If you loved the last one, and I know you did, you’ll really love this one too. I don’t hold back anything. I’m always talking about receptors. I’m always talking about mechanisms of action. Again, to explain why, to help you remember why, some of these things. Vasopressors and inotropes, these are some things that you have access to. I want give you why is one drug preferred over another. Not because somebody told you so, but to tell you, physiologically speaking, why. Granted, it’s probably going to match your protocol. So what. And now you know why. And if you ever had to deviate from protocol, granted you’d get whipped and yelled at, maybe you would at least hypothesize why you would need to deviate.

Or maybe I need to call for med control and ask for something. Objective– compared and contrast some of these things. Obviously, volume status in your critically ill patients. Kind of talk about what physiologically is going on when someone is actually in shock. There’s a couple different shocks. They’re hypotensive. That’s what you know. Why are they hypotensive? There’s different reasons to be hypotensive and in shock. List some of these blood pressure or cardiac output things. Talk about lactic acid and some of the other things that we would be looking for in the hospital. And I’m giving it to you and you’re like, but we don’t do any of this. I know. What happens if you pick a patient up and transfer him to another hospital? Then you may have some of this at your disposal. I’m not saying you’re doing anything with it, but it’s there.

I want you to know why is it there. What else can you possibly be doing, right? Just taking an intense person from one place to another, right? If I’m wrong, I can just shut up now. And don’t tell me I’m wrong because you want me to shut up. I’m wiley. Also describe the catecholamine vasopressors and inotopres. What makes them somewhat different. And what are some clinical endpoints you need to look for when these are running. Pretty much what that is all saying, what is shock? I’m shocked. No I’m not. Because if I was shocked it would be a life-threatening condition that occurs when the body is not getting enough blood flow. So, there’s many things that can cause not getting enough blood flow. Can lead to, obviously if left unchecked can lead to your organs not doing well. Because they’re not getting enough blood flow. As blood is going to be shunted, and blood is always shunted to your brain. You can live without kidneys, your body knows this. Your brain, not so much. So everything always tends to shunt to the brain.

Brain, heart, but you know, you don’t do well without liver, all these other things. Shock requires immediate medical help. Types of shock. Hypovolemic. That’s a big word. What does that mean? Yeah. Low volume– hypovolemic. Low volume. They either lost blood, paid for college by plasma, I don’t know. They lost blood. Cardiogenic shock. What does that mean? It generates from the heart. The heart is the problem. So you’re not getting enough blood flow because the pump’s broken. If your sump pump is broken, your basement is flooded. Kind of same thing with this. We’ll talk about it. Distributive shock and obstructive shock. Obstructive shock could be a massive clot. Or, if we have a massive clot in our lung area, we like to call it a PE.

You don’t tend to live long with a massive PE. So these things are obviously of major– So what will affect blood pressure? This is not rocket science. I am not telling you anything that is not painfully obvious. If your pump is not working, as we talked about, your sump pump is not working, you’ve got a backup. Your blood flow is not going if your heart is not working. You’ve get an MI, some arrhythmia, acute heart failure, some valvular disease. Heart’s not working well. Hypovolemia. Hemorrhage. Intractable diarrhea. You always forget about that. You think there’s no way they’d poop themselves– you can lose a lot of volume in stool. Funny, it’s funny, we always talked about poop from when we were little. We’ll still laugh a little bit about it. Not so funny when you poop out four liters or more. You can lose a lot of water, and a lot of salt. Heat stroke, same thing. Lay out in the sun, do a lot of work in the sun, technically could be going into shock. We kind of forget about those things. Like yes, OK, we know about them, we pick these people up.

It can be very dangerous as well. Decreased cardiac output and vasodilation. This happens in sepsis, or sometimes is drugs induced. Anaphylactic shock is the same thing. And neurotrauma. If you actually wind up shocking or damaging your spinal cord, you will become hypotensive enough because the nerves supplying the vessels stop and those vessels open up, and they become hypotensive. And for a short period of time, you need to give them a pressor to get those back.

They’ll bounce back eventually. But if you don’t recognize it, the person can actually die on you. Now you go from a neck injury you can go into a shock, because the vasculature will open up. Because they’re not getting that neurotone. Everything that leads someone to death is always a vicious cycle. To get this vicious cycle, whatever it is, you’re not supplying enough blood.

So you have inadequate blood flow to the organs, your tissues become hypoxic. We’re a dual-fuel system, so if you don’t get enough oxygen, what’s it going to do? You’re going to switch to anaerobic metabolism. Anaerobic metabolism makes lactic acid. In a short period of time, when you’re running really hard, that’s OK. You can stop and you start breathing and it’s good. But when you can’t, and you keep building up lactic acid, it becomes a problem. Then you get a metabolic acidosis, which causes cardiac depression, which then causes inadequate blood flow to the tissue. Which then causes more, and more, and more, and you can spiral yourself right out.

So you’ve got to break this somehow, in any of these places, stop that cycle. So how can we break this cycle? Where is the system broken? Try to figure out, hey, they are low blood pressure. Where’s the system broken? Where can I intervene? Trying to figure out where is it initiating from is of great help. It’s very hard to do, especially in the field. But it’s something that we’re all trying to do. Do I need a vasopressor? Maybe. Maybe not. What happens if I add a vasopressor and it’s really the heart? Am I helping the heart out? I’m adding stress to the heart. Oh, well, the heart was actually sick. We’ll talk about that in a little bit. How much of a vasopressor is too much? When I start making the heart sick and sicker.

Let’s say the heart wasn’t the sick part, but I can make the heart sick with my vasopressors. Sorry, this is more of a joke, if anybody knows the movie, Sure Thing. Unfortunately it’s from the ’80s, and I’m old. Anyway. Who made liquid soap and why? We’re going talk about monitoring. And we’ll go quickly through the monitoring. This is a lecture I give to many people, so I apologize. Some of this monitoring stuff may not always apply to you. But it will apply if you pick patients up from one ICU to another. So we’ll talk about and answer five of the six. I don’t know who made liquid soap and why. They probably made a lot of money. Hemodynamic and oxygen transfer monitoring. Blood pressure is the gold standard. Mean arterial pressure is what we’re really looking for, is more of a mean than systolic. You want to know what that average is. That’s what your mean gives you. What is the heart rate? If I can figure out cardiac output. To get cardiac output, I need an invasive line placed.

I can’t get cardiac output in the emergency department either. So I’m in the same boat you are. I can’t get that. I can just kind of go by my other signs and symptoms. Well, I don’t think their heart’s working too good. You look at how they’re oxygenating, stuff like that. Cardiac index is actually your cardiac output. And I’ll talk about all these. Over body service area, stroke volume is how much squeeze, how much volume is being ejected when their heart is beating. Central venous pressure. That is how much pressure is in your venous system. When we look at your blood pressure, that’s how much pressure is in your arteries. As your blood goes from your arteries to the capillaries, the capillaries are large, very spacious. You lose a lot of pressure. When we talk about like 120 over 80 is what we look for in a blood pressure. On the venous side, we’re looking like 10. That’s how much pressure you lose as it goes into your venous side. And 10 is actually a great number. You’re topped off. You’re looking good. You’ve got enough volume onboard.

You can also look at systemic vascular resistance. If I take your blood pressure right now, let’s say it’s a garden hose, and you’re doing fine. And the spigot is turned on and I’m able to knock that knob off so I can’t turn it up anymore. You’ve got great pressure with the garden hose. I’m able to take off the garden hose and now I put on the fire hose. It was a great stream before. How is that streaming out now? And that’s what your SVR gives you. Systemic vascular resistance. You didn’t lose any volume. The vasculature just went ughh. This is what you see in sepsis. The heart’s fine, the pump’s working. The volume didn’t go anywhere. I just put on some fire hoses.

Pulmonary, this a wedge pressure. A very, very special catheter gets this one. We almost never see this anymore. But it is of great value. Pulmonary artery pressure would get on an echo. When you’re looking at oxygen purposes, when you look at someone’s pulse ox, you’re looking at their arterial oxygenation saturation, your SaO2. That’s what you’re looking at in a pulse ox. You like to see that 100%. Somewhere in the 90s is fine by me too. But you’re looking at 80s– if they have COPD it may be OK. I’m not necessarily happy. You get a mixed venous, that becomes a lot more complicated. Some of these other oxygenation stuff. You can actually get to a point where you can find out how much oxygen you are delivering to the end cells. Which actually gets to that whole vicious cycle thing, when we’re talking about we didn’t deliver enough oxygen, which causes it to switch to a different fuel system.

Lab values. CBC tells you how much blood somebody has. Electrolytes can kind of point to how well the heart’s working. Metabolic panel, blood gas, lactate level as well. Your mean arterial pressure is very good for us to know. And your mean arterial pressure technically can be calculated. I know machines give it to you, but it can be calculated. Your heart is actively beating a third of the time. So you take your systolic blood pressure times one third. And guess what? It’s not beating 2/3 of the time. Voodoo math there dude. I know. I know it’s hard. But if it’s a third of the time it’s beating, 2/3 of the time it’s not. So you get a diastolic pressure, when it’s not beating, times 2/3’s. That will give you your mean arterial pressure. That’s how you calculate it. Why is the mean arterial pressure more so when you’re evaluating this? It’s because the arterial pressure is an endpoint. You want to get that average pressure up high enough that you’re delivering enough oxygen to all the end cells. So if you’re looking at it systolically speaking, let’s say you’ve got 120 over 2.

My mean pressure stinks. Not really delivering enough oxygen. And if you’re in bypass surgery, they’ll put you on a pump. Let’s say they put you on pump, your pressure is 50 over 50. It’s a constant pump. It’s not like a heart beating. It’s a constant pump. So it’s really focusing on what we’re looking for. We need restoration of adequate perfusion, is really what you’re looking for . Coronaries, also your brain. MAP’s less than 50, you’re not getting enough delivery. SVR is your system vascular resistance. You’re going to see this more in sepsis. Don’t worry about calculating for central CVP. We talked about it already. Skip that. What will affect your CVP? Blood volume. What else? Also if you’re in some sort of right heart failure.

Will this make sense to you? If my pump is broken, will I see the backup before the pump or after the pump? Before the pump. So if my right heart is failing me, say I had my RCA occluded and I blew out the right side of my heart and my right heart is failing me now, where will I see the backup? In the body, the vasculature. So this should make some sense, if my central venous pressure, which normally is low, is starting to get pretty high, there’s a chance that your right heart is failing. Eventually right heart failure will lead to all heart failure. The left side as well. Heart rate we know. Cardiac output is simply calculated if you know stroke volume. You know how much volume is being ejected, you take that times your heart rate. That gives you cardiac output.

That is an OK determinant on how your heart is doing, but it’s not the best. The best determinant is cardiac index. Why? Cardiac index is based on body surface area. [INAUDIBLE] Exactly. It’s geared towards how much mileage that heart has to beat against. You take a very, very small person with that same output, it doesn’t have to travel over all that mileage.

You take someone very tall, very large, that’s a lot of vasculature mileage you need to pump against. Same thing as with hoses. If I link as many hoses as I can, will that pressure be as good as if I only had a really short hose? No. The really short hose is really firing out from the source. So intuitively it should make some sense. So when I’m looking at– granted these numbers you can’t get in the field, I can’t get in the emergency department. But if I’ve got someone in an ICU the probably have this hooked up. They probably have an immediate monitor, a catheter, that’s giving them cardiac index. It’s giving them cardiac output as well. But what you really want to look at it not output. You want to look at index. We don’t get these anymore. Wedge pressure is very important as well.

It tells you how much backup you get. And what it is doing, I will tell you. You get it from a Swan-Ganz catheter, not that you need to know that. Swan-Ganz catheter, what they would do is they would put the catheter in the right atria, put it in the right ventricle, blow up a balloon and have it float into the pulmonary artery. Pretty dangerous. Yes it is. That’s why we don’t do it too much anymore. Because if you blow out any of those things, you’re probably hurting your heart as in permanently hurting your heart and not living.

But what that will tell you is how much pressure is in your lungs. If the left side, which is the biggest side of my heart, is failing me, where’s my backup going to be? In the lungs. I’m going to have a lot of lung backup or pressure. This Swan-Ganz catheter would tell me that kind of pressure. It will also tell you how much volume the person has on board. Your CVP is less invasive, and it will tell you the volume as well. But we used to use the Swan-Ganz catheter with this wedge pressure to find out how good the left heart was working and see how much volume somebody had on board. Oxygen delivery. We will blow past this. Lactic acid we already talked about. If you’ve got someone who is hypotensive, and it could be shock, what would you look for? Well, primary labs you don’t necessary worry about. What do you worry about for a patient history? What do you want to know? What meds they’re on? Have they been eating? Have they been pooping a lot? Has the poop been diarrhea? Has it been blood? These are things that help you and help us when the he gets there.

You guys tell us this stuff all the time when you’re dropping people off. He pooped a lot of blood, because I have to hose out the rig I can tell you that right now. You’re telling us this. So he could be hypovolemic. Could be septic. They’re feverish, they’re hot. You’ve got to know if someone has got somewhat of an infection. They were in the hospital and had some kind of surgery.

And now that side is oozing with some pus. It doesn’t take rocket science to go, there could be an infection there causing the hypotension. So some of these things are just painfully obvious as a possible source. Things to think about. Cardiogenic is harder to see, unless they have a known CHF. Cardiogenic shock and CHF are fairly similar, fairly close. Cardiogenic shock tends to be, you weren’t expecting it. Somehow the heart took a shot, took an unexpected turn. CHF tends to gradually come on. They didn’t take enough Lasix. They’re already on treatments more than likely. Obstructive causes. Trauma, that’s obvious. GI bleed tends to be obvious. Intractable diarrhea tends to be obvious. Delivery or miscarriage, all these things are going to be obvious. You will know these upon picking the person up. Get them some fluids on board. Cardiogenic causes. MI, that’s obvious.

Like boy, I did an EKG and it’s tombstones. If the pharmacist can recognize it’s an MI, you guys can too. Trust me. An arrhythmia, you can recognize that. Acute heart failure, taught to recognize. If it’s an unknown heart failure, it is tough to recognize. So then you’re looking at some of those other things and weeding out. Well, they’re not bleeding to death. It’s a guy. He didn’t have a miscarriage. You go through all the other things. Valvular disease. You listen to the heart and it seems like one is really loud or regurging really well.

If you can hear it without the stethoscope, that’s probably the problem. If you hear the swish, swish of the heart without the stethoscope, that’s a six out of six murmur if you’re looking at the grading. Yeah. That’s where it doesn’t take much. That means their valve is pretty much shot. Sepsis. Bacterial, fungal, or viral tends to be the cause. Things you need to look for. Very quick facts– and again an aside. Brought you through all that terrible stuff that you rarely look at to get you to some of the stuff that you do look at. Your best vasopressor in the world within normal limits– fluids.

If blood pressure is low, the best thing you can do is give them some fluids. As long as they don’t have CHF. Even if you give someone 500, even with CHF, that ain’t gonna do much of anything. They’d have to be so brittle of a CHF person that you– to put them into full failure, they’d be living in the hospital on IV drugs. Trust mt. So you’re not going to hurt anybody with 500. Maybe not even a liter. Whatever your protocols are. Your best pressor in the whole world is always fluids. Always. Catecholamine receptor is less responsive when the patient is acidotic. That’s a physiological fact. So let’s say you have to start somebody on a pressor and you know they’re acidotic.

It may not work real well. Let’s say someone is coding. Let’s say you come upon somebody who has already been coding and somebody is doing CPR. And you give them some epi. And it doesn’t necessarily work right. They’re probably acidotic. Even though somebody is doing CPR, and it’s great CPR, it’s not as good as the heart is ever going to be. They’re gradually getting more and more acidotic.

You give somebody a milligram of epi, the body will respond at less than a milligram. I can’t tell you how much less, but it’s less than what it would normally be. So maybe the next epi may work. I’m just letting you know some of these things. If something goes down in front of you. Like they were fine and all of a sudden they go down in front of you, that epi may work. Because they’re not maybe as acidotic. So some of these physiological facts may help you to know maybe I need to work this a little longer. Maybe I need to keep doing the things I’m doing to get to that same endpoint. May need ludicrous amounts of catecholamine vasopressors. When I’m talking to some of my pharmacy students and I’m like, OK, let’s say I want to start somebody on an epi drip. They’ll want to start them at two.

Normally I would like two. But if they’re really acidotic, no. I don’t want to start them at two mics a minute. I want to start them at four, eight, something. Or titrate it quickly, knowing that their body is not going to see the same amount. So it helps you to know, I need to move faster with these drips, then slower. Because the person is probably acidotic. So some of these are just tricks of the trade.

Just things to know physiologically. Once you know that, you can get somebody better, faster. What you have learned about heart failure really will apply in this cardiogenic shock stuff. It just applies. What I ask myself when I’ve got somebody who’s hypotensive, my first question is, is the heart OK? Is it a pump issue? That’s always my first question. Because the other stuff is obvious. You’re seeing blood fall out of somebody, yeah that’s obvious. I know it’s hypovolemic shock. I don’t even have to ask is it a pump issue? Because that’s something that’s going to kill them right away. Is it an arrhythmia, is it somewhat like that? Is the heart OK? Heart seems like it’s OK. All right. Then I’m looking hey, is the piping OK? Is my vasculature OK? And is it a supply issue? Supply issue is always the last for me because it’s obvious.

They’ve had a miscarriage, they’ve had something. It’s so obvious, it seems. Not always. The GI bleed that bled out well before you got there and he cleaned himself up. He bled out so much that he doesn’t have much more to give. We start giving him fluids, all of a sudden he starts going again. Oh! That’s why he’s hypotensive. I thought it was something else. It wasn’t obvious. Have I seen that? Yes. It wasn’t obvious until you get the fluids back in him. Let’s talk about some of these drugs that you can use. Yay. Dobutamine. You don’t have access to it immediately on a rig, I’m assuming. But you can pick somebody up who’s on dobutamine. Dobutamine affects catecholamine receptors, so obviously it is affected by acidosis. All it does is help the heart squeeze. Dobutamine just affects the beta. Going through all this. All it will do is have the heart beat faster and stronger. That’s all it does. Yay. That’s great. Right? Downside is can produce hypotension. Whoops. You know I don’t want hypotension. Right. So you normally are not going to dobutamine itself. Rare case would CHF. What happens is you’ve got stretch receptors on the aortic arch.

Once they feel that pressure that activates them, they relax their vasculature. If you’ve got CHF, they’re already stretched out. You can give a CHF patient dobutamine. They won’t respond like that. They’re already stretched out. You see CHF patients getting dobutamine boluses, maybe even at home. It can happen. Dopamine. Dopamine’s effect is three stage. It depends on your rate. Going back to dobutamine. You can still use dobutamine as long as you take into account their hypotension. So if you put on another vasopressor that’s going to block that hypotension. Put on norepi, put on dopamine. When do you want increased contractility? When do you want the heart to beat better. When in those shocks do you want it to beat better? Cardiogenic shock. Which granted, you might not necessarily 100% know. But we may finally figure it out. I’ve actually done this. I don’t have these monitors to find out if they’re in cardiogenic shock.

But I”m watching their pulse ox get better when I give them a slight bolus of epi. Hey, the pulse ox will get better, then it falls off. The pulse ox will get better, then it falls off. Because I’m helping the heart beat a little better, then it falls off. I’m like, I think it’s cardiogenic. Should give some dobutamine. Doesn’t work all the time, but when you can see it. Dopamine has an effect that’s based on your rate. Do you guys have access to dopamine? Yes. You know the various rates that it’s at will give you different effects. All right. So at low dose we used to call it renal. We don’t do this anymore. It in theory would help the kidneys be supplied. It doesn’t. In practice it doesn’t work. So anybody that says they’re doing renal dose dopamine, they’re wrong. Intermediate rates, 2 to 10, it stimulates the beta. Which just means heart. So you get increased contractility, cardiac output, your heart’s beating better. And you also get better perfusion all around in your heart. So between 2 and 10, you’re really looking at kicking the heart better. You don’t really get that hypotension like you do with the dobutamine.

That’s why dopamine is a little bit better when you’re looking at just cardiogenic. You can go anywhere between 2 and 10 and get that almost same response you get from dobutamine. Almost the same response. Not fully. At high rates, now you’re clamping. Any time you see alpha, that is vasculature clamp down, or causing hypertension, or trying to increase someone’s blood pressure. So you get less of that beta, you get more vasculature squeeze. So you get less heart kick, more vascular squeeze. Let’s say I don’t have cardiogenic shock, let’s say I’ve just got septic shock. So the vasculature is big. Instead of garden hose, I’ve got the fire hose. Higher dose dopamine. Don’t start at two. Don’t start at ten. If you know it’s not cardiogenic. If it’s sepsis, start at ten. Very high rates, then you’re really actually decreasing renal blood flow.

That’s all you’re doing. Epinephrine. We all know epi, epi boluses. Anybody know how we came up with a milligram for code purposes? How we cam up with a milligram? Anybody? It’s the dose that they would use to restart a heart, on average, when they did open heart surgeries back in ’60s, ’70s, whenever it was. So kind of like a dose on average that would help kick start a heart that they had stopped. So that’s how we came up with a milligram. Is it really science that it’s a milligram? No. It might even be weight-based. Who knows. We haven’t really found their science. Because it’s tough to do a drug study on people dying. It’s tough to get the volunteers, know where the volunteers are. And you definitely can’t get college students to sign up for near-death experiences.

They find that bad. Any time you see alpha, think of vasculature squeeze. Any time you see beta, think of heart squeeze. This squeezes both. Alpha, so you get vasculature squeeze, and you get the heart to kick. Epi is great for getting the heart to kick good, and also to get the vasculature to squeeze. Downside is, if you’ve got a sick heart, yay, I got that to squeeze better. Wait, I’m working against this resistance. You can actually make a sick heart sicker. Because yes, you got it to beat harder against a lot more pressure. It’s like taking your water pump that’s not quite good in your car and flooring it.

It always works better. Your pump is probably pumping faster. Until it dies, because it’s probably going to. Because it was already weak to start. You mechanics out there, I’m trying to give you a visualization. So epi is good when you look at getting the heart to work. But think about the effects afterwards. You will make a sick heart sicker. So as long as they don’t have a cardiogenic issue, epi is not poor. Cardiogenic issue, you’re going to make it worse. You’ll notice it. They look better, then they tail off quick. Start thinking maybe the heart is sick. Maybe I need my dopamine at 2 to 10. Norepi is epi-like. Its alpha and beta gives you that vascular squeeze. Uses that beta, but a little less tachycardia. So a little less squeeze on the heart.

But same thing you get with epi, you pretty much get with norepi. You don’t have that access to you in the rig, but you’re transporting patients. Sepsis protocols, norepi is the drug of choice. Phenylephrine is another drug you don’t have on the rig, but you may be transporting. All it does is affect the alpha essentially. It doesn’t do anything at all to the heart. So you just get vasculature squeeze. You can increase someone’s blood pressure. It doesn’t do anything to the heart at all. If they don’t have a sick heart, fine. They’ve got a sick heart, you made it sicker really fast. Because it doesn’t do anything for the heart at all. You just stressed the heart out. Follow? Everyone’s with me? Boring as heck, right? Staying awake? Wish I had my amphetamines to spread now. Vasopressin. You have vasopressin available for you, right? Vasopressin does not affect the catecholamine receptor at all when it’s working.

So is it affected by acidosis at all? The answer is no, if you wish to look ahead. Remember I said your catecholamine receptor is less responsive when you’re acidotic. Your vasopressin is not. So say you come across somebody who has been down, someone’s doing CPR. You don’t know how long they’ve been down. V-fib, V-tach, whatever. You shock them, certainly. They’re still in it. Your assumption, because you don’t know how long they’ve been down, could be that they’re acidotic. Your protocol says reach for epi. Maybe reach for vasopressin. Because it will work the same potency no matter what. Downside is, if it’s a sick heart, you’ve caused a lot of vasculature resistance, a lot of stress on that heart.

And you haven’t helped the heart at all. Because it doesn’t do anything for the heart at all. That’s the give and take. Works no matter what. Acidotic, nonacidotic, doesn’t matter. But if there was a heart issue– you don’t know if there’s a heart issue. Obviously you think it’s a heart issue because the heart’s not working well. But you don’t have to worry about, hey, they’re not getting the full thing. So trying to give you some hints when you’re out in the field doing what you’re doing. There’s all that alpha, beta stuff that I talked about. You kind of link the drugs to where they are affecting. That’s for your own benefit when you go home. A loose diagram of what the drug’s alpha was affecting the beta in that visual graphics look. So you’re going to link it up to where is it working. Because you’re going to clamp down on any of these. You’re clamping down on something. You’re even clamping down on gut and stuff like that. Until you clamp down so hard, so long– we have some patients in the ICU, we start to worry about, are we starving the gut of blood supply because we’ve been clamping down so long.

It can cause more damage with this stuff. Yes, their body is alive. But eventually we’re going to kill off something possibly if we overstretch stuff. Cardiogenic shock treatment. We need to increase their cardiac output, AKA index. Possibly increase or decrease there resistance. If they’ve got a sick heart, I’ve got to worry about how much resistance they have. Goal is, I want the cardiac index about 2.2. Granted you don’t have that index marker. I don’t have that index marker, either. But you can see that they’re delivering oxygen better.

You can just see that. And a CVP of 10 and a wedge pressure of 15. Same thing like CHF. Cardiogenic shock is like CHF. Luckily there was somebody back in the– well I don’t know when this was. Forrester’s hemodynamic classification, kind of did with CHF. They don’t necessarily teach CHF much like this anymore. But if you know what their cardiac index is and you know what their wedge pressure is, and you take this point right here and you put it on where they are. And you want them less than 15 and above 2.2, follow the arrows.

A cave man can do this. It’s not rocket science. It’s look at a graph. Some people don’t look at the graph and they wind up guessing and spit-balling and stuff like this. There’s science out there, and why not use it? So if you’ve got somebody who is not beating well. It’s almost like heart failure. Heart failure would be over here. Fluid loaded and heart not working well. Get their heart to work better. You can use dopamine, whatever, to get the heart working better. And you give them diuretics. You get them over here. What about in the field? You’ve got someone who has bad CHF? Where do you start? Where do you start? You start nitro? Nitro moves you this way too. Where you want to be. That’s why you start nitro. You’re decreasing that resistance on that heart and having the heart work a little bit better. Supplying blood to the kidneys so they can actually pee. That’s why you’re doing nitro.

I can show you a graph why you’re doing nitro. Do the nitro to have the heart beat better. Before you do, if anybody has a diuretic that they’re able to give, do not give the diuretic until the nitro’s been on for like 10 minutes or so, please. Have the heart beat better and supply the kidneys before you actually give a diuretic. Or else the diuretic is not actually getting to the kidneys like you want it to. Have the kidney supply be better before you give the diuretic. There are some units out there that have diuretics. Start the nitro, let that run for a little bit, then do a diuretic. Ideally. There are ways that we can actually dose stuff once we know some of these numbers. That’s why I’m telling you some of these things. Any questions on cardiogenic shock stuff? Realize if you stress the heart with the resistance, you’re going to make the heart sicker.

But you need them also to have a good blood pressure. Yes. I don’t have a good answer for you. You give them a lot of fluids, that’s not necessarily your friend either. I know. I don’t have a good answer for you. Start with dopamine. Start with some other stuff like that. Dobutamine sounds good, but you’ve got to cover for that reflex hypotension. Septic shock. There’s other guidelines out there as well. Don’t have to even think about this stuff. Make sure they have enough volume. I’m really over-explaining this. I’m making it where a doctor will punch me in the face that it’s too simplified. But it is mostly true. If I take a dirty, disgusting nail and scratch your hand, it gets inflamed right? Why? What? [INAUDIBLE] And your white blood cells need to come out and fight it, right? So it gets inflamed to limit, to try to enclose that exposure, and to get the white cells there. Now let’s say I put dirty and disgusting stuff in your vessels.

What does that do? Same thing. They expand out. That’s really what’s going on with septic shock. Heart’s fine, the volume’s fine. Vasculature just got really huge. OK. Well how can you fix that? Best fix in the whole world– fluids, fluids, fluids, fluids, and fluids. Until their CVP– granted you don’t have that monitored. I don’t necessarily have that monitored until the doc puts it in. Until their CVP is about like 10. Is somewhere between 8 and 10. But it’s going to be a while. It would be a couple liters in before they may come close to that. Unless of course they’ve got CHF. You’ve got somebody who’s history is like, they had an infection, they have hypotension, you can get a couple liters in probably, to get their fluid up. Because the garden hose that was good, now they’ve got the fire hose. The reason why? The bacteria is in there.

Your body is doing what it should do. It just happens to be, oh yes, we also need blood pressure. Oh darn. That vicious cycle thing we need to. Break Make sense, what’s going on with septic shock? CVP less than eight, you give a lot of fluids. We look for mean arterial pressure of 65. Anything less than 50, you’re not supplying enough blood. 65 is really your best bet. If their heart rate is greater than 100, which most of the time it is, if you’ve got somebody with low blood pressure and their heart rate is not greater than 100, they might have a drug onboard causing that, like a beta blocker.

More than likely it is. So you would add norepi. Norepi is your drug of choice for sepsis. So if you’re picking up somebody who is septic and they’re not on norepi, and they’re somewhat tachycardic, I’d be suspicious why they’re still on norepi. Not that you need to ask for something else. Hopefully you’re just transporting from one place to another. We realize that person is not on probably the best pressor they should be on. There might be a reason they’re on that one. But I’m just letting you know it’s not ideal for you. If the heart rate is less than 100, it could be because beta blocker, something else, or just because.

You could give them dopamine. And you’re really looking for the mean arterial pressure, like I said. When you get to a point where you get their blood pressure stabilized, and they’re still– you get a mixed venous, this gets very complicated. I’m telling you too much. Now we’re really to the point where we’re fine tuning. Where the person is going to live, but boy, we could make them so much better. You can possibly add just a little bit of the dobutamine to have the heart beat better to actually get a better supply. It’s like a recipe. You follow the recipe, the person’s better. Sometimes people don’t follow the recipe and then you have to pick them up and maybe take them somewhere else. Or whatever. Just trying to let you know what is normally the case that should occur. If you pick up somebody who’s in septic shock, there are things you should be seeing unless there’s some other comorbidity, some other reason why.

What do I want you to take away from this? You can give epi. You can give dopamine, all those things. Realize the difference on the dosing of the dopamine will cause different effects. A little more cardiac and then a lot more vasculature. You can stress out the heart. Clamping on the vasculature is not helping the heart. Epi does help the heart, but only for a short period of time. You can actually overpower that. Back in the day, sometimes people would do high dose epi. The reason why it fell out of favor, and it really wasn’t in favor to begin with, is yes you can get somebody back because you overpower that acidosis. You could see the reason why they wanted to use high dose epi. The person’s been acidotic. I want to give them more epi to equal a milligram. They don’t know how much more to give them, but they give them more.

But it causes so much resistance, you’re going to cause someone’s heart to fail. So that’s why you really shouldn’t do it. As long as you understand [INAUDIBLE] of why some people do it. Any other questions at all? That’s stuff you already knew? Trying to explain the why. Granted yes, your med person told you, because I said so. And maybe explained it. I’m trying to really give you the science why. So if you have to go off reservation, or are asked to call, maybe you have an idea what you can ask for. All right. That’s it. I don’t have anything else. I’ve bored you enough..