LUIS DIEGO PACHECO: This talk, what we're going to talk about is sepsis. And I have no interest in talking to you about like what you hear all the time, which is seven slides on chorioamnionitis and the bugs that cause chorioamnionitis and the antibiotics for chorioamnionitis. Or for pyelonephritis or for endometritis, because you all know that better than I do, and better than anyone else.

The main issue here is most of the people that deal with obstetrics know what to do with the infection, know what needs to be drained, which antibiotics you need to give and so on. But when the patient actually starts being a little bit different than the rest and you start having some hypertension, and you start having some leaky lung, and the patient develops pulmonary edema, and the kidney stops working and you become oliguric, then people start feeling a little bit uncomfortable about fluid therapy about vasopressors, and so on.

And that's what we're going to talk about. And we're going to talk about here is actually reflects the latest guidelines on how do you treat sepsis. If anyone has any question as we go just feel free to raise your hand and ask it and then we'll clarify it if I can as we go.

So these are actually the main objectives is going to be. First of all, understand how do you define currently sepsis. And what is the pathophysiology of sepsis, and then know what to do about it. And then acknowledge how do you apply these things to pregnancy. I think we need to stop, and this is something that it's going on nationwide now, we need to stop this thing about well, there's no evidence that works in pregnancy. Or there's no there's never going to be evidence that any of this critical care interventions actually work or don't work in pregnancy, because all the trials exclude patients.

There is no reason whatsoever to think that the use of vasopressors is going to be different in a pregnant patient than in a non-pregnant patient. There's no reason to believe that one fluid which is harmful for non-pregnant is going to be non-harmful for the pregnant, and so on. We just need to start learning about these things, people that take care of high risk pregnancy need to start. Because there is a huge lack of intensivists in this country, and it's just going to get worse and worse and worse and worse. You're going to see a lot of hospitals that are going to have the surgeon and the OB person taking care of these sick patients because there is not enough intensivists for all the hospitals.

So if you go into an intensive care unit in this country, if you're going to die of something it's going to be sepsis. The mortality of sepsis actually has is extremely high. Couple of things have dropped the mortality, but not enough. And still if you get severe sepsis you have like a 20% to 30% chance of dying. And if you have septic shock you have probably around a 40% chance of dying. So it's still pretty high.

And the important thing here is early diagnosis and early intervention. And when I talk about early intervention it's as simple as giving an antibiotic fast, and giving two or three liters of fluid fast. In most cases, that actually makes a huge difference. As opposed to just waiting and not giving the fluid for one or two hours, that's going to actually worsen the outcomes.

So in the past this used to be the definition of sepsis. It used to be like the systemic inflammatory response syndrome, right. So it was actually proposed that you had systemic inflammatory response syndrome if you have two of these four things. So if you have tachypnea or you have tachycardia, or you have a change in your white blood cell count, or if you actually had a change in your temperature then you would have two of these. We'll say you have systemic inflammatory response syndrome.

This is extremely sensitive, but it is extremely nonspecific, right. I mean, if you look at patients, any patient I'll bet you that you just did surgery on yesterday, you go and round on them, they're going to have SIRS. Because if you have a heart rate of 92 and you have a white blood cell count of 12,100, then you have two criteria, and you have systemic inflammatory response syndrome. So if you actually have two of these you're say to have an inflammatory response syndrome, correct?

Now if this systemic inflammatory response syndrome happens in the setting of an infection, or you suspect that this patient has an infection. For example, you go in there and you see someone with pyelonephritis, clinically you think they have pyelonephritis. And they are tachycardic in the 110s, and they have a temp of 38.2, then that is sepsis. Because it is systemic inflammatory response syndrome secondary to an infection, right.

Now this actually changed, part of this is still that sepsis what we talk about, right. And still many people use this. That's sepsis, then what's the difference between sepsis and severe sepsis? Severe sepsis is when you have sepsis with an organ dysfunction, like one organ failing.

So which organs can fail? Well, I mean there's some obvious ones. For example, if you have sepsis and you start having trouble breathing then you have pulmonary edema, right. That's usually called noncardiogenic pulmonary edema because it's not necessarily a problem of the heart. It's not that you have an ejection fraction of 5%. It's because if you have an infection, you have pyelonephritis, the inflammation is not localized to the kidney, right. You have a massive inflammatory response. And these neutrophils, all these inflammatory cells, they injure your endothelium.

Same thing that happens in preeclampsia, right? You have diffuse endothelial, that's why you third space. That's why you become edematous. Well you third space everywhere in the body. And you third space in the lung and you start having some tachypnea. So that will be your lung failing.

But then also, there's a lot of other things, for example, obviously if you become oliguric then your kidney's failing already because he's been hypoperfused. Because if you're third-- remember in sepsis, what happens here is this massive inflammation produces a lot of substances like nitric oxide and so on that are going to vasolidate you.

So you're going to be hypertensive because you're a profoundly vasodilated, but on top of it your endothelium is injured. So your third-spacing your albumin, and that's pulling water out and plasma out, right, fluid out. So you're hypovolemic and that's why you hypoperfuse all the organs. So you hypoperfuse the kidneys and you become oliguric. So that will be your kidney failing.

If you hypoperfuse your gut how does that manifest? Ileus, so if you have someone with an unexplained ileus it can be a marker of sepsis. If you hypoperfuse your kidney, I mean your liver, what are you going to have? You're going to have elevation in the LFTs, you're going to have elevation in bilirubin. So that's going to be your liver failure. If you hypoperfuse your brain what do you get? Confusion, that's why when you get called to the ward and someone is confused the first thing that's got to come to your head is going to be hypoxia, hypocarbia, and sepsis. Because you hypoperfuse, and so on.

So if you have any organ failing then that will already be severe sepsis. If you have thrombocytopenia or you have a prolonged in your INR or your APTT, that's your hematologic system failing now. Why does it fail? Remember that if you have diffuse endothelial injury, when you injure the endothelium you exposed the subendothelial collagen, correct? And if you expose--

[BACKGROUND LOUD SPEAKER]

All right, if you expose the subendothelial collagen then what are the platelets going to do? They're going to start adhering to it to try to create a clot, right. And then it's going to activate your clotting cascade, you're going to start developing all these little clots all around your body. How do you call that?

AUDIENCE: DIC.

LUIS DIEGO PACHECO: DIC, OK. And so that will be your DIC and your hematologic system failing. So as you see, any organ pretty much can fail. So that will be severe sepsis, you need one of those. Septic shock is going to be that same patient that you go in there, you give them fluid, and you cannot bring their blood pressure up. So then what do you need to do? Give them vasopressors, something to squeeze the vessels. Because the main problem here is the vessels are dilated. OK?

So that's this concept still most people use them. What people don't use is the serious thing that I told you before. So nowadays, the definition of sepsis is-- [MUSIC PLAYING] I like that. Evanescence, right? Anyways, the thing here is nowadays what they tell you is sepsis is-- the important thing here is not to sit there and say let me just sit here with this checklist to see if you have sepsis. And then like when you go to 20 boxes then oh, you have sepsis, and now the patient is very sick. The idea here is to think it, early treat it early.

Just like preeclampsia. I don't know if you guys know, but you know that you don't need proteinuria anymore to diagnose preeclampsia. That's coming in The Green Journal next month. The five gram thing for severe preeclampsia is gone. It's not a criteria for severity. you can diagnose preeclampsia in the absence of proteinuria. That's the same principle.

There's a lot of patients that-- a lot of people that sit there and say, well, you have this headache, and you're hypertensive. And you have epigastric pain, and nausea, and vomiting, but you don't have protein. So go home and then when you have the proteinuria then you have preeclampsia. And that happens, that happens a lot. So proteinuria is out of the picture and you're going to see it in The Green Journal next month.

So same here, here the idea is if you suspect that someone has an infection, someone comes in postpartum and they just had a c-section a week ago and you think they might have an abscess and they look bad. The definition of sepsis is going to be you suspect an infection and you have some of this, and that's how it says, some of this. It doesn't say you need to have two, three, four, five, six, or seven. You don't need to learn these by heart. Everything actually makes sense. It obviously, I mean, the systemic findings like fever or hypothermia, tachypnea, so it's kind of the same, the inflammatory response syndrome.

Positive fluid balance, so if this is someone that came in and you already gave them two liters, and they're still not improving their blood pressure, then what we just talk about is happening. You're just third-spacing the fluid, and the fact that you're becoming, requiring more and more fluids should alert you and say this is not simply dehydration. This is probably have a leaky vasculature.

Abnormal white blood cell count, these things are just marker, source of inflammation, you can get them if you want to. Hypertension, low system vascular resistance, decreased urine output. So you have your kidney failing, or you have someone that actually has elevated liver enzymes like we talk, or thrombocytopenia, or the normal clotting times, or hypoxemia. Or they are confused, or they have an ileus, any organ that you think what will happen if this organ gets hypoperfuse. Starts failing, then you say this patient has some of these that will go with infection.

Now in terms of, just feel them. I mean, if you just look at their extremities and their extremities are actually cold and modeled, then they're being hypoperfused. Or they have a capillary refill of less than three seconds they're being hypoperfused. The physical exam is the most important thing, right? And then if you get a lactate level. You can, if you don't have to make the diagnosis. Once you have sepsis you're going to have to get it because it's going to guide your therapy.

But the bottom line is, just look at the patient and if you see that some organs are failing, the GI tract, the liver, the lungs, the kidney, et cetera. If you see that something is actually wrong in the setting of inception-- of infection, then just go ahead and make the diagnosis of sepsis. You probably will not kill anyone by giving broad spectrum antibiotics and a couple of liters of fluid really fast. But if you don't, and it was sepsis, then you will regret it. Because once this gets ugly it's very hard to improve it.

So if you, once you actually have the patient, and let's say this is the patient that had the-- came post c-section day 7, and you think they have an abscess. And their blood pressure is 80/30. So you say, well, this is likely an infection. So how do you start treating them?

So this is going to be pretty much the same for every patient. And everything I'm going to tell you here comes from critical care literature. It doesn't really come from the obstetrical literature, but there's no difference. There's pretty much no difference. Remember even if most of these patients are going to present postpartum, as you know. The vast majority of them. But even if they're pregnant, if you don't treat the patient you're going to end up with both mom and baby dead.

You cannot just hang out with a mean arterial blood pressure of 30 and expect the baby to survive, and say I'm not going to give you vasopressor because he might hurt the baby. Right, I mean you need to improve the hemodynamics of the mother to improve the perfusion to the baby. OK?

So the things you're going to do is get as many cultures as you can before you start the antibiotics. Now don't delay the antibiotics. If someone comes in let's say from the EMS with a peripheral line already working and no one can get blood cultures after 20 minutes of poking, go ahead and start the antibiotics and then get the cultures. But ideally, get all the cultures before you start the antibiotics. You're going to start with broad spectrum antibiotics.

And remember there's more than ampi/genta/clinda. I mean obstetricians and gynecologists tend to use these antibiotics, everything is ampi/genta/clinda. Those are not even good antibiotics. And gentamicin hurts your kidneys, and then clindamycin, for example, it's not even, doesn't even give you very good coverage for anaerobes. Metronidazole gives you very coverage compared to clindamycin according to the infectious society Infectious Disease Society of America.

So there's other antibiotics, and we're not going to talk about antibiotics, but just know that there is a lot of other options. So start broad spectrum antibiotics and then surge control. If this patient comes in, has an abscess, then drain it. Drain everything that needs to be drained. Always choose the least invasive ways of draining. So a CT-guided or ultrasound-guided drain is way superior than opening the patient and draining the abscess.

OK, so now here comes the problem. Not necessarily the problem, this it's actually easy. You gave the antibiotics, you got your culture, you gave your antibiotics, and you already drained the abscess, let's say. But then the patient doesn't really look good. So the name of the game in sepsis is you need to resuscitate early, and the first line of resuscitation is going to be fluids.

Now the main problem here is going to be, there's three components in the resuscitation. Fluids, vasopressors, which are going to be the medicines that will work mainly by squeezing your blood vessels and increasing your systemic vascular resistance, and then inotropes. Which are going to be the medicines that will increase the cardiac output.

So we'll talk about them and all of them together, but if anyone has a question just let me know because see if we can go back and see. This paper here is a paper that was published probably 13 or 14 years ago, which is the early goal directed therapy. And this is actually in the emergency room. And what they did was they got these patients that came in with suspected sepsis and they randomized them into this protocol, or standard of care.

So the patients that got the standard of care that was kind of unfair. Because if you go to an emergency room you do know how it works. You go there, you sit there for a while, and then you get seen by the intern. And then the intern actually comes to the resident, because intern doesn't know what to do. Talks to the resident, the resident doesn't know what to do. Calls the fellow, the fellow doesn't know what to do. And then the fellow does-- when someone knows what to do, it's been already three hours. So there's a lot of delay in care.

Versus the people that actually came here, they had an ICU doctor come and see them right away. So maybe just that accounted for the difference. But this actually was accepted and pretty much everyone does this. So this applies for the first six hours of sepsis. You come to the hospital, if you're within the first six hours you probably should be doing this.

We're going to talk about this because this is useless, the central venous pressure is useless to predict fluid responsiveness. It's completely useless. You might as well get an aluminum level to see if someone needs fluid or not. It's as useless as that. Having said that, the guidelines still say you should use a CVP just to make things simple. But hopefully by the end of the talk you'll know that this is not that good.

Patient comes in and then you're going to, they're hypertensive, you're going to give them fluid. Which fluid are you going to give them, crystalloids or colloids? Remember that the crystalloids, I mean, we all have the same ones, right. Either normal saline, or lactated ringers, or Plasma-Lyte. You can use either. And that is the first line recommendation for fluid resuscitation in sepsis. That's what the sepsis surviving campaign in the guidelines of 2012 tells you to use, crystalloids.

Now, if you say I want to use colloids. No problem, there is no difference in outcomes. You're not going to save anyone's life by giving a crystalloid or a colloid, and whoever tells you that albumin is better than normal saline is lying to you. The literature does not show that.

Now out of the colloids if you say, no, I don't want to use crystalloids, I want to use albumin. You can use albumin, there is no problem with that. Do you guys use Hespan, hydroxyethyl starch? All right, don't use it anymore. Hespan, we use it a lot. But in sepsis it's been associated to increase mortality, mortality and kidney injury. So it should not be used in sepsis. And somewhere around there you're going to see the reference there.

There's actually two papers in the New England Journal of Medicine in the last year addressing Hespan. So don't use Hespan. So you're going to give them fluid, don't make your life complicated. Either a crystalloid or albumin, OK.

Now the problem here is going to be when do you stop giving fluid. Because you start giving fluid, fluid, fluid, fluid, and these patients might need a lot of fluid. But if you give them more than what you need you're going to hurt them. If you give them less than what they need and you start of a vasopressor you're going to hurt them as well, right.

So what they did here was they started giving fluid and they used a central venous pressure. It is easy to use a central venous pressure because it's an absolute, it's a number. That's why the guidelines still use it. Because it's very easy just to write it there, this is the number. So they will say give fluid until you get a CVP of 8 to 12. And the idea here is going to be to maintain a mean arterial blood pressure of more than 65.

So your first goal initially is going to be give fluid to achieve a mean arterial blood pressure of 65. A urine output of more than half a cc per kilo per hour, OK. And that's pretty much it. That will be your immediate goal, to give fluid. And still the current Surviving Sepsis Campaign guidelines tell you to use the CVP of 8 to 12. They do make an acknowledgment afterwards, and we'll talk about it later. But anyways, you're going to give fluid until you get this.

Let's say you give fluid, you get a CVP of 12, and your MAP is actually more than 65, and your urine output is more than 0.5 cc's per kilo per hour. So then you're happy there with fluids, right? Now if you give the fluids and you reach this arbitrary point of 12, and you have not achieved a mean arterial blood pressure of 65. And we talk about 65, that's an arbitrary cut off. All the literature in sepsis tells you to maintain a mean arterial blood pressure of 65. That's just as arbitrary as it gets.

Because it's the same for an 80-year-old who has atherosclerotic disease, or a 19-year-old who is otherwise healthy. The guidance says you use, an MAP of 65. You and I know that probably the person who is 80 will need a higher MAP to maintain perfusion to his organs because he has all these vessels with atherosclerosis, versus the young person that probably needs a lower MAP. But it just makes things too complicated, so 65 is pretty much what's accepted. And that should be your angle.

Now if you give the fluids and you cannot achieve that then what do you do. You're going to give them vasopressors, like Levophed, norepinephrine, to squeeze the vessels. Does make sense so far? OK. Now regardless of if you were able to maintain an MAP only with fluids, or if you reached 12, this was below 65, and you gave the pressor, then they did this measurement, which is called the SevO2.

And the SevO2 what it is simply, how saturated is the hemoglobin that comes back after it oxygenates all your body that comes back here into your neck. Obviously you need a central line for that which you have already placed because you need a central line for the central venous pressure, correct? Does that make sense so far?

So the principle of this SevO2, this is easy to understand. All these things if you just don't see them often it sounds like, oh my God, this is so complicated. It's easier than all the trisomy 21 thing there, the quad screen, and the triple, the fifth screen, and all those. This is way easier.

So imagine that blood comes from an artery pumped by your heart, and then the hemoglobin comes here. And then all these these little lines are like oxygen. So these hemoglobin here normally leaves your lungs, what saturated like 100%, and then it goes to your left atrium, left ventricle. And you pump it to the tissue. This is the red cell coming here. As it goes through the tissue the tissue is going to extract oxygen.

Now normally you only use like 25% of the oxygen that goes to your tissues. The body's too smart. So you have 75% of the oxygen that you deliver, you don't need it. You're just going to use it if you run in trouble, if you actually get hypoxic or whatever. So when this red cell goes here and the tissues extract the oxygen, and the red cell comes back all the way into your neck here, the superior vena cava going into your atrium, before you go into the lung. The saturation of these hemoglobin should be more than 70%. Does that make sense?

So it was saturated like 97%. It delivered the oxygen that you needed. And then when it comes back still you have 70% saturation Does that make sense? Now, the idea of measuring this is that if this is lower than 70%, what it tells you is that there is ischemia going on in the tissues.

This is like if you're poor and they let you go into a grocery store, and you have your little cart there, and you're hungry. You're going to get a lot of food in there, right? You can just kind of get as much as you can. They give you one minute to get food. You're going to get everything you can. But if you actually happen to just have a huge meal and you're not hungry and you go to the grocery store. You go, you might get two things.

So same thing with the tissues. If the tissues are hypoxic, or hypoperfused, when that red cell comes through here it's just going to get as much oxygen and pull as much oxygen as it can. And then when the hemoglobin comes back here it's going to be 54% saturated. And what that tells you is you need to increase oxygen delivery to the tissues. Even if your MAP is 65, still you're not perfusing the organs. That makes sense?

Now, if you happen to have a SevO2 that is less than 70%, everything is easy so far, right. You gave the fluid, and then let's say you reach a CVP of 12, we'll talk about that in a little bit. And let's say the MAP is not good, you start to Levophed, now your MAP is 65. Everything is good, and I say, hey, let's send an SevO2.

Say the SevO2 comes back at 60%, you know it's got to be more than 70%. So now is, how do I improve oxygen delivery to the tissue? There's only two ways. Either increase the cardiac output, or increase the hemoglobin.

So in terms of transfusion, this protocol here within the first six hours of sepsis, only within the first six hours, tells you that you can transfuse to a hemoglobin of 10. So if they have a hemoglobin of eight you can give them two units of blood. This only applies for the first six hours. Once you hit the ICU or your OB antenatal special care unit, whatever that is, once you're there and it's been more than six hours, you would not transfuse unless you drop below seven. That's what all the guidelines say. Do not transfuse, because blood is bad for you.

We think we are increasing oxygen consumption with blood, that's not true. The blood in the blood bank that you have right now is not the same blood that your bone marrow produces. And it doesn't liberate oxygen, but that's a whole different topic.

Anyways, you can give blood or let's say you give you're still within the first six hours. Hemoglobin was eight, you give two units. Or you are past the first six hours and the hemoglobin is six. So you say, OK, it was less than seven I can give one unit of blood. Now your hemoglobin is 7.3, past the first six hours, or 10.1 in the first six hours.

And then you send another SevO2, and let's say it is 63%. So you increased it a little, but still you want it to be 70. So now you cannot give any more blood. What do you do now? Give a medicine to increase the cardiac output. It's called the dobutamine. So you just start them on a little dobutamine.

Low dose, like 2.5 to 5 mics per kilo per minute of dobutamine, that's going to make your heart increase the contractility, and it's going to increase the heart rate. And it will increase cardiac output and subsequently oxygen delivery. Does that make sense? So that's pretty much how you actually treat according to this. Yes, sir?

MALE SPEAKER: So that's one indication to use dopamine or dobutamine versus [INAUDIBLE]?

LUIS DIEGO PACHECO: All right so the norepi is mainly a vasopressor. So that one you're going to use here if you remain hypotensive despite the fluid. Then here you will do norepi. And that is actually, the current guidelines say norepi first line pressor, second line, epi. Dopamine, don't use it in sepsis. Should not be used in sepsis anymore.

So here you would use the vasoconstrictor, Levophed. Here remember that what you're trying to achieve is you already have an MAP, an acceptable MAP. What you're trying to do here is increase oxygen delivery. And to increase the oxygen delivery you don't need the medicine that squeezes, you need a medicine that helps contractility. And the best ones, the inotropes pure kind of inotropes, are dobutamine and Milrinone, that's it. And dobutamine is the one that has more evidence for sepsis. That makes sense? OK.

FEMALE SPEAKER: Why would you not use vasopressin?

LUIS DIEGO PACHECO: Come again, ma'am?

FEMALE SPEAKER: Why would you not use vasopressin?

LUIS DIEGO PACHECO: We're going to talk about vasopressin in a little bit. First line is Levophed, and we'll talk about vasopressin in little bit. It's a good question. All right, the question was why would you not use vasopressin? I was told I have to repeat that. OK.

So this is pretty much what we talked about. This is what we talked about and these are the references on how-- this is the paper here, the 2004 paper. That's the SAFE trial, that's the paper that shows that there is no difference between albumin and crystalloids. There is a subgroup analysis of that trial, saying that if you use albumin it might be better for sepsis. That's a subgroup analysis. That is the trial is negative and then people just sit there to see what actually will be positive so you can publish it again. You cannot make decisions based on subgroup analysis.

OK, that's what I told you about the Hespan. Don't use Hespan because it kills your kidney in sepsis. And you should have all those.

So we're going to talk a little bit more about fluids. The thing here is let's say you gave the patient three liters of fluid or four liters. And still your blood pressure is less than 65. And then you start Levophed, right, norepinephrine. That's pretty much what we've been talking about. Now people might stand there and say, and this happens every day, you stand there and you say, well, should I give more fluid or not. So if the patient needs fluid will certainly benefit from it. When you give fluid what's the one thing you're looking for?

There was a curve in physiology, remember the starting curve. That says if I give you preload you will increase your cardiac output. And remember the curve is like this, something like this, goes up like that. This is preload and this is cardiac output. So what I want to be sure is that the heart is on the steep portion of that curve. So that if I give you preload you will increase your cardiac output and that will increase your blood pressure. That's the only thing you're looking for when you give fluid.

Now, if the heart is on the flat curve, in the flat part of that curve, you will not respond to fluid. Doesn't matter if I give you fluid, I will not increase your cardiac output. Does that make sense? Yeah. So this is the problem if you give fluid to people that don't need it. That fluid will only third space. Remember in the setting of sepsis you have diffuse endothelial injury, you're third-spacing everywhere, right.

So all this fluid is going to go to the third space. And if I'm not going to increase the cardiac ouput then all I'm doing is just sending it to the third space. So you can get worsened cerebral edema, and pulmonary edema, heart edema. There's something we're going to talk about when we talk about hypertensive emergencies, there's something called diastolic dysfunction.

You can have a heart that squeezes perfectly, 65% ejection fraction. But it is, let's say, someone with chronic hypertension. The muscle is so hypertrophied, it has concentric hypertrophy, and it's not compliant. When you give fluid a normal ventricle will expand like this and then squeeze, expand and squeeze. Well if you have a thick muscle there then during diastole you cannot expand. And then the fluid will accumulate and backwards and you develop pulmonary edema.

That's called diastolic dysfunction. You cannot expand the ventricle doing diastole. So it doesn't matter if you squeeze well, you cannot relax. Same thing happens here if you give people tons of fluid that they don't need and they start third-spacing, just like you become puffy in your face and in your hands and in your feet, the left ventricle becomes edematous. And when it's edematous, it's going to be noncompliant. So it cannot relax during diastole, and when you give them fluid they develop pulmonary edema.

Gut edema, when you give tons of fluid that you don't really need you start third-spacing everywhere, the gut is not the exception. You're going see the third space through all this plasmic circulation, you start developing ascites there. And then when you have an edematous bowel it's, the perfusion pressure decreases. You develop an ileus, and what can you develop if all that happens together? Abdominal compartment syndrome, you can die from it.

And then if you have a wound you don't want that wound to be edematous because of excessive fluid, or a graft, or someone transplanted or organ in you, or a vascular anastomosis. So lots of fluid that you don't need is very bad for you. So the problem is if you use the central venous pressure that we're talking about, which is still in the guidelines as your endpoint of giving fluid, the problem is that both the central venous pressure or the pulmonary occlusion pressure, like putting a Swan a PA catheter in someone, they are useless to predict fluid responsiveness.

All these things are doing is just telling you what is the pressure in a certain part of the vascular tree. Central venous pressure you have a line that gets right there into the superior vena cava, right, where it drains into the right atrium. All it's telling you is what is the pressure there. So let me just give you an example. And there's actually trials, I think it's this one here, that actually shows that the positive predictive value of a low CVP or a low wedge, low pulmonary occlusion pressure, for predicting fluid responsiveness is 50%.

So out of the patients that you have there and they have a low CVP, let's say they have a CVP, the central venous pressure normally a zero to eight. Most people will say less than five or whatever, in these recommendations less than 12, you give fluid. But let's say someone has a CVP of four and they're hypertensive, everyone would say you need fluid.

All that is telling you is that the pressure right there in the right side of the heart is four mercury millimeters. So, yeah, the patient maybe might be dry, I agree with you on that. But let's just take the example of someone that has what we just talked about the heart, diastolic dysfunction, right. So imagine it's someone that has had three MIs. And they have a very fibrosed left ventricle. And that ventricle, when it's not muscle and it's just scar, it cannot do this. Fill and then expel, fill and expel, it cannot expand that much because it is all fibrotic. Right, that's diastolic dysfunction what we're talking about.

So you can have a CVP of three which will urge you to give fluid, and you will give the fluid. Well you're not able to recruit cardiac output because you cannot put that fluid inside the ventricle. So the ventricle will expand and it squeeze harder. Does that make sense? So even if you have a low CVP or a low wedge, same thing, how do you know that this is going to increase your cardiac output? That's the question.

You need to know before you give the fluid if you will be able to increase the cardiac output. And these measurements do not tell you that. So what people do right now to see if you need fluid or not are one of two things. Something called passive leg raising or pulse pressure variation. We're going to talk a little bit about pulse pressure variation, and we're going to talk a little bit of passive leg raising.

And this is the key here, passive leg raising. Especially you guys that have a hospital, you make a lot of money to how many deliveries you're making. You should buy these little devices to measure cardiac output non-invasively. And we'll talk about that in a little bit. And then you can know if you need fluid or not.

So let's just talk, when you-- let's say you have your patient that came with the abscess. There's going to be mainly two groups of patients. One is going to be the group of patients that are going to be intubated. Most patients that are going to be intubated for sepsis they're going to be in sinus rhythm. This is not a cardiac ICU. They can have AFib occasionally or something, but most patients are going to have sinus rhythm.

And they're going to be intubated, and they're going to have an A-line, right. Putting and A-line and is very, very easy, right, it's just like putting a peripheral IV. Well those patients that are intubated, and you are debating if you need fluid or not, those are very easy to know if they need fluid or not. And what you're going to do is you're going to do something called pulse pressure variation.

So this patient is going to be on a ventilator, is going to be in sinus rhythm. Because if they're not intubated and they are not in sinus rhythm this thing that we're going to talk about doesn't work. You need to be under a ventilator and in sinus rhythm. They need to be not triggering the ventilator. Triggering the ventilator means let's say you're on the vent, I put the rate at 10. But the patient is breathing 20. So on top of the 10 the patient is doing this, [DEEP BREATH] when the patient takes in inspiratory air for the ventilator senses and delivers a tidal volume.

So that will be triggering. How do you keep her from triggering? You just go to the bedside, increase the rate to 20, increase the tidal volume like to 8 to 10 mLs per kilo. So if it was 400 increase it to 600. And then you take over the breathing. Does that make sense? So the ventilator will give more than what the patient wants. And then you just sit there and in a matter of a minute the patient is going to stop breathing because the vent is doing more than what she needs. She's going to lose the desire to breathe because the vent is doing it for her.

That's a requirement. Because if the patient triggers the vent and generates a little negative pressure it's going to affect what we're going to talk about. OK, so that makes sense so far? And you need to have an arterial line. And if you meet these criteria what you're going to do is you're just going to look at the A-line tracing.

Say the red one on the monitor, right, when you have an A-line. And then this is what you're going to do. You're going to look. The pulse pressure is systole minus diastole right. So like everyone is 120 over 80, so your pulse pressure would be 40. So in an A-line the pulse pressure is going to be systole, that's the systolic pressure, minus diastole there.

So what you're going to do is, when the patient is on the vent and they're on the A-line, you're just going to look at the tracing. And if you look at this, look the difference between this one here, systole is really high compared to the diastole, and this one. The pulse pressure here is higher than the pulse pressure here. Does that make sense? The spike here is way higher than this spike. That means that during the respiratory cycle there is variation of the pulse pressure.

And that tells you with a positive predictive value of 80% to 90% that you need fluid. If the variation between one and the other is more than 13% then you need fluid. And if it is less than 13% you don't give them fluid. Two minutes just to talk about this, why is it that this happens?

When you have, if you're on the ventilator, when the ventilator fires right, and it actually gives you a tidal volume, that increases your pressure in the chest. When it increases the pressure in the chest the lungs are like sponges and they're full of blood. When you increase the tidal volume and increase the pressure inside the chest you squeeze those lungs. And when you squeeze that it's like getting a sponge where you're taking a shower, and then you see all the water come out. Same thing happens with the lung. You squeeze it, where is that blood going to go? To the left side of the heart.

Because that's the drain by the pulmonary veins. Go to the left atrium, the left ventricle. So the left ventricle gets more preload. And if he gets more preload it will squeeze more and you will have an increase in your stroke volume. Here you see the increase in the stroke volume. Versus during expiration when the tidal volume comes out, you're not squeezing the lungs anymore. The left ventricle lets less preload, and then you will have a smaller stroke volume. Does that make sense? So just by looking at these you know that you can recruit cardiac output.

And then the other way is, the other group of patients are going to be the patients that don't meet that criteria. And this is actually most of the patients you're going to have. These are patients that are in the postpartum unit, they have an infection, they're not that terribly sick. They are slightly hypertensive. You already gave them three liters of fluid. Since they're not on the ventilator, you cannot use what we just talked about.

So then you say, well, how do I give you fluid? How do I know if you need fluid? So the classic teaching is put a central line and get a CVP. Don't do that. We already talked about it, that doesn't work. So that's what I'm telling you since you have the money, then otherwise it's [INAUDIBLE] fault if you don't get it. There is a lot of machines right now that are non-invasive cardiac output machines.

The one we have is called the Cheetah. And what it is it works by a thing called bioreactance. And what it is is you just get these electrodes, they are like EKG pads, and you just put them here in the neck and in the chest. Put three electrodes there, and hook it to the machine and it gives you the cardiac output bit by bit. That's it.

Now a lot of people criticize these machines because they say, well, it doesn't correlate with the PA catheter. Well, the PA catheter is no gold standard. The PA catheter has a lot of problems. Plus, you're not really interested in what is the cardiac output. I don't care if the cardiac output is five and it's measuring seven. I don't care about that.

What I want to know is with that measurement that I have, I want to know if I can increase that some way before I give you the fluid. Meaning I can recruit cardiac output. Does that make sense? How can you do it?

Lay the patient in bed, like 30 degrees like all patients are in the hospital. And then you just hook the machine, and you get their legs, and you raise them like 30, 45 degrees for one minute. Normally you have up to 300 of blood, 300 cc's of blood in your legs. And when you raise them now you're injecting 300 cc's, it's like a unit of blood back into the central circulation. And look at the machine. And if you increase the cardiac output by more than 15%, one- five, 15%, then you need fluid.