what is going on wonderful people it's meticosis Perfection Ellis where medicine makes perfect sense welcome back to my pharmacology playlist in the last video we talked about sympathomimetics or drugs that mimic the sympathetic nervous system they were adrenergic agonists as for today we'll talk about the exact opposites medications that antagonize the sympathetic they antagonize the adrenergic receptors what are the adrenergic receptors Alpha receptors and data receptors so today we'll talk about alpha blockers or Alpha antagonists as well as beta blockers or beta receptor antagonists so smash the like button click the Subscribe button and let's get started for more videos like this one please refer to my pharmacology playlist it has more than 200 videos this video was made possible thanks to the generous support of Maria so please people take a moment to say thank you to Maria in the comments in the last video I've told you about the story of the Two Worlds the insulin world and the glucagon World insulin alone is on one side every other hormone that you can imagine is anti-insulin and I mean glucagon epinephrine cortisol and thyroxine all of them hate insulin so it makes sense that epinephrine I.E the sympathetic nervous system try to decrease insulin release so what does the sympathetic nervous system want it wants to decrease insulin it wants to break down glycogen into glucose I.E sympathetic loves to stimulate glycogenolysis which is anti-insulin because insulin prefers the opposite insulin likes glycogen synthesis or glycogenesis what else does my sympathetic nervous system wants it wants to break down triglycerides into free fatty acids I.E lipolysis which is an anti-insulin action because insulin wants the opposite insulin wants me to build up free fatty acids into triglycerides the moral of the story is sympathetic hates insulin for the most part epinephrine inhibits insulin release from the pancreas now what if I'm taking a sympathetic antagonist what if I'm taking an alpha blocker a beta blocker a sympatholytic an adrenergic antagonist well well well then the inhibitory effect on the insulin will be prevented and Insulin will be secreted if this is my post-ganglionic sympathetic fiber it releases norepinephrine or nor adrenaline hence adrenergic fiber and when you secrete noradrenaline you can act on Alpha receptors or on beta receptors recall from the previous video that after norepinephrine is released from its adrenergic nerve Terminus it can act on Alpha receptor beta receptor or the presynaptic alpha-2 receptor and recall that Alpha 2 is n toy N2 sympathetic anti-sympathetic meaning if you stimulate Alpha 2 you will reduce the release of norepinephrine also in the previous video we have talked about the fact that Alpha One is GQ meaning calcium meaning increased contraction of smooth muscles Alpha 2 is GI I for inhibitory because when I stimulate Alpha 2 I inhibit norepinephrine release all the betas are GS coupled meaning they will increase cyclic amp which is very important if I stimulate GQ calcium increases if I stimulate GS I stimulate a delayed cyclase which converts ATP to cyclic amp so cyclic amp goes up but if I stimulate GI which stands for inhibitory rather than stimulatory then I get decreased cyclic amp in the last video we talked about the sympathetic agonists today we'll talk about those sympathetic antagonist I.E sympatholytics or adrenergic antagonists or adrenergic blockers we'll also talk about Alpha 2 agonists because Alpha two agonists are anti-sympathetic so let say that I have a patient with high blood pressure what is blood pressure well blood pressure equals cardiac output multiplied by the total peripheral resistance the cardiac output depends on what cardiac output equals heart rate times stroke volume and the total peripheral resistance depends on what it's the inverse of radius as radius goes up resistance goes down and vice versa so how about giving an alpha to Agonist to treat a patient with hypertension if you give Alpha to agonists what's going to happen you will reduce the release of norepinephrine and you will decrease the heart rate stroke volume which means you will decrease the cardiac output and you'll also decrease the total peripheral resistance when this goes down and this goes down blood pressure will decrease what else can I do you can give that patient Alpha One blocker if I give Alpha One blocker what's going to happen you will not constrict your vessels instead you will dilate them the radius goes up resist distance goes down when resistance goes down blood pressure goes down which means we can use Alpha One blockers to treat patients with hypertension what else how about beta blockers if I block the beta I will lower the heart rate and stroke volume and therefore lower the cardiac output and the blood pressure will decrease so the moral of this story is Alpha 2 agonists can treat hypertension Alpha One antagonists can also treat hypertension and don't forget beta antagonists can also treat hypertension please pause and review this beautiful chart that we talked about in the last video if I give you an alpha to Agonist you will reduce your norepinephrine release I can also block the alpha receptors with alpha blockers I can block the beta receptors with beta blockers I can prevent the entry of norepinephrine into the vesicle by giving reservine alpha-1 receptors are GQ coupled when you stimulate alpha-1 receptors you can strain affect your vessels and raise your blood pressure conversely beta 1 beta 2 and beta 3 are GS coupled they increase cyclic amp and when you do this you will relax your vessels decreasing the resistance and decreasing the pressure so when I stimulate alpha 1 I raise my blood pressure but when I stimulate beta 2 I lower my blood pressure vasoconstriction versus vasodilation so tell me about this adrenergic antagonists you can block the alphas such as blocking the alpha one with Perez Center as a syndaxa is a sin as glucent tamsulosin or you can block the alpha two receptors such as uhmbin and Mirtazapine how about the Alpha 2 agonists include clonidine Alpha methyl dopa and others then help me block the beta receptors we have many many beta blockers all of them and n o LOL what are the medications that can treat hypertension well well let's talk about the sympatholytics some of them are centrally acting which means they act on the presynaptic neuron and these include the Alpha 2 agonists clonidine Alpha methyl dopa and Dex medatomide and we cannot forget Reserve pain which inhibits vmet or the transporter of norepinephrine into the vesicle after the centrally acting what do we have we have peripherally acting on the post-synaptic membrane we have the alpha and beta receptors Alpha 1 beta 1 beta 2 Etc we can block the Alphas with alpha blockers praso Center resuscentox asosen tamsulosin we can block the beta receptors by any drug that ends in olol as in Propranolol metoprolol there are many other ways to manage hypertension today we're just focusing on the sympatholytics as well as quick review on the calcium channel blockers remember that calcium is the hero of contraction so when you block the calcium you block the contraction so you will relax and lower your blood pressure see medicine makes so much sense once you understand what the french toast you're talking about sympatholytics again we have centrally acting and peripherally acting centrally acting let's reserve the norepinephrine I mean restricted I mean prevent it from entering the vesicle by inhibiting the vmet transporter protein and this is the function of reservine or let's stimulate the Alpha 2 receptors to inhibit the release of norepinephrine so that I can lower my blood pressure clonidine methyl dopa dextmedatomide it's the infamous Triad of CMD clonidine methyl dopa dexmedatomide then the peripherally acting you can block the alpha or you can block the beta let's start by talking about the centrally acting sympatholytics what's going to happen well whether you inhibit norepinephrine from entering the vesicle or you inhibit norepinephrine from leaving the axon Terminus the end result is the same there is no norepinephrine available to function so what do I get without the stimulating effect of norepinephrine in my brain sedation drowsiness depression and low libido because everything is depressed this is the central effect the peripheral effect well there is no norepinephrine available to act on alpha-1 or beta1 no acting on Alpha 1 your blood pressure will drop every time your blood pressure drops you trigger a baroreceptor reflex to cause the reflex tachycardia which can also happen when I inhibit the alpha-1 receptor what's going to happen I inhibit vasoconstriction including Vino constriction when the veins cannot constrict they will be dilated like this lots of blood will pull into them and away from the right atrium decreasing the venous return and I can get postural hypotension every time I stand up blood pulls down not in the heart but in my ankles I get postural hypotension because I could not constrict the veins why do healthy adults not suffer from postural hypotension because they have robust sympathetic fibers constricting the veins in the lower extremities to push the blood upwards towards the heart but if I'm taking a centrally acting sympatholytic or if I'm taking an alpha blocker I can get postural hypotension moreover remember the urinary bladder yes I remember that it had a sphincter I remember that how can we constrict and contract that sphincter Alpha One stimulation so Alpha One can constrict the sphincter which prevents the retrograde movement of the semen or the sperms or seminal fluids back into the bladder okay so it's the constriction of the sphincter that prevents the retrograde ejaculation but what's going to happen when I inhibit the Alpha One or what's going to happen when I lack nor epinephrine stimulation to Alpha One I cannot do this I cannot constrict the sphincter so the semen will go back to the bladder and this is called the retrograde ejaculation one of the infamous side effects of alpha-1 blockers or centrally acting sympatholytics when you inhibit your sympathetic nervous system who is going to take over who's going to have the upper hand pair a sympathetic nervous system will be unopposed and unhinged it will do its parasympathetic stuff rest and digest secret to mortar all kinds of secretions and motility in my gut I get diarrhea I can get nausea vomiting of course I can get urinary incontinence and stool incontinence because my bladder is pushing too much and my colon is pushing too hard rest and digest also the parasympathetic is the hero of secretions including gastric acid secretions so I can worsen my previously existing peptic ulcer disease send to the acting sympatholic number one recipe and how do you work I work on your reserve I restrict the entry of norepinephrine into the vesicle by irreversibly inhibiting the mat vesicle monoamine transporter norepinephrine cannot exit the vesicle it will be unable to leave the vesicle later the end result is no norepinephrine in the synapse decreasing the stimulation of alpha-1 so I get decreased vascular tone I get hypotension decreasing the stimulation of beta 1 I get decreased heart rate or bradycardia so when should we use reservine in some cases of hypertension at least theoretically today almost no one uses reserving ever side effects well think about it nausea vomiting diarrhea there is no norepinephrine so I get depression drowsiness decrease libido no Alpha One stimulation I can get retrograde ejaculation in hours though static hypotension no beta 1 stimulation I can get ready cardi and heart block that's why almost no one uses this today next clonidino we're starting the Triad clonidine Alpha methodoba indexed medatomite how do they work they stimulate Alpha 2 receptors in the presynaptic neuron decreasing the release of norepinephrine same thing you get hypotension and bradycardia why hypotension because you're not stimulating Alpha One why bradycardia because you're not stimulating beta 1. when should we use it well think about it it lowers your blood pressure so I can use it if I have high blood pressure clonidine might alleviate the withdrawal symptoms of opiates think of opiates as depressants when I remove the depressants I get excited oh I'm so excited how can I inhibit this super excitation you can take an inhibitor such as clonazine to decrease norepinephrine see it makes sense what if I have too much excitation in the form of Tremors oh then you need to inhibit the CNS a little such as by taking clonidine side effects well too much inhibition of my CNS I get sedation drowsiness delusion it can also lead to dry mouth Vaso dilation and high potential because I'm not stimulating alpha 1 or beta 1. remember anytime a professor asks you about the side effects of a medication and you can remember absolutely nothing just say the following four nausea vomiting diarrhea zerostomia and that's how you game the system next methyl dopa very similar to clonidine okay when do we use the same thing hypertension such as hypertension in pregnancy whether it's gestational hypertension chronic hypertension or preeclampsia side effects toxic to the liver can lead to elevated liver enzymes such as ASD and ALT also known as increased liver trans aminases it can lead to warm autoimmune hemolytic anemia with positive direct Coombs test it's one of the medications that can give me drug-induced lupus with positive anti-histone antibodies some argue that it can lead to hyperpolact anemia which can lead to galactorrhea and amenorrhea in females impotence and gynecomastia in males how do I remember Alpha methyl dopa I remember two errors going up and two positive signs I am increasing your liver function test because I'm toxic to the liver I also cause hyperpolactonemia two positives you get positive Coombs test because of the hemolysis and you get positive antihistone antibodies from the drug-induced lupus what's the drug of choice for hypertension during pregnancy especially mild to moderate hypertension Alpha methyl dopamine what is the drug of choice to treat beta blocker toxicity don't forget the glucagon for reasons that we'll discuss shortly how do I manage hypertension during pregnancy just remember that hypertensive moms love nifedipine what's the H hydronozine what's the m alpha methyl dopa what's the L laboral and was the n in the Philippine it is in the Philippine this is a vasodilator this is an alpha to Agonist labetta LOL LOL is a beta blocker and Alpha blocker nephedepine is a dihydropyridine calcium channel blocker there are three medications contraindicated in pregnancy that you need to memorize ACE inhibitors and utensil receptor blockers and LS chirin these same three medications cause hyperkalemia as well how about the third one is in the Triad we talked about clonidine Alpha methyl dopa let's talk about dextmedatomide same exact thing I lower your blood pressure I lower your heart rate my Half-Life is about 2 hours when I decrease nor epinephrine I decrease the excitation of your brain that's why you are sedative and I have some analgesic effects side effects I can be toxic to the liver a large bolus of text meditumide can lead to paradoxical hypertension how do I remember dextmedatomite everything here is D it starts with a d it's Half-Life or elimination Half-Life is 2 hour or two it is a sedative and it can cause paradoxical hypertension we're done with the centrally acting sympatholytics now let's talk about the peripherally acting starting with alpha blockers Alpha receptor antagonists these are the doozies that we'll talk about some of them block both alpha 1 and Alpha 2. some of them block only the Alpha One others block the alpha 2. these two are non-selective because they block everybody these are selective Alpha One blockers and these two are selected Alpha two blockers Alpha receptor antagonists include fintolamine and phenoxybenzamine they block both Alpha 1 and Alpha 2 which means they are non-selective because they block everybody next press Center as a syntax Asus sen alphozen tamsulosan all of these are alpha 1 selective antagonists you him being selective on Alpha 2 Mirtazapine selective on Alpha 2. if I am blocking the alpha what's gonna happen well you can load lower my blood pressure If you block the alpha one yeah so we can use them to treat hypertension especially those who act in Alpha One how about those who act on Alpha 2 well remember that Alpha 2 is anti-sympathetic Alpha 2 decreases the release of norepinephrine so when I block the Alpha 2 I boost the release of norepinephrine I can raise my blood pressure so I can use this to treat hypotens when I raise nor epinephrine I can use this to excite my brain and treat depression but as for the Alpha One blockers they block the vasoconstriction so your vasodilate so my blood pressure drops amazing and the vessels in my fingertips dilate so that they are not ischemic anymore and they are not red white and blue so they can treat Raynaud's disease the difference between phentolamine and phenoxybenzamine is the fact that phentolamine is a reversible antagonist but phenoxybenzamine is an irreversible antagonist what do I need to know about phentolamine well it is reversible non-selective alpha 1 and Alpha 2 blocker when you block the Alpha One you will vasodilate when you vasodilate your blood pressure will drop which can trigger a reflex tachycardia and arrhythmia when you block your sympathetic like this who is going to predominate parasympathetic secret to motor baby increasing your GI motility diarrhea abdominal pain you name it for the phenoxive enzamin its non-selective Alpha and Alpha 2 antagonist irreversibly blocking them which means you cannot go back once you get phenoxybenzamine you cannot reverse it oh what should I do then you gotta wait until the patient metabolizes all of the phenoxybenzamine that's the only way to get rid of it so phenoxybenzamine can accumulate with repeated dosing so be very careful if I can lower your blood pressure what can I do you can cause orthostatic hypotension when you block the sympathetic who predominates the parasympathetic and I can get meiosis or constriction of the pupil of my eye when the parasympathetic predominates it is secretary to motor it can increase my nasal secretions and give me some nasal congestion and stuffiness phenoxybenzamine can be used to treat pheochromocytoma and the half-life is 24 hours how do I treat theochromocytome well the acromocytoma is a tumor in the adrenal middle secreting too much epinephrine norepinephrine and dopamine oh oh oh so how do I block the effect of epinephrine for example epinephrine acts on alpha-1 it also acts on beta 1. that's true so how do I block the Alpha One give me an alpha blocker how do I block the beta 1 give me a beta blocker and this is a freaking tumor in my Adrenal medulla what should I do surgical excision Alpha One Agonist preso-center rhizosindoxaso centamsulosin they block the alpha one that's why we can use them to treat benign prosthetic hyperplasia how come well here's the deal here's the urinary bladder urethra and then they are surrounded by the prostate gland in patients with with benign prosthetic hyperplasia or prostatic enlargement the prostate is going to press on my urethra making it harder to urinate oh so how can we treat this we'll try to prevent the constriction of the urethra oh one way to do it is to relax the sphincter how do I relax the sphincter since the sphincter responds to Alpha One stimulation you dilated or relax it by Alpha One blockers such as presenter as a syntaxis a centamsulosin but when the sphincter dilates too much what can happen is retrograde ejaculation is there any difference between Prezzo Center syndoxation and tamsulosin the answer is yes the first three can lower my blood pressure and that's why we use them to treat hypertension but tamsulosin usually keeps me normotensive without altering my blood pressure so if a patient comes in with benign prostatic enlargement and hypertension you give one of this today but if the patient comes in with benign prosthetic enlargement with normal blood pressure go with temp solos next beta blockers beta blockers block the beta receptor including beta 1 and or beta 2 receptors when I block beta 1 what's going to happen you will decrease your heart rate contractility and conductivity what's going to happen to cardiac output it decreases stroke volume it decreases blood pressure can decrease as well so when should I use beta blockers to treat hypertension because they do lower my blood pressure to treat tachy arrhythmias because they do lower my heart rate to treat chronic congestive heart failure because they decrease my blood pressure which means they decrease the afterload on the poor ventricle they decrease heart rate and blood pressure oh so we can benefit from this in a patient who has thyroid storm or thyrotoxicosis in a patient with theochromocytoma and they also block beta-2 receptors when they block related to I cannot relax my bronchi and I cannot relax my vessels if I cannot relax my vessels they will not dilate and cause headache in my brain so we can use them to prevent migraine headache but when you block the beta I'll be unable to dilate my bronchi oh so I worsen the asthma when you block the beta to unable to metabolize stuff metabolism is toast when I block beta 1 my heart rate can never go up which will mask the symptoms of hypoglycemia what does that mean think of my blood sugar dropping and suppose that I am a healthy person anytime my blood sugar drops the sympathetic nervous system gets activated this is a dangerous situation fight flight so what's gonna happen the sympathetic will raise heart rate stroke volume blood pressure Etc I'll start sweating etc etc and this will alert me hey doofus maybe your blood sugar is low you need to eat something oh so I go and eat something however if this happens to me and I blocked the beta 1 do you think tachycardia will happen no you will have hypoglycemia and you will not feel anything do you think increased stroke volume will happen no you'll feel no palpitations whatsoever so I'll have low blood sugar but my body cannot alert me because I block the betas and this is what we mean by masking the symptoms of hypoglycemia in patients with diabetes when you block the beta 2 you cannot relax your vessels so you are vulnerable to vasoconstriction and vasospasm vasospastic diseases such as friends metal angina Raynaud's phenomenon can get worse let's say that I have acute heart failure that is not caused by tachycardium it's caused by something else well acute heart failure means that my stroke volume is very poor oh why would you give me beta blockers to make my stroke volume Porter and my heart rate lower not a good idea so be very careful in some instances of acute heart failure not all of them next when I block the beta 2 I'll be unable to dilate my vessels oh so my vessels tend to constrict okay and what else makes my vessels constrict viachromocytoma cocaine overdose oh so now cocaine when the beta is blocked will act more on Alpha 1 receptors cause severe vasoconstriction which can kill me from the hypertension fear chromosytoma is the same thing if you give a patient with fake chromosytoma beta blockers without blocking the alpha receptor first all of that epinephrine or epinephrine will act on the alpha one causing severevasive constriction and severe increase in blood pressure so in which Trade Fair chromocytoma alpha blockers first then beta blockers then you go to Surge some effects of beta blockers when you block the beta 1 you decrease heart rate and stroke volume and you decrease the cardiac output so the blood will pile up and pull up behind the poor ventricle increasing the preload most students will get this wrong remember beta blockers increase preload because they slow down the heart when I block beta 1 there is no more renin when I block beta 1 I decrease aqueous humor secretion in my eyes that's why temolol one of the beta blockers can actually be used to treat glaucoma which has increased intraocular pressure beta blockers decrease myocardial oxygen demand which is awesome that's why we can use them in patients with myocardial infarction when I block beta 2 I cannot dilate my bronchi I get bronchospasm I cannot dilate my vessels I get vasospasm and I cannot metabolize anything say goodbye to glycogenolysis and gluconeogenesis so be very careful in patients with diabetes because they already have a metabolic dysfunction if I block beta 3 say goodbye to lipolysis so some lipids might accumulate in the blood because I could not break them down some beta blockers have have something called the intrinsic sympathomimetic activity they are beta blockers but they can boost the sympathetic to a certain extent they are partial agonists they will give you less bradycardia because they are more sympathomimetic they can give you some bronchodilation because they are sympathomimetic they cause minimal change in your blood lipids which is awesome clinical uses of beta blockers if I have angina or myocardial infarction give me beta blockers if I have tachyarhemias give me beta blockers beta blockers are anti-angina and anti-arrhythmic medications if I have glaucoma I can benefit from them if I have hypertension I can benefit from them if I have thyrotoxicosis or essential tremors or performance anxiety or migraine headache I can benefit from propranolol side effects of beta blockers are many they can cause nervousness they can lead to some Tremors they can cause palpitations they can worsen Reynolds phenomenon and Prince metal angina because of all of the evasive spasms they can increase triglycerides and lower HDL they can worsen asthma symptoms and peripheral vascular disease which is Reynolds they can mask the symptoms of hypoglycemia in patients with diabetes they can cause severe bradycardia and heart block they are anti-sympathetic so they cause CNS depression they can cause sedation and they can lead to erectile dysfunction giving beta blockers before giving alpha blockers can worsen the symptoms of a chromocytoma and cocaine overdose beta blockers clinical uses they are antihypertensives they are anti-hard failure they are anti-angina anti-arhemics they are anticodic remodeling in patients with CHF they decrease sympathetic flow from the brain they are anti-renin they lower cardiac output and they are anti-vasodilation you tend to constrict more when should we use them for glaucoma thyrotoxicosis migraine headaches essential tremors performance anxiety at cetera side effects are many I can get bronchospasm wheezing I can get erectile dysfunction and sedation my asthma or COPD can get worse if I'm taking a non-selective beta blocker that blocks the beta-2 receptor my peripheral vascular diseases can get worse such as renounce phenomena they mask the symptoms of hypoglycemia they can lead to heart block from the bradycardia they can lead to cardiogenic shock from the bradycardia and the decreased stroke volume and ejection fraction and they will worsen my renault's phenomenon and Prince metal angina I.E they worsen vasospastic diseases beta blockers is one of those medications that you should not stop suddenly because if you stop them suddenly you get the opposite of their desired effect you get sudden hypertension rebound hypertension you can get rebound arrhythmia and much more beta blockers end in a lot but if you have a medication that ends in alol such as sotalol then that's a potassium hand blocker with some data blocker activity chronic use of beta blockers well I have been blocking this receptor for years and years and years my body will make more that's a negative feedback it causes up regulation of the beta receptors and that's why you should not stop them suddenly sudden withdrawal of beta blockers can lead to rebound effects rebound hypertension rebound attacking arrhythmia Etc if you want to withdraw gradually taper the dose baby steps not suddenly beta blockers have additive bradycardic effects with Johnson adenosine or calcium channel blockers if I take beta blockers and calcium channel blockers together I am more likely to develop bradycardium if I have beta blocker toxicity what should I do I should take glucagon why is this because beta blockers block the beta I.E they lower the cyclic amp but the glucagon raises cyclic EMP oh so it's kind of an antidote beta blockers classification the non-selective beta blockers I.E the ones who block the beta 1 and the beta 2 they block everybody they do not care are drugs that start with n or start with any letter between n and z and end in olol such as natalol Propranolol timolol Etc as for sotelol it is a beta blocker and a potassium channel blocker be very careful with Propranolol because it's about 95 percent bound to plasma proteins which means it can interact with other medications that also love to bind plasma proteins we have selective beta1 blockers they block beta1 only and not beta 2 for the most part and these are the beta blockers that start with letter A all the way through M such as attendul betoxylol bisoprolol esmolol metoprolol then we have the beta partial agonists which are beta blockers plus some intrinsic sympathomimetic activities how do I remember the partial Agonist I think of an ace chord partial really coming in front of a pendulum acetylol and pendulum then I have beta blockers that block the beta and the Alpha One also known as third generation beta blockers labetalol and Carvedilol then beta blockers plus nitric oxide relators this is nebulolol nitric oxide with an N nebulol with an N can we use beta blockers for Angina yeah for every kind of engine I can imagine except Prince metal engineer because it has vasospasm try to avoid the use of the partial beta agonists in case of angina such as acipidalol and pendulum beta blockers improve longevity and reduce mortality post Mi beta blockers as anti-anginal avoid in transmetal angina avoid the partial agonists and avoid in acute heart failure not caused by tachycardium can we use beta blockers to treat arrhythmia yes beta blockers are Class 2 antiarhythmics they slow down your AV node and a node what are the beta blockers that can be used for arrhythmia especially s model metoprolol and Propranolol these beta blockers can be used post Mi as well as to treat supraventricular tachycardia but don't forget that they can slow down my heart leading to a heart block let's talk more about s model it is a selective beta1 antagonist it starts with a letter that's before the N from a to M it has a rapid onset short duration which means rapid onset rapid opposite Easy Come Easy Go it gets metabolized into methanol but that's not very significant to cause toxicity when should we use it we can use it to prevent arrhythmia or to treat arrhythmia sometimes arrhythmia happens when we're intubating the patient or with direct laryngoscopy so we can use S model to prevent the arrhythmia the half-life of asmolol is short it's about 9 Minutes easy come easy go when should we use it again thyrotoxicosis vicromocytoma gain induced toxicity of the heart only after you give an alpha blocker it can also treat the hyper cyanotic spells in tetralogy of Philo which we have talked about it before in my video on tetralgia follow you can find it in my Cardiology playlist next let's talk about labetalol it is non-selective beta as well as alpha-1 blocker so it blocks beta it blocks Alpha One when you block alpha 1 you cause vasodilation when should we use labetal law we can use it to treat congestive heart failure to treat hypertension to treat angina can I use this during pregnancy yeah remember that hypertensive mom's love nifedipine the L was the labetalol the half-life is about 6 hours and if I have liver disease be very careful because it will take me longer to metabolize it is it affected by kidney disease no it's not just deliver disease when you decrease my blood pressure I can get orthostasis especially since you block the Alpha One and when you block the beta 2 I can get bronchospasm and there you go everything about the toxicity of beta blockers in one slide how do I treat this toxicity remember it's emergency so your ABC is first the antidote is a glucagon beta blockers lower cyclic amp but can glucagon raises cyclic amp and that was the story of the beta blockers or beta receptor antagonists they are peripherally acting sympatholytics how do we treat hypertensive urgency or emergency let's say that my systolic blood pressure is 200 and my diastolic is 120. well we can give you a nicodipine clevideopin we can give liberal or esmelon we can give phenoldapam we can give hydralazine Etc so today you learn about a category of medications that inhibit postsynaptic receptors you learn about alpha blockers and beta blockers Quake review on calcium channel blockers remember that calcium is the hero of contraction contraction of cardiac muscles and contraction of smooth muscles in vessels but when I give you a calcium channel blockers your heart contractility will decrease and Your Vessel will not constrict instead Your Vessel will dilate your heart rate will decrease your stroke volume will decrease so if my heart rate will decrease if my stroke volume will decrease if my vessels will dilate can I use calcium channel blockers to treat hypertension yes there are two types of calcium channel blockers those who focus more on vessels I.E smooth muscles and those who focus more on the heart I.E cardiac muscles which ones focus more on vessels the dihydropyridine calcium channel blockers look at the name nifedipine rhymes with dihydropyridine pneumodipine nifedipine amlodipine and much more which ones focus more on the heart Verapamil is the most important followed by deltiazem calcium channel blockers can be used to treat hypertension they can also be used to treat arrhythmia because they slow down your SA node and AV node just like the beta blockers nifedipine acts more on vessels Verapamil acts more on the heart Delta azim is kind of in between more closer to the heart than two vessels the Philippine is gonna decrease my base a constriction which decreases my total peripheral resistance the rapid metal will decrease my heart rate it will decrease my stroke volume and the conduction in the SA node and AV node when I say calcium channel blockers which calcium channel am I referring to um I'm referring to the l-type calcium channel remember L is in the ventric L so calcium channel blockers block the l-type calcium channels they're also in the smooth muscles of Your Vessel how about the T-Type calcium channels no the T-Type calcium channel was involved in the thalamus and we talked about them in my video on the anti-seizure medications if I take in the Philippine what's going to happen to my blood vessel my blood vessel will not constrict it will dilate when I dilate the veins what's going to happen preload will drop when I dilate my arteries what's going to happen after load will decrease so this decreases the cardiac work and decreases the oxygen demand when I dilate my coronary I increase oxygen supply to the heart which is awesome how about they focus on the heart so they decrease heart rate they decrease contractility which decreases stroke volume this also decreases oxygen demand and that's why we can use these calcium channel blockers to manage hypertension and to manage hypertension with angina we can also use them as antiarrhythmics side effects of calcium channel blockers gingival hyperplasia when I decrease my blood pressure I get hypotension anytime I get hypotension I can develop reflex tachycardia how can I prevent The Reflex tachycardia block the beta-1 receptor on your heart what else can they do well well well if you slow down your heart a lot you can get heart failure if you slow down your heart a lot you can get AV nodal block from the severe bradycardia if you slow down your bowel you get constipation varam ml can also lead to hyperprolactinemia which causes amenorrhea and galacteria in females impotence and gynecomastia in males and there you have it today we'll learn about of the sympatholytics and we have learned about the calcium channel blockers please take a moment to pause and review we use spintolamine and phenoxybenzamine to treat hypertension and pheochromocytoma present to resistant oxycin treat hypertension and benign prosthetic hyperplasia terms of those and traits benign prostatic hyperplasia you him being might treat hypotension or postural hypotension Mirtazapine might be beneficial in depression the beta blockers are antihypertension anti-angina and Mi antiarrhythmics and anti-chf the calcium channel blockers are anti-chf antihypertensives and anti-arrhythmics if you want to learn more about autonomic pharmacology I have a complete course on this topic on my website meticosisperfectness.com it comes with videos cases and notes to learn more about the anti-arhythmics anti-anginal drugs anti-hyperlipidemics digoxin and the diuretics download myocardiac pharmacology there are more than 300 premium videos available on this channel when you click the join button and choose the highest tier Please Subscribe hit the Bell click the join button support my channel on patreon PayPal or venmo go to my website to download my courses notes and cases or if you would like me to personally tutor you be safe stay happy study hard this is medicosa's perfectionist where medicine makes perfect sense