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0:00
I envision airs in this video we're gonna talk about beta-blocker so let's just go and get started alright so before we start talking about beta blockers I really want us to understand just the basic autonomic nervous system physiology primarily focusing on the beta receptors beta 1 and beta 2 okay because a lot of the beta blockers that we're going to talk about some of them are very selective they only bind to beta one some are non selective so they can bind to beta 1 and beta 2 and
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there's one other group that we'll talk about a third generation consisting of labetalol car veda law that they can bind to alpha and beta receptors okay well we're primarily going to focus on the beta receptors in this point here so beta receptors they can be found on multiple different target organs the ones that we're gonna focus on are here and what I want you guys to remember is that we're gonna talk about how the sympathetic nervous system works on these target organs during a fight or
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flight situation so during a fight-or-flight mode what basic like gray matter structure inside of the central nervous system particularly within the diencephalon is simulated as the hypothalamus right when hypothalamus is stimulated it sends these descending action potentials down through the spinal cord through the brainstem through the spinal cord to these pre ganglionic motor neurons located within the thoracolumbar portion of the spinal cord particularly t1 to l2 it stimulates
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these pre ganglionic motor neurons in t1 to l2 and sends that out flow and if you guys really want to be particular here technically it goes out and synapses on a post ganglionic motor neuron right the cell bodies there and then those post ganglionic motor neurons will then go to the effector organs our target organs well let's think about some of the organs that are defects let's start with the top we look at the eyes what do we know that it does to the eyes if you
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guys remember it works particularly on the ciliary processes right and the ciliary body and the overall effect here is that it actually causes an increase in aqueous humor production which is that fluid that fills with in the anterior a segment of the eye right and the other thing that it can do is a connection caused pupillary dilation what is that called what's this special fancy word for that's called madhurai Isis so it can cause pupillary dilation and also if
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you guys really want to know it can make can control the effects of the ciliary muscles which can accommodate the lens in a specific way for distant or far vision now the next thing that we have to talk about is that this can act on beta receptors on the heart right particularly the ones that I want you to know are the beta 1 receptors and these are located on the conduction system as well as located on the contractile cells now when epinephrine and norepinephrine
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are released onto these beta 1 receptors here if it works on the conduction system like the SA node the AV node what's the overall effect it's going to increase the heart rate anything increase heart rate you technically increase cardiac output and therefore increase blood pressure if we affect the contractile myocardial cells we're gonna increase the calcium loading into those right we'll increase calcium loading into those contractile myocardial cells and increase the strength of the
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contraction through that sarcomere unit if we increase contractility what does that do so you increase contraction if you increase contraction you increase stroke volume if you increase stroke volume you increase blood pressure right if you increase heart rate you increase cardiac output and if you increase cardiac output you increase blood pressure and if we really want to be specific here technically an increase in stroke volume will actually increase cardiac output and then that will
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increase blood pressure right either way we're increasing blood pressure why are we increasing blood pressure because in a fighter flight situation we want good perfusion to those tissues like the muscles in the brain simple thought there right what else there's also beta 1 receptors that are present here in the JG cells of the kidney nor the juxtaglomerular cells they respond to epinephrine and norepinephrine and whenever they're released onto those beta 1 cells they release
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renin Renan if you guys remember eventually leads to converting angiotensinogen to angiotensin one and then angiotensin one is converted through a called ace angiotensin converting enzyme into angiotensin 2 and through multiple different mechanisms the overall goal here is that angiotensin 2 increases blood pressure through vasoconstriction through increasing the aldosterone production which causes more sodium and water retention increasing ADH production which increases water retention
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the overall goal though is increased BP okay so again that plays a role in perfusion let's go down to the next one the lungs these are actually beta 2 receptors and again I didn't put up here I should actually go back up here for a second technically if we look here on the eyeball the ciliary body is controlled by beta 2 receptors and the pupil is actually controlled by alpha 1 receptors if you guys really wanted to know that ok since we were mentioning the receptors here but again we're
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primarily going to focus on the beta ok so beta 2 primarily I want you to remember regulates accommodation of the pupil as well as also regulates the aqueous humor production if you really want to the alpha one does control pupillary dilation are we go back to the lungs there's beta 2 receptors on the lungs particularly in the bronchial smooth muscle whenever epinephrine and norepinephrine act on this what does it do it causes bronco dilation and if you cause bronchodilation what's the overall
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effect the overall effect is that you could potentially increase ventilation and if you increase the insulation what does that do that increases oxygen supply and if you increase oxygen supply you increase the oxygen delivery to the tissues and we need that oxygen because it helps to make ATP ATP is good for muscle contraction as well as important for action potentials within a central nervous system pretty simple stuff right let's go to the next thing not only do
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we need oxygen and good perfusion but we need energy we need glucose as well so there's also beta 2 receptors on the liver cells and beta 2 receptors on what's called the pancreatic alpha cells so I'm actually gonna put here alpha cells when epinephrine or epinephrine act on the liver beta tubers it increases glucose through two primary mechanisms I'm just gonna tell you that it's gluconeogenesis right gluconeogenesis is the formation of glucose molecules through non
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carbohydrate sources the second way is glycogenolysis which is the breakdown of glycogen into glucose either way we're gonna increase those blood glucose levels if it acts on the beta 2 receptors on the pancreatic alpha cells who does that stimulate that stimulates what's called glucagon and you guys know that glucagon works on the liver right and how does it work on the liver well it stimulates the liver to make more glucose how their gluconeogenesis and glycogenolysis pretty cool stuff right
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so that's one way we increase the glucose we increase that ability to perform anaerobic and aerobic respiration to make ATP pretty cool stuff what about on the particularly the blood vessels now remember we're talking primarily about beta receptors we're talking about beta there is beta-2 adrenergic receptors that are present on the vascular smooth muscle that's supplying the brain as well as the muscle so these two primarily well I'm gonna tell you one of
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the things about the adipose tissue in a second so if we act on the beta 2 receptors remember what do I want I want good perfusion as well as oxygen and nutrients to be delivered to the brain and the skeletal muscle so what I'm gonna do is is in order to increase blood flow to these two organs alright if I want to increase blood flow or perfusion what do I have to do to these vessels I got a vasodilator so the overall effect is vasodilation to increase perfusion or blood flow into
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the capillary structures that are supplying these two organs and therefore give them more blood more oxygen more nutrients and therefore the ability to perform better there's something else is really cool though in the capillary endothelium the beta adrenergic receptors can activate capillary endothelial cells to increase the expression of an enzyme called lipoprotein lipase let me write that down it's called lipo protein lipase what this enzyme does is is you have
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triglycerides flowing through the bloodstream right these triglycerides and the triglycerides can be found in what's called chylomicrons if you really want to be specific but just for the simplicity here triglycerides are broken down via lipoprotein lipase into what's called free fatty acids and if you really want to remember it's also glycerol now what happens is these free fatty acids are another nutrient source - what tissues these free fatty acids can actually be delivered to our
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skeletal muscle and cardiac muscle because now we're giving it more fuel to produce tons of ATP for energy as well as some of this also can lead to free fatty acids being taken up by the adipose cells as well okay alright so now we know that there's vasodilation to increase perfusion as well as activation of lipoprotein lipase enzymes to break down triglycerides unto free free fatty acids and glycerol to deliver more energy to the muscle tissue what about the GI tract
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there's beta 2 receptors that are found on the gastric smooth muscle not the sphincter is the gastric smooth muscle now if we talk about this sympathetic nervous system do you want to be digesting food expending energy for that kind of activity in a fight or flight situation No so let's decrease a lot of the energy going into contraction of smooth muscle and motility as well as secretions and by doing that we can divert a lot of that energy as well as blood flow to
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other more needed tissues like the brain and the muscles ok so let's go ahead and do that and by doing that we decrease GI motility and we decrease a lot of this accretions okay now before we move on to now talking about how beta blockers work in the next diagram I want us to have an idea of how these adrenergic system work on the beta 1 receptors that are present on the heart ok and the reason why we're primarily focusing on the beta 1 receptors on the heart cells is because
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a lot of beta blockers that we're prescribing are primarily used for cardiovascular diseases and we'll talk about those indications later but we're going to focus on two cells one is we're gonna talk about a pacemaker cell which is basically like your AV node your SA node your Purkinje system and then we're going to talk about the non pacemakers which are basically the contractile cells these are the ones that if we were to kind of draw it here they would have
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that sarcomere like structure right with all the myosin and actin filaments as well okay so these are ones that produce contraction these are the ones that generate action potentials do you guys remember super briefly whenever a pacemaker cell wants to generate an action potential on its own intrinsically what channels are literally open a little bit these are called funny sodium channels we'll put F here first the funny sodium channels these allow for a little bit of
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sodium to trickle in now normally resting membrane potential is pretty it's negative maybe negative 90 millivolts somewhere on there right as we bring in this sodium we bring positive ions into the cell what happens to that resting membrane potential it starts becoming less negative maybe let's just say we're making up numbers here but just for simplicity sake maybe goes up to negative 70 millivolts as it does that that potential is high enough to open up another voltage-gated channel
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and these voltage-gated channels are t-type calcium channels and they allow for calcium to also trickle in and as calcium trickles in we bring in more positive charge maybe we go up let's just say maybe we go up to negative 40 millivolts okay we're becoming more positive as we bring in more cations as that happens these more positive ions actually stimulate another voltage-gated calcium channel a really important one and this one is called the l-type calcium channels and they allow for
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calcium to flow in and to bring that actual membrane potential from negative 40 maybe bring it all the way up to like plus 10 or something so they really flipped that membrane potential this creates a depolarization of this cell and then when depolarize it helps to allow for some of those cations to flow from other pacemaker cells as well as to contractile cells through these specific structural units called gap junctions and technically there's gap junctions and little proteins that anchor the
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cells together called desmosomes which make up intercalated discs now once these cations start flowing in to this actual non pacemaker cell or contractile cell what happens it brings maybe resting membrane potential it's just used the same number negative millivolt 90 millivolts by having this it brings it up let's just say it brings it up to negative 70 millivolts that might be just enough to activate these voltage-gated sodium channels and allow for sodium to rush into the cell as
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sodium rushes into the cell through these fast sodium channels the inside of the cell starts to become extremely positive maybe it goes all the way to like plus 10 millivolts what happens then is once we have plus 10 millivolts this channel shuts down and potassium channels open and a lot for potassium to start leaking out now the cell membrane now if we're having positive ions leave the cell what's happening to the inside of the cell membrane now now the charge
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might becoming more negative maybe it drops to zero millivolts around anywhere between zero to positive 10 millivolts this calcium channel this l-type calcium channel is very sensitive to that voltage and it opens and when it opens it allows for calcium to flow into this actual muscle cell and stimulate this little endoplasmic reticulum structure which has specific types of Rea entity and receptors on it and that causes calcium to come exploding out of this sarcoplasmic reticulum into the
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sarcoplasm where is that calcium go to the actual sarcomere and induces muscle contraction so how does this adrenergic system work to affect this pacemaker cell remember I told you to increases heart rate right well what happens is through a long process right it basically helps to activate a g-protein which activates adenylate cyclase converts ATP to cyclic AMP II and activates what's called protein kinase a and that protein kinase a phosphorylates these proteins on these l-type calcium
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channels and opens up the channel now more calcium can flow in if more calcium can flow into this pacemaker cell it generates action potentials must much quicker and if the action potentials are occurring quickly and more at a faster rate what happens to the overall rate of that conduction and increases therefore if increased conduction rate there's an increase in heart rate same way epinephrine norepinephrine bind onto the beta-1 adrenergic receptors on the contractile
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cells are the non pacemaker cells what do they do it activates again G stimulatory protein converts the ATP and activates G stimulatory which activates adenylate cyclase which converts ATP to cyclic GMP cyclic AMP II eventually used two protein kinase a when an activated protein kinase a guess what this guy does phosphorylates these l-type calcium channels if i load this myocardial cell with more calcium it's gonna stimulate the sarcoplasmic reticulum to release more calcium more calcium in the
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sarcoplasm means more contraction more contraction you increase the intensity of the contraction and therefore there's an increase in contractility simple concept right so now that we've talked about this we can now understand exactly how these beta blockers work alright so now that we've pretty much laid the groundwork for how the beta receptors play a role in all these different target organs all we got to do is just pluck every effect so remember what it did on the beta 2 receptors remember
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primarily beta 2 I know we did say that there was alpha 1 on that basically the iris muscle but I want us to focus on beta 2 remember that it caused madrassas right which is what threw the alpha 1 but for the beta 2 and the ciliary processes it increased equation reproduction if we block that we're going to decrease aqueous humor if you decrease aqueous humor what does that do to the intraocular pressure it decreases intraocular pressure you'll see that there are certain drugs that actually
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can do that beta blockers like timolol that we use for people who have high interact of the pressure and what kind of conditions glaucoma I'll talk about that alright it acts on the beta 1 receptors that are on the conduction system and the beta 1 receptors that are present on the ventricular myocardium if we block what this these receptors remember used increase heart rate increase contractility well if we block it we're gonna decrease heart rate and we're gonna decrease contractility and that
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has multiple effects one of the big effects that I want you to remember out of this is that if you decrease heart rate and contractility are you using as much oxygen to supply that myocardium now no so it's not having to work so hard all about downtime so if you're not having it work so hard all the time it's oxygen demand starts to decrease and that's important and also if we decrease oxygen demand that's important in conditions like heart failure that's important conditions to where people
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have myocardial infarctions after that effect or if they just have coronary artery disease angina pectoris and here's another thing if we drop high heart rate and contractility we drop blood pressure so this is also good in patients who have hypertension and if you decrease heart rate by blocking that AV node guess what else you can do you can decrease the actual conduction effects and patients who have what's called arrhythmias we'll talk about that next thing if you inhibit the JG cells
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the beta 1 receptors on the JG cells you decrease renin production if you decrease random production you decrease angiotensin 1 production and decrease angiotensin 2 production what does that do that decreases blood pressure through what way inhibiting the vasoconstrictive mechanisms inhibiting aldosterone and ADH production if you inhibit aldosterone and ADH production you don't reabsorb a lot of sodium and water you instead excrete that out of the body a
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second thing is you're not causing basal constriction so the pressure is going to start dropping because there's not as much resistance of the vessels pretty cool all right what about in the lungs well remember it caused bronchodilation if we block that on the beta 2 receptors especially if we use non-selective beta blockers they can bind onto these beta 2 receptors and if what does it normally cost bronchodilation what's the opposite of that bronchospasm so it can lead to
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Bronco constriction and that bronchoconstriction could lead to a potential spasm of the bronchi which is not good if somebody has an underlying COPD or asthma okay now let's block the beta 2 receptors that are present on deliver cells as well as the beta 2 receptors present on the pancreatic alpha cells remember what this eventually did it caused glucose production right there gluconeogenesis this led to glucagon production from the pancreatic alpha cells which stimulated glucose
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production right there gluconeogenesis and glycogenolysis if we inhibit glucagon production we inhibit glucose production through gluconeogenesis and glycogenolysis and if we inhibit the liver cells we decrease glucose production this is important especially if someone has what's called diabetes we'll talk about it's called hypoglycemia unawareness next thing what about the beta 2 receptors that are present on the vascular smooth muscle supplying the brain and these skeletal
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muscles as well cardiac muscle primarily skeletal though if you block this it caused vasodilation what's the opposite of a so dilation vasoconstriction but here's the key thing I want you to remember it's mild vaso constriction it's not that severe where it's going to significantly alter the pressure going to these tissues there's a mild vayzosa so because of that there's a minor drop or bump in the blood flow to these tissues okay as well as if you block the capillary
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endothelium from expressing the production of what's called lipoprotein decreasing the expression of lipoprotein lipase what does that mean remember triglycerides that were found within the chylomicrons or vldls that's going to have less conversion into what's called free fatty acids so if you inhibit this process you can't break down the triglycerides so what happens to the triglyceride content it goes up it makes sense right all right what about the beta 2 receptors that are
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present on the fat on the actual gastric smooth muscle the one that plays a role in peristalsis and segmentation and things like that well if you inhibit this you're actually going to have the opposite effect it usually decreases GI Mattila t so what's the opposite of that increase in geometry so there's a moderate bump in GI motility that may be responsible for a little bit of diarrhea maybe a little bit of increase in secretions as well okay now that we've
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understand all of that let's look at how these beta blockers affect the inside of the cell common questions that come up on like board exams is how they affect particular phases so if you guys just a basic diagram here let's say here on the y-axis you have millivolts here on the x-axis is milliseconds you guys might remember this kind of graph here might look familiar right this is basically the conduction potential through the pacemaker cells and if you remember there was different
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phases to this right so you have phase four phase zero you have Phase three okay now phase four is basically where these funny channels are open and it's also where those t-type calcium channels are open and just a little bit towards the end as you approach this what's called threshold potential as you approach that these l-type calcium channels start slowly opening and allowing calcium ions to leak in just a little bit remember what I told you with basically how epinephrine and
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norepinephrine act on these beta 1 receptors remember what they did eventually they increased protein kinase a production which was designed to stimulate those l-type calcium channels and increased calcium influx what if we inhibit this if we inhibit it by giving a beta blocker we block the effect of it on this beta 1 receptor we effectively do what to the protein kinase a production we decrease it if we decrease that we decrease the stimulation of the l-type calcium channels if you decrease
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calcium loading into the cell that's going to decrease the conduction potential and if you decrease that conduction potential it's gonna slow down that heart rate we already talked about that right but in what phases a primarily effect you're gonna notice that it actually slows phase four and phase zero because zero is also where this l-type calcium is flowing in very powerfully so it slows phase four and phase zero it's a common question on your boards the other thing
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is again remember here and the non pacemaker cells here's millivolts on the y-axis milliseconds on the x axis here we have resting membrane potential here's threshold potential let's say here's your peak potential remember it starts off kind of flat then it starts to rise up drops down plateaus and then drops down again here if we look at this one you have a bunch of different phases here right there's phase four there's phase zero there's phase one and phase two and phase three here right now
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phase four is basically where the cell is repolarizing okay potassium is leaking out of the cell but then phase zero is when these sodium channels are open and they blast in and increase the action potentials on the sarcolemma that leads to the activation of these calcium channels eventually right the l-type calcium channels remember what happened before as sodium influx in we went up to peak potential maybe positive ten millivolts remember that channel that opened up on
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the cell membrane around positive ten millivolts it was the potassium channels and when potassium leaked out what happened to that membrane potential remember we said we made up a number went from plus zero to about plus ten to zero millivolts then what happened is you drop down it stimulated the calcium channels and the calcium flew in stimulated the ryanodine receptors which were on the sarcoplasmic reticulum that led to calcium release which led to contraction right well
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phase two is when the calcium is rushing in and where potassium is exiting guess where the beta blockers primarily work remember they decrease protein kinase a because they block the effect on that receptor if you decrease protein kinase a you inhibit the activity of the l-type calcium channels where did the l-type calcium channels primarily occur in Phase two because remember phase one is when the potassium is leaving four - is when calcium is coming in and potassium is going out if we inhibit
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this there's less calcium coming into the cell less stimulation of the ryanodine receptors less calcium release and less contractility right so what phases are primarily effect it slows phase - and again this is in the non pacemaker cells and then slows phase four and phase zero and the pacemaker cells alright so now we've talked about the physiology of the actual beta receptors we talked about how beta blockers work mechanistically at the overall organ and a cellular level right
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now what I want to do is I want to mention the different types of beta blockers but we have to be specific on the category that they belong to so three main ones first generation second generation third generation why are they different okay first generation what I want you to remember is that these are nonspecific okay so these are non-selective beta blockers so what does that mean that means that these beta blockers that we're going to mention here combine on to beta one or it could
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bind on to beta two okay so it can bind on to both of them alright what are some of these first generation beta blockers some of these are going to be things like timolol and interestingly or not this one is actually used to treat glaucoma you can put that on topically or opthalmic wise another one it's called propanolol also brand-name inderal and another one is going to be called sotalol so again these kinds of beta blockers you can give for multiple different reasons and
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we'll talk about the reasons for beta blockers in general and then we'll mention a couple that are a little bit more specific to certain kinds of conditions but again if you give these the overall thing that you have to remember is that they can bind to beta 1 and they combine to beta 2 so because of that they might have some of the side effects because of the beta 2 effect like what bronchospasm okay they might also drop your glucose which can lead to hypoglycemia unawareness and
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we'll talk about some of the other side effects the second generation blockers the ones are selective okay these are selective what does that mean they only particularly bind to beta one but I need to make sure that we make a little disclaimer here these yes these second generations primarily are a beta one but there is notices on these drugs that say at higher concentrations they do have the capability to bind on to beta 2 receptors so yes they are primarily beta
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1 but at higher concentrations of the drug they do have the potential to bind on to beta 2 receptors what are some of these drugs well atenolol is one ace butyl law is another this sopra law asthma law and a very common one metoprolol these are a lot of your second-generation beta blockers and again these are gonna be more for beta 1 which means where they going to primarily act heart and kidneys so what are the primary functions we're gonna see here a little bit that they're
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primarily going to be helping with hypertension super ventricular tachycardias may be heart failure after someone's had an mi things like that okay the last one that I want to mention here is your third generation beta blockers what is the difference with these these are also non selective but we have to be a little bit more specific because the first generation was also non selective these combine on to beta 1 they combine on to beta 2 and they can also bind on to alpha 1 receptors
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remember what alpha 1 receptors do with the vascular smooth muscle they cause vasoconstriction right whenever they're stimulated by epinephrine norepinephrine if you give these kinds of beta blockers like carve a DeLong labetalol they block the alpha 1 receptor so basically what normally is basal constriction if you block that will lead to phaser dilation once the others are overall effective dropping on vasodilation it drops the resistance and therefore drops the
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pressure and decreases after load on the heart as well right so what are these kinds of drugs these are things like labetalol as well as carve ADA law another an actual nice thing to know about these especially labetalol labetalol is commonly given during hypertensive emergencies so whenever somebody has blood pressure that is according to the age a greater than 180 systolic over 120 diastolic with and organ damage we calmly give labetalol like a drip carve a toll oo carve a doe
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law is actually going to be a little bit specific in the sense that you can give this especially in patients who have heart failure or hypertension because it actually has antioxidant properties so what it can do is it can actually decrease reactive oxygen species and by doing that remember reactive oxygen species play a role within the oxidation of the LDL particles and that plays roles in atherosclerosis technically you can decrease a thorough sclerosis with
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this and therefore help with patients who have heart failure or hypertension that's a pretty cool thing another thing I want to make sure for labetalol not just for the hypertensive emergencies but it's also safe in pregnancy okay so it's not teratogenic which is nice alright so again these are things I want you guys to remember first generation second generation third generation big overarching view first generation is non selective for beta-1 beta-2 second generation selective for
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beta one but at high concentrations it can't act on beta two and lastly third generation is non selective for beta 1 beta 2 but also has alpha 1 antagonistic activity as well okay now let's move on to the indications alright so the next thing we got to talk about is the indications of these beta blockers we've kind of already done that a little bit right remember what it did to the heart it decreased oxygen demand within tissues because it's dropping the heart rate and contractility so it's not
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consuming as much oxygen what would that be good for what kind of conditions where you basically need a lot of oxygen to be delivered to the tissues and you dropping the demands a little bit helps with that kind of situation what if there's ischemia to the heart what if somebody has an underlying coronary artery disease that could be a reason so if someone has CA D whether that CA D be due to having myocardial infarction previously or whether it be due to angina pectoris
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right chest pain what else would it be good for well another thing that you have to think about is that not only are you decreasing oxygen demands and therefore decreasing the ischemic pains as from coronary artery disease but also remember it slows down the heart rate and if we slow down that heart rate by either decreasing the SA node action potentials or blocking conduction at the AV node we can potentially decrease a lot of those arrhythmias that are originating in the atria like a fib and
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a flutter so we can also treat tachycardias particularly atrial fibrillation and atrial flutter right and again that's because we're decreasing the heart rate blocking the AV node or decreasing conduction conduction potentials right the next thing also if you're also inhibiting the inotropic action right decreasing contractility of the heart that technically can help in particularly situations where the blood pressure is really high because technically if you
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decrease heart rate and you decrease the contractility the overall effect is a drop in blood pressure so this could be good in patients with underlying hypertension the other thing which is also really helpful for and again there is some controversy on this but it can be helpful by decreasing the oxygen demand right and also by helping to decrease a lot of the preload on the heart particularly beta blockers can help in conditions like heart failure as long as they are not decompensated so
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these are also good for heart failure but just make sure that you remember there is controversial evidence saying that not in decompensated heart failure okay the next thing that we also have to talk about here is it can also be used in situations like protecting the heart whenever there is may be an aortic dissection so if patients have what's called an aortic dissection it's also a port important for that because if you decrease the blood pressure right you're technically
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going to be decreasing the action decreasing a lot of that tearing forces through the actual tunica media right so it's going to decrease the risk of actually having that any order dissection getting worse so it's good for treating aortic dissections that haven't don't need to be treated surgically at this point time and we can try to manage medically same thing with someone who has a aortic aneurysm if someone has any or two aneurysm obviously if we continue to allow for
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that pressure to be high it's gonna continue to keep exerting excessive forces on that blood vessel wall which can potentially produce a rupturing of that aortic aneurysm which can lead to exsanguination and therefore hypovolemic shock and death so we can also try to control a or t'k aneurysms as well the other thing that's also important for is that we can also use this in situations where someone has an arrhythmia like atrial fibrillation atrial flutter we can use
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it to rate control them at that point time or we can use it for prophylaxis for SVT so it can also be used for SVT prophylaxis so basically if someone has an afib atrial flutter exacerbation we can rate control them at this point in time if they come into the ER we can rate control them with a beta blocker but then long term we can put them on a beta blocker to prevent them from developing another atrial fibrillation or atrial flutter exacerbation okay next
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thing we have to talk about besides the heart is its effect on the vascular system remember we talked about two particular drugs to particular drugs that are going to be important here right one of the big ones here is labetalol right so we know labetalol is going to be acting here at the actual vascular smooth muscle cuz remember it can act at the beta receptors as well as the alpha one receptors here on the vascular smooth muscle Dupree capillaries fingers if it works here
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what's the overall effect if you basically inhibit vasoconstriction what does that allow for that allows for vasodilation and increased blood flow but also if you decrease the vasoconstriction mechanisms it'll decrease the total peripheral resistance proximal to this which will help to decrease a float on the heart so labetalol is really good for helping with these kinds of situations when people have high blood pressure by reducing the total peripheral resistance
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that one as well as carve a Dalal okay so that is important so I want you guys to remember it can help labayda long carve a Dalal can help with particularly systolic hypertension that is caused by increased resistance right from the adrenergic system if we block those alpha one receptors then we can allow for that decrease in total peripheral resistance decreasing the blood pressure and afterload here's the thing that you got to remember these kinds of drugs except for maybe
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labetalol car beta law regardless though you shouldn't really do this if you're giving a drug like a beta blocker a primary beta blocker that doesn't have an alpha blocker activity if someone comes in and they have what's called a they're you they're using cocaine or they have what's called a pheochromocytoma which is where they produce a lot of epinephrine or epinephrine it is a contraindication to give beta blockers why let's make sense of this you have an alpha 1 receptor here but
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guess what else sometimes you'll have what's called beta receptors right so you can have beta receptors over here if you're using beta blockers what are they doing they're blocking the beta receptors right so if I give a beta blocker it's blocking the beta receptor so that means that epinephrine and norepinephrine can't bind to that beta receptor where can they now bind then they can come over here and bind onto the alpha 1 receptor because they don't have to buy onto the beta receptor they
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can't now a lot of their concentration is being drawn towards that alpha 1 receptor if it binds to that alpha 1 receptor what happens to that now it increases it causes vasoconstriction which increases the total peripheral resistance and increases the blood pressure even more leading to worse situations so the basic idea is you never give beta blockers do not no beta blockers for these patients with cocaine use or pheochromocytoma because there's what's called unopposed
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alpha-1 agonism okay and so because of that you can't actually block that alpha 1 receptor because you're actually having so much beta blockade that the epinephrine norepinephrine are finding another receptor site at the alpha 1 receptor causing the increased phaser constriction increased total peripheral resistance increasing the blood pressure which might even lead to an aortic dissection because now the blood pressure is out of control so you see what's a contraindication other things
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that these beta blockers can be used for especially propanolol is it can be used for anxiety you guys know basically that whenever the sympathetic nervous system is activated a lot of some of the symptoms that the patient can develop is physical symptoms of anxiety palpitation chest tightness shortness of breath diaphoresis things like that right so if we can give specific drugs we can inhibit the sympathetic nervous system to decrease a lot of those physical
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symptoms a common one that's given for this is per panel okay so we can also use the frame of the treatment of anxiety particularly like panic attacks another one is you can use it for migraine prophylaxis I believe it does this by regulating the blood flow through the central nervous system right because if you give a beta blocker that technically can cause a little bit of vasoconstriction of the blood flow going to the brain and that can help with basically that the migraines that people
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can get related to that blood flow and again this would be purple law they also see that that ones are helpful another thing is that you guys know there's beta 2 receptors almost called the muscle spindles right and whenever epinephrine and norepinephrine bind onto these muscle spindles they increase the contraction on the muscle spindles which increases the action potentials right through these sensory receptors and therefore increases the efferent potential through
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the motor fibers and what happens as a result of this is that you can get tremors so whenever there's the sympathetic nervous system activity it can increase muscle spindle activity that can lead to tremors if we give a beta blocker we block the effect of epi and neuropathy on these beta 2 receptors therefore blocking tremors who is that important in people who have essential tremors so we can also use some of these beta blockers against what's called a central tremors
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and again this would be something like propanolol the other thing you guys remember that there was these beta 2 receptors on the ciliary body and ciliary processes remember they helped to play a role with aqueous humor production well if I have someone who has a lot of aqueous humor which is leading to high intraocular pressure because so much of that fluid is building up within the anterior segment or particularly anterior chamber the anterior segment that can cause a lot of
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pain right that's called glaucoma so if we give someone a drug like timolol that's going to inhibit that beta 2 receptor that will decrease decrease aqueous humor production and decrease intraocular pressure so this is also a drug that can be used in glaucoma okay so again remember timolol particularly for glaucoma so the last condition I want you guys to remember thyrotoxicosis okay which is called thyroid storm right and so basically with this condition there's an increase in thyroid hormone
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and if you guys remember if there's an increase in thyroid hormone it increases the receptor sensitivity of the sympathetic nervous system right so it increases the activity on beta 1 receptors and on alpha 1 receptors so if we give a drug that can block the activity of that increased sympathetic nervous system activity on beta 1 and adrenergic receptors we're gonna help with in situations where someone s thyrotoxicosis obviously if they have thyrotoxicosis you have to treat other
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underlying symptoms drop their fever give them fluids and again you might have to give them something like per panel law or another type of beta blocker to try to drop that pressure drop the heart rate and also basically just control a lot of their other symptoms as well okay so again that's the indications of beta blockers alright so side-effects pretty simple we've already gone over a lot of this stuff it should make true sense again you give a beta blocker right they're gonna block the
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AV conduction potentially if you give too much of a beta-blocker what could that do it could block the AV node enough that it leads to potentially a heart block so there is the potential of leading to a heart block maybe prolonging a PR interval maybe potentially leading to a second-degree heart block we don't know it depends upon how much that beta blocker you give as well as another drug interaction never give a beta blocker over the calcium channel blocker
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why because you double blockade that AV node and if you double blockade that you're gonna lead to a severe heart block the patient become pretty syncable or syncopal and that's not something we want obviously with any antihypertensive drug if you're using too much of it there is the potential of hypotension so that's another side effect that you also have to watch out for another thing to watch out for especially with labetalol or car beta law because they act on
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those alpha one receptors and they block it they could potentially lead to ortho stasis so I'm just gonna write a little note in here ortho stasis for third gen okay beta blockers so don't forget that last thing here on the lungs here right it also acts on those beta 2 receptors the non selective type but even the selective at higher concentrations if it acts on those beta 2 receptors and blocks it which normally causes bronchodilation you can get bronchoconstriction that bronchospasm is
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not good whenever someone has an underlying disease it can even be potentially contraindicated in patients with asthma or COPD because it could exacerbate it even more and it could make it worse so we don't want to give patients beta blockers who have severe asthma or COPD all right what about activity on the GI tract remember what the sympathetic nervous system does it decreases much GI Mattila T if we block that we're talking on an alien to an increase in geometry and an increase in
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geometry could potentially produce diarrhea okay also we block that lipoprotein lipase enzyme we decreases expression if you decrease that you decrease triglyceride into free fatty acid conversion so if you decrease free fatty acids and increase triglyceride what will happen you need to a lipid panel they're gonna be like me and they're gonna have my glycerides okay the other thing if you give a beta-blocker remember the act on those beta 2 receptors that supply
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blood to the muscle tissue and to the brain tissue if you block that beta 2 receptor which causes vasodilation you're gonna get vasoconstriction and therefore there'll be a slight drop in blood flow to that muscle what can happen with that it can lead to fatigue because you're not getting enough energy to the muscles so there's a potential of fatigue another thing you have to be aware of is that it acts in the central nervous system right there sympathetic activity in the central nervous system
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okay usually it's a part of your fight or flight system if you blunt that sometimes it can lead to potentially nightmares and also maybe even insomnia they've even shown it in certain situations where can even maybe be a cause of sexual dysfunction or Edie last thing big big big one it can lead to what's called hypoglycemia unawareness simple concept here right when someone's diabetic whether they have a decrease in insulin or they have insulin resistance right one of the other what's the
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overall effect that they can have what increased blood glucose levels right because they're not able to take that glucose into the cells over time as a result that high glucose levels lead to polyuria and lead to excessive amounts of urine which is high in glucose and high in water eventually that will lead to hypoglycemia okay if someone develops hypoglycemia how does the body react whenever there's hypoglycemia it's supposed to stimulate the sympathetic nervous system the sympathetic nervous
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system is supposed to cause particular symptoms that make the patient aware that they're low in their blood sugar like what maybe they start having tremors maybe they start having palpitations maybe they start sweating because the sympathetic nervous system does that maybe they start getting a little bit anxious maybe they actually start adding a little bit of confusion right so those are some of the sympathetic nervous system signs but if we give a beta-blocker which blocks that activity
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are they going to be aware of those symptoms like increasing heart rate palpitations diaphoresis tremors no and so because of that they can be unaware that their glucose levels are actually low and they could go into a potential coma so that's something that we don't want and that's something we got to be careful of when we give beta blockers in patients with diabetes last but not least if you give someone too much of a beta blocker and they start exhibiting symptoms on any of these things heart
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block side hypoglycemia unawareness what can we do well first thing is given tons of fluids so start off by giving lots of fluids and you can do two drugs atropine why because atropine is a acetylcholine receptor antagonist so it's basically going to block the acetylcholine effect at the receptor site which at the heart it's going to actually oppose the Seigle choline which tries to drop that heart rate and blood pressure so therefore if we block the acetylcholine effect we technically even
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lead to an increase in heart rate increase in blood pressure so we're trying to oppose all the effects of that beta blockade so we can get atropine the other one is glucagon okay because glucagon it also helps to be able to override the effects of this beta blocker block beta blockade alright so again answer do't in situations where there's high beta blocker fluid atropine and glucagon okay inez year so in this video we talked about beta blockers I hope this video
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made sense I hope you guys really did enjoy it if you guys did stick out there at the entire time of this video we can't thank you guys enough you guys are awesome greatest fans in the world also if you guys get a chance down in the description box we have links to our Facebook Instagram patreon account go check those out make sure you hit that like button comment down the comments section and please subscribe re-engineers as always until next time [Music]
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