate. It lowers your parasympathetic response. So now you tell me what is true of the mechanism of action of epi. and atropine.
I'm going to give you five seconds. Five, four, three, two, one. Remember, here it is.
Epinephrine is an agonist that is a sympathomimetic and it's going to act and turn on the alpha one, beta one, beta two receptor. Thus, we get vasoconstriction, increased heart rate, bronchodilation. Right.
Atropine. Atropine is a parasympatholytic. It's going to be the roadblock at our vagus nerve. So the parasympathetic response goes down.
Thus leads to the heart rate increasing. And this is why atropine is given for bradycarnias with symptoms. Because it is able to raise that heart rate. And there it is.
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