Full disclosure: this is a brutal topic to learn. I did my best to simplify it. Remember to pay special attention to: 1. Cardiac action potential changes 2. Main adverse drug reaction (ADR) 3. Classification (Class 1A, 1B, 1C, II, III, and IV)
I'm just riding your top comment, but I also wanted to add that we need to know refractory recovery/AP changes with class I. I just had a question about it. If you keep them in CAB order, you can say "No long shorts" imagining some weird club where they don't want to see long shorts anywhere: C - NO change A - LONGer B - SHORTer I know he was just trying to keep it simple, but as he just drew them in based on phase 0 slope change, the diagrams are sort of wrong in terms of AP length. Also, I feel like it's pretty easy to just pop in your memory, but it's interstitial lung disease in particular for which amioderone can show up in test questions.
My mnemonic for class IA :queen(quinidine) die(disopyramide) fast after doing cocaine(procainamide) Class III : LOL(sotalol) till I die(ibu-til-ide, dofe-til-ide) Amigo (amiodarone) Both class mnemonic has dying part :D so they can cause torsades de points by increasing the effective refractory period (ERP) -->> QT prolongation (Action potential prolongation) For class IC: proper(propa-fenone) cane(fle-cain-ide) slaps the sodium channel the hardest but stabilizes ERP.
Calcium channel blockers and beta-blockers work on the nodal action potential, so the shape of the original AP curves should be different. Thank you for another great video!
I was looking for this comment... you don't need to memorize 0,3,4 for class 4 because you already know there are no phases 1 and 2 in nodal action potential .. I guess he's just trying to simplify and avoid the physiology 🤷♀️
Additional UWorld facts: 1) Amiodaron has partial Class 1,2 and 4 effects too. It also has an homogenous effect on K channel hence lowest risk of TdP among Class 3 agents. 2) Sotalol has partial B-cloker effect 3) B-Blockers reduce PR interval (obviously) 4) Adenosine acts on A1 receptors---->Potassium outflow--->Nodal conduction delay
My med school professors are terrible and it's exhausting as a learner. I binge-watch Dirty Medicine after every topic we cover to actually understand the material. Thank you for helping my mental health stay afloat.
I've realized that it's not our faculty's job to keep us happy. They just have to have presented the info at least once, so that when they test you on it you can't say you didn't "learn" it in class; how that info manages to stick in your brain is all on you.
Did that help? YES! That was beautiful. You are a gem, seriously. I learn way more from you than I did in my two years of med school. Any chance you could do some more drugs with us? I'd love any obgyn/repro stuff you feel like doing too. Thanks!
The reason you give glucagon in a beta blocker overdose is not because of the hypoglycemic masking. Glucagon stimulates cardiac ionotropy via a separate mechanism than beta blockers.
These pneumonics also help solidify the info: For the K-Channel (Class III) he mentioned the AIDS pneumonic "Kant Kure AIDS with Potassium" Also class II - Bets Blockers Two B's / double B's = class two Calcium channel blockers Verapamil and diltiazem are the only Non-dihydropyridines in the CCB class They are "Very Different" (since they are the only two that have a significant impact on cardiac conduction / heart rate)
Thank you so much for taking your precious time to simplify stuff for us Dr. DirtyUSMLE. Can you make a video on how best to recall all these fun facts from all your videos. I don't mean to sound ungrateful for everything you're doing for us🤭 Oh, I'm quadrupling the amount I'd pledged on your patreon. What I'd have paid a tutor is what I'll donate I hope others can do the same, to show appreciation for your hard work you put in to making it easy for us. Thank you Dr. DirtyUSMLE sir.
Not sure if this helps anyone, but a way to remember what blocker goes with what class is that for the chemicals it goes in the order on the periodic table and for beta blocker, beta = 2nd = II. Just my II cents.
@11:10, I would suggest the fact that they're class II can be related to the rule of 4s in that 2squared is 4; class II, 2squared adds to the rule of 4s ;)
Class 1a and class 3 has increase Tdp so they prolong Qtc so they are high yield Class 1c is like c for chooter (shooter)so like in video games First Person shooter(Flecainamide, and P) Procainamide has more A then propafenone So more A goes higher so A grade So class 1A and later is class 1C
🤣 WoW 😂 Great job man Another way to remember the names. If youve heard heard the song "Hotel California" in that main chorus rhythm sing the following Smoke (Sodium) Better. (Beta) Pot. (Potassium) (In) California. (Calcium) Adenosine Mg Hope this helps
If you had a vid to help keep a1, a2, B1, B2, mAChR stuff straight, that would be bae. FA has it diagrammed out, but it's not as sexy. Relevant to pretty much every system and it kicks my butt in all of them (currently in cardio and had it in msk and GI)
One pro tip; class 1 and 3 act on contractile cell & class 2 and 4 are for Nodal Cells. So while looking at those graph on first aid don’t get confused it just different cells.
Thank you very much for this video,,, very detailed explation Loved the Salty Cab 🚕 idea 😉 but I wish you explained use dependance and reverse use dependance 😊
thank you perfect video can someone answer this : slowing down the influx of sodium ions into cardiac muscle cells causing a decrease in the excitability of the cells it has a beta adrenergic blocker which can cause bradycardia and bronchospasm : sotalol propafenone verapamil mexitilene
HI! I've seen from many questions that non-dihydros CCBs (verapamil & Diltiazem) are adverse effect constipation. And Dihydros (Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine) are edema. Just something to consider!
Correction: in the Na blockers, the tipe A prolong the action potential, the tipe B have no effect and the tipe C shorten the action potential, in the image shows like if the more inhibition of the phase 0 the longer is the action potential. This is a important fact.
all lectures are a treasure. I also concluded that quinidine causes a lengthening of the QT interval (torsades de pointes) because it blocks potassium channels, and quinidine and K channel (potassium channel) also sound the same in the first letter.😬😬😬😬
Full disclosure: this is a brutal topic to learn. I did my best to simplify it. Remember to pay special attention to:
1. Cardiac action potential changes
2. Main adverse drug reaction (ADR)
3. Classification (Class 1A, 1B, 1C, II, III, and IV)
Thank you so so much. This is really hard!
What time zone will you be airing this topic?
How about antidiabetic drugs?
How about anti diabetic drug?
I can’t believe my eyes! Thank you so much dirty. Thank you so much!! You’re the BEST!!
Very Very important that Amiodarone messes with your TSH (it can cause hypo or hyperthyroidism). Appears in the questions every time
He mentioned it here with TFTs. Thanks for the reminder again tho
Hypo and hyper
Double track drifting
I had this exact question on my exam yesterday, thank you so much 🥰🥰
I'm just riding your top comment, but I also wanted to add that we need to know refractory recovery/AP changes with class I. I just had a question about it. If you keep them in CAB order, you can say "No long shorts" imagining some weird club where they don't want to see long shorts anywhere:
C - NO change
A - LONGer
B - SHORTer
I know he was just trying to keep it simple, but as he just drew them in based on phase 0 slope change, the diagrams are sort of wrong in terms of AP length.
Also, I feel like it's pretty easy to just pop in your memory, but it's interstitial lung disease in particular for which amioderone can show up in test questions.
freaking Uworld gets me every time with that question
My mnemonic for
class IA :queen(quinidine) die(disopyramide) fast after doing cocaine(procainamide)
Class III : LOL(sotalol) till I die(ibu-til-ide, dofe-til-ide) Amigo (amiodarone)
Both class mnemonic has dying part :D so they can cause torsades de points by increasing the effective refractory period (ERP) -->> QT prolongation (Action potential prolongation)
For class IC: proper(propa-fenone) cane(fle-cain-ide) slaps the sodium channel the hardest but stabilizes ERP.
Did you make it up by yourselves?
Do share if it was from some website
Amiodarone = Am(iod)arone = iodine = Thyroid Problems.
Dronedarone = No “iod” so = No thyroid issues.
Calcium channel blockers and beta-blockers work on the nodal action potential, so the shape of the original AP curves should be different. Thank you for another great video!
I was looking for this comment... you don't need to memorize 0,3,4 for class 4 because you already know there are no phases 1 and 2 in nodal action potential .. I guess he's just trying to simplify and avoid the physiology 🤷♀️
Saaaaame thought omg
I studied this on Uworld and it took me an entire day to master it, but you’re simplifying it into just 20 minutes, huge thanks sir!
Thought the same
Additional UWorld facts:
1) Amiodaron has partial Class 1,2 and 4 effects too. It also has an homogenous effect on K channel hence lowest risk of TdP among Class 3 agents.
2) Sotalol has partial B-cloker effect
3) B-Blockers reduce PR interval (obviously)
4) Adenosine acts on A1 receptors---->Potassium outflow--->Nodal conduction delay
Beta blockers increase pr interval
My med school professors are terrible and it's exhausting as a learner. I binge-watch Dirty Medicine after every topic we cover to actually understand the material. Thank you for helping my mental health stay afloat.
please, keep making these videos man. This is gold. This and the other videos as well.
Thanks!
It's so impressive how easy you and palatable you've made this topic. Thanks again
You could remember that beta-blockers are class II by thinking of beta being the second letter in the Greek alphabet
So logic, I guess i will never forget it 👍
or B the second letter in our alphabet
@@MedicineGod no is it really???
@@Jimbo292yess!!! i’m glad ur up to date now !
Christ imagine if medicine were taught like this. It might even be possible to do it in three years and be HAPPY?!
I've realized that it's not our faculty's job to keep us happy. They just have to have presented the info at least once, so that when they test you on it you can't say you didn't "learn" it in class; how that info manages to stick in your brain is all on you.
@@masterimbecile don't know about you, but our faculty figured out food = happy. Every event had food lol
Did that help? YES! That was beautiful. You are a gem, seriously. I learn way more from you than I did in my two years of med school. Any chance you could do some more drugs with us? I'd love any obgyn/repro stuff you feel like doing too. Thanks!
Na Channel blocker pneumonic for class 1 drugs...
Class 1A: DQP; Double Quarter Pounder
Class 1B: ML; Mayo Lettuce
Class 1C: FP; Fries Please
Mnemonic
The reason you give glucagon in a beta blocker overdose is not because of the hypoglycemic masking. Glucagon stimulates cardiac ionotropy via a separate mechanism than beta blockers.
Thank you for not brute forcing this and actually teaching the info!
I remember the mechanism of each of the classes though the phrase, "Never BET the Kitchen Counter". Type I, II, III, IV = Na, BETa, K, and Ca.
I love your lectures. Thank you:) The way I remember Beta blockers are class II by remembering that B is the 2nd letter of alphabet.
These pneumonics also help solidify the info:
For the K-Channel (Class III) he mentioned the AIDS pneumonic
"Kant Kure AIDS with Potassium"
Also class II - Bets Blockers
Two B's / double B's = class two
Calcium channel blockers
Verapamil and diltiazem are the only Non-dihydropyridines in the CCB class
They are "Very Different" (since they are the only two that have a significant impact on cardiac conduction / heart rate)
this has to be the most helpful and actually efficient way to read pharmacology omg thanks
Your effort is so greatly appreciated!
POLICE DEPARTMENT QUESTIONED THE LITTLE MAN FOR PUSHING ENCAINIDE
this help u to remember Class 1A 1B 1C
Thank you so much for taking your precious time to simplify stuff for us Dr. DirtyUSMLE.
Can you make a video on how best to recall all these fun facts from all your videos. I don't mean to sound ungrateful for everything you're doing for us🤭
Oh, I'm quadrupling the amount I'd pledged on your patreon. What I'd have paid a tutor is what I'll donate
I hope others can do the same, to show appreciation for your hard work you put in to making it easy for us.
Thank you Dr. DirtyUSMLE sir.
Gingival Hyperplasia and Ca Channel Blockers seems to be high yield for my Q banks.
some block potassium channels - sodium (I), beta (II), potassium (III), calcium (IV)
gingival hyperplasia is also an important side effect of CCBs.
thank you so much
Β blockers also elongate the floor (sounds like four). The floor being phase four.
Not sure if this helps anyone, but a way to remember what blocker goes with what class is that for the chemicals it goes in the order on the periodic table and for beta blocker, beta = 2nd = II. Just my II cents.
I see what u did there :D
@11:10, I would suggest the fact that they're class II can be related to the rule of 4s in that 2squared is 4; class II, 2squared adds to the rule of 4s ;)
Class 1a and class 3 has increase Tdp so they prolong Qtc so they are high yield
Class 1c is like c for chooter (shooter)so like in video games First Person shooter(Flecainamide, and P)
Procainamide has more A then propafenone
So more A goes higher so A grade
So class 1A and later is class 1C
Thank you!! You can also remember that Beta-Blockers are class II because Beta is the 2nd letter in Greek alphabet.
Beta = 2nd letter = Class II
🤣 WoW 😂 Great job man
Another way to remember the names. If youve heard heard the song "Hotel California" in that main chorus rhythm sing the following
Smoke (Sodium)
Better. (Beta)
Pot. (Potassium)
(In)
California. (Calcium)
Adenosine
Mg
Hope this helps
😂😂😂 thanks!
If you had a vid to help keep a1, a2, B1, B2, mAChR stuff straight, that would be bae. FA has it diagrammed out, but it's not as sexy. Relevant to pretty much every system and it kicks my butt in all of them (currently in cardio and had it in msk and GI)
10:13
Isn’t the red graph a nodal action potential graph?
One pro tip; class 1 and 3 act on contractile cell & class 2 and 4 are for Nodal Cells.
So while looking at those graph on first aid don’t get confused it just different cells.
You are very hard working teacher - Respect!
I really hope u make more videos on pathology amd pharmacology pleaseeee
Ty so much . Best video ,easy understanding and great pneumonics.
Thank you so much.Really helpful class.Thank u for explaining with tips ,mnemonics,images and voice all sounds pretty gud for a lecturer.
I'm not going to lie, when you said your mnemonic for CCB's I felt like Jimmy Neutron experiencing a brain blast. 20/10 video
My IQ definitely jumped a few points after hearing it 😂
Thank you very much for this video,,, very detailed explation Loved the Salty Cab 🚕 idea 😉 but I wish you explained use dependance and reverse use dependance 😊
Tyvm. I’m going to watch it over and over. 👍
Thanks Dirty you rock!!!...For Beta Blockers, you can also say SE: affects Breathing, Balls, Blood glucose masking
thank you perfect video can someone answer this :
slowing down the influx of sodium ions into cardiac muscle cells causing a decrease in the excitability of the cells it has a beta adrenergic blocker which can cause bradycardia and bronchospasm :
sotalol
propafenone
verapamil
mexitilene
HI! I've seen from many questions that non-dihydros CCBs (verapamil & Diltiazem) are adverse effect constipation. And Dihydros (Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine) are edema. Just something to consider!
Beta blocker s/e = B - b0ner block (impotence), B - bronchospasm (COPD exac.)
Thank you so much,your videos are so helpful 😊.
You’re videos are great but this one the way you simplified it its amazing 👏🏻👏🏻
Procainamide => SLE
"it's HIP to have lupus"
HIP: Hydralazine
Isoniazid
Procainamide
Extremly helpful; thank you
lots of love you made it a peice of cake
why did you draw nodal and ventricular APs interchangeably?
noticed that too... great video but those should definitely be different APs
Omg thank you so much Dr Dirty..you are amazing.....this topic has been such a nightmare for me since the med school
Hi, could you please make a video comparing different types of benzodiazepines? Thank you!
Nice work.
Correction: in the Na blockers, the tipe A prolong the action potential, the tipe B have no effect and the tipe C shorten the action potential, in the image shows like if the more inhibition of the phase 0 the longer is the action potential. This is a important fact.
Very Informative..3/17/23 Educational purposes for work
Thanks a tonne!!😊
Wonderful
which antiarrythmic causes tall t wave? amiodarone, digoxin or ibutilide? best ans?
Thank you Dirty Medicine
You are awesome
I had given my Step 1 yesterday and had few questions from this topic
You are lovely
Keep it up.
You are a saviour!
You’re the best ❤
are all these affecting the myocardial action potenital? beta blocker and phase 4 slow depolarization sounds more like the pacemakeer potential
YOUR BEST VIDEO. THANK YOU
He save me literally 😢❤
how is phase 3 affected in CCB's when phase 3 is for potassium efflux
Great 👍 👌 👍
Beta is the second Greek letter, it is also class 2 antiarrhythmics
Great presentation, hard core over-acronymaged!
You are amazing!! You made it so easy and simple.
Very useful intro to cardiology medications!
Thank you so much😭😭😭😭😭❤❤❤❤❤❤
Dirtyyyyyy, you’re a gemmmmmmm my guy ❤
took me 5 years to remember the D in class I antiarrhythmics is Dysopyramide and the D in class III is dofetilide
Thanks a lot for your awesome work!!
Amiodarone has the least chance to cause TdP (but still can), high yield.
Why did u switch from dirty USMLE to dirty medicine?
Thanks you so much , i learn antiarrythmics Drugs quickly in a easy way,
U made it too easy for all of us..great upload👍
THANK YOU SOOO MUCH
You are smart!...
Thanks for this video 😊
Thank you, thank you, thank you
You could say, that beta is the second letter in the greek alphabet, there by completting the class II mnemonic
"How do you remember xyz? Well unfortunately you have to memorize" ... yeaahh. that's basically entire medicine *eye roll*
thanks a lot !! ❤❤
all lectures are a treasure. I also concluded that quinidine causes a lengthening of the QT interval (torsades de pointes) because it blocks potassium channels, and quinidine and K channel (potassium channel) also sound the same in the first letter.😬😬😬😬
IB antiarrhytmics: Post MI, I'd rather B (IB) on the lido (lidocaine) in Mexico (Mexilitine) (with a SALTY margarita)
amazing content, as always!
You my friend a legend
thank you i love the mnemonics
Thank you!
Thank youuu so much for this video it was so helpful ❤️
🙇♀️regards to u!!
please make pneumonic for alpha-blocker graph given in FA pharmacology. Thank you
Already have one, check the channel
Mnemonic
knowing how these change EKG is also important
majestic thank you
Good shit.
Great shit, even.
thanks a lot