Short-Acting Beta Agonists Explained: Pharmacology & Clinical Use

[00:00:00]Well, welcome to this pharmacology drug class  review on the category of bronchodilators with   a specific focus on those short-acting beta  agonists (SABA). You know the short acting   beta agonists are well-known lifesaving  treatment for acute bronchospasm leading   to that respiratory distress as we've seen in  patients with asthma and COPD. Furthermore,   they also work in other life-threatening  conditions that I'm going to cover. Hey guys,   I'm Dr. Busti, thank you so much for joining me  on This Is Why, a show dedicated to helping us   as health care professionals really dig in and  understand the why behind the decisions that we   make. That includes pharmacology and the drugs  that we use. Because when we understand the why,   the how becomes easier and that mechanism starts  to explain the therapeutic effects that we see,   what we should be looking for, the side effects,  modern parameters, and some of our counseling   points. Now, as with all my drug class reviews,  we cover core content. We hit the agents that   make up that class, common indications and uses.  Not all of those are FDA approved necessarily,   but they're commonly still used off label. What is  the net benefit? Why am I grabbing this drug class   over something else? Get into the pharmacology.  How does it work? Making that mechanism really   come alive? And then transitioning that clinical  knowledge, application, the clinical pearls. Okay.   Okay. So when we look at these agents, we have  albuterol. That's the obvious classic identified   agent in this group. Now when I put that up there,  this is the understanding that this is both the   formulation with the R&R. The R anantimer is the  active form. Okay. Um, Lev albuterol is just the R   enantiomer, the R albuterol. All the manufacturer  did is just filter off the S enantiomer and it   just became Levalbuterol. Okay. Um, I included  racemic epinephrine here simply because they are   short-acting, and there is some beta agonist  activity. Now epinephrine also interacts with   other receptors. Okay, including alpha receptors,  beta 1 receptors, but I I listed it here just to   be complete. We're not going to spend much time  on it in this particular lecture because we're   talking about in the context of mainly asthma,  COPD. And then lastly, we have terbutaline. Also,   again, I'll talk about it intermittently, but  terbutaline is kind of one of those older drugs   that has fallen down in its use and acceptance  in clinical practice. A lot of potential side   effects because we're typically administering it  in a fashion, in a manner that is systemic. So,   we get systemic manifestations as a result  of using it. Okay. Now, we're going to pivot   over to the indications and uses. And this  is where I'm going to mention a few of the   non-traditional things that we don't think about  or always think about when we talk about asthma,   COPD. Um, but it's important that these drugs are  understood in their context outside of that. So,   you can see here obviously asthma they are used,  but it should not be as just PRN like it used to   be historically where patients you know that may  have been the only thing they were given. I still   see to this day patients only on a short  acting bronchodiilator like this and that   is inappropriate for asthma. Remember the main  state of treatment for asthma that we'll see here   in a minute is really centered around the use of  inhaled steroids. Then you add on beta agonist so   that we treat the underlying problem mainly COPD.  There are some patients that we'll see here in a   minute that have symptoms and manifestations of  hyperactive airway disease. It mimics asthma and   and again this would be where patients can have  overlap and they have inhaled corticosteroids or   they benefit from one agent over another. Okay.  So we typically think of antimuscarinic drugs   okay or muscarinic antagonist anticholinergic  drugs as being the mainstay in COPD. But there   is a role for obviously albuterol in the acute  phase. And then third is that exercise induced   bronco spasm. It can relieve it if it begins  to happen in patients participating especially   in aerobic activity where their minute ventilation  is causing some irritation. Then there's that last   bullet where some other causes. Okay, bronchospasm  from anaphylactic reactions. And that is really   important, right? Next would be probably the  other one is Croup with some stridor trying to   do everything we can to relax that. That's where  sometimes that racemic epinephrine is commonly   used to reduce the constriction of those vessels  trying to maximize the airway opening in that in   that small airway in a pediatric patient which  typically has more croo than adults. And then the   other one is hyperkalemia. Um, patients with uh  come in with their their potassium over at five,   maybe they're having EKG changes, maybe they're  not, but we've got to be able to sometimes drive   that potassium back into the cell. And one of the  ways that we do that is with albuterol. And then   lastly, there's tocolysis. Basically, pre-term uh  labor symptoms. I put plus or minus there because   it's really not recommended. uh there may be  more harm in doing that because again you're   exposing people it's usually a subcutaneous  injection. You're exposing people to systemic   beta agonist activity. So they get tremors,  tachycardia that can lead to other other   problems. U and we typically don't want that to  happen in pregnancy. But if you end up using it   uh just realize that it should be very limited in  its use. Now I like to put tables together and I   like to talk and teach about drugs in the context  of the disease at a basic level. This is obviously   not a disease state review but I put this table  together which is available at thisiswhy.health   for you for free download. The link is for this  episode is available in the description if you're   watching this on YouTube or if you're on Spotify,  Amazon or Apple for our podcast channels. it's   there for you to be able to access that for your  own personal use. Feel free to share it. This is   looking at what are some of the variations  and characteristics between asthma and COPD   recognizing there is some overlap which I'll  talk about here in a second. But the cell type   in asthma it is eosinophils, COPD it's going to be  neutrophils. Those neutrophils in particular are   going to cause a lot of more inflammation damage  and remodeling of the airway. Why does all that   matter? because the underlying airway activity  problem influences the bronchodilator response in   row three there. So you see the asthma typically  has a better bronchodilator response especially   with these beta agonist than COPD patients.  That doesn't mean COPD patients have none.   It just means it's less and that has to do  with the hyperreactivity the spasms that is   occurring at the level of the bronchiole. And  then of course asthma's main state of treatment   is that inhaled steroid, treating the underlying  mechanism to control those eosinophils. Whereas   in COPD there's limited benefit unless they have  overlap syndrome. And that's what I wanted kind   of to show you next. So this kind of Venn diagram  is meant to say okay there are things that overlap   and share some of those qualities. Why does that  matter? Because some patients may need extra drug   therapy or certain combinations, because that's  their underlying problem. And the way we know   that in some respects is their symptoms. As we add  on, takeaway, do things with their medications,   we we try to tweak it to maximize their quality  of life and the reduction of their symptoms. But   you can see that on the top one there's asthma.  On the bottom two circles there, there's chronic   bronchitis, which is usually the earliest phase  of COPD. and then which are then left untreated   constantly being exposed there's that remodeling  that occurs that leads to emphysema but if they   overlap that's something called ACOS asthma COPD  overlap syndrome where patients can res benefit   from one agent over another okay now let's move on  to our what is the net benefit of the drug class   then why would I pick this agent uh or this class  of drugs and compared to something else. Well,   remember this is nice to have something as needed.  When my symptoms get flared up even despite being   on those preventative or maintenance medications,  it's good to have that because patients will   have eczema or asthma exacerbations or COPD  exacerbations and they need something to provide   a bronchodilatory effect when they need that. In  the context of hyperkalemia, the net benefit is   that it basically changes the location of that  potassium in the hopes to temporarily provide   you transition time until you get to dialysis or  find some other way of eliminating the potassium   maybe out through the bowel. Uh but you got to  shift that potassium into the cell. Remember   potassium is the major intracellular cation and  so in uh albuterol is known to turn on those   transporters that drive it in. But remember it  can be doing that can be harmful especially with   EKG changes already present from the hyperkalemia.  So remember they get those peak T- waves. I mean   not just peak T- waves by the way that's what we  classically teach but they have a lot of variable   uh effects on their EKG. So that's where we would  typically before we drive that potassium into the   cell we would give calcium and then we would  administer the albuterol or if we were using   insulin dextrose conic combination we we would  use the calcium first to stabilize the cardiac   membrane as we drive this positive cation into the  cell and change electrical potential inside of a   heart that could be bad. All right. Now, we're  going to pivot and move into uh the pharmacology.   But in before we jump into the the the mechanism,  which is important, we need to make sure that we   understand some of the basic uh lung anatomy um  and some of the physiology that is happening there   because the reason it matters or the why is that  if you don't get the drug to the sight of action,   it's irrelevant. sitting in your mouth is  not going to help you down in the area of   the bronchi of your airway. So this diagram that  I'm showing you here shows the kind of the visual   of the oropharyngeal area going into the trachea  down into the lungs. But you'll see a lot of like   ring-ike structures as you go through that extend  many and many of the branches on both sides of the   lung. And those are cartilagynous rings and  they're rigid and they hold the airway open   otherwise you would die if they spasomed. So those  are important anatomical features that yes there   can be some swelling and mucus production in that  area but they're not going to collapse typically   because of those cartilaginous rings. But when you  zoom in at the very distal end so you got to get   way deep down into that lung field. you get to the  bronchioles where there's the smooth muscle tissue   wrapping around that airway and that relaxation  contraction of that smooth muscle especially in   the acute is what regulates the air flow in and  out of that bronchial. Where's it going? Well,   it's going to the alveoli. Why does that  matter? Well, because when you zoom in on   the alveoli there's a lot of blood vessels coming  in because you've got to carry deoxygenated blood   to the alveoli to get oxygenated from the air  you've breathed in. But you also have to expose   the alveoli to CO2 that was delivered from the  cells after their metabolism as a byproduct. And   you need to be able to get rid of it. So there's  something called oxygenation which is that air   coming in and being able to diffuse across the  membranes into the blood passing by. But you   also have to facilitate ventilation, the removal  of CO2 because if you retain CO2 in the blood,   you're going to facilitate a shift in an acid base  disturbance and put the patient in a hypercapneic   state which can increase their risk of acidosis.  Well, okay. So that's fine. Dr. Best, why are you   talking about all this? Well, because if I occlude  or spasm this airway at that very distal end   because I can't get the drug down here by whatever  method or formulation I'm using or I don't have   the underlying right treatments on board, then I'm  going to reduce the airway flow. So I will reduce   oxygenation, but I will also reduce ventilation  in these patients. And so we get both hypoxia with   retention of CO2 putting the patient into more  respiratory distress. And this gets worse as time   goes on. That's what this visual is trying to show  you. So in the normal otherwise healthy airway,   we have that relaxation contraction depending on  our needs. Okay? Uh you see that the mucus area,   the smooth muscle tissue is relatively normal in  size. But as you start to have inflammation and   irritation from uncontrolled asthma in particular,  you get this swelling and edema. And so that   airway, the lumen of that airway is now smaller.  So less air can get in. And if t's hyperreactive,   it spasms. And so you've got to get the drug  way down here in order to relax this. And the   problem is is as it gets worse then you start  making more the inflammatory cells kick in start   making more mucus and that's when they can develop  obstruction. That's why asthma is an obstructive   airway disease. The constriction followed by the  secretions obstructs the airway and there's no air   movement going distal to that point trying to make  it to these alvei for gas exchange. So you air   trap whatever's stuck in these alveoli. they get  trapped in there the air so it can't get out and   then the gas exchange going by is not happening  because there's no concentration gradient being   created and so you reduce the oxygenation to  the blood and you reduce the removal of CO2 okay   uh in COPD patients they go through phases again  that chronic bronchitis phase where the tissue   really just is irritated makes gobs of mucus right  and over time if left untreated evolves into a   remodeling of the airway that causes damage and  those airways lose their compliance and strength   and they just collapse and so they trap air in  though it's an obstructive airway disease as well.   But the reason that it obstructs is different  than an asthma. And that's why it's important   to recognize the difference and to have these  visuals because when we are administering these   medications, we have got to get it down here.  Sitting in the oropharynx is not going to do   you any good. Now, once we get it there, it's  got to bind to some receptors on those smooth   muscles to create the bronco dilation that we're  seeking. Okay. So what is that? Well, R albuterol   remember is the active form. It's the active  enantiomer. The S enantiomer which is mirror   image of it is the inactive. It does nothing.  All right. And so that's where levalbuterol   this is basically levalbuterol. Okay. It is the  R enantiomer isolated. So it binds to this beta   2 receptor which turns on adenylate cyclase which  is an enzyme that converts ATP and and facilitates   increases in cyclic AMP that drives up our protein  kinase A activity and the effect on that is that   it does two things. It reduces the phosphorylation  of myosin which is necessary to interact with   actin to contract muscle but it also reduces  the cytosolic calcium concentration. So it has   two different very important effects inside that  cell and that recauses an overall decrease in the   interaction of that actin myosin in that smooth  muscle and so it relaxes. It breaks the spasm.   It bronchodilates because of that net effect on  those two things. And the reason I spend time   talking about it is that you if you memorize a  drug as being oh it's just a beta 2 agonist. Well,   that doesn't tell me how it works. That tells me  what it receptor binds to or the class of drugs.   But why does it cause bronco dilation? That is  what that mechanism is trying to show you is   why does it translate into a relaxation of those  bronchioles where there's no cartilaginous rings   at where we get the desired therapeutic effect  that we need that improves the symptoms of the   patient. And that goes back to the very thing I  said at the beginning. When you understand why   you do what you do and why something works the  way it does, the mechanism then makes sense of   the therapeutic effects that we're looking for and  then the side effects and monitoring parameters   that we have to consider. Now I want to take  a moment and talk about the structures of our   albuterol. Um so when you order regular albuterol  and whatever whether it's nebulized form or a   meter dose inhaler you know type of formulation it  doesn't matter it has the the albuterol has an R   and an S enantiomer in it. So when we look at the  R enantiomer which is what this structure is for   albuterol it is the active one. The S enantiomer  is not helping us. We should technically remove   it but this drug's been around for a long time.  So the drug company basically filtered off the   S enantiomer formulated it as only the R&R called  levalbuturol and that drug is the active form only   there's no s an enantiomer in it so it's literally  half the dose or half the concentration of plain   old racemic or albuterol okay and so when you look  at the structures they're identical because they   are so if Someone tells you, "Oh, Levalbuterol is  better than regular albuterol." That's not true.   There's no ounce of evidence at all that proves  that. The totality of the evidence actually says   there's absolutely no difference. And in some  respects, if you look at the product package   insert, Lev Albuterol has been reported to have  even more side effects. Go figure. Okay. So,   I I drive that point home because a lot of people  get this thing confused. They've they get they   they don't understand the evidence. They don't  understand the mechanism. The medicinal chemistry   just that level alone makes that clear. Okay.  All right. Now you are affecting receptors. Blood   vessels have beta receptors in them as well.  Okay. uh when you activate beta 2 receptors in   the vasculature that can cause some vasodilation  which is why beta blockers cause vasoconstriction   and are not really great blood pressure lowering  medicines for that reason. Okay. When you couple   that with the drug being absorbed in the body  a little bit even though you've inhaled it,   they can also activate beta 1 receptors in the  heart but also beta receptors in the kidney. that   matters. Like why does that matter Dr. Busty? Who  cares? Well, because when you activate the beta 1   receptors in the kidneys from systemic absorption,  you release renin. And renin then turns on the   renin angiotensin aldosterone system (RAAS) that  leads to sodium water reabsorption that increases   plasma volume and raises your blood pressure.  Stimulation of the beta 1 receptors turns on your   pulse. Both of those two things together can raise  your blood pressure and affect pulmonary vascular   flow. And so they're actually coupled together,  this can lead to um increases in blood flow   through poorly ventilated uh lung and may actually  theoretically cause a little bit worsening of the   hypoxia initially. Okay. Now this is only usually  at the beginning and then it typically goes away.   But it's a it's an aspect of the mechanism that  becomes important once you start absorbing the   drug systemically. Now I mentioned racemic  epinephrine earlier at the beginning. I said   I wasn't going to spend that much time on. I'm  not u because it interacts with other receptors,   alpha receptors, beta receptors, both beta 1 and  beta 2. And so its beta 2 effect is the reason we   use it in anaphylaxis. We're primarily trying to  bronchodilate them. But if they're hypotensive,   then we also get that alpha stimulation that  raises their their blood pressure. Well,   in CORO patients, which are typically pediatric  patients, their their airways are small, really   tiny, and we don't need engorged blood vessels in  that already engorged edematous, inflamed airway   from the infection. Okay. So we give these racemic  epinephrine which will bind to alpha receptors   will vasoconstrict those blood vessels and that  reduces the airway edema theoretically and that's   one of the reasons why we use it in there to  reduce that subglottic edema that is causing their   predominant symptoms and respiratory distress.  Now in the context of tocolysis remember again   I put the plus or minus here um you're relaxing  smooth muscle in the airways of your lungs. Yes,   it will work to bronco dilate but it also relaxes  muscle in other places and that's why people   consider it or think about it and historically  have taught it to be used in to as a tocolytic   basically patients in pre-term labor their their  uterus is contracting muscle the myometrium is   contracting of the uterus and so we can relax  that just like we would relax it in the airway.   Uh this is again ad ministered in a parental  formulation usually subq and we should only   do it if we're going to do it at all because you  really don't have anything else or you're there's   some reason you need to delay and the benefits  outweigh the risk. But most of the evidence would   suggest and most experts say we shouldn't really  be using this. This is not our main effort to be   tool for a tocolytic. All right. Now again we're  kind of thinking about the therapeutic effect   when we think about it in context of asthma of  these broncodilators. I told you at the earlier   in that table that asthmatics have a hyperreactive  component with a decent or better bronchodilatory   response than COPD patients. And that's true in  the context of asthma. We have criteria that tells   us on a when we're doing pulmonary function test  if they have an adequate bronco dilator response.   And I've defined that here for you. there's  usually a change in the FEV1 or FC by 12%   from their baseline before the bronco dilator is  given or or at least 200 or mls or more of airflow   improvement after giving the bronco dilator. So  that is a positive bronco dilator response that   we desire and helps us to know this patient has  hyperactive airway disease and they are going to   respond. The only way you know that is a pulmonary  function test. And again, so for patients with   ACOS, that asthma COPD overlap syndrome, that's  where it becomes a little bit, you know, hard to   um to know until you do these tests. Okay. Next is  um receptor crossover and the risk of tachycardia,   blood pressure elevation. I've kind of alluded to  this a little bit, but no, very rarely are drugs,   especially that interact with receptors like  this adrenergic receptors are they pure only   beta 2 only this remember. So when you give enough  drug even of albuterol which is preferentially a   beta 2 agonist you will get crossover binding to  beta 1 and that's why patients will experience   palpitations or an increase in their pulse. They  will also increase t have tremors and anxiety   sometimes and feel like anxious. Okay, that is  the systemic absorption and the interaction and   the crossover to those other receptors and that's  really important to remember including also the   kidneys where that renin is going to be released  from the juxtaglomerular cells in that those JG   cells of the afferent arterial going into that  glomerulus they sense that that will trigger the   renin angiotensin aldosterone system that will  increase plasma volume but and and also known   angiotensin two which comes from that activation  is a potent vasoconstrictor. So you raise blood   pressure. So that's why you can see people's blood  pressure pulse go up after they've administered   short acting beta agonists in any form. Obviously  topical is going to be less than something like   terbutaline okay or epinephrine that was given  subq or IM. All right. Now we're going to shift   over to the clinical knowledge. And this is where  I'm going to really kind of start to dive in on   the mechanics method of getting those drugs  down into that airway. Please do not ignore   this section. Do not bypass it. I cannot tell  you how many patients do not know how to properly   administer the medications that we prescribe.  We as a health care team, nursing, pharmacy,   respiratory therapy, pharmacy, and physicians  all need to take the moment and reaffirm proper   technique because that translates into getting  the drug to the right location to exert the   effect that we just talked about. Okay. So, we  have a number of different dosage formulations   that are out there. Um when we talk about short  acting beta agonist, we're primarily over here   in the aerosolized MDI with our pressurized and  the nebulizer treatments, dry powder inhalers,   whatever. This is just one example. It's not the  end all be all. It's just trying to point out the   different varieties of dosage formulations that  occur. When do we want a you know a certain how   to drug a certain drug to work a certain way?  um when you use a dry powder inhaler like this,   you have to generate much greater inspiratory flow  rates to get the drug down to those airways. Well,   sometimes in acute exacerbation or symptoms,  you can't get a patient to do that. And that's   where they get something to help propel the drug  where they don't need the same inspiratory flow   rate. In fact, they should use it a little less  like slow continuous deep inhalation as much as   possible so there's no oropharyngeal deposition  or deposition of the trachea. But we want to get   it down to those bronchioles. Now, sometimes the  coordination and the timing of that is affected.   And that's where spacers can be very helpful at  holding that drug so that you're ready. You've   blown out. We'll see there the technique here in  a minute. And then you and then you inhale when   you're ready to maximize the timing and the drug  delivery and deposition to those bronchioles. I   cannot stress that enough. And the other thing  that I wanted to point out here is that there   are a lot of people uh who unfortunately believe  that the nebulizer is better. There is no evidence   that proves that. Most of the evidence, the  totality of the head-to-head trials and studies   that looked at using a meter dose inhaler, even  in acute exacerbation in multiple age groups,   is equally effective and sometimes more effective  than a nebulizer treatment, which is just spewing   drug everywhere. Doesn't necessarily mean you're  getting the right amount of drug delivered to the   side of action just because it's on your face  and making a bunch of noise and gas. In fact,   it can get in your eyes and cause side effects.  So, what is the proper technique recognizing that   our patient might have nebulizer which they  can't carry around with them to the grocery   store as you know on their back, right? So, they  have to have multiple dosage formulations. Well,   they have to use the right technique for the  dosage formulation that they're administering   to themselves. And so, it varies, right? So you  you heard me talk about the dry powder inhalers   have a different inspiratory flow rate whereas  metered dose pressurized inhalers (MDI) like these   on this diagram here require slow continuous deep  inhalation. So you remove the cap, you shake the   inhaler, rotate it. Okay? And the idea there is to  again maximize the pressure inside there so that   the pressurized dose that's released is equal each  time before you administer the medicine. After   you've shaken it, you blow out. So you exhale  the air and then you put the device up to your   mouth. Okay? And then you begin to inhale and the  propellant or the pressurized activation of that   device is pushing the drug out and into your  airway. And so it's expecting at the timing of   that that the air is already flowing in so that it  as it comes out it continues to move down and it's   got to get way down here in those bronchioles.  That's why I went and showed that to you. So   there's different techniques even of how you put  it up to your mouth in that step. You can see here   in this one where the mouth is open and the if  the propels out into the oropharyngeal that is   appropriate as long as your lips are not blocking  the propellant or the pressurized activation and   release of the medication. And then there is  the method of wrapping your lips kind of around   the outside again not occluding the opening.  So, you have to be careful in both. They're   both appropriate ways to do it. People go to the  nebulizer simply because it seems easier, and it   is. There's an element of putting it in there, put  it on your face, walk away. But the reality is all   this gas that's floating around here is getting  in this guy's eyes. It's getting out into the air.   It's it's bronchodilating the the drape over here  and and the pole. No, I need it down here inside   that guy's airways. So when when he has got to be  bringing it down in there appropriately. So he has   even the technique of slow continuous deep breath  in and blowing it out is really important to get   that drug down there. Just putting something on  someone's face doesn't make the drug work better.   You still have to do something. And that's where  for using a a a spacer is so important. But it's   inconvenient to carry that thing around. I mean,  who's going to put that in their pocket? Even in   a purse sometimes. I mean, you know, there's a  lot of things sometimes in purses. So, it creates   difficulty. So when we come back, when we get the  drug in, whether it's by nebulizer or pressurized   canister, we then need to hold our breath at step  five for at least 10 seconds. And that allows the   aerosolized drug to deposit on those bronchioles  where they're going to work. We don't want to   just blow it right back out. We got to give it  time to deposit on the airway. And that's hard   when you're having acute shortness of breath,  isn't it? Right. And then when you blow it out,   you blow out slowly. So it's not these extreme  movements of air that people It's like kind of   shocking sometimes to watch people inhale. Like  the more dramatic it is, the more effective.   No. Right. Proper techniques. Now when we get a  and we're using short acting in the most common   context is acute symptoms exacerbation. So is  there a maximum dose? Well, not really. You just   keep going until either the symptoms resolve or  they develop side effects, right? But clinically,   remember as the bronco spasm increases, the  severity of it, that swelling of the airway goes,   it's harder. You need more drug to exert the  desired duration and effect of bronchodilation.   So it makes it harder. And that's even worse if  they're already on a long acting beta agonist   at the time you're trying to administer because  there's receptors are occupied. So sometimes we   do have to use much higher doses and repetitive  or even continuous nebulized treatments for that   very reason. Now I mentioned Levalbuterol and I  mentioned that because they remove half of the   drug that's not active and they just keep the R  in the product. It's half of the dose. You know   there's really no again evidence when you look at  the totality of the published studies they do not   say that lev albuterol causes less side effects.  There was one particular study that suggested   that but that is not consistent with all the other  studies. So the story was inconsistent concern of   potential internal validity uh of that study. Do  we have something available over the counter? Yes,   we do have options that have uh utilized racemic  um epinephrine. I know that sounds a little crazy   but sometimes patients don't have access to  things and you know it this can save their   life. There is a meter dose inhaler. Primitine  mist. Uh Asmanephrine is another one of those.   It's a bulb kind of nebulizer uh device that you  can technically get without a prescription. It's   not recommended. We don't desire this. Remember we  don't want patients treating just their symptoms   especially if they have asthma because that's not  treating the underlying problem. They need to be   on inhaled corticosteroid. If you're using this  terbutaline for tocolysis, as I mentioned before,   it really should not be used past 48 to  72 hours um you need to get that patient   to the right location. This is not something you  should be seeing used in uh outpatient ambulatory   care practice. A lot of risk of tachycardia,  cardiac dysrhythmias, sudden cardiac death,   all these things is not recommended. You're also  lowering um the the potassium. That's that's one   of the things that we use to lower potassium in  hyperkalemia is a high doses nebulized treatment   uh with albuterol. So adverse effects we can see  some temporary hypoxia because that redistribution   of blood flow remember that goes away and  improves. Uh we can see drops in the potassium   because we're shifting it into the cell. Okay.  This lactic acid levels here we're talking about   is because of the small elevation and that uh  effect on the hypoxia again it's not very common   tachycardia because of that beta 1 stimulation  right tremors because of the again systemic   absorption and making people feel nervous. So  from a lab standpoint and monitoring we do need   to consider if we're using a lot of it right  more in the acute setting we do need to check   potassium okay um we do need to consider even AG  if someone's really out of control but that's not   really from the medicine but from a medicine's  perspective it's at potassium with the short   acting not with the long acting beta agonist the  short acting ones and then really we're monitoring   patients response their symptoms oxygenation  ventilation right that's where sometimes we   get an AG we're adding on drugs but they should  not be ever used all by themselves in asthma   patients with nothing else that's not appropriate  management of patients with airway disease even   even many respects COPD okay so short acting  beta agonist primarily albuterol we have lev   albuterol which is really just the active form of  albuterol we have racemic epinephrine terbutaline   okay these make up the short acting beta agonist  and bronchodilators predominantly used for acute   asthma symptoms bronco spasms even also including  in COPD yes we also use them for hyperkalemia   uh and nebulize form for to try to drive that  potassium in and again historically some people   would try to use it for tocolysis but it's really  not recommended binding those beta receptors   lowering the cytosolic calcium concentrations  lowering the interaction of actin and myosin   that causes that relaxation. Now, obviously, you  can absorb it systemically. You get tachycardia,   tremors, shakes. Again, you're driving the  potassium down. So, all of these things,   you know, are good and bad depending on what  we're using it for. Sometimes they're desired,   sometimes they're not. All right. So, I hope that  helped you to put the kind of the perspective   of short acting beta uh beta agonist and bronco  dilators in the context of long acting agents and   in the context of asthma versus COPD. Um, again,  some of these images and tables are available at   thisiswhy.health along with access to collections  playlist that we don't have in other places. Um,   there's also coupons there for um, board prep  material if you're in need of that. So, I'm   Dr. Busti. Thank you so much for joining. Again,  never stop learning that why behind the decisions   that you make and that we do every day and that we  see. It makes sense of why we do what we do. You   don't need to memorize things anymore. It sticks.  And then you actually end up managing patients   likely more effectively or at least that's my  experience. So we'll see you next time. Take care.