DIP Episode 104 - ACLS, Arrhythmias, and HY Cardiac Pharm

Okay, welcome. My name is Divine. I am a PGY-1 transitional year resident. That's ultimately going into a geology. And this is episode 104 of the Divine Intervention Podcasts. And in this, hopefully what is a quick podcast I'm going to be describing are ECLS algorithms. I'm not just basically going to essentially explain how to run a code. And I mean pretty much, right, a lot of this is also exam testable. This is something you'll likely see on most of the US Meli exams and whatnot. But there's also something that will probably help you in a clinical practice. Okay, so let's begin. Right, so let's assume you literally hear it overhead, right? Code blue, right? Code blue is like crap. It's personas coded, right? So your next step is to then run to the code, I guess. So when you run to the code, right, you get to the door, right? The first thing you have to ask is who is running the code, right? Whoever is running the code should not be doing anything. If there's no one running the code and you are able to run the code, then you go ahead and take over and say, identify yourself and say, you are running the code. And usually by the time you get there, right, a person would already be there during chest compressions. And I will sort of, I'll talk about like, oh, let's see, a patient code's like right in front of you. What do you do? I'll talk about that in a quick second.

But I just want to go ahead and just talk about like some good general things to do if you're the person running a code. And then we'll talk about how to run the code itself. Right? So let's assume you're the guy running the code. The first thing you do when you get into a room is you need to identify yourself. You need to say, oh, my name is divine. I am the one that's going to be running this code, right? After you identify yourself, the next thing you really want to do is to assign tasks to people, right? Assign tasks to people. So you need to have someone that is going to be doing your chest compressions, right? You need someone to be doing that. You need someone that is going to be your electricity guy, right? So the person that going that's going to be handling a defibrillation or like cardio versions. And then you need to have someone that records, right? So who is going to be recording like, oh, like this is what happened here. This is what happened here because believe it or not, at the end of the day, nursing is going to need that, you're going to need that documentation. And then you're going to need a timer, right? Because timing is extremely important when you're running a, when you're running a code, right? You basically need someone to say, oh, you know, okay, we're getting on the two minute mark. It's time to give the next drug where I'm in the two minute mark. It's time to defibrillate again, right?

So you need someone on that, those, uh, on that those are circumstances. And then, um, you also need pharmacy, right? Who do you think is going to give you those drugs that you're using a code? It's going to come from somewhere. It's not going to come from failure, right? So you need pharmacy, um, under those are circumstances. So you need a recorder, need a compressions person, you need pharmacy. And I'm not sure you need it. Someone that's going to be pushing your drugs, right? So basically like the pill pressure, president is going to like push the drugs into those into that patient. Uh, you need those people, okay? And the thing is again, you don't need millions of people in a room to run a code successfully. I will encourage you to have as few people in the room as possible when you're running a code. And the thing is, as the leader of the code, you want to become, you want to be gentle, right? Because the tone of the leader sort of sets the tone for the entire team. So if you're freaked out and you're like, ooh, are you raising your voice at everyone, right? Then that's not very productive for a code. Okay? So just calm down. Be gentle. Take a deep breath. You have that two seconds to take a deep breath and think, okay? Go in and just follow the protocol. You know, and again, if you forgot in the protocol, it's not bad to whip out your book and look at the protocol as you're running the code. Okay? No one is going to fault you for that. Okay?

So if a person codes right in front of you, right? The first thing you're supposed to do is to tap them, right? You tap the patient and say, are you okay? Try to see like if they can respond. If they cannot respond, your next step, right? So again, like literally this podcast, just sort of follow these steps, right? Next thing you do is you try to fail for a pause, right? So you feel on the coordinates for a pause. If you don't feel a pause, you say, I don't feel a pause, blah, blah, blah, I'm starting CPR. And you call for help immediately. Right? So I don't know, like you pull the code blue button in the patient's room or whatever, where you call for help and you start CPR, right? So you start CPR, bam, bam, bam, bam, bam, right? So let's assume you start CPR, right? And help then comes in, right? Obviously they will try to hook up the patient to like the monitor, right? So like hook up the patient to the zoo and try to identify whatever they're in, right? So let's assume that the patient's, and again, while all this is happening, someone is doing CPR, right? I remember CPR, you're doing it at a rate of like, like 30 to two, right? So I'm not describing any of the pediatric stuff here, but CPR in adults, you do it at a rate of 30 to two, right? So you do 30 compressions, right? And in between those 30 compressions, you provide a two breaths. Okay? So 30 compressions and then two breaths, 30 compressions, two breaths.

So 30 compressions, two breaths, very important to remember that. And remember that your compressions, right? You try to do it at a rate of about 120 per minute, right? And remember the stain a life song, right? So it's like the, you can find the song online. It works perfectly. Just follow those, follow those rules, right? Then usually you want to compress to a depth of like 2.4, 2.5 of their mouths. So just sort of keep that at the back of your mind. Then again, about 120 per minute. Now, so let's assume the, they analyze the rhythm, right? And the person is in V-fib, right? So V-fib is what's identified on the monitor? So the patient is in V-fib or like postless V-tack, well, for that, those are shockable rhythms, right? So once you analyze the strip, and you see the person is in V-fib or postless V-tack, continue your CPR, but the next thing you should be thinking about is delivering electricity to the patient. And by electricity, you're going to defibrillate the person, right? Another name for defibrillation is unsynchronized cardioversion. Synchronized cardioversion, I'll talk about that shortly, but those are, that is for completely different, that's a different kind of electricity that you're delivering to the patient, right? So V-fib or postless V-tack, you're going to cardiover the, you're going to do an unsynchronized cardioversion, also called the defibrillation.

And the thing is, when you, excuse me, when you do that, right, to your using like a bi-physic defibrillator, you basically can give at 200 joules. If you're using a monophysic, you can give like 360. But for the most part, I'll say 200 joules, like most of the joules you see in most hospitals, these days, 200 joules for V-fib, postless V-tack. So you shock the person, right? And how often are you supposed to shock the person? You're supposed to shock them every two minutes, right? You're supposed to shock them every two minutes. And then, so we've dealt with the electricity part, that's the thing you want to do as quickly and as efficiently as possible, right? Because that's really the thing that can restore the person's rhythm, right? And then in terms of pharmacology, right? You, the first drug you try to give is epi, right? And the epinephrine dose is 1 milligram. And then, after two minutes, basically just remember that you can give drugs every two minutes. So you give epinephrine more, one milligram first, two minutes afterwards, you give a mutoron, okay? A mutoron, the initial dose is 300 milligrams, right? As an IV push, right? And then after those two minutes, you give epi again, one milligram, the dose is 1 milligram. And then after that, you give a mutoron again. But the subsequent, I'm going to run doses are 150 milligrams, right?

So, and I'll summarize all this at the end, just to make sure you remember all of this, you give a mutoron 150, next you give epi 1 milligram, after that a million 150. And the thing is, you actually allow to give a lidocaine, right? After you've given a few doses of like amoea, you actually allow to give a lidocaine. I believe the dose is like 1 milligram per kilogram. So, I don't know, like the average person, let's say like 100 milligrams pretty much, and you should be solid there. I know before this, to say you can substitute your first dose of epinephrine with vasopressin, that's no longer a thing for V-fibre bolsteles v-tech. Okay, so, so quick summary, you do a defibrillation every two minutes. The defibrillation is the first thing you want to try to accomplish as quickly as possible. Although remember that in the meantime, when you see the patient, you're doing your chest compressions, 32, right? About 120 per minute, keep bringing in stainless-living your head. So, so defibrillation every two minutes. And before you defibrillate, you want to do like a pulse check on a rhythm check, right? Because what if the patient has moved from a shockable rhythm to one that's no longer shockable, right? So, every two minutes, basically, there are three things you want to do. You want to do a pulse checker in check. You want to shock if it's indicated and you want to give one drop. If you remember that, like, oh, every two minutes, I got to do three things.

It makes it a lot easier to, it makes a code a lot easier to run. So, every two minutes for V-fibre bolsteles v-tech, you got to do a pulse rhythm check. You shock if it's indicated and you give a drop. And the drop is alternating every two minutes between epi and amyol. Epi and amyol. The epi dose is always one milligram. The amyol dose, the first one is three hundred milligrams. And then afterwards, it's one fifty. And down the line, you can give light, okay, at one milligram per kilogram. So, about a hundred milligrams, okay? So, that is really how you run a code. Now, what if same deal, right? You call, you, let's assume you feel, you don't feel a pulse on the patient. So, let's, so basically right all the steps I talked about where you patient is, you call, they're not responding. And let's say like you feel a pulse, right? I mean, sorry, you don't feel a pulse. So, you say, I'm studying CPR, right? And let's say that on the monitor, you see like some squiggles, right? So, it's not easy, it's in like some squiggles that looks like normal sinus rhythm, but a patient doesn't have a pulse, right? That patient obviously has pulse, let's electrical activity, right? So, pulse is electrical activity. The heart is beating, actually, but those patients don't have enough squeeze to generate a good cardiac output, right? So, for that, actually managing PAA algorithm is a lot easier.

There's not many decisions you have to make, because can you shock PAA, you cannot, and actually I'll go ahead and see this right now. The management of PAA and A-sisterly is basically the same, right? So, PAA sisterly, you just study a high quality CPR, right? High quality CPR. And then, you give EPI at your earliest opportunity, right? And the dose of EPI again is 1 milligram, okay? You give EPI, and then you just continue your CPR at a rate of 30 to 2, as I described already, 30 compressions, 2 breaths. And the thing is, remember, like I said, for V-Fed, postless V-Tack, where you can alternate between EPI and AMIO, EPI is your only option in PAA sisterly, right? In fact, one of my friends gave me this, a treat, he said, all roads lead to EPI. In a code, you usually have to give a person EPI in some way, shape, or and it's 1 milligram, right? So, you give EPI and you basically wait like every, I mean, the official guidelines, every 3 to 5 minutes, right? But I like remembering that, like, oh, like every 2 minutes sort of deal. So, just tell yourself, you know what, every 2-minutes intervals, so 4 minutes total, you go ahead and give EPI. You don't give AMIO in PAA sisterly, and you don't shock PAA sisterly. And again, remember, every 2 minutes, you make those 3 sets of decisions, you do a pulse check and a rhythm check, right? You shock if it's indicated, so if let's assume you switched from PAA to like V-Fed, right?

You shock them on those circumstances, and then you also give one drug, right? But remember that you basically like, if a person is in PAA sisterly, you're not giving a drug every 2 minutes, you're giving a drug like every 4 minutes, so every 2-minutes intervals, okay? And remember, you're supposed to run through your differential of the 5-heaches and the 5-Ts, right? So, the 5-Ts, like the Tensionium of thorax, the thrombosis, so like a PE, the like toxins, trauma, there's another T, let's see, so thrombosis, trauma, toxins, tension, hemotherax, tampona, that's the 5-T, right? And then in terms of your heaches, right? So like hypohyperchylemia, hypothermia, hypo glycemia, hydrogen ions, so that's like an acidosis, and then like a hypovolimia, okay? So those are the things you sort of want to work through and rule out. Okay, so that's really ACLS in a nutshell, right? But let me just talk about some other Rhythmias real quick, I'll talk about these in like bigger like more dedicated podcasts, but let's just do a quick drive by through the like a lot of the other Rhythmias, right? And to say like high-yield exam testable slash clinical things that you'd need to know about that, right? So, let's assume a patient has like a white complex attack here with me, right? So like a regular, white complex attack here with me, the very first thing you should assume is that the patient is in V-TAC, okay?

Now, if the patient is in V-TAC, there are three decisions you need to make basically. The first decision you ask yourself is, does the patient have a pulse or no pulse? If the patient has no pulse, that's ACLS, right? You need to go down that epi-ami-o, epi-ami-o shock every two minutes pathway, right? That's it, your job is done. Now, if the patient has V-TAC and they have a pulse, the next thing you have to ask yourself is, are they stable or unstable, right? And by unstable, I mean, are they hypotensive? Are they altered? Are they symptomatic, right? If a patient is symptomatic and they're in V-TAC, right? Your next step for those people is electricity as well. But electricity is different this time. It's not a defibrillation, it is not a, it is not an on-synchronized version. This time, these people have a synchronized card diversion, okay? Synchronized card diversion. Synchronized card diversion is what you do if a patient has V-TAC and they have a pulse or they aren't stable, okay? Synchronized card diversion. And let's see, what else do I want to mention there? Yeah, that's pretty much it. You do a synchronized card diversion. Occasionally, on MBM Es, you may see that referred to as a direct current card diversion, it's the same thing. On MBM Es, you may also see that referred to as direct current counter shock. So just something you want to keep at the back of your mind. Okay, now, so you do a synchronized card diversion, right?

Then literally a synchronized card diversion. The difference between a synchronized and an on-synchronized card diversion is you're trying to not shock the heart when the person's heart is going through repolarization, right? So that's like the R on T phenomenon you hear about because the thing is, if you drop a QRS complex, right? So if you shook the heart when the heart is repolarizing, that can basically go from, you can go from one rhythm to like V5 or like really bad VTAC and then patient and die, right? So you don't want that. So that's why you do a synchronized card diversion, right? So like that's the whole point behind the sync button on the on the cell. Okay, so the third decision for VTAC, right? Let's assume they have VTAC, they have a pulse, they have really no symptoms, they're like super stable. Then your next step in management is immuter, that's it. Okay? Immuter. Okay. Now what if you have a patient, right? And this patient has narrow complex regular TAC here with me on the monitor, right? So like narrow complex regular TAC here with me, right? So the first thing you want to assume is that they have an SVT, right? They have a super ventricular TAC cardia. For patient as an SVT, right? You can try the VEGLE crap, right? You can dunk with your head in cold water, turn them blow into straw, massage their carotids. But let's assume that's not working, right? So after that, you proceed to, you want to go ahead and proceed to to drugs, right?

So the first drug you can give, you can give a denocene, right? And the dose is like six milligrams, right? The first one you give is six milligrams. After the six milligrams, if that's not caught in it, you can give 12 milligrams. If that's not caught in, you can give another 12 milligrams. Okay? So give a denocene and you can try to like basically slow your heart down and see if you can sort of get them back to like a no more of them or slow the heart down enough to be able to see the arrhythmia they're going through, right? But basically for SVT, right? You, you basically pursue like, like you try to control the arreets, right? So you can put them on like an IVB to blocker or calcium or calcium channel blocker, right? So you can put them on like a beta blocker like my tuberloil or like a beta law liven or you can use a beta blocker. Okay? So just, I mean, sorry, a calcium channel blocker. So those are the things you want to keep in mind there. But I mean, if the patient is unstable, the thing I just tell myself is one easier to remember is if a patient is unstable for any reason and they have like a rhythm that is not PEA or AC study, you need to give them some kind of electricity. And that electricity is a synchronized cardioversion. The only exception to that rule is V-FAP, POSLS V-TAC. That's why that's called ACL is in the first place.

The only exception is V-FAP, POSLS V-TAC where you, where you do an unsynchronized cardioversion, which is also again, like I said, called a, called a different relation. So, yeah, so those are the decisions you make for an SVT. Okay, so if they're unstable at the same time, synchronized cardioversion. Okay? But for medication, you can give something a basically slow conduction than the even like a beta blocker or a calcium channel blocker. And the calcium channel blocker I'm referring to is a non-dihydroperiodine calcium channel blocker, like Vera Pamell or Deltaia Z. I'm not talking about like your naefer the pin, I'm not a pin, clevida pin and whatnot. Those are mainly for those are your dihydroperiodine calcium channel blockers. Those are mainly for block pressure control. Okay, now what if a person has you know they're 6, 6, 6, you look at the monitor and you're seeing a feb, right? A feb is like your classic irregularly irregular whatever. Basically the way to identify, the quick and dirty way to identify a feb, you're looking at the QRS complexes and the spaces between them are not equal and you're not seeing p-waves. If that's what you're looking at, then it's, that's a feb, right? And a feb, right? Again, if they are stable, you, you can start them on like a beta blocker. So you can post you like a rhythm control strategy, you can start them on a beta blocker, or a non-dihydroperiodine calcium channel blocker.

Another option you can explore is, you can use a mute or run, right? So that's a rhythm control strategy. Remember a mute or run is a class 3 anti-rhythmic, right? So you can use a mute or run for those people. But if a patient has a feb and you're unstable, believe it or not, your next step in management for those people is a synchronized cardio version. Okay? So definitely give that at the back of your mind. A flotter, basically the same deal as well. A flotter, sought to pattern on an EKG, okay? Again, if they're unstable, cardio version, synchronized cardio version, if they're stable, same treatment, beta blocker or non-dihydroperiodine calcium channel blocker like Verapamell, they'll tie us up, right? And remember if a patient has a wolf Parkinson white, you don't want to give them an even auto blocking agent. So in those patients drugs like beta blockers, non-dihydroperiodine calcium channel blockers, the joxin, those are all contraindicated in those people because if you basically block the even odin those people, you're like saying, oh, you know what? Arithmia, I will encourage you to go through this bundle of camp more, right? Which is obviously a bad idea because those patients can degenerate in the beef and die. You don't want that, right? So under those circumstances, the things you, the drug of choice for for WPW, right? It's Prokina mite, right? Prokina mite, Prokina mite, don't forget that Prokina mite.

Okay, in fact, if a patient has A Fib with a WPW, you want to go ahead and give a Prokina mite under those circumstances. Okay, now, and remember, for WPW, you have the classic Delta wave, very short PR interval, right? That tells you what you need to do. Now, what if you have a patient and they have like a multi-focal atrotachic cardiac, right? So MFAT, on exams, that was right. So you see like three or more different P wave morphologies. Remember, MFAT, you don't, you really do not shock for the most part. Those people, you just treat them on the line disorder, you can also give them like a beta blocker or a non-dihydroperiodine calcium channel blocker and tell them who stops smoking. If they stop smoking, chances are that MAT order is off. And then what if a patient has like a breathing arrhythmia, right? So let's say they're breathing like in the, I mean, their heart rate is like in the thirties, right? For those patients, right, you can consider pharmacology, right? So like atropine, remember atropine is a most chrynic receptor antagonist. So speed up conduction through the EV node. Alternatively, you can, you can consider, what is it called? You can consider pacing those people, right? So you can sort of like paste them. So yeah, you just pace. You can set it at a reasonable rate, I don't know like 70 bits per minute, whatever, but you can pace those people. So just something to keep at the back of your mind.

Remember, I've been saying, oh, if a patient is on stable and it's not V-fib, it's not a POSLS V-TAC or it's not a PA system where you obviously don't give electricity. I say, oh, do synchronized code version. The synchronized code version dose is like 100 drools, okay? 100 drools. Not 200. 200 is generally what's used for V-fib POSLS V-TAC. So just something to sort of kind of keep at the at the back of your mind. Okay. And then just sort of running through some high yield cardiac drugs real quick, right? So remember your anti-rhythmics, right? Amuletaronis, like the big, big one used in ECLS. Remember, it's a class three anti-rhythmic, it's a potassium channel blocker, right? Remember, amuletaronis can tank a person's pressures. So just sort of keep an eye on your patient's blood pressures. And remember that amuletaronis can cause many problems, right? It can cause both a hypo or hypothyroidism, right? So if you remember that fancishmancy wolf check-off effect on like your daze-dough phenomena, it can cause a hypohypothyroidism through those mechanisms. Amuletaron can cause like a blue discoloration of the skin, right? That's another high yield thing you want to know. And amuletaron can also cause a pulmonary fibrosis, right? So it can cause restrictive lung disease. So like reduced lung volume, snomal, FVV1, FVC ratio, normal low increased FVV1, FVC ratio. And because it causes a pulmonary fibrosis, the DLCO will be decreased, right?

And then don't forget your your class one each inch, right? So you have your class one E1 B and one C, your class one E drugs, right? So you have so like that, come on divine, really? You have your dysoperemit, you have your quinidine, then you have your perquinamide. Those are your class one, class one agents, class one A agents, and then your class one B, you have like your lidocaine, your mixility, and your tokenite, and then your class one C agents, you have your flaky night and propaphenol, okay? Remember that your perquinamide, right? It's the one they use in WPW, and remember that perquinamide is also associated with drug induced lupus, right? With those fancy anti-histonantibides, right? Something you want to keep at the back of your mind. Remember that finitoin kind of works almost like a like a class one, a anti-rhythmic, right? So that's why finitoin can have per-rhythmic side effects, so that's something also when they keep at the back of your mind, and remember your class one agents are your sodium channel blockers, and they can prolong the QRS, right? They can increase your risk of corsag, the point, and stuff like that. And then don't forget your class two agents, right? Those are your beta blockers, right? So like my topper lol, a beta lol, and what not, and then your class four agents are your non-dihydropyidine calcium channel blockers, like Verapameo, Deltiasm. Remember that those drugs, right?

They also slow down conductors, and through the EV node, they basically affect like phase four of the of the peacemaker potential, right? And then don't forget your the juxtaposition, remember the juxtaposition, it does not improve survival, like beta blockers doing heart failure, but you can use the juxtaposition certainly for E-fib, because the juxtaposition in addition to being a positive I-notrope, right? So it will increase your stroke volume, it will increase your cardiac output, the juxtaposition also has a most chrynic receptor agonist activity, right? So it's slow conduction through your EV node, right? And remember the way the juxtaposition works, right? The juxtaposition inhibits the sodium potassium ATP's pump, right? So when you do that, you decrease the intracellular concentration of sodium, right? Because remember that, sorry, you will increase, I take that back, oops, because remember the sodium potassium ATP's pump, right? It pumps three sodiums out of the cell and brings two potassiums in, right? So if you block the sodium potassium ATP's pump, sodiums will no longer be extruded out of the cell, if the sodium is not lung extruded out of the cell, they'll sort of build up, right? And if they build up, right, that sodium calcium exchanger that you learn to well study for step one, it won't work anymore, right? You won't work as well.

Remember the job of the sodium calcium exchangers to bring sodium into the cell and then extrude potassium out of the cell, right? So bring sodium in extrude calcium, bring sodium in extrude calcium. So if your sodium calcium exchanger is not working because remember, sodium calcium exchanger is kind of like a secondary active transport mechanism, right? It brings sodium down, it's gradient into the cell and then use that gradient energy of sodium to pump calcium out of the cell. So if you've blocked the sodium potassium ATP's pump with your friendly digoxin, the amount of sodium inside the cell builds up. So that gradient no longer exists between like sodium that is usually very high on the outside and very low on the inside. That gradient doesn't exist. The sodium calcium exchanger basically stops working. So you do not extrude calcium from the cardio, from the cardiac myocyte. So calcium builds up interestingly, right? And that causes better contractility. And remember that if your hypochylinia make you have a higher risk of dig toxicity, right? Because remember that on that sodium potassium ATP is pump. Basically the juxtapine is to like the potassium site on that pump. So if your hypochylinia make it's like there are more open size for the juxtapine to bind. So hypochylinia predisposes you to the juxtapine toxicity.

But the thing is your friends at the MBM or whatever board exam you're taking, they know people, they try to mess with your head with another potassium issue relating to the juxtapine. So if your hypochylinia make that increases your risk of dig toxicity. But if dig itself causes hyperchylinia as a side effect, right? So why is that? Again, again, pharmacology is something you never really should be memorizing. It's something that makes perfect sense. If you just sort of think through it, right? So I just told you that the sodium potassium ATP is pump brings three sodiums out of the cell and two potassiums into the cell. Well, guess what? If you block the sodium potassium ATP is pump aka, which is what the juxtapine does. You will not be able to bring potassiums into the cell. If you don't bring potassiums into the cell or persistent side of the cell, they get a hyperchylinia, okay? So the juxtapine by virtue of its mechanism of action can cause hyperchylinia as a side effect. But being hypochylinic predisposes you to the juxtapine toxicity. So the classic example should be a person that's like on diuretic, like ferozomide and dig right, heart failure, heart failure, right? And then that ferozomide causes hypochylinia and then the get dig toxicity. And remember that dig toxicity, right? You treat that with, you treat that with anti-deger phabapragments, right? So anti-deger phabragment, I believe it's called a digibund, okay?

And then some other hyalurde, uh, drug stuff you want to know. Remember your, basically I'm just run my go with this podcast was just to go through ACLS arrhythmias and then just talk about like random hyal cardiac drugs, right? So, um, not a drug, you can remember your beta blockers, right? They've been shown to improve survival in heart failure. Remember beta blockers, you don't want to give those to a person that comes in like a cocaine overdose, right? Because of that unopposed alpha crap, right? Where they can get like superhypertensive. So the person comes in with a cocaine overdose, you, you know, want to consider um, giving them like a benzo or you can give them like an alpha blocker like a phentolamine or you can give them an alpha beta blocker like a labeta law or carvedi law, right? And again, remember beta blockers, the improved survival in heart failure, uh, but remember it's only three beta blockers that have been shown to do that, right? So like metoprolol, carvedi law and pisoprolol, those are the ones that have been shown to improve survival in um, in heart failure. Okay. Now what are the other drugs that have been shown to improve survival in heart failure, right? Spirinolactone is one. Remember Spirinolactone is an outdo stone receptor antagonist, right? So remember the classic gynecomastia side effects because in addition to blocking out dose stone receptors, it also blocks um, um, angrogen receptors, right?

So you can get kind of gynecomastia side effect with the Spirinolactone. Remember Spirinolactone, um, you can also use it as prophylaxis, right? In patients that have like really badly vertezides and viruses. Okay. And you can also use Spirinolactone to treat PCOS, right? Because it inhibits five alpha reductives in the skin, right? So you can use that under those circumstances. Okay. What other drug has been shown to improve survival in heart failure, right? In heart failure, another drug is um, by deal, right? So the combination of isosorbide and um, and the hydrolyzing, right? But it's in African-Americans that that has been shown to improve survival. And then in terms of other drugs that improve survival, remember your ACE inhibitors, right? So like your lysinoprile, captoprile and whatnot, uh, basically the, uh, those drugs, right? ACE inhibitors, right? The inhibit and your tensing convertible enzyme. Remember that if a person has bilateral or other stenosis, you don't want to give those drugs, right? And then those, uh, your ACE inhibitors are almost always the correct answer on NBM Es or any board exam. If they give you a question about like a diabetic, um, and they see, like reduce the risk of like renal failure in the future and all that crap, give an ACE inhibitor, right? Because remember, uh, by giving a, by giving an ACE inhibitor, you decrease the formation of angiotensin two.

If you think back to your preclinical coursework in med school, remember that angiotensin two, right? Uh, it varies selectively, uh, when you act on its type one receptors, right? It, uh, uh, it preferentially constructs the efferent arterial, right? But remember that if you're constructing your efferent arterial, that can cause, uh, because again, think about your kidneys, right? Afferent arterial, glomerulus, efferent arterial. If you construct your efferent arterial, uh, the pressure, the hydrostatic pressures in your glomerulus will increase, right? So you have like intraglomerular hypertension. And over time, that can cause a hyperfiltration injury, right? Hyperfiltration injury. That can, you can just crop your kidneys. So you clearly don't want that, right? So that's why you give ACE inhibitors in the abedies, right? Because by giving ACE inhibitors, your decrease angiotensin two, you sort of keep the efferent arterial open, right? And by doing that, you can sort of decrease that intraglomerular hypertension. So you sort of exert a protective effect on the kidneys, okay? And remember, your ACE inhibitors, you can actually also use them to treat the peripheral edema. That's associated with, um, with, uh, come on divine thing, think, think, think, think, with your dihydroperidine calcium channel blockers, right? So like your, I'm low-depean, fellow-depean, whatever, your depends, right? Those drugs, remember those drugs can cause peripheral edema, right?

And reflex tachycardia has a side effect. The reason they cause the, um, reflex tachycardia is the viso-dialit. So because viso-dialit, your heart is like, hmm, what's going on here, right? So your heart begins to be a lot faster as a, sort of like, as a, as a reflex, right? And again, if you want a deep, real deep into pato phase, um, you can basically think about your viso-dialit, your bowel receptor sends the low pressures, they're like crap. Let's try to, um, respond to this. So you have like a massive sympathetic discharge, you got the video, a bit of one receptors and boom, the heart starts going a real, real, real, real fast, right? So your dihydropinidine calcium channel blockers, yes, you use those for, uh, they can cause, um, um, reflex tachycardia. The reason they cause peripheral edema, right? So again, if you think about your vessels, right? So remember your vessels, you have like your arteries, bam, bam, bam, bam, they decrease, your formaterials, and then from materials, you have capillaries where you have like absorption and all that crap taking place. And then after your capillaries, you have venules, right? So the thing is your arterios come before your capillaries, and the thing is your dihydropinidine calcium channel blockers, they cause a dilution of your pre-capillary arterios. So the arterios that come before the capillaries did I leave them, right? So if you dilute the pre-capillary arterios, that will send more blood to your capillaries, right?

So you're basically increasing the hydrostatic pressure in your capillaries. If you have that, you can have like fluid extroversition, you can get peripheral edema. However, if you're like, okay, let's fix this peripheral edema, right? You can do that by trying to decrease that hydrostatic pressure in those capillaries, right? And the way you do that is by diluting, because remember I said, arterios, little capillaries, capillaries, into venules. So if you go by some magic, dilute those venules that come after the capillaries, that will basically cause drainage of those capillaries, and that will decrease the hydrostatic pressures in those capillaries, right? So that's where your friendly ACE inhibitors come in. Your ACE inhibitors, they work specifically by diluting those post-capillary venules. So that's the pathophysiology behind them being used in the treatment of the peripheral edema that's associated with the use of your dihydroperidina calcium channel blockers, right? And then remember your nitroperside, right? You can use it to treat like a hypertensive emergency, works pretty well, although don't forget that you can leave a person on a nitroperside drop for a long time, right? That can cause like bad, bad, bad, bad, a cyanide toxicity, right? That's usually not a great outcome. Okay, and then remember hydrolyzing, right?

Hydralazine, it's an awesome viso-diiliter, remember because it's a viso-diiliter, it can cause reflex tachycardia, and don't forget that hydrolyzing is also associated with the drug induced lupus, right? With those anti-histonantibodies, right? Let's see, what other cardiac drug can I talk about? Well, let's assume a person is in cardiogenic shock, right? You could consider giving them like dobitamine, right? Dobitamine. So remember dobitamine, it's a beta-1 agonist, right? You remember you can use it for those pharmacological stress tests, but remember from the ebi, literally like the most recent podcast I meet where I said, if I present like a bad arrhythmia, bad tachycardia, those are contraindications to using dobitamine for those pharmacological stress tests, but basically dobitamine is a beta-1 agonist, right? So it will increase your heart rate, it will increase your stroke volume, right? So ultimately it will increase your cardiac output, you can use that for cardiogenic shock, right? Another drug you can use cardiogenic shock, you can use merino, right? Remember merino is a phosphodistory in hebeta, right? So if you inhibit phosphodistory, that will increase your cyclic AMP, right? Remember cyclic AMP is broken down my phosphodistory, so inhibit phosphodistory, you will increase cyclic AMP. The thing is, if you remember from your preclinical course working med school, where cyclic AMP does many different events, right?

Depending on the kind of muscle you're dealing with. So if you're dealing with cardiac muscle, cyclic AMP actually causes in contraction of cardiac muscle, but if you actually have high levels of cyclic AMP in smooth muscle, that actually causes a relaxation of smooth muscle. So that's the pathophys behind merino, being called an I know dilator, you hear that classic mantra in critical care circles, I know dilator, I know dilator, I know dilator. The reason it's called an I know dilator is by giving it info for diastories, it increases the cyclic AMP in muscle, but in cardiac muscle by increasing the cyclic AMP will cause increased contractivity, in smooth muscle by increasing the cyclic AMP will cause reduced contractivity. So you have like smooth muscle dilation, and if you dilate smooth muscle, remember smooth muscle is what lines your blood vessels that will decrease your systemic vascular resistance, right? But if you increase cardiac contractivity that will increase your like your stroke volume, right? My ocradia couple goes up, okay? So merino is an awesome drug because it increases your cardiac output, it decreases after load as well, right? By decreasing your systemic vascular resistance. Okay, so it's about four minutes to when I need to prepare to start going to work. So have a wonderful day. I hope you found this podcast to be helpful.

This is again, one of those podcasts that will generate you some points on pretty much any USM and pretty much any like medicine related board exam, right? So as I round up, right? I always say this, I offer one on one tutoring for all the USM exam, step one, two CK, two CS, step three, and even like the complex exams, I don't have actually tutored a bunch. I don't know why I've never mentioned that, but actually tutored a bunch of people on those are complex exams. And then like the preclinical exams in med school, the third year shelf exams, and then the medicine in training exam, right? And the medicine board exam, I'd offer one on one tutoring for those. And then if you're not a college student that needs tutoring like physics, general chemistry, organic chemistry, biochemistry, physiology, histology, I offer tutoring and all those things, right? Those subjects, thankfully I still recall from college. Okay. And then if you're a med student applying to residency, so like an ERAS application or a college student applying to med school, so I'm amcass application, I do offer like consulting and one on one guidance for that. I mean pretty much everyone I worked with this last admission cycle, they all matched into their residency. Most of them matched that in first choices. So take that for what you will, but I've actually been on the admissions committee of top two med school for like a year.

So I've sipped it through thousands of applications and I know the things that people watch out for and admissions are committing. So if you need any help with that, feel free to reach out to me through the website. So you can send me an email at Divine Intervention Podcasts. So podcast with an S at the end at gmail.com. Okay, so have a wonderful day. We'll see you in the next podcast and God bless you. Thank you.

To maintain calm leadership by identifying yourself and assigning specific tasks (compressions, electricity, recording, timing, pharmacy).

100–120 compressions per minute.

At least 2.4 to 2.5 inches (6 cm).

Unsynchronized cardioversion (defibrillation), delivered every two minutes.

1) Rhythm check/Pulse check, 2) Shock if indicated, and 3) Administer the alternating drug (Epi then Ami).

High-quality CPR and administering Epinephrine 1 mg every four minutes (or following protocol guidelines for repeat dosing). No shocks or Amiodarone.

Adenosine; initial dose is 6 mg IV push.

Beta-blockers or non-dihydropyridine calcium channel blockers (Verapamil/Diltiazem).

Procainamide.

Tension pneumothorax, Tamponade, Toxins, Thrombosis (PE/DVT), and Trauma.

Any AV nodal blocking agent (Beta-blockers, non-dihydropyridine CC Bs). The preferred drug is Procainamide.

They decrease Angiotensin II formation, preventing excessive constriction of the efferent arteriole and thus maintaining intraglomerular pressure.

Amiodarone.

Synchronized cardioversion must be timed to avoid shocking during the vulnerable period of repolarization (R-wave), whereas unsynchronized cardioversion delivers energy regardless of the cardiac cycle.

Digoxin.

All three (Metoprolol, Carvedilol, Bisoprolol) are proven beta-blockers that improve survival in heart failure; Propranolol is generally avoided due to its lack of proven benefit.

Tension pneumothorax, Tamponade, Toxins, Thrombosis (PE/DVT), and Trauma.

Any AV nodal blocking agent (Beta-blockers, non-dihydropyridine CC Bs). The preferred drug is Procainamide.

They decrease Angiotensin II formation, preventing excessive constriction of the efferent arteriole and thus maintaining intraglomerular pressure.

Amiodarone.

Synchronized cardioversion must be timed to avoid shocking during the vulnerable period of repolarization (R-wave), whereas unsynchronized cardioversion delivers energy regardless of the cardiac cycle.

Digoxin.

All three (Metoprolol, Carvedilol, Bisoprolol) are proven beta-blockers that improve survival in heart failure; Propranolol is generally avoided due to its lack of proven benefit.