Critical Care Paramedic 7: Hemodynamic and Cardiac Monitoring

So quickly we’ll just go through, finish up on some labs. I’ll be honest, a lot of it is what I would say– you don’t even draw some of this stuff in the emergency room, and it’s rarely drawn in critical care. It’s nice to know, not need to know. We’ll see how much of it is on the test. But just to kind of recap what we talked about last time, I introduced these terms “specificity” and “sensitivity”– how it relates to lab work. If a lab test, a blood test, has a lot of specificity, it’s very good at telling a particular issue, a particular problem. If it has a high sensitivity, that means that it’s also really very good at detecting something. We talked about the complete blood count. We talked about the differential– the breakdown of the white blood cell count. You’ve probably heard that term before. I think I explained it to you maybe in a way that is easy to remember– the idea of a left shift versus a right shift.

A left shift of the immature white blood cells indicates a bacterial infection. A right shift indicates, oftentimes, a viral infection. Most of the time, what we see is a left shift. Somebody says to you the patient had a left shift on their differential, that should mean to you this patient probably has a bacterial infection, breaking it down. We looked at all the different coagulation studies. The most commonly drawn ones, the PT, the PTT, the INR– the International Normalized Ratio, which is a very common blood test now. People that are on Coumadin, they go into the hospital frequently when they’re on Coumadin, especially when they start taking it. And what’s measured to ascertain the effect of the drug is an INR, just to make sure that the Coumadin is doing what it’s supposed to be doing in their body.

We talked about all the electrolytes. We talked about what an anion gap was. We looked at some of the kidney function tests. And then we looked at the cardiac labs. And what’s the one that is most– I’m going to grill you a little bit here this morning– what’s the most commonly used cardiac troponin level? Yeah. And there’s reasons for that. It rises very quickly at the early part of somebody having an acute coronary event. What’s the downfall of a troponin? What happens if somebody comes into the hospital with an acute MI, they’re there for two days, and they have another MI? It’s still elevated. It’s still elevated. All right. So it’s useful for that first insult to the heart, but it may not be that useful if the patient continues to have further infarction or ischemia or has another ischemic event. So that’s the downfall of that. How long does that stay elevated? It’s like two or three days, and it starts to trend down.

So you can make some decisions. If somebody’s troponin was 4 and then two days later it’s 10, obviously something’s going on. But that’s getting into this specificity and sensitivity. At some point, some of these tests aren’t as good as they are at another point. Because now you’re providing blood to that area of the heart that is ischemic, and while it’s ischemic, it’s releasing these enzymes, these troponins, into the surrounding tissue. And then when I [? re-profuse ?] that area of the tissue, those metabolites are then released into the circulation. And yeah, your troponin actually goes up a little bit. Absolutely. So there’s all those things that are important to understand if you’re taking care of those patients at various intervals. Just a couple of other things, and I really tried to hit a lot of the slides because I just don’t think it’s important for you to know these things.

And I can’t imagine that somebody’s going to test you on some of these things at this level. But understanding how creatinine clearance is used. Creatinine clearance is a very common test that is used to really look at kidney function. We have other things that we’ll talk about– the BUN and creatinine– but this test really tells us how well the kidney is able to function. It’s looking at the urine creatinine level, the serum creatinine level, and the total volume of urine. Your body produces creatinine. It’s a byproduct of muscle and cell tissue breakdown. Your body also produces urine by volume, and we expect that a certain amount of that creatinine is cleared by your kidneys. That’s what this test is all about. So if I measure a certain volume of urine, I expect a certain amount of creatinine in it, because it’s the kidneys’ job to do that. If I have that same volume of urine and it’s very low in creatinine, there’s something wrong with the way the kidneys are clearing that.

So that’s how that test is used. That’s what nephrologists do. Serum osmolality. It’s another very commonly ordered test in critical care. It has to do with the amount of total dissolved solutes in the blood. So everything that you can possibly have dissolved in your blood, we measure an osmolality level. If you’re dehydrated, the stuff that’s in your blood volume becomes very concentrated, so your serum osmolality goes up. If you’re overhydrated, your blood is dilute, so the concentration of everything in your blood goes down. So it’s a measurement of the dissolved solutes in the body. The higher it is, the dryer the patient.

The lower it is, the wetter the patient is– the more fluid overloaded the patient is. It’s used very commonly when we’re taking care of patients with traumatic brain injury. In the acute phase of their brain injury, we’re trying to limit the amount of cerebral edema, brain swelling, that is occurring. And we’ll be giving medications to help remove fluid from the bloodstream. You give mannitol. That’s done in the field sometimes in the helicopter with somebody with a traumatic brain injury. Mannitol is an osmotic diuretic. It’s a concentrated solution administered into the bloodstream. It causes the fluid from the cells to go into the vascular space to sort of dilute that out. In the case of traumatic brain injury, it pulls fluid from the brain. The kidneys then get rid of that urine. When we’re using that drug, we have to be aware of the fact that as we’re giving mannitol, we’re going to be causing a diuresis that could cause the patient’s serum osmolality to go up to a dangerous level.

Why do we care? The more concentrated your blood is, the more likely you are to have a clot form, as just one example. And it can cause electrolyte abnormalities and those kinds of things. So that’s how those tests are used. I mean, ultimately, if I give somebody enough mannitol and they diurese enough, their blood pressure is going to be low. But it’s not necessarily the intention of how it’s used.

Generally, you don’t want to lower people’s blood pressure with traumatic brain injury. We want to keep it nice and regulated, because as the brain swells, it is compressing the blood vessel, so blood isn’t getting to the tissue. If I let their blood pressure get low, that’s going to compromise it further. So we actually sometimes will make patient’s blood pressure who have a traumatic brain injury who have increased intracranial pressure problems, we’ll actually use drugs to make their blood pressure higher than normal. We’ll use epi and dopamine drips to elevate their blood pressure above supranormal levels in order to try to profuse the brain under those circumstances.

So yes, mannitol, being a diuretic, ultimately can make your blood pressure go lower, but it’s not necessarily the goal. We talked about this the other day, the difference between a BNP and a BMP. A BMP is a basic metabolic panel. Every hospital has their own version of what a BMP is. But it basically is the most common electrolytes that we would worry about and care about that can be abnormal that we can do something about. So that’s what a basic metabolic panel is. And you have to know wherever you’re working what their version of this is. Blood glucose test. In critical care, we care very much about blood glucose. In EMS, you care about it if it’s really too high or it’s really too low. That’s how we understand it in EMS and even in the emergency room. But in critical care, we care very much to maintain someone’s blood sugar within a very narrow range.

There are a fair amount of decent studies that say it’s really important to keep a critically ill blood patient’s blood sugar less than 150 at all times. Reasons for that are most people believe and understand that that will help prevent many complications that we see when you’re critically ill– the big one being infection and poor wound healing. So if you’re a traumatically injured patient and you have all these sores and open wounds and devices in your body, you’re at high risk of infection. And they’ve been able to show that, in fact, if we keep your blood sugar below 150, during that time, you’re less likely to develop some of these infection complications.

So that’s been a real huge push in the last 10 years is to control, regulate, critically ill patient’s blood sugar. So it’s not uncommon that you’ll see a critically ill patient who doesn’t necessarily have diabetes, and they’re on a continuous insulin infusion. Doesn’t mean they’re diabetic. It just means that we’re trying to control their blood sugar at all times. It has more to do with that you’re over-providing glucose to the cells.

So they don’t function the same way as they would if the blood sugar level was controlled, and they are much more susceptible when they’re not functioning well to infection and poor wound healing, just as two really good examples. So does that help? It’s less to do with the concentration of blood sugar in your body from a thickness standpoint. It has to do– and boy, this starts getting into this really complicated world of things that people are just starting to understand– but what we also see is that in diabetics, which is different than just a critically ill patient who needs to be on insulin, in diabetics, it’s a lot of things just beyond their high glucose levels.

Because we see complications in diabetics even when they’re well managed from a blood sugar perspective. So there’s other stuff going on in their body that is very different if they have diabetes, as opposed to when I’m just trying to control a critically ill patient’s blood sugar. When you’re critically ill, it’s a stress response. So it’s absolutely anticipated and normal after any kind of critical illness that your blood sugar is going to shoot up– 180, 200, 220, not unusual at all. It is a stress response. And what happens when you’re critically ill is you are undergoing the stress response for many, many, many days, not just the short term, I need glucose for an hour or two.

And it’s that long term elevated glucose that starts to create a problem with cellular metabolism. It’s interesting. I just sent one of our endocrinologists, [? Sed ?] [? Fraiderd, ?] who’s a really good guy, an article that came out just yesterday that showed that there was no difference in controlling critically ill patient’s blood sugar at the 150 level than if you didn’t. It was a small study, but it was done by the same physicians that did the original study that showed tightly controlling these blood sugars was beneficial.

So I just said, hey, what do you think about this? What are we going to do about this? Did they justify the shift? The article talked about the fact that they really didn’t have a control group at the beginning of the time when they initiated the study. So they just did it because they felt it was the right thing to do, and there was a smattering of literature out there that said, yup, you should control blood sugar in critically ill patients. The pitfall of starting somebody on an insulin drip who is critically ill– and again, if you’re transporting critically ill patients, you need to be aware of this– they’re on an insulin drip. The pitfall of that is we can easily induce hypoglycemia by giving insulin to somebody who isn’t diabetic. So if I’m tightly controlling their blood sugar between 80 and 130 because they’re critically ill, and I’m going up and down on their insulin drip every hour based on their blood sugar. If I’m not careful, I can cause the patient to slip into a hypoglycemic event, which is way worse than being a little bit hyperglycemic when you’re critically ill.

So that’s the other thing that people have always balked about, this idea of getting too crazy about how we control blood sugar in critical care. Way more than I wanted to say about it, but it’s important because you’re absolutely going to see this in critical care. Hemoglobin A1c, are you familiar with that, how it’s used? A hemoglobin A1c level is basically used to determine how well a diabetic is controlling their blood sugar, or how well we’re able to control a diabetic’s blood sugar. So as you see down below the normal values, a non-diabetic, if I measure their hemoglobin A1c, it’s going to be about 4% to 6%. A diabetic who is well controlled has a well controlled blood glucose level, I would expect their hemoglobin A1c level to be less than 7.

Anybody that is higher than 9 tells me that they are not a well controlled diabetic. Now, it may be that they aren’t doing a good job, or it may be that the medications that they’re on aren’t effective. So don’t make any judgments about patients. If you ask a diabetic what their hemoglobin A1c last was, and they tell you 9, don’t think, well, you don’t know how take care of yourself. Don’t make those kind of judgments. It just tells you they’re not being effectively managed, one way or the other. They’re not doing it, or the meds that they’re on are not effective for whatever reason. So to me it’s an important question to ask when you’re taking care of a diabetic because it gives you an idea of how well they are managed right now. The lipid tests. These are probably most familiar to us because we have them drawn on ourselves. Cholesterol levels. I’m not going to talk a whole lot about these things.

Triglycerides– obviously, we want these levels, cholesterol, total cholesterol, triglycerides, total triglyceride levels to be normal– not particularly low, and definitely not high. These things contribute, as we understand things today, to coronary artery disease and other vascular type diseases. So we’d like to keep those things low. The HDLs– the high-density lipoproteins– what we consider to be the good cholesterols, that one we want to see on the higher side. We know that exercise and weight loss allow you to have higher HDLs. That’s why there’s all that literature that’s out there that talks about moderate alcohol intake, glass of wine, a cocktail a night is actually beneficial from an HDL perspective. It helps elevate your high density lipoproteins. We see low levels of HDL in people with diabetes. Well, that helps us understand why they have so much vascular disease– peripheral vascular disease, coronary vascular disease. The LDL– the bad cholesterol– we want that to be within normal ranges as well. We see high levels of this in multiple different disease processes, particularly diabetes again. This is why diabetics have so many vascular problems– why just controlling blood sugar is not necessarily the answer for a diabetic.

They could still have all of the complications. Liver function tests commonly drawn in critical care. Any time you go through a situation in which you’re hypertensive, a shock situation where you’re not profusing your vital organs, one of the things that can happen is that your vital organs take a hit. So this test is commonly measured as a way of assessing hepatic function– liver function.

There are some others that are probably more important to draw, which we’ll talk about in a minute. But this measures the total amount of bilirubin in your body. Bilirubin is a byproduct of the breakdown of red blood cells. It’s metabolized and conjugated in your liver and excreted through your GI tract. If you have high levels of bilirubin, that’s indicating that the liver is not doing its job of getting rid of that breakdown of red blood cells. I’m going to skip that one. These are all different liver function tests. They are drawn frequently. As far as what you need to know about this is if I have elevated liver enzymes in general– my SGOT my SGPT or my ALP or my GGT, those are all liver enzymes– that’s indicating to me that my liver has taken some sort of a hit.

It’s very common. Somebody arrests in the field or they’re in a bad car crash. The next day– so they’ve been hypotensive or asystolic for a while and resuscitated, not uncommon at all to see the next day when we draw these labs that their liver enzymes are elevated just from being underperfused for that period of time. So we use it as a guide to tell us globally what organ– how the organs have been affected by this insult. Ammonia is generally drawn very specifically when we know the patient has liver failure.

Ammonia is normally present at extremely low levels in our body. Our liver metabolizes it. It occurs in our body as the result of a combination of many different metabolites that accumulate in the body that normally the liver would get rid of. So if the liver’s not working, your ammonia level becomes high. And we used to think that the confusion that occurs when somebody is in liver failure is a result of high ammonia levels. Well, it probably contributes to what makes people with liver failure confused and agitated and have all of these neurologic findings.

It goes beyond just having a high ammonia level. But an elevated ammonia level is very common in patients with fulminant liver failure. So they give examples here– it just says liver failure, but acute hepatitis, alcoholic liver cirrhosis, things like Reye’s syndrome, which we don’t really see too much anymore– but anything that causes acute fulminant liver failure is going to cause a rapid rise in your ammonia level. Amylase is a pancreatic enzyme. It is frequently drawn, again, much like we will draw liver enzymes after somebody has a cardiac arrest or is involved in a car crash and we want to ascertain the function of their organs, Amylase will be drawn.

And it’s going to tell us about the function of the pancreas. Amylase is elevated for certain in patients with pancreatitis. So if somebody does have acute pancreatitis or chronic pancreatitis, very commonly they’re going to have elevated amylase levels. These pancreatic enzymes are normally released into the bloodstream. They help with digestion. In the case of pancreatitis, they’re produced at a very high rate, and they actually leak into the surrounding tissue. Instead of going into the GI tract, it leaks– so it irritates the pancreas. It’s a digestive enzyme that’s now kind of eating away at the pancreas. That’s what acute hemorrhagic pancreatitis is. So we do measure these levels, and it’s just an indicator of how angry the pancreas is. Lipase is another one of those. Functions sort of the same way.

Seruologic testing. We talked about serum chemistries. We talked about the hematologic studies. Seruologic testings are mostly things that I would say are not going to directly affect what you do in advanced transport or critical care transport. But a couple of things that you should be aware of and just be exposed to– blood banking is one of those things that involve seruologic testing so we can do ABO typing to determine someone’s blood type. ABO typing is the most common worldwide way of typing blood, matching blood from one person to another. There’s like six or seven other ways to do it, but this is the most acceptable way of doing it. Rh factor is looking on the red blood cell for the Rh antigen.

So that’s what gives you your O positive or O negative. Positive and negative is the Rh factor that’s on red blood cells. Just in short, blood typing is obviously very specific. I think everybody knows that you have to give the right blood type to a patient. It has to do with the antigens that are on the surface of the red blood cells, depending on your blood type. So if you’re type O, you don’t have any surface antigens. If you’re type A, you have surface antigens type A. You carry antibodies for the B. So I can’t give a patient who has type B blood to a person with surface antigen A because it’s going to have a reaction.

It’s not going to be compatible. What that means, what that compatibility is, is that the red blood cells will be agglutinate. They’ll clump up. This works for most patients. 99% of the time if I match a patient’s blood type, determine it, and give that patient that blood type from another patient, it’s going to be fine. Understand that there are other things on these red blood cells that may still cause a patient to have a reaction. So the type O blood is the blood that can be given to anybody because it doesn’t have any surface antigens.

So even if you have antibodies to something, you’re not going to respond to type O blood. So in a trauma room setting, when we don’t have time to type somebody’s blood, we can give them type O blood. Specifically, we give O negative blood. is, if a woman is post-menopausal, or if it’s a male patient, we can actually give O positive blood to that patient. Because the RH factor doesn’t matter if you’re not going to have a baby or can’t have a baby. So most commonly, at [? Fraiderd ?] in the ER when the trauma patient rolls in, they bring uncross-matched blood to the trauma room and it’s just a bunch of O negative blood that they give to patients. Sometimes if it’s a male patient and we’re low on O negative blood, they’ll bring O positive blood. Because it’s OK to give O positive blood to a male patient.

Do you all understand what typing and cross-matching means? If a patient is typed and cross-matched? So if I type somebody’s blood, that means I figure out what kind of blood type they are. They’re AB positive. Cross-matching is taking that patient’s blood and a sample of some banked blood. And mixing it together and looking at it under a microscope and making sure that it doesn’t have any kind of reaction. That’s blood that is now typed and cross-matched. So I can give type-specific blood. Meaning I know what the patient’s blood type is. I’ll just grab some patient’s O positive. I’ll grab some O positive blood off the shelf and give them O positive but without cross matching it. That’s a little dangerous because there’s other things on the blood that can cause a reaction. If I cross-match, it takes a couple extra steps– couple extra minutes. Take that blood off the shelf. Take a little sample of it. Take a little sample of the patient’s blood. Mix it together. Look at it. And now it’s typed and cross-matched.

It’s specifically OK for that patient. So that’s the difference. Other serologic tests that you may be familiar with or exposed to. A bunch of tests for syphilis. Syphillis is becoming more and more of a commonly transmitted sexually-transmitted disease. Now, don’t fool yourself. It’s back. Kind of back with a vengeance. So that’s something that, as you’re caring for a patient, that you generally need to be worried about. But it is, from a public health standpoint, it’s out there. Other types of serologic testing. Some of these you’ve had done on yourself. You’ve got your hepatitis vaccine. And then you went in for serologic testing to make sure that you developed the antibody for hepatitis B. We do those sorts of things for measuring hepatitis A and hepatitis C antibodies, as well. To see if somebody’s been exposed to, or has had, an active hepatitis infection. That’s how it’s used. HIV. Commonly drawn blood test. That’s to determine whether or not somebody is HIV-positive or not. Other tests for patients with HIV that are commonly drawn are things like viral load in T cell counts. That’s going to go allow people to understand how well we’re managing someone’s HIV.

CMV is another virus. It’s called cytomegalovirus. Very common virus. Most of us probably had CMV as a child. It comes across as an upper respiratory infection in most cases. It can be very devastating to somebody who is immunocompromised. So if somebody is a transplant patient or an HIV patient, if they have never been exposed to cytomegalovirus as a child and develop an active CMV infection when they’re immunosuppressed, that can be a real life-threatening problem for them. Mono– mononucleosis test. I think everyone is familiar with that. Some other tests that are commonly used in critical care that are related to the endocrine system. Cortisol levels are frequently drawn in critical care.

I don’t know that it’s impactful for you, transporting a critically ill patient, to know what their cortisol level is. Understand, though, that it’s one of those hormones in your body that is in incredibly important in just the functional level of all your cells. So if your cortisol level is very low, your cells aren’t going to function very well. And in fact, critically ill people oftentimes will have low cortisol levels. And we’ll treat them to boost their cortisol levels back to normal levels. But in a short-term transport of a critically ill patient, you’re not going to worry about it.

We should have taken care of that and recognized it before we put the patient in the back of an ambulance if it was that important. TSH, or thyroid-stimulating hormone. This becomes elevated when the patient’s thyroid is not functioning properly. So again, just like the cortisol is produced by your adrenal glands and your kidneys. Thyroid-stimulating hormone is produced by your pituitary gland. This stimulates the production of two other hormones– T3 and T4– don’t worry about them. What you should understand, though, is if somebody has a high TSH level, they are not producing enough of the necessary hormone. And that’s important to know in a critically ill patient. Because just like cortisol helps maintain normal function of all cells, so does the thyroid. And if the thyroid is not working, what we see is a high level of TSH, because the pituitary gland is trying to get the body to make more of the necessary bioavailable hormone.

So that can be an issue in a critically ill patient, as well. Where we might recognize it and treat it. Not something you’re going to be treating on the back of an ambulance, though. But that’s what those tests tell us. Blood cultures. How many of you have drawn blood cultures before? Blood goes in special bottles. It has a broth in it, usually. Or a gel substance in there. The idea is that if there’s bacteria present in the blood or a virus present in the blood, that it’s going to grow in this biologic medium– this broth. Understand that when we draw cultures, it can take up to three days for the bacteria to grow. So it’s not like I can draw blood cultures and in 20 minutes know that the patient has an infection. It takes time. There are some devices out there– and I’m not bragging about this, I just know this to be true. That [? Fraiderd ?] actually has one of the devices now that, within a matter of hours, it can measure bacterial count in blood cultures. It’s new technology. I’m sure within a matter of months, all of the hospitals are going to be up on it.

It was something that we beta-tested there with one of the companies that came up the device. But the idea is that we want to be able to recognize that the patient has an infection, whether it’s bacterial or viral. And we want to know what exactly that bacterial infection is. Because this idea of using broad spectrum antibiotics– and does everyone know what that term, “broad spectrum” means? Like, it’s an antibiotic that kills a whole bunch of stuff.

That’s a broad spectrum antibiotic. The idea of using broad spectrum antibiotics nilly-willy is why we are in a big mess right now with these resistant infections. So MRSA and VRE. All of those things are as a result of historically– in the ’70s and ’80s and ’90s– using broad spectrum antibiotics nilly-willy. So the goal is, now, to quickly figure out, is there a bacterial infection. What is it, specifically. So that we can use an antibiotic that only acts on that infection, instead of using a broad spectrum antibiotic. Or what we do if someone comes into the ED in septic shock, we’ll get blood cultures. We’ll start them on broad spectrum antibiotics. And as soon as those blood cultures come back, we’ll switch them very quickly to antibiotics that are specific to that organism. So that’s the goal of blood cultures, now, is to really nail what the organism is and see what antibiotic is most appropriate for it. Rather than using broad spectrum antibiotics. OK But understand that it can take days. 48, 72 hours– depending on the level of bacteria in the blood at the time the specimen is drawn– before something grows out.

A low level of infection the bloodstream is going is going to take a long time for the cultures to be positive. A lot of bacteria in the bloodstream– those blood cultures are going to probably be positive in a matter of four, six, eight hours. Because they grow quickly. Once the bottles are determined to be positive for bacterial growth, they take a sample. And probably still under microscope, in many situations, but now this stuff is getting more and more automated. But they take a sample of that broth from the blood culture bottle. Put a staining solution on it. And this is where they come up with this terminology of, this is a gram stain-positive infection– this is a gram-positive infection or a gram-negative infection. It has to do whether it stains on the slide positive or doesn’t stain on the slide.

And there are different bacteria that will stain and bacteria that won’t. And that’s what helps us start to really figure out what is the most appropriate antibiotic for the patient. Ultimately, we’ll be able to know exactly what the organism is. But knowing how it gram stains– either negative or positive– is going to help us decide very early on what is a more appropriate antibiotic. So that we’re avoiding the use of these broad spectrum antibiotics.

Urinalysis. Commonly done in an emergency room. Commonly done in an ICU. How much of it is meaningful to you, as critical care paramedics, I’m not sure. Obviously protein in urine is not good. It can indicate kidney disease is the most common thing that we understand is going on. Or women who are preeclamptic will have high protein levels in their urine. If you don’t have any protein your urine, it’s usually a good thing. Blood sugar in the urine.

It’s a pretty non-specific test. I’m not going to treat someone’s blood sugar based on their urine glucose content. But obviously patients who have diabetes, they have an excess amount of glucose their bloodstream and the kidneys work to get rid of it. So their urine screens positive for glucose. If I had a urine glucose-positive sample, that would just trigger me– if I hadn’t done it already– to do a blood glucose measurement on the patient. Nowadays, because we know how important it is to control blood glucose, we’re skipping this step and just actually measuring the blood glucose.

Ketones. Ketones are not normally found in urine. Ketones are a byproduct of anaerobic metabolism, or alternative metabolism. So we see ketones in the urine in patients who are malnourished. Very commonly, we’re most commonly seeing ketones in the urine when somebody has DKA, diabetic ketoacidosis. Alternative metabolism, right. Or someone that’s excessively dieting. Low value of ketones not anything to worry about. But if I didn’t know what was wrong with a patient who presented in the ER and I dipped their urine. And it was positive for glucose and ketones. I’m probably thinking that this patient is in diabetic ketoacidosis. But I need to do other things to really figure that out. White blood cells in urine.

Indicative of infection. That’s the most common reason why anyone would have white blood cells. And a genito-urinary infection. So from the kidneys all the way through to the bladder and outward. Red blood cells are, if present in the urine, often indicate trauma to the kidneys, trauma to the bladder, trauma to the urethra. It can be seen as also an infection. And very commonly in kidney stones. Toxicology. A lot of things can be done on urine. I’ve listed some of them, here. I think you guys are familiar with that concept.

Some of the newer drugs that are out there– not able to really pick up on the most common urine tests. So they might be drawing blood tests, as well. Everybody knows what an x-ray is, right? I think you’ve seen them. Bone is most dense. It’s white on the film. Air is least dense, so it’s black on the film. Lots of x-rays taken for a long time. I’m not going to belabor that. Fluoroscopy is another x-ray technology. But it’s a live video image that’s taken. So the cardiac cath lab. Those images that they take when they’re floating the catheter into the coronary arteries. That is fluoroscopy. So it’s an active live video image of x-ray. A lot more radiation when we’re doing fluorscopy than just for a standard chest x-ray, as an example.

CT scan. Everybody knows what that is. Gives us these cuts. And now, with the technology that’s out there, they can actually do three-dimensional reconstruction of the body with these CAT scans. It’s quite amazing. That’s sort of the default for when we’re trying to figure out what’s wrong with the patient. It’s the next best thing before we open them up to see what’s going on inside. All trauma patients get– multiple trauma patients get scanned in the ED. It’s not even a question. Most hospitals now, in their emergency rooms, have a CT scanner. Because it has become the way to quickly assess for major life threatening illness. It also is x-ray. Higher radiation dose than a standard plate x-ray. But certainly I can run somebody through a scanner in less than 15 minutes and be able to get a full understanding of what’s going on with them. Ultrasound. Also used a fair amount in health care. Most of us are familiar with ultrasound when it’s used like on pregnant women to look at the fetus.

But ultrasound is used in many, many other ways on the inpatient world. You do fast exams now. You’ve probably seen– in most ERs, they’re doing fast exams. It’s an ultrasound looking for bleeding that’s going on the belly. So it’s looking for fluid, and looking through fluid to see you see what’s going on. Nuclear med studies. We used to do– we still do a fair amount of these. It’s not that important for you to know what all those things are from a critical care transport perspective. But it involves injecting a radioactive isotope into the patient. And then measuring where that goes into the body and how fast it’s picked up in different areas of the body.

That can tell us things about the patient. MRI. Everybody, I think, is familiar with that. Most of us have probably had an MRI for one reason or other in our lifetime. It’s not radiation. It’s a strong magnetic field. It causes the water molecules in the cells to orient themselves in a certain way and show up. Lots can be determined with an MRI. More than I could even talk about in an hour. It also has become sort of the mainstay of diagnosing for patients, short of operating on them. The difference between CT scan MRI is I can’t put everybody in an MRI scanner. If they have devices in them that are metallic, obviously they can’t go into a giant magnet. That would be a problem.

The magnet can heat it. It can rip it through the tissue. So in critical care, while MRI is used, we are oftentimes selective about when we can use it on a critically ill patient. Because if they have things in their body that don’t allow them to be safely scanned in MRI, we might not be able to do that test. So maybe a day or two until we can get that stuff out. Until they’re more stable. Before we can actually do the MRI.

CT scan, doesn’t matter. They can be hooked up to anything and I can put them in the scanner. PET scans. Becoming more and more a common. It’s generally not something that’s used in critical care. But just for your own edification, a PET scan is used to help determine, most commonly nowadays, looking for cancer in various organ systems of the body. So it measures the uptake of a glucose solution that’s given to the patient, in the body.

And we know that cancer cells metabolize much faster than normal cells. So if I put a glucose solution into the patient’s bloodstream and then scan their body looking for where the glucose is taken up most quickly, I can sort of anticipate that, gee, if the glucose uptake in the lungs faster than it normally is, there’s probably some cancerous activity in there. Because the cancer cells are absorbing the glucose faster because of their high metabolism. So that’s how PET scanning is used. It can be used for a variety of other things. But I will just tell you that, in most instances, the way PET scan are used is looking for cancer and– the word just flew out of my head– metastases.

That’s how it’s going to be used. How are you with blood gases? Pretty good? Not so good? Let’s just go over it quickly. And hopefully it’ll be a little bit of a refresher for you. No matter where you work, a blood gas involves pretty much the same test. It’s going to measure your pH. It’s going to measure your dissolved oxygen level in your bloodstream. It’s going to measure the dissolved carbon dioxide in your bloodstream. It’s going to measure the bicarbonate level in your blood. And your oxygen saturation.

And there’s a couple other things that can be added to that. But those are the most common things. pH– normally between and 7.45. And we’re talking about arterial blood samples when I do this. Although if I drew venous blood, you would see that the values are pretty close. With one exception, and that’s the amount of dissolved oxygen. It’s going to be much lower in the venous blood. Understand that to 7.45– we’re not kidding. Your cells are very dependent on that pH. And as soon as the pH is less than that or more than that, cellular function changes. And the more acidotic you are or the more alkalotic you are, the more significant the changes are. So for example– and this is partly why vassopressin is a ACLS resuscitative drug. I’ll give you a good example. If you are acidotic– let’s say your pH is 7.16. Not uncommon for someone who’s arrested in the field.

Epinephrine isn’t going to work as well as it would if your pH was normal. So that’s why vassopressin became a second-line drug. Because vassopressin is not affected by pH. So it works as well on someone’s pH who’s as it does on someone who’s to 7.45. So drugs don’t work as well. Some drugs don’t work as well when you’re very acidotic. So long and short of this is it’s very important for normal cellular function that your pH remain somewhere between and 7.45. Because bad stuff starts to happen when you’re outside of those ranges. If you are above the 7.45, the term we use is alkalosis. If you’re below 7.35, we say acidosis. PaCO2, or PCO2, measures the partial pressure of carbon dioxide in the blood. So how much carbon dioxide is in the bloodstream. Where is most of the carbon dioxide– how do we get rid of most of the carbon dioxide in our body? We breathe it out.

We exhale it. So when we see high levels of PCO2, that tells us, usually, the patient’s not breathing enough. Because it’s now accumulating in their bloodstream. So we have a normal range of 35 to 45 millimeters of mercury. A high value– so above 45– is going to in be indicative of respiratory failure. And if the pH is low– so I have a pH of and a PCO2 of 50. The cause of that acidosis is the accumulation of CO2 in the bloodstream. CO2 is an acid. So the more CO2 in the bloodstream, the higher the acid level of the bloodstream, the lower my pH is going to be. That’s why when you stop breathing and your PCO2 goes up, you become acidotic because CO2 is a volatile acid in your bloodstream.

Low values of CO2, so less than 35, that’s called respiratory alkalosis. That’s seen in hyperventilation. So if somebody’s hyperventilating, if I measure their blood CO2 level, it would be low. That’s a result of them just blowing off more CO2. PO2 is the amount of dissolved oxygen in your bloodstream. It’s what’s free-floating in your bloodstream, not what’s attached to the red blood cells. It’s what’s dissolved. It needs to be dissolved in order to get to the cells. The red blood cells just carry it around. Then it free-floats. And then it gets into the cell. Normal is 80 to 100. High values are indicative of a over-oxygenation, like just being too crazy with how much O2 we’re giving the patient. Or in hyperventilation, low value is indicative of hypoxia. I’m either not giving the patient enough oxygen or they’re not able to get– because their lungs are working– get enough oxygen into their bloodstream. Bicarb is the measurement of the bicarbonate ion in the bloodstream. Normal is 24 to 30 milliequivalents per liter. If the patient has a high bicarb level, that is going to be indicative of a metabolic alkalosis. So it’s going to make the pH be elevated.

A low value is metabolic acidosis. O2 saturation. Again, most of us are familiar with that. That’s the amount of hemoglobin saturation, saturated with oxygen. It’s a misleading value. We get very comfortable about– feeling comfortable about patients when their O2 saturation is 95% or 100%. But it really doesn’t tell us much. So if I have two red blood cells in my body and they’re both saturated with oxygen, my saturation is going to read 100%.

But that’s not enough oxygen. Obviously two red blood cells is not enough to carry oxygen to all the cells in my body. So that’s an exaggeration, but to drive home a point to that, just in looking at someone’s saturation isn’t really telling us the whole thing. The lower their hemoglobin level, the more concerning it is, even when they have a normal saturation. Because they don’t have enough red blood cells to carry around the required oxygen, all right. We talked about hemoglobin. So there’s four scenarios when you’re interpreting a blood gas, four basic scenarios. And it has to do with– the first one is respiratory acidosis. So in respiratory acidosis, the pH is going to be below 7.35. The pCO2 is going to be above 45. And the bicarb is going to be less than 25. That’s going to be a respiratory acidosis. A respiratory alkalosis is the pH of 7.45. My total pCO2 is going to be low. And my bicarb is going to be low. From metabolic acidosis my pH is 7.35, bicarb is going to be low, and my pCO2 may be normal or low.

And then metabolic alkalosis, so pH is 7.45. I look at the bicarb and the CO2 levels. If the bicarb is elevated and my pH is elevated, that is a metabolic alkalosis. So something that is outside of what you definitely do in the field normally, and even outside of what most emergency rooms do, is this concept of invasive hemodynamic monitoring. But if you’re transporting critically ill patients, they’re going to have these devices in their bodies. So you’re going to have to have– in most circumstances in the state of Wisconsin, if you’re transporting a critically ill patient, , you’re going to have an ICU nurse along with you, right.

But you’re going to be there to help. You’re going to be there to hook up. You’re going to be– and you still need to have an understanding of what is it you’re doing. In other states that’s different. Paramedics take care these kinds of patients. But most of the time in the state of Wisconsin, there still has to be in RN there for this kind of patient. So when we talk about hemodynamic monitoring, it’s a lot of stuff you already do. But you do it in a non-invasive way. So you do EKGs.

You do blood pressure monitoring. Those are basic, non-invasive ways to monitor someone’s hemodynamics, hemo meaning blood, dynamic meaning the flow of blood in the body. That’s what hemodynamics is. OK. In critical care, we’re going to be more interested in the subtle changes in the patient’s hemodynamics. Because if I can recognize a number changing, a very subtle number changing, and I’m going to give you lots of examples of this, before the patient’s blood pressure actually changes, and I can treat the patient before they actually have a systemic change in their status, that would be good, right? Why would I wait until somebody gets actually hypotensive and shockey if I can recognize that this is about to happen because of an invasive line.

And treat the patient before they actually get into trouble. That’s where this concept of hemodynamic monitoring comes in. I can anticipate things that are going to happen to the patient that are obvious to anybody but very harmful to the patient, treat them before they get out of hand. I don’t know if you know this, maybe you do, maybe don’t, but like 5, 10 minutes of hypotension, where your mean arterial blood pressure is less than 60 for more than five minutes, your organs are taking to hit.

You are not perfusing your vital organs. And the next day in the ICU when I measure your liver function, and your pancreatic function, and your cardiac function, I’m going to see those enzymes rise in the bloodstream. Because for 15 minutes, that patient was hypotensive in the field, or hypotensive in the trauma room, or hypotensive in the operating room. It absolutely makes a difference. And what ultimately makes a difference, what you have to understand in all of this is it’s not the numbers.

It’s not the blood pressure that’s the issue here. It is the fact that we’re not getting oxygenated red blood cells to those vital organs. That’s what shock is. Don’t let anyone tell you any differently. It’s not the numbers. It’s the idea that we’re not getting oxygen to the brain, the liver, the spleen, the kidneys, I said the liver, all of the gut. And when I don’t do that for more than 10, 15 minutes, I am already compromising those vital organs. And it’s going to show up the next day when I my measure somebody’s lab tests that we talked about. That’s how we use those lab tests. How much of a hit did that patient take when I let– because they were hypotensive for 15, 20, 30, 40, 50 minutes in the field. In critical care transport, you’re going to be getting patients that have these lines in. You’re going to be required most of the time to keep an eye on them during transport. And then, and how to handle them safely, all right. So the idea is that I want to introduce you to some of these concept of these different numbers that maybe you are not expose– haven’t ever been exposed to before, so that you can learn to interpret them.

And maybe think about how you could intervene on a patient before they actually become shockey. That is going to be the concept that we’re going to work with. So we have things like EKG. Well, we’ve got that one down pretty well. We measure arterial blood pressure. We measure that with a cuff. We can take a manual blood pressure, or most of us now. Do you guys have automated blood pressure cuff devices, NIBPs? There’s some pitfalls with those, right. And I’m sure you’ve experienced it. They all pretty much work the same. But they can be misleading. You’re bouncing down the highway. You can get a blood pressure reading on a dead person, right.

Or sometimes it’ll only display the mean pressure. It won’t give you a systolic or a diastolic. What does all that stuff mean? We can sort of talk about that here. I want to introduce you to this concept of central venous pressure, or also, and I’ll explain the difference in a little bit, right atrial pressure. The right atria, meaning the right atrium of the heart, OK. There’s a difference between central venous pressure and right atrial pressure. But they are similar. Understand that. This idea of cardiac output, this idea of measuring blood pressures in the pulmonary artery as a way of determining what’s going on with the patient, and then talking about stroke volume, and then talking about oxygen delivery, which is ultimately what we’re trying to maximize at all times with the critically ill patient. So I heard you guys and Marcus talking this morning. I know you all know what a [? 12 lead ?] EKG is, what you do with, it how it’s used.

It to form of hemodynamic monitoring. We know that there are also 15 lead and 18 lead ECGs. That basically– you know, a 12 lead gives us a view of the left side of the heart over to that lateral wall of the left ventricle. But there’s other parts of the heart other than the LV. Why do we worry so much about the LV function? That’s the one that’s pumping blood everywhere, right. So if that one goes down, we’re going to be in trouble. Quick. You can still get in trouble if your right ventricle isn’t pumping well as well. So these 15 lead and 18 lead ECGs give us a more direct view of the right ventricular muscle mass and the backside of the heart. OK. I can see that stuff on a 12 lead by we see the changes that are happening on the right side on those 12 leads. But it’s difficult to really understand what’s going on the right side. So we use these other EKGs. How many of you have ever seen a 15 or an 18 lead ECG done? It is done.

It’s not done that commonly. It became sort of fashionable to do it for awhile. I would say most patients are not having 15 and 18 lead ECGs done when they show up in an emergency room. Most. So we talked about this indirect, non-invasive blood pressure monitoring with NIBPs and sphygmomanometers. We know that putting the wrong size cuff on the patient has an impact with those devices– user error, a lot of environmental factors, bouncing down the highway. Also, what you should know about these non-invasive blood pressure cuffs is when they’re cycling, so you start it and it’s ticking its way down, if the patient’s heart rate or blood pressure changes dramatically during the time that it’s cycling, a lot of times it will not display a systolic or a diastolic.

And it gives you a mean pressure only. And that has to do with that the patient’s vascular, their cardiovascular status changed while it was cycling. What you should know about that is if it’s just displaying a mean arterial pressure, you can usually believe that mean arterial pressure. What is a normal mean arterial pressure? What do we want someone’s mean arterial pressure to be? So you get the systolic. You get the diastolic. And you get the mean on those devices. Anything above 65 is what’s acceptable. So 65 to 85 is what a mean arterial pressure is going to typically be. We know that if your mean arterial pressure falls much below 65 for an extended period of time, 10, 15 minutes, you’re not getting oxygen to your cells. So that is going to be– and in fact, when we’re taking care of critically ill patients, a lot of time we’re treating them, not on what their systolic and diastolic is, but what their mean pressure is.

So there’ll be orders that say run the dopamine drip. Titrate it to keep the mean arterial pressure greater than 65, or greater than 70. I don’t care what their systolic and diastolic is. I care what their mean arterial pressure is. Because that’s the driving pressure in the microcirculation all the timeline does that mean arterial pressure. Invasive pressure monitoring is a little bit more involved. Now I’m sticking a catheter in some place in the body, and I don’t mean a urinary catheter, I mean a vascular catheter, into a blood vessel. Or in some instances, I’m sticking that catheter directly into the chambers of the heart to directly measure pressures in a blood vessel in a chamber of the heart.

That’s what invasive hemodynamic monitoring is. This requires some sophisticated equipment, right. I have to have the right kind of catheter to shove in that blood vessel. I need to have a transducer. And this is just one example of a transducer. But a transducers is a transducers is a transducer. I’ll pass this around so you can look at it. It gets attached to a bag of normal saline that gets put in a pressure bag. It gets flushed, just like IV tubing would. And what you’ll notice when I pass this around, pay attention to this, is from the– this is the actual transducer itself. Inside of here is a little rubber diaphragm that has electrical wires on the backside of it. And when this is hooked up to a catheter, the pressure from that vessel or that space actually pushes on that diaphragm.

And it moves those little pins. It’s cabled to a monitor. And that converts– the transducer converts that fluid pressure signal to an electrical signal, sends it to the monitor. And I get a waveform and numerical display. That’s what a transducer does. What I want you to notice about a transducer is that this is the back where the cable comes off. This is what I would call the back side of the transducer, what goes to my bag of fluid. This tubing is very soft and pliable, just like regular IV tubing. It is regular IV tubing. But from the transducer forward to what I hook up to the patient is a very different kind of tubing. So I can just take this tubing right here and kink it right over, occlude it. If I try to do that with this tubing, it doesn’t ever kink. It’s called high pressure tubing. Why would I want that kind of tubing between the catheter and the transducer, and not care about the tubing that goes back to the IV solution? What do you think the benefit is of having tubing like that between– [INAUDIBLE] Right.

I don’t want the pressure that’s coming from the patient to be absorbed by the tubing. I wanted it to be– the integrity of that pressure wave form to be as the same as it is at the tip of the catheter that I’m measuring that pressure from. All right. So that’s why. And the length of the distance between the transducer and where I’m connecting it to the catheter are also matters. You never want to have more than about four feet of, and this is called pressure tubing. So if I was going to put an extension on this because I needed more length, I would need to put similar IV tubing, pressure tubing, on here in order to maintain the integrity of that fluid wave to the transducer. I don’t care about behind the transducer.

The monitoring is occurring forward. So I’ll pass us around. Just take a look at what a transducer is. They all look the same. I don’t care what company they come from. They’re all very similar. The other thing that has on it is this little pig tail. Some of them have a squeeze valve on them. It’s called a rapid flush device. So when I pull on this or squeeze it, it forces fluid through that line very quickly to flush the line. That’s what that is. Just kind of take a look at it. [INAUDIBLE] You should always put saline on there. Yup. Some old school places will put a little bit of heparin in the saline bag. But you wouldn’t want to using anything that contains dextrose, because dexterous is sticky. And after awhile, it’s going to kind of muck up the function of the little diaphragm inside that transducer, OK, also cause the line then to clot off. So that’s basically how it is, how it’s set up. I’ve got the fluid bag under pressure. The fluid bag under pressure needs to be at 300 millimeters of mercury. So that’s really why you have that little gauge on those pressure bags, is when you’re using a transducer system.

When that thing is pumped up to 300 millimeters of mercury, that transducer will infuse at three ml per hour automatically. So that’s done to keep the line patent. All right. If the fluid pressure goes below 300 millimeters of mercury, it’s going to not infuse and the line’s going to clot off. And you’re going to have a really irritated ICU nurse and a really irritated physician, all right.

We get excited about these lines, because they’re invasive. If the line clots off, that means I have to put another one in, all right. It’s not like it’s just easy to do that in some cases. So we get a little freakazoid about these invasive lines. So you saw what– so any pressure that I’m monitoring, I have to have that transducer. That’s going to provide me this this electrical interface between the fluid- filled vessel or chamber back to my monitor to give me a waveform and numerics.

The transducer to that does that. So whatever vessel I’m monitoring, or chamber I’m monitoring, I’ve got to have it. So if I want to monitor someone’s arterial blood pressure, I’m going to put a catheter in their artery. I’m going to hook up a transducer to it. And I’m going to be able to directly, invasively monitor their arterial blood pressure. All right. If I want to monitor somebody’s right atrial pressure, or their central venous pressure, I’m going to put a central line them with the tip of that catheter sits in the vena cava or in the right atrium, hook a transducer up to it. And now I’m going to be able to see what the pressure is in the right atrium or the central venous pressure in the vena cava. All right. So that’s how these all work. The way these monitors work is if I turn the monitor on and tell the monitor that I’m going to be monitoring arterial blood pressure with this transducer, it’s going to show me a systolic, a diastolic, and a mean pressure.

If I hook that transducer up to that monitor, and I tell it that this is a central venous pressure waveform, it’s only going to display the mean arterial, the mean pressure for that waveform. And monitors are smart. They know if I’m monitoring this pressure, I don’t need its systolic and diastolic. I just need the mean to come across, all right. How many of you have seen an arterial line and seen an arterial waveform? So not new information for you. I sort of talked about all these sorts of things already. A 500 cc bag of saline, or heparinized saline. The key thing with the transducer system– I’m not going to belabor this too much– but the key system is you learn very quickly that if there’s a little air bubble in the IV tubing, it ain’t going to hurt anybody.

All right. It takes a significant amount of air intravenous before it actually is harmful to a patient, most patients. When we have a transducer system, I don’t want any air bubbles between the catheter that’s coming out of the patient’s body and that transducer. Because that little tiny air bubble in there is going to affect the integrity of how that waveform is displayed or transmitted back to that little diaphragm in the transducer, OK. So while we don’t care about little air bubbles with IV tubing, we do care a lot about air bubbles in these transducer systems. So when they’re set up and flushed, we’re going to take a lot more care to make sure there’s no air bubbles in them. Even little teeny tiny air bubbles can have a negative effect on the waveform. If I’m monitoring an arterial blood pressure where the blood pressure’s 120 over 80, or 190 over 70, a little tiny loss of integrity isn’t going to be a big deal, right.

Oh, so the blood pressure is reading 150. And it’s really 158. Who cares, right? But if I’m monitoring a pressure in a chamber where the pressures are really low, like three millimeters of mercury, a little tiny air bubble is going to have a bigger effect on that situation. I love this, because firefighters get this stuff, right. It’s fluid, it’s flow, and it’s pipes, right? You can talk to nurses about this for days and they still don’t get it. But firefighters are like, oh yeah. I get that. It makes sense. The other important piece of using a transducer is not just hooking it up and having it read a waveform, but it has to be leveled and zeroed in order to be maintained accurate. And it has to– the transducer itself has to be maintained at that place where it was leveled and zeroed, all right. So we generally strap it to the patient’s arm. Because the point of leveling and zeroing– let me go back to the slide, because it’s a good example. It is level and zeroed at the phlebostatic axis.

How many of you have ever heard of the phlebostatic axis before? All right. The phlebostatic axis is the distance between the top of your sternum and your back, it’s the midpoint of that, and we say it’s the mid axillary space, so right down near your chest, down your armpit at the fourth intercostal space. That is the phlebostatic static axis. If I drew a horizontal line from my phlebostatic axis through my chest, it actually– that line, that’s approximately where your aorta is, and where your atria are for your heart. So these transducers are so sensitive that subtle changes in the atmospheric pressure from here to here to here make a difference in the readings. So we’re going to level and zero these transducers at the patient’s phlebostatic axis, so that we know we know that we’re at the same level atmospheric pressure-wise as is the chambers of the heart of the vessel that we’re monitoring.

Does that kind of make sense? All righty. When I have a– so it’s leveled at the phlebostatic axis, it’s going to be zeroed, which means I’m going to take away the effects of atmospheric pressure on the system. And then the third piece of this to ensure its accuracy is to make sure that it has a good square waveform. What the hell is a square waveform? So this is showing you an arterial pressure waveform from an arterial line. And what this is here is me pulling the pigtail, or squeezing the little valve on the transducer, and introducing rapid flush through that line, OK. That’s the change on the waveform that I see. So I pull the little pigtail. On the example of the transducer they there, the waveform squares off. And when I let go of the pigtail, the waveform bounces very sharply and then goes back to the arterial waveform. That’s a good square waveform test. All right. Here is a bad square waveform test. I pull the pigtail. It’s squared off. And when I let it go, there’s no bounce. It just kind of goes right back into the waveform.

When I have this situation here, it’s called an overdamped waveform. And what it does is it makes the pressures on the monitor that you’re looking at lower than what are actually going on in the patient. The most common reason for an overdampened line is an air bubble in the transducer system, or a pressure bag that’s not pumped up to 300 millimeters of mercury. And it’s causing the tip of the line to start to clot off, because there isn’t flush through that line.

All right. So what does that mean? That means I can treat the patient for being hypotensive when they’re really not. And it’s because of the transducer system. OK. Not anything wrong with the patient. It’s I didn’t set up the transducer system properly. [INAUDIBLE] Not pumped up to 300 millimeters of mercury. So what happens when that pressure bag starts to empty out or it causes the pressure to go down, that transducer is dependent on 300 millimeters of mercury pressure in order to keep it infusing at three ml per hour. There is a little valve that opens up when that pressure bag is at 300 millimeters of mercury that allows three ml per hour of flush through the system.

A different transducer might do two ml per hour. A pediatric one does one ml per hour. The idea is the pressure still has to be behind the system in order to keep that flush going through the system. All right. So here’s an– this is another example of a bad square waveform test. This is called an underdamped square waveform. So I pull the little pigtail. It squares off. And then when I let it go, it bounces like crazy and goes back to the waveform. This will exaggerate the patient’s blood pressure. So my patient can look hypertensive, when in fact they’re really not. And it’s just a fault of the transducer. All right. So the transducer is leveled at the phlebostatic access, zeroed to remove the effects of atmospheric pressure, and then maintained at that phlebostatic axis, and then a square waveform test is usually done once a shift, or any time you question the values that you’re seeing.

You’re going to do a square waveform test by just pulling or squeezing on whatever rapid flush mechanism there is on the transducer. So there’s a variety of different catheters that we can use. We can use arterial catheters. We can use central venous line. And then we could also introduce a catheter that goes all the way through the heart into the pulmonary artery. Obviously, this is dangerous, right. We’ve got these big, huge catheters sitting in arterial blood vessels under high arterial pressure. So if that line became disconnected from that transducer, patients can bleed out in a matter of 5,10 minutes, depending on what catheter it is that we’re talking about, all right. So they are dangerous. They can cause hemorrhage. That catheter that we put into the heart or even a central line, if it’s in too far, it can cause dysrhthmias.

So it can be the cause of why the patient’s in v-tac right now. It can cause pulmonary injury. The Swan catheter that I’ll show you when we get there sits all the way in the pulmonary area. It has a balloon on the end of it. That can cause rupture of the pulmonary artery and you can die when that happens. You oftentimes do die when that happens. It can cause cardiac injury. Putting a Swan-Ganz catheter through the patient’s heart can actually cause a right bundle branch block on the EKG.

So if somebody already has bifascicular block on the left side– are you with me, you know what bifascicular block is– and now I put a Swan-Ganz catheter in and it causes their right bundle branch block to occur, that patient’s now in complete heart block because I put this catheter in their body. It’s a contraindication to a Swan-Ganz catheter is bifascicular block. Also, these catheters can become dislodged. I have an agitated patient. I have a radial arterial line or a femoral arterial line. They’re moving around and flaking around on the bed. That catheter comes out, they could start to hemorrhage from having that catheter come out. This Swan-Ganz catheter that’s sitting in the pulmonary artery can dislodge. And the tip of it– instead of being in the pulmonary artery– can wind up in the right ventricle.

That can cause ventricular tachycardia. So part of caring for the patient is always knowing where the tip of that catheter is by looking at the waveform and knowing what you expect to see. I haven’t shown you that yet so don’t worry about it. So here’s an arterial waveform. The upstroke is what’s listed as the a. b, the point b on that waveform on the monitor– that’s what the monitor’s going to determine as the systolic pressure, the highest of the pressure. The lowest point on here is going to be considered the diastolic blood pressure. And then we calculate a mean arterial pressure mathematically, very different than the way the monitor calculates the mean arterial pressure.

So if you did it mathematically with your calculator and compared it to what you get on the monitor, it’s going to be a little bit different. Don’t get freaked out about that. It just does it a little bit differently. This little notch on an arterial waveform– and you may or may not see it, I don’t flip out if I don’t see it– but what it is, is it’s a bump in the waveform that occurs when the aortic valve snaps shot. That’s what the dicrotic notch is. So depending on the patient’s vascular tone, if I have this little old lady with all this bad personal vascular disease and I put an arterial line in them, I’m probably not going to see that little blip on that waveform.

But if I put an arterial line in a 25-year-old, healthy guy with great vascular tone and no peripheral vascular disease, I might very well expect to see a dicrotic notch. You should know, for purposes of when we talk about balloon pumping that all of this is systole. So the heart is still contracting through all of this until the dicrotic notch. The relaxation phase or diastole starts at the dicrotic notch down. So the heart is squeezing, relaxed. It’s the dicrotic notch that is the start of diastole. File that away for later, OK? People think, oh, diastole starts when the waveform start to go down. Uh-uh. The heart is just squeezing. There’s no more blood left in the ventricle so the pressure starts to go down, but it’s still squeezing. There’s just not enough blood left in it to generate the same pressure. So we talked about what square waveform testing is. Any time you have a transducer, with one exception, we use those transducers when we’re monitoring pressure on the inside of the brain.

We use that transducer, but we set it up very differently. We don’t hook it up to a 300 millimeter pressure bag. I don’t want to be infusing normal saline into somebody’s brain, right? So I can’t do a square waveform test when I’m doing that, but a transducer like that is used. When I have a transducer in a vessel or a chamber, I’m going to be able to do that square waveform test, because I’ve got a pressure bag that I can do a rapid flush test. So why do we put lines in? The most common reason is we want to, very closely and continuously, , monitor the patient’s blood pressure. And we don’t want to be dependent on whether or not a cuff is too big or whether or not we’re bouncing down the highway or the patient’s moving. I can see what their blood pressure is under all of those circumstances and– provided it’s leveled, zeroed, and I have a good square waveform test– I can trust it.

We compare the cuff pressure with the arterial line. And what we generally say is if the cuff pressure is within 20 millimeters of mercury of an arterial line, I believe them. They’re accurate. How can you do a square waveform test? Is that like an [INAUDIBLE] type thing? If I was you and I’m transferring a critically ill patient, here’s what I’d do. I’d walk into that room, and I would check to make sure I have enough saline in that bag, that that bag is pumped up to 300 millimeters of mercury. I would level and zero it to my monitor when I get them hooked up and I would do a square waveform test at the very beginning so that I know that during that transport I can believe what I’m seeing on the monitor. I teach people that. If you don’t do any of that stuff, if you just pack up the patient and go, now they’re hypotensive or hypertensive in the back of the ambulance.

I got to start from ground zero. Is this a technical problem or is there really something wrong with my patient right now? If I rule out all those technical issues before I start taking care of the patient, I know that it’s not the technical problem, it’s the patient. And I can deal with it quicker. So the bag is no more, no less than 300? It’s pretty tough to get it more, but I wouldn’t try to overdo it. Just keep it right at 300 millimeters mercury. Yes. OK, you’re doing the test usually when you’re leaving [INAUDIBLE] the hospital. What happens when you MedFlight this patient? Good question. In a helicopter, the changes in atmospheric pressure are not significant enough to make a big difference. If I had a long flight, I would re-zero the transducer when I was at altitude. In a fixed wing aircraft, it’s a big deal, because we’re artificially changing atmospheric pressure at various points in the flight, until we get up to altitude. So you have to be a little more aware of that sort of stuff on fixed wing transport, because they’re flying higher. Helicopters generally don’t fly, well, not generally, they never fly as high as a fixed wing aircraft so it’s not as big of an issue.

The idea is, though, that I still have leveled and zeroed it at the phlebostatic axis so the changes in the atmospheric pressure are the same changes that the patient is undergoing. So it’s less worrisome on a rotor wing device. In the picture on here, when you’re zeroing it, are we looking at like a 45…? Good. Despite what you might be told by somebody in your career, the patient has to be supine. So they have to be on their back. They can’t be side lying. But they can have their head of the bed up as high as 40 degrees. So they can have the cot up at 40 degrees. As long as they’re on their back, I can level and zero at the phlebostatic axis. Any higher than that, sitting up or side-lying, uh-uh that’s not acceptable. Old school physicians, cardiologists, in particular– because how is a patient positioned in the cardiac cath lab? They’re flat on their back.

They’re never sitting up. In their world, that’s how transducers are leveled and zeroed. They’re the ones that are most stickler about it. In reality, as I said I can provide you with all the literature that you want, if you’d ever care to see it, that patients– as long as they’re supine– can be as high as 30 degrees and it’s still safe to level and zero that transducer at that level.

So you don’t have to get all freaked out about that. Good question. So arterial lines– blood sampling is another reason why we can check ABGs very frequently without poking the patient over and over and over again. If I’m titrating an insulin drip and I need to get blood glucose levels every hour, now I don’t have to stick the patient every hour, I can just take a little sample off the line. Multiple reasons why an arterial line is indicated. You’re, most of the time, not going to be responsible for placing an arterial line. It’s possible. In some hospitals, nurses and paramedics place arterial lines. But, again, in Wisconsin, given our laws and other regulations, nurses don’t routinely do this, nor would paramedics, but it’s not outside the realm of possibility. Common placement sites for arterial blood pressure monitoring, for arterial catheter placement: Radial artery is the most common. The ulnar artery, rarely, rarely, rarely used. It’s too hard to find.

Brachial artery has become sort of more in favor now, because it’s a great big artery and so if a little blood clot or something forms on the catheter, it’s less likely to compromise circulation. And then femoral artery… Femoral artery is usually cannulated for blood pressure monitoring after a cardiac arrest situation, because the patient is going to be so peripherally clamped down. When an art line is placed, it’s not done by visualization. All right? It’s done by palpating the artery. So if you can’t palpate a pulse, it’s going to be almost next to impossible to get an arterial catheter in. So post code, they’re hypotensive, I can still feel a femoral pulse, I’m going to put the femoral arterial cath in there because I can.

All right? Because I can feel it. Other factors that go into this is the patient’s history. If I don’t have good pulses on my right side of my body, I shouldn’t be putting an arterial line in there, right? So that is going to be a reason of why we pick different sites on the body as an example. Complications from an arterial line are pretty rare. The biggest one that you would need to worry about is hemorrhage. If you notice on that transducer, it has a stopcock on it. If that gets turned the wrong way or if the tubing becomes disconnected, patients can bleed right out of that line. In an ambulance, where you’re watching the patient you’d catch that right away.

In an ICU, when you have two patients and you’re stuck in another patient’s room for two hours, if that art line became disconnected for 15, 20 minutes, you’d have a big puddle of blood on the bed. Trust me, I’ve seen it happen. Most of the monitors in the ICU now have an alarm system on it that when it suddenly recognizes that the pressure is lost, it crisis alarms, so it brings your attention to it right away. Transfer monitors are not so sophisticated like that, but you’re right there. Other things that can happen with arterial lines are circulatory compromise and peripheral nerve damage, but that’s pretty rare. Basal spasm is common with arterial lines. And when that happens, it can cause the blood pressure values that you see on the monitor to not be accurate.

So that’s something to be aware of. How would I know that someone is having basal spasm from their arterial line? I can usually see that the circulation in their hand, where that line is, is compromised. It’s pale, they don’t have good capillary refill. That’s usually an indicator that the patient is having an arterial spasm. In adults, that’s not that common. It’s much more common in kids with radial arterial lines. They actually give them medication to prevent spasm from happening. We talked about dampening and overdamping and underdamping. I don’t want to get too much more in depth with that. But here’s an example, even without doing a square waveform test, of a good arterial waveform and a dampened arterial waveform. I can just tell that by comparing these two. I’m going to just… There’s nothing here that I really… I think we know what normal blood pressure, systemic pressures are, right? I don’t have to tell you what a normal blood pressure is and we’ve reviewed this concept of mean arterial pressure.

And in critical care it’s very much viewed as very important. It should be viewed as important everywhere, but in critical care we really embrace this idea of managing someone’s hemodynamics off of their mean arterial pressure for obvious reasons that I mentioned to you. So other types of, now, invasive pressure monitoring… The book calls them central circulation catheters.

A central line. The definition of a central line is any catheter, any venous catheter that’s tip lies in the superior vena cava or at the junction of the SVC and the right atrium. That is a technical definition of a central line. So a PIC line, that’s here, typically lies at the junction of the superior vena cava and the right atrium, it’s a central line. Any time I have that tip of the catheter at that level, I can now monitor pressures in this central venous circulation. OK, and I can measure central venous pressure, CVP.

Or if the tip of that catheter is actually in the right atrium, I can measure right atrial pressure with that catheter. If I have a double lumen line or a triple lumen line, I would always pick the line that I’d hook the transducer up to that leads to the most distal tip of the catheter. All right? So there’s a distal tip and a proximal lumen that’s telling you where that catheter lumen opens up on the vessel. So I would always choose the lumen on the vessel that is this distal lumen, because that’s the one that’s going to open up at the very tip of that catheter where it’s sitting inside the body.

Make sense? Do colors vary on that? Yup, they do. Most of them say distal, proximal, medial. You’re always going for the distal. I’ve yet to come across one that actually doesn’t say distal. Depending on the catcher you use, a distal might be the brown lumen or it might be the red lumen. Don’t go by color. Go by what it says on the catheter itself. Other types of central circulation catheters are going to be the pulmonary artery catheter that we’ll talk about as well. Although I hesitate to almost talk about Swans too much, although it’s in your book and you need to know about it, because they’re being used less and less. There’s a lot of controversy surrounding the use of these types of catheters, because– not so much central venous lines, but PA catheters, because they’re very dangerous– more harm can be done to patients than good, especially if you don’t know what you’re doing with them. All right, so now we know what the technical definition of a central venous line is: a central venous catheter whose tip lies at the junction of the SVC and the right atrium or actually in the right atrium.

That’s a definition of a central line. There is a good example of a triple lumen central line. And here’s where I could determine whether it’s distal, proximal or medial. Always going to choose the distal for transduced monitoring. Historically, central venous pressure has been used as a guide to the patient’s volume status. So if the central venous pressure was low, we would say, oh, they needed volume. And if the central venous pressure was high, we would say, ah, they have enough volume. Maybe we need to [? diurete ?] some a little bit. This whole concept of too much fluid, not enough fluid– what you have to understand about this is not so much what the pressure is in the vena cava.

It’s what the pressure is in the right ventricle at the moment in time right before the right ventricle contracts. OK? Have you ever heard that before? Have you ever heard the term preload before? What we’re really trying to measure when we’re measuring right atrial pressure or central venous pressure is the amount of stretch on the right ventricle right before it contracts, Otherwise known as preload. So if I have a catheter whose tip is in the right atrium and I look at that waveform at the right time during diastole when the tricuspid valve is open, my heart on the right side is really one chamber, because the valve is open.

So if I measure the pressure in the right atrium at the time when the tricuspid valve is open, I’m measuring the amount of stretch on the right ventricle. Why is that stretch important? Why is preload important? [INAUDIBLE] Starling’s law. The farther I stretch it, the harder it’s going to contract within reason, within parameters. I can overstretch. Some people can’t stand that much stretch. But, yeah, that’s the idea. So when we measure right atrial pressure, central venous pressure, what we’re trying to get at is this preload, this stretch on the right side of the heart. And if you have a normal, functioning heart, the amount of stretch on the right side of the heart is pretty much the same as the amount of stretch on the left side of the heart. This gets really tricky when your left side isn’t working the same as your right side.

Because the amount of stress on the right side might be too much for the left side. And that’s when we start putting more invasive catheters in where we can start to monitor the filling pressures on the left side of the heart, because now there’s this mismatch. Concept’s making sense? OK? Understand this, though. That for the last 40, 50 years we’ve been hanging our hat on central venous pressure and right atrial pressure as a way of really getting at this concept of preload, but it’s invasive. There are other ways that we can figure this out that are noninvasive. I can do an echo and look at that. There are Doppler devices that I can place on the patient’s neck and on their chest that measure the stretch, without putting a catheter in the patient, that probably work a little bit better in a lot of circumstances. So there’s this idea of central venous pressure and right atrial pressure– while it’s still taught and you have to know it– people are really starting to call that into question.

Is this really the best way to ascertain somebody’s volume status and how they’re going to respond to food if I give it to them? It is being called into question. That’s what a normal central venous pressure waveform looks like. It has little undulations in it. Those Little undulations are actually something. And I would not expect to just see a CVP going across flatline on the screen. I would question the patency of the line if I didn’t see those little jiggles. Those little jiggles, if I line them up to the patient’s EKG are the contraction of the atrium, the closure of the tricuspid valve, and the squeezing of the ventricle against the closed valve. The valve bulges back and makes the pressure go a little bit higher. That’s what all those little undulations are. We don’t care about that. At your level, even at my level, most people don’t care about knowing all of that, the detail of it. Suffice it to say, though, I don’t want to see a straight line going across the screen.

I want to see these little undulations, because there is mechanical activity happening very close to the tip of that catheter that I expect to see some little fluctuations in it. When I’m monitoring CVP, the monitor knows to just display the mean value of that waveform, OK. Normal CVP what does your book say a normal CVP is? I have in my head what it is. Normally, we typically will say somewhere between 8 and 12 millimeters of mercury is a normal CVP. Why I asked you what does your book say is because… Two to Six. [LAUGHS] Two to six. All right. Two to Six is a 24 year-old college student in 1972 who volunteered his time to have a catheter put in his body and they measured his CVP while he was laying flat in bed not doing anything.

That CVP would not be normal for 90% of the population. All right, so CVP, right atrial pressure becomes relative. Some people need more stretch in order to maintain a good cardiac output. So you almost have to know what is normal for your patient. And that’s why, in my brain, I think, yeah, somewhere between 8 and 12 for most people is what it is. You need to know for the purposes of the test what the book says. I guarantee you you’re not going to be transporting a critically ill patient around with a CVP of two without doing something about it under most circumstances. On the contrary, most of the time they might even be higher than 12, because that’s what their heart needs to maintain good contraction.

Indications for CVP monitoring: Mostly, it’s related to vascular access into a central line. Large fluid volume administration, medication administration. Pressures, it’s safer to give pressures through a central line than it is through a peripheral line for obvious reasons. The patient’s peripheral vascular access might be limited, because of other health problems, their body habitus. Or the patient may need long term central access. Normal CVP, my slides say, five to eight. Suffice It to say, you’re going to find a lot of variance in what is a normal CVP. I like to hang my hat on somewhere between 8 and 12 millimeters of mercury for a critically ill patient. All the sepsis guidelines talk about keeping a patient’s CVP at least eight millimeters of mercury and giving them fluid until it is eight millimeters of mercury if they’re spontaneously breathing. Twelve if they’re on a vent. That’s a discussion for another day. We have historically always said that if you’re CVP is low, it’s either related to hypovolemia or venodilation.

Your veins dilate out like in septic shock, for example. Increased CVP– we’ve always understood it as indicative of right ventricular failure. If the right ventricle isn’t squeezing blood out into the pulmonary artery and it’s backing up, your right atrial pressure’s going to get high. It’s failure of the right ventricle. You can also see increased CVP in vasoconstriction, volume overload, cardiac tamponade, chronic lung disease, tricuspid valve insufficiency. And any time a patient is on a mechanical ventilator, because of intrathoracic changes with positive pressure ventilation, that’s going to cause the CVP to go up a little bit. Not a whole lot, but by three or four millimeters of mercury. Their CVP is going to go up just by putting them on a ventilator. And now because it’s positive pressure violation versus negative inspiratory ventilation.

Changes the intrathoracic pressures. Central venous lines– this is a big deal. I’m not going to get all into this. But central venous lines are very dangerous from an infection standpoint. This is very closely monitored in hospitals. It’s part of the publicly released information that all hospitals have to provide at the state level and the national level is what’s your central line infection rate? So these lines are placed under very sterile conditions under ideal circumstances. Even in an emergency, we’re going to do this this like we’re in the operating room. Because the risk of having an infection grow on that catheter can immediately lead to a systemic blood infection. So it’s a big deal. So we deal with this very carefully. These are the most common sites for central venous catheters. We have the internal jugular, external jugular in the neck. We have the subclavian vein in the chest.

And then we have the femoral vein as well. We really try to avoid putting central venous lines in the femoral vein for obvious reasons. Not necessarily a clean site. So if we’re worried about introducing infection, this is not the best place. But in a resuscitation, in a code, post code when patients are hypovolemic, it’s difficult to see the veins in the neck. And you don’t see these at all. They have to be nice and full to find them. This might be the easiest place to put it. So I’m not saying that you’re never going to see a femoral venous catheter.

You will, especially in a really sick patient that might be transported from one hospital to a higher level of care. They may have a femoral venous line temporarily. It’s fine. Realize that when we get the patient to the new hospital, we’re probably going to take it out after putting another one in. Because we know this is not great for infection reasons. Most frequently used, I will say, is the internal jugular vein. That is by far the most commonly– common placement position for a central venous catheter. Other places are the subclavian vein. That takes a pretty adept, usually a surgeon who knows how to put a subclavian line in, because it’s a blind technique. It’s placing a line based on anatomical location of the blood vessel, as opposed to seeing the blood vessel. Most central lines now, it is required that they use an ultrasound to find the vein. So you will see, if you work in an ED, or in critical care areas, the docs are putting this ultrasound on so they can find the carotid artery in the jugular vein, so that they aren’t accidentally putting the central line in the wrong place, which happens.

Complication rate for central line placement can be very high in people that aren’t good at doing it. Complications specifically with central venous lines, venous perforation, accidental arterial puncture, cannula dislodgement. Particularly with subclavian lines, there’s a high risk of causing a pneumothorax. If they miss the vein and nick the top of the pleural space, the patient’s going to get a pneumothorax. That’s why most people, unless they’re really good at putting subclavian lines in aren’t even going to try it, because they know that they could cause a pneumothorax as a result of it. We talked about the fact that they can cause dysrhythmias if the tip of the catheter gets in too far, infection. And just because somebody said it’s in the vein, doesn’t necessarily mean that is in the vein. So I’ve seen some horrific things where vasoactive meds have been run through the central line because that was the best place to do it. And that line actually wasn’t in the vessel. And that epinephrine infused into the neck and chest for three hours before somebody figured it out.

So we get into the habit in critical care of transducing that distal lumen to look for that CVP waveform so I can verify that the line’s in good position. Because even on an x-ray, it’s hard to tell sometimes where exactly that line is. You can see it there, but is it in the vessel? Or is it not in the vessel? That’s why ultrasound has become the mainstay of placement of these lines, so we can rule out this accidental misplacement of the line. I can see the catheter right inside the blood vessel with an ultrasound. So PA catheters. I brought one. This is a pulmonary artery catheter. Swan-Ganz catheter is the less generic name. It was invented in the 1960s and ’70s by Dr. Swan and Dr. Ganz out of Texas. Dr. Ganz was a female physician. Actually, she just died last year, interestingly enough. But they designed this catheter that is placed through a short central venous line called an introducer. And it is advanced into the patient’s first right atrium, right ventricle, to the tricuspid valve, out through the pulmonic valve into the pulmonary artery.

And then when it’s home, the tip of this, the distal tip, is sitting in the pulmonary artery. So notice it’s shape. What does that look like? The right ventricle. And when it’s placed, this shape helps it get in the right spot very easily. OK. When it’s been sitting in the body for a couple of hours, it warms up. And if I pull it out, it’s going to look like this. It’s like spaghetti. As it heats up, it loses its natural shape. So it gets a little bit more flexible. Right away when they take it out of the kit, it’s got this nice curve to it to help in placement.

The other thing that it has, so it has three lumens on it. And this is one type of Swan-Ganz catheter. There are about four or five different kinds. This is the most common, the most generic of the Swan-Ganz catheters. It has three infusion lumens on it. And they’re labeled. The blue one is labeled proximal. This one is labeled medial. And this yellow one is labeled distal. So this distal one opens up at the very tip of the catheter. So if I hooked up a transducer to this when this is sitting inside the body, I’m actually transducing the pressure from the pulmonary artery continuously on the monitor.

All right. So three lumens. The blue lumen, if I trace it all the way down to the end, when the catheter is in position, the blue lumen opens up in the right atrium. So if I hook a transducer up to it, I can monitor right atrial pressure with that. The medial lumen actually opens up right around the tricuspid valve. It’s typically used for infusing vasoactive medications. It’s a really teeny tiny little line. So I can start up a drip at a really low infusion rate. And it’s going to quickly get into the patient because it’s so tiny. The other thing that’s on this catheter at the tip of it is a one and a half cc latex balloon. This balloon is used to help guide the catheter into position during insertion. It’s like a drag parachute. So I’ve got the curve of the catheter.

I’ve got the balloon. It helps with blood flow, drag it into the right spot. Once it’s in position, though, we rarely inflate that balloon ever again, right. Years ago we used to. Nowadays we don’t so much. Because if I inflate this balloon when the tip of the catheter’s in the pulmonary artery, I’m inflating the balloon against the wall of the pulmonary artery. What do you think could possibly happen when I do that? I can rupture the pulmonary artery.

You better believe it. So we don’t do that so much anymore. All right. Once it’s in, we leave the balloon deflated. It’s a special syringe. It’s a three ml syringe, but it only pulls back to 1 and 1/2 ml. That’s because that balloon holds ml, no more, no less. All right. Well, it could hold less. But its maximum is 1.5. The other connection on here is a thermometer. It’s called a thermistor. It gets connected to a temperature cable that goes to your monitor. It is reading the temperature at the tip of the catheter. So at the tip of the catheter, I have a balloon. I have a lumen that opens up that I can transduce. And I have a temperature cable. When I inflate this balloon, I want you to notice what happens there. I can still see the tip of that balloon. So in the pulmonary artery, if I inflate the balloon and occlude the pulmonary artery, the distal tip is still looking forward into the pulmonary circulation. It’s called wedging the catheter. We don’t do that anymore much at all. But if I do this, I can look through the pulmonary vasculature all the way through to the pressures of the left atrium.

So with this catheter, I can indirectly monitor left atrial preload. That was the goal of inventing this catheter. We don’t like sticking things in the left atrium and the left ventricular or the aorta if we don’t have to. It’s pretty dangerous to do that. So if we could figure out a way to measure the left sided filling pressures, especially when we have this conjugate or discoordinate relationship between right ventricular function and left ventricular function, like we have in left heart failure. How nice would it be to be able to indirectly monitor those pressures. So that’s how AP catheter is used. The last thing that it does, and I’m going through about 15 slides here, so that’s fine. It’s easier to talk about it than look at slides. The last thing that we can do with this catheter, and we do it, is we can inject a known volume of a solution and a known temperature at a precise rate and introduce that into the right atrium.

So it’s going to go through this blue line. And time how long it takes that now subtly cooled blood, because I’ve introduced 10 ml of room temperature IV solution into the as a bolus, how long it takes that bolus of IV solution to get from the right atrium to the distal tip in the pulmonary artery. And in doing so, I can calculate the patient’s cardiac output off of that. It’s called thermodilution cardiac output. It’s the most standard, traditional way of directly measuring a patient’s cardiac output. There are other ways. It is typically the most standard way of measuring cardiac output, thermodilution. Timing how long it takes 10 ml of room temperature saline to get from the right atrium to clear all the way past the distal tip of this. It’s a big, long mathematical formula that you would never be expected to know. But suffice it to say, it gives us our cardiac output.

So with this catheter, I can measure right sided preload, left sided preload. I can measure pressures in the pulmonary artery. And I can determine the patient’s stroke volume and cardiac output. So I can really see how the heart is functioning, but in an extremely invasive way. We talked about some of things already. This can cause an arrhythmia. It can cause a right bundle branch block, because it’s resting on the bundle branch, the bundle of His.

It can develop clots on the end of it. So now the patient’s got a blood clot sitting right in their pulmonary artery, waiting to become a pulmonary embolism. It can puncture the right ventricle. It can puncture the pulmonary artery. Lots of bad problems with it. But that is the purpose of this catheter, to sort of optimize my cardiac function. So when I said to you, well, if I could identify a problem with the patient before they actually get hypotensive, this is where this comes in. I can see that the patient’s right atrial pressure’s starting to get low. Well, I know the last time it got that low, they got hypotensive.

So lets not let them get hypotensive now. Let’s give them a fluid bolus, because I know their right atrial pressure is at such a point, where as if it gets any lower, they’re going to get hypotensive. So let’s treat it before they actually get there. I can see that when I give that fluid bolus, that it has an immediate effect on the patient’s cardiac output.

So I can see the immediate effect of stretching the right ventricle, stretching the left ventricle a little bit more with some fluid, because now my cardiac output is better. I can see that with this catheter. OK. If I’m using drugs to do that, I can titrate up on the drugs or titrate down on the drugs and see immediately what the effect is on preload and cardiac output. All right. I blasted through all these slides. So this is what the catheter looks like when its positioned in the pulmonary with the balloon inflated, which I said we don’t really do that anymore. We use the balloon inflated just for insertion. And then never inflate it again. The waveforms that we see when we’re transducing this distal tip as we’re advancing it into its home position are shown here.

The first one that you see is the right atrial pressure. Looks like a CVP waveform. Makes sense, right? That’s what we would expect to see in the right atrium. When it gets into the right ventricle past the tricuspid valve, the pressures change dramatically. And I have what almost looks like an arterial waveform. It doesn’t have a dicrotic notch. And the diastolic blood pressure almost gets down to zero. As a matter of fact, if I really measure this out carefully, I would find that the lowest point of my right atrial pressure is the same as the lowest point of my end diastolic pressure. Because remember we said the tricuspid valve is open, it’s one chamber right before it contracts. So the pressures are going to be the same when that tricuspid valve is open. I don’t want to confuse you. Maybe should’ve have said that. But that’s what we’re getting at here. That’s what we care what somebody’s right atrial pressure is.

It’s their end diastolic pressure, the stretch on the myocardium before it contracts. When it gets into the pulmonary artery, the wayform– oops– the waveform changes again. It looks kind of like an arterial waveform. But notice the pressures that we’re seeing here. We’re seeing it’s a low pressure system– systolic in the 20s, diastolic in the teens. It has a dicrotic notch. But that dicrotic notch not closure of the aortic valve. Its closure of the pulmonic valve. But it has a distinctive arterial appearance. Just the pressures are much lower. So this slide is showing you what we used to do, how we would use this. If I inflate the balloon and I’m transducing that distal tip, I’m looking forward to all of the pulmonary circulation all the way over to the pressures inside of the left atrium. Now we use the pulmonary artery diastolic pressure. What you will find is in most patients, the pulmonary artery diastolic pressure is the same as the wedge pressure that I would read.

So rather than inflating the balloon, I’m just going to look at the PAD and go, yup. That’s the filling pressure on the left side of the heart. It closely approximates that. Much safer than inflating that balloon. So here’s a right atrial waveform. Very closely approximates CVP in many people’s minds. Right atrial pressure is the same as CVP Just understand that CVP is sort of at the door of the library. And right atrial pressure is standing at the counter of the library with your library card and book. All right. You’re in the right atrium. I’m measuring right atrial pressure. Right ventricular pressures. I’m going to just kind of glance over this. There’s your right ventricular waveform again. And here’s your pulmonary artery waveform. Systolic in the 20s to 30s.

Diastolic in the teens. It has a dicrotic notch. Normal systolic PA pressures is 15 to 30 millimeters. Diastolic is about 8 to 15. The diastolic blood pressure, the pulmonary artery diastolic, or PAD, is an indirect measurement of left ventricular filling pressure. And then we have pulmonary artery mean pressure. Normal is 10 to 20. Most of the time when you are transporting a patient with a PA catheter, your job is going to be to make sure that the tip of that catheter is still in the pulmonary artery.

When you’re moving patients around, sliding them over to the gurney, sliding them onto the CT scanner, the catheter is designed in such a way that it can move, much more than a central line, a typical central line will move. So any time you move the patient, it is possible that the tip of this catheter is either going to go into too deep or slip back into the right ventricle. And if it does either of those things, if it moves in too deep, it can puncture the pulmonary artery. If it slips back into the right ventricle, this is going to– this sharp tip is going to be bouncing around on the inside of the right ventricle. What do you think could happen? Arrhythmias. Perforate. So your goal in taking care of a patient with a pulmonary artery catheter in transport mostly is just knowing where the tip of that catheter is. And knowing what the patient’s normals are. And where you would start to get excited about doing something before the patient actually got hypotensive. You’re probably not going to be doing shooting card– I know you’re not going to be shooting cardiac outputs in transport.

You’re just going to want to know what it was before you left. Most of the transport monitors do not have the capability of doing what I described to you. That’s going to happen in the ICU. But that’s what we do with it. So cardiac output– this becomes very important. Because this is sort of moving us into the end all, be all of what we’re always doing with our patients, even when you were just checking somebody’s blood pressure and checking their heart rate. What you’re really trying to get at, even though you maybe didn’t think about this, was what’s their cardiac output. What’s your stroke volume. How are they moving oxygenated blood around their body. That’s what this is.

Normal cardiac output is four to eight liters per minute. All right. Eight liters per minute in me is probably not enough for somebody who’s six foot four, 300 pounds. So having cardiac output in liters per minute can be very misleading. It does not tell us what’s appropriate for the patient. So what we generally do is we take the patient’s body surface area and divide the cardiac output by the body surface area and, get what’s called a cardiac index. Now I have cardiac output value that’s stratified for that patient’s body type. And so basically what that means is a cardiac output of less than two in a toddler, it means the same thing as a cardiac output of less than two in someone who’s six four and 300 pounds.

It means cardiac failure. OK. So the cardiac index is used to normalize the value for all body types, So that I only have to remember that a cardiac output of less than two is bad. It doesn’t matter how big or small the patient is. If I don’t get the indexed value, if a cardiac output is five, that may be enough. Or it may not be enough for that patient, depending on their body size. So the cardiac index is the value that we mostly talk about.

That’s the one that most everybody cares about. Normal cardiac index is to liters per minute. So what determines your cardiac output index? We’ve talked about a couple of these things already. You know this already. Your heart rate affects your cardiac output. The faster your heart rate goes to a point, so will your cardiac index go up. Your output and index will go up.

But if I get the patient’s heart rate too fast, like in SVT, or rapid atrial fib, and I don’t allow enough filling time, what happens to your blood pressure? It goes down. That’s because your cardiac output and index have gone down. That’s what’s really happening. So heart rate can be used to manipulate the patient’s cardiac output. That’s one thing. Preload. We’ve been talking about that now for about a good hour.

That’s the amount of stretch on the ventricles, either the right or the left ventricles. And we determine that by looking at right atrial pressures, CVP, or pulmonary artery diastolic pressures. That’s what we’re going to do then. So preload, the amount of stretch, is another influencing factor on the patient’s cardiac output, cardiac index. I’m going to say cardiac index from now on, because I hate saying cardiac output, cardiac index.

And we all know what I’m talking about now, right? OK. So preload affects cardiac index. Heart rate affects cardiac index. The next thing is contractility. We understand that as Starling’s law, we think about preload. But there are drugs that I can use on patients that are going to increase its contractile state, drugs like epinephrine, dopamine, milrinone. Those are drugs that increase the force of contraction. So I can change somebody’ cardiac index by changing their heart rate, by changing their preload, and by changing the contractile state of their heart directly with a drug. The other thing that you less have thought about, I would imagine, up until this point that is an influencing factor on cardiac index is the amount of resistance that the left heart has to pump against to eject blood out of it.

That is called afterload. It’s another thing that we can measure with that Swan-Gantz catheter. It’s a calculation. Normal SVR, systemic vascular resistance, is between 900 and 1,400 dynes per meter squared. I don’t care that you remember the dynes per meter squared. Just remember 900 to 1,400, all right. That’s the amount of total resistance that the left heart has to pump against. So if there’s a lot of resistance, if the patient is very vasoconstricted, and the left heart is trying to eject blood out of it, it’s not going to be able to. So my stroke volume falls. So I have these four things that at any given time are controlling my cardiac index. I have my heart rate. I’ve got my preload. I’ve got the overall contractile state of the heart.

And I’ve got this resistance to blood flow, because I’m vasoconstricted. Or like in the case of septic shock, where I lose all my vascular tone, I will have a very low vascular resistance. I think the lowest SVR that I’ve ever seen a patient in fulminant septic shock was an SVR of like 200, 150. Normally, it’s 900 to 1,200, 1,400. Somebody in cardiogenic shock. And this is why a catheter like this was so important. Somebody in cardiogenic shock, what’s the compensatory mechanism from your blood vessel standpoint when the heart is not pumping effectively? What are your blood vessels doing? They constrict, right? So if somebody is in left heart failure, in cardiogenic shock, and their heart can’t pump, it’s not ejecting enough blood out. Immediate compensatory mechanism that the body puts forth is to vasoconstrict. Well, that raises my resistance. Now my heart is pumping against my heart that can’t pump already is pumping against all this resistance. So when you go out into the community and you’re taking care these cardiac patients in the field, they’re all on all these meds that are vasodilators, that slow their heart rate down.

What they’re trying to do with all those meds is to lower the amount of resistance the their left heart has to pump against every time. We think of it as well, they’re on blood pressure medications. What they’re really trying to do, yeah, we’re trying to lower their blood pressure. But what we’re trying to get at is to lower the amount of resistance that the heart has to pump against, all right. The resistance that the left heart has to pump against is the diastolic blood pressure. Because every time the left ventricle contracts, it has, in order for the aortic valve open, it has to generate a pressure that is higher than the diastolic blood pressure. So if my diastolic blood pressure is 100, the aortic valve is going to stay shut until the left ventricle generates at least 100 millimeters of mercury. This is all going to make sense when we start talking about balloon pumps. Trust me. OK. That amount of force of contraction is using up a lot of oxygen to generate that pressure. And so one time, two times, three times, who cares. but when your left heart is working 100 times a minute for hour after hour after day after week, that is putting a considerable amount of stress on the left ventricle.

That’s what afterload is. It’s the workload that the heart has to overcome. And when the heart’s working hard, it’s using more oxygen. And if I can’t get enough oxygen to the cells because I’ve got coronary artery disease, I can really get into trouble with a patient. So things that alter preload, hypovolemia and hypervolemia. Pretty common sense. Other things that will alter preload are any time you alter the vascular space, so like in septic shock.

You vasodilate. You haven’t lost blood volume. It’s just hanging out in places where it doesn’t usually hang out. It’s not getting back to the heart to increase preload, all right. Spinal cord injury, acute spinal shock, does the same thing. Profound vasodilatation, patient gets hypotensive. Hasn’t lost any blood. It’s just sitting out in the periphery not getting back to the heart.

Those are things– things that can cause. Anaphylaxis is another one. There are also drugs that cause profound venodilation. A big one is nitroglycerin. That’s why your patients, when you give them nitroglycerin, they drop their blood pressure, because it’s a venodilator. Why you’re careful when you give them nitroglycerin. The ACE inhibitors, the ARBs, all those things are venodilating drugs. Conditions that alter afterload. So how do we manipulate the resistance that the heart has to pump against. Well, sepsis– we’ve already determined that. Anything that causes vasodilatation is a way of manipulating afterload. A lot of drugs can be used to manipulate or lower afterload. Most of these things are things that you encounter every single day, on every single run that you go on, right. They’re on calcium channel blockers. They’re on ACE inhibitors. All of this is this idea of making the left ventricle work less hard the pump against that– not having to pump against that high diastolic blood pressure. Other drugs, maybe I want to increase afterload, so like in septic shock and in spinal shock. I want to cause vasoconstriction, right. I don’t want them to be so vasodilated.

So I can use drugs to cause vasoconstriction. So epi, norepinephrine, dopamine, vasopressin– those are all drugs that cause vasoconstriction. So I can alter afterload by drugs. Conditions that alter contractility. Most of what we do to increase contractility is something that we’re doing by administering one of those drugs that’s mentioned up there. Decrease contractility, on the other hand, is usually not something we’re trying to do, under most circumstances. We can do it, as is shown it the list of drug below. But most of the time when we see decreased contractility, it’s because something’s really wrong. Myocardial infarction, obviously– not getting enough blood. The cells, muscles don’t contract. Cardiomyopathy, ischemia, hypoxia, and acidosis– in and of themselves, cause decreased contractility. So when your patient’s pH is 6.9, their ventricle is not contracting as well as it would contract if their pH was normal. It’s a direct myocardial depressant, when your pH gets that low, or when you get profoundly hypoxic. I can put patients on– and the term that we use is inotropic drugs. Inotropes are things that affect contraction of the heart. So a positive inotrope increases contraction.

Negative inotrope decreases the forced contraction. So acidosis hypoxemia are negative inotropes. They decrease the force of contraction. There are drugs that do that. And in some circumstances, we’ll put patients on drugs to decrease the force of their contraction. If we know that somebody is coming in for surgery, they have a cardiac history, I don’t want their heart working like crazy under the stress of anesthesia when they have surgery, so we put all those patients on preventative beta-blockers around time of their surgery. Because studies have shown that they’re less likely to have a cardiac complication when they’re having surgery. So we can do that, but generally when a patient is very sick, we’re not interested in decreasing the contractile state of their heart. We’re usually trying to fight getting more contractility. So we talked about the thermodilution technique. I explained how that’s done by injecting a known fluid to the right side of the heart at a known temperature, and timing how long it takes. The other thing that we can determine by that is stroke volume.

That’s the amount of blood that’s ejected with each contraction. Just for your information, I don’t think that you need to necessarily know how to do this, but to calculate an SVR, you need the following information. You need to know the patient’s mean arterial pressure. You need to know what their cardiac output is, not their index, but their output. And you need to know what their central venous pressure is. And it’s this mathematical formula. This 80 is a constant, a mathematical constant, so it never changes. Every patient, it’s always 80. If you do that calculation, you take their mean arterial pressure, subtract the CVP from it, divide that by the cardiac output, multiply by 80.

That’ll give you that SVR and [INAUDIBLE]. So I don’t need– if I know all those numbers by some other means, I can still calculate the patient’s total vascular resistance. Nice to know, not need to know, I don’t think. The other– the sort of the final endpoint of all of this hemodynamic monitoring is our ability to move oxygen around, right. If my cardiac index is low, I can have my red blood cells 100% saturated. If they’re not moving around and getting to the tissues, I’m not doing any good by having those cells 100% saturated, right.

The idea is that we need to understand, can we oxygenate the red blood cells. And can we move them around in the body. And the moving around piece is all this stuff– preload, afterload, resistance, cardiac output, stroke volume. All that stuff is, how am I moving this stuff around? Am I able to move it around sufficiently? And what can I do to manipulate the patient’s contractility, resistance, preload, heart rate. What can I do to manipulate those numbers to optimize cardiac index, so that I optimize oxygen delivery? That’s what we’re thinking about when we’re doing hemodynamic monitoring. That’s what it’s all about. Why people stand at the bedside like this for hours and think about what number are they going to manipulate next to optimize that patient;s flow.

OK. That’s all I’m going to say about that. Do you understand the concept of arterial oxygenation versus venous oxygen saturation, so arterial saturation and venous saturation? Have you ever encountered a time when they’ve drawn a blood gas, and they’ve also asked to get a venous blood gas, arterial blood gas and venous blood gas? So this is what it’s all about, really. This is what we care about. If I– and I’ll just use simple, basic, commonplace levels. If my arterial oxygen saturation, if I put a pulse ox on my finger, my arterial saturation right now is 100%. All that’s telling me is how much oxygen I can get from my lungs into my arteries.

It does not tell me at all, am I getting it around? Is it being used? And how much is being used. If I put a catheter in, and we can do this, into a central venous vein, and it has an oximetry probe on it, I can continually measure the venous saturation. If my arterial saturation is normally 100% on the arterial side, what do you think normally if I measure the saturation of the blood after it’s been through all the tissues, what do you think the saturation in the blood is when it comes back to the right of the heart to be re-oxygenated again? How much of a drop do you think there is? If it starts out at 100%, how low does it get after it goes through the whole body? Any– take to stab.

That’s usually what people say. Here’s what it is. It’s 70% saturated still. What that means is your body has this incredible reserve all the time for increased oxygen requirements. So if I ran up and down the hallway few times, I’m going to dip into that reserve. But my body will quickly get my venous saturation back up to 70%, so I have that reserve there.

So we only use, under normal circumstances, a normal, healthy person only uses 20% of the saturated hemoglobin, the oxygen off that. 20% of the oxygen off those hemoglobin molecules– very little, in other words. All right. Let’s now put this– extrapolate this to a critically ill patient. So now I’ve got a patient with pneumonia. I can’t get oxygen into their lungs well across to the arterial. So my O2 saturation is 85%.

If I use, under normal circumstances, 20%, what is that going to make my venous saturation? 65. Guess what? That’s a critical venous saturation. That patient is in trouble. I don’t care if their saturation is 85 over here. I’m dipping into that reserve that the patient has. For a couple minutes, not a problem. For a long time, hours, that’s going to be a big problem. So now let’s take this one step further. In a patient with pneumonia who now has septic shock and cardiac failure, their saturation is 80% arterially on their pulse ox. Their in a high metabolic state because of their sepsis.

And their heart’s not working. So I’m not pumping those hemoglobin molecules around very well. So the ones that are present in the peripheral circulation have a longer time to give up their oxygen. So now when it comes back to the right side of their body, we can see venous saturations of people in the 40– 35, 40, which is close to death, even though my arterial saturation is still 85%. In my mind, meaningless. It’s great for a stable patient who’s got one problem and one problem only. But when you’re talking about a critically ill patient who’s got all these other issues going on with them, heart’s not pumping well, they don’t have– they’re bleeding.

They don’t have enough hemoglobin in their body to carry oxygen around. That’s when these patients get into this really this imbalanced state of how much oxygen we’re delivering. And how much is left over. And anytime the what’s left over is low, below 70%, some textbooks will say it’s below 65%, that patient is in trouble. You need to think about what can I do from a contractile state, from a preload state, from an after-load state, from a giving them blood state, to optimize oxygen transport and delivery to those cells so that I get the patient back into the reserve side of things.

You’ve been doing that since the day you set foot in the back of an ambulance. You just didn’t know you were doing it. OK. Every intervention that you’ve always ever been taught to do, giving volume if somebody’s bleeding, getting them transported quickly to somewhere where they can give them blood, stop the bleeding, giving them oxygen. All of those things were to get to this end result of delivering enough oxygen and having enough left over in the reserve at the end. Because if the reserve is OK, that means I’m meeting the patient’s oxygen requirements at any given time, no matter what’s going on. One step further, not need to know, nice to know– when somebody is in end stage organ failure and they’re dying, if their venous sat is, let’s say, it’s been 60, 55% for hours, and they’re dying now. Their cells are dying, riddle me this. Why might I see the venous saturation start to go up? The organs are dying.

They’re not utilizing the oxygen. So it stays [? honest, ?] and the venous sat will go up. So if you riddled me that, you get what I’m saying about all of this. That’s really all we’re trying to do with all this monitoring pressures, transporting oxygen, oxygenating the patient well. I hope you understand the limits to pulse oximetry now. You already knew of some, right. Somebody has carboxyhemoglobin. Their stats are going to read normal.

And it’s not really carrying oxygen. It’s carrying carbon monoxide. You know that sort of stuff. But there are other pieces to this. The fact that it’s really just telling you how well you’re getting oxygen into your arterial system. It doesn’t tell me anything about how my body’s using it. Or how it’s getting back to the right side of the heart. Very limited view of things. It’s fine for a non-critically ill patient to just know their pulse ox, someone with just a breathing problem. Fine. Great. When I have a patient with multi-system problems, who are critically ill, that becomes a very limiting piece of information, that just knowing that pulse ox. OK. In the field, you’re really limited. You can’t be doing all these fancy tests. There are Swan-Ganz catheters like this that have an oximetry probe on them, on the distal tip, in addition to the balloon in them. [INAUDIBLE] measuring the saturation of the blood when it comes back to the pulmonary artery. So all the way through the heart continuously.

So I can monitor the patient continuously. I can see what their arterial sat is. I can see what their venous, it’s actually called their mixed venous saturation. Because it’s in a pulmonary artery, it’s mixed venous. That’s the name it’s given. So it is– I don’t think it’s possible right now with any transport monitor to continuously view mixed venous saturation. So in the field, you’re not going to have that. But what would I want to know when I go to get the patient is what is their mixed, what is their venous saturation right now at the start of this transport.

Once what’s their sat. And what’s their heart rate. And what’s their blood pressure. And what’s their right atrial pressure. And if everything is looking good right now, during this transport I’m going to try to maintain all those things. Because if their venous saturation was good when all those other things are OK, their venous sat is probably still going to be good, even though I can’t see it, if I can maintain all these things.

Good? Done. So in various states of shock, and then we’ll take a break– and any time you want to getup and go the bathroom if you’ve got to go, just go. I don’t care about that. Cardiogenic shock– this is what we’d see a patient. Decreased cardiac index, elevated CVP, because blood is not moving to the system, my SVR, my vascular resistance, is going to be elevated. I’m going to have poor oxygen delivery. Forget the DOT and the VOT. Suffice it to say, I’m not going to be delivering enough oxygen to the cells if my heart is not pumping effectively. In hypovolemic shock, in late hypovolemic shock, we’re going to have decreased cardiac index, decreased CVP, or right atrial pressures are going to be low. Compensatory mechanism to shock is to vasoconstrict. So my SVR goes up. And I can have low oxygen consumption. In distributive shock, like sepsis or spinal shock, I have an increase in my cardiac output.

Why would my cardiac index go off in things like spinal shock? So the volume is OK. I am a little bit vasodilated. And if I’m young and healthy and have a great heart, my response to having less resistance is our hearts will pump more effectively, all right. So in septic shock, what you oftentimes see in early sepsis is that the patient will have a really low SVR and a very high cardiac output. Because their heart is just pumping away like crazy to no resistance. So the output stays very– it actually is elevated. What happens though, in septic shock, is as the patient get sicker and you get into late septic shock, when the heart starts to fail, then cardiac output will fall. And that’s the end result of septic shock as is cardiac failure. But very early on septic shock, if you measure someone’s cardiac output, it’s actually normal to high, because the heart is just pumping against no resistance.

And while it’s still healthy, it’s able to generate a very high cardiac output index. So the intra-aortic balloon pump. How many of you have seen a patient on a balloon pump ever? It was initially designed for short term management of patients that are having an acute cardiac event. It’s broadened its scope a little bit. But it still is basically used for short term management of somebody undergoing some sort of acute cardiac event. So they may have had an acute MI. They may have had cardiac surgery and not recovered well after that from stunned myocardium from having been cut into, and whatever else they did to it. This device can be used. It is a device that is placed in the femoral artery.

And I meant to bring one day. And I apologize for forgetting the catheter. Because it’s quite impressive to see when you look at one. The catheter itself is about this long. The balloon on it is about that long. It’s a very stiff, thick catheter, thicker than that is even. That is introduced into the femoral artery. And it’s threaded all the way up the aorta, so that the distal tip of the balloon sits just shy of the subclavian artery on the left hand side. And the base of the balloon sits right above the renal arteries If the balloon was in too far, it can obstruct blood supply to the left arm, including the subclavian artery. If it sits too low, it can obstruct the blood supply to the kidneys. And you can develop acute renal failure for it. Why is that being told to you? Because when you move a patient around with a balloon pump in them, that’s when the balloon pump shifts. It can move inside the body. We want to be able to move, because we don’t want it to get stuck in a certain spot.

We want to be able to adjust it if need be. So it is a mobile catheter. You cannot sit a patient up bolt upright, above, much above 30 degrees. Otherwise that cause the catheter to advance and the balloon will get obstructing the subclavian artery.V So that’s where it’s positioned. It’s approximately a 40 ml balloon that is filled with helium. The gas helium is used because it’s light. And it shuttles back and forth from the balloon to the machine and back and forth very quickly because its a light gas. And it’s basically an inert gas. So if the balloon ruptures inside of the patient’s aorta, which it can, helium is dissolved very quickly out of the vascular space. So it’s not going to like get into somebody’s head and have a big air bubble. It just– poof. It just disperses. So it’s a very nice– hydrogen would be better probably, but as you know, hydrogen is a non– it’s a pretty volatile gas.

So that could be a problem, right. It gets lighter and moves faster, but it’s not a safe gas to use. And it’s safer than using air, because air does not dissolve as quickly if the balloon ruptures. So that’s how they came upon helium. Plus it doesn’t move around. These have been around since the late ’60s, early ’70s, and are still fairly widely used today. It is a mainstay if a hospital doesn’t do open heart surgeries and they have a cath lab, they have to have the ability to put a balloon pump in. So that’s where you start getting into critical care transport of patients with a balloon pump. Because now they have to go from this small little community hospital where they had to put a balloon pump in, and now they have to get this patient somewhere where they can do open heart surgery on them.

Because it’s a temporizing measure for somebody who needs to have an open heart procedure. Balloon pumps do two things, and two things only. And don’t let anyone tell you otherwise. They increase coronary artery perfuse. And they decrease afterload. Now you know what afterload is, right. Specifically, the afterload that it’s decreasing is it’s lowering the diastolic blood pressure. So every single time a the left ventricle contracts, instead of having to overcome 100 millimeters of diastolic pressure before the aortic valve opens, it lowers the diastolic pressure. And now the left ventricle only has to have 90 millimeters of pressure generated in order for the aortic valve to open. That doesn’t seem like a lot. But when we’re talking about every single contraction of the heart over minutes, hours, days, that 10 millimeters, five millimeters change in the diastolic blood pressure, making it easier for the left ventricle to open that aortic valve, makes a difference on how much oxygen requirement the left ventricle has. Yes? [INAUDIBLE] Does it do that. [INAUDIBLE] On average, how long [INAUDIBLE] So that’s complicated. Around here, in this state, very short, three, four, five days max. Why do you think that that would be– what do you think is the most limiting factor to leaving a catheter like that in somebody? No.

Complication rate. Having a big, huge catheter like that in the femoral artery– clots, vascular compromise distal to the catheter. That’s why you can’t sit them up. It can move and it takes up a huge portion of the femoral artery. So if I’ve got femoral artery peripheral vascular disease, I’ve seen patients lose legs from having had a balloon pump in. Infection is another big one. It’s in the groin. You better believe it. So that’s sort of the limiting factor.

Having said that, there are centers around the country that use balloon pumps for people with chronic cardiac failure while they’re waiting to get a heart transplant. It’s one of the strategies that are used. You’re going to learn about others. You’re going to be learning about ventricular assist devices, which are probably– long term have less complications. But they’re more difficult to put in. Requires a surgery to put in a ventricular assist device. I can put this in in a cath lab. So it’s easier to put in than it is a ventricular assist device. But there are centers that keep these in patients for months. They actually put them in what’s called a retrograde. So they put them in through a sternotomy incision into the aorta upside down so the patient can be up walking around with their balloon pump in. I’m not going to get into all the wheres and whys and hows and what the hell are they doing this for. It has a lot to do with insurance reimbursement. It has a lot to do with how quickly you can get a heart transplant. In big cardiac transplant centers, they do stuff to try to move patients along quickly.

And the trajectory of being able to get– if you’ve got a balloon pump in, and you’re on the transplant list, you’re going to get a heart before somebody who doesn’t have a balloon pump is who’s on the list. So this is very complicated. I’m not trying to sound like it’s nefarious, but it might be. No, I’m just kidding. So long answer to a very short question. In our world, four or five days max because of the complications associated with that. So it does two things. And this is an absolutely need to know. It increases coronary artery perfusion and it decreases afterload. It increases coronary artery perfusion by inflating during diastole. I’m going to go back to this picture. So what position is the aortic valve during diastole? Open or closed? The aortic valve. Closed. You had a 50/50 chance of getting the right answer there, but during diastole when the left ventricle is relaxed the aortic valve snaps shut. What did we say on the arterial waveform was the beginning of diastole? The dicrotic notch.

What did we say the dicrotic notch was? The closure of aortic valve. So the balloon inflates at the dicrotic notch. At that point in time, that’s the beginning of diastole when that aortic valve is shut. The balloon inflates then. So the blood between the end of the balloon and the aortic valve is going to be pressurized by having that balloon inflated in that closed space. Are you with me? Where does the blood come from in the coronary arteries? Where are the openings to the coronary blood vessels? Right above– Just above the aortic valve.

So during systole the aortic valve is open. The leaflets of the valve cover up the coronary sinuses so very little blood gets into the coronary circulation during systole. Under normal circumstances, during diastole when the leaflets close that’s when all the coronary artery perfusion occurs. And it occurs because during systole, the valve is open and the aorta is being stretched. And during diastole, the valve closes shut and the aorta recoils and squeezes blood into the coronary arteries.

So if I can, during diastole when the coronary sinuses are open, increase the pressure in the aorta above what is there because of the stretch by inflating a balloon in a closed space, I can increase coronary perfusion in the coronary arteries. So that’s how it works to increase perfusion. You might surmise that the timing of that inflation has to be pretty precise because if I happen to inflate the balloon during the time of systole and the balloon is in the way, that’s going to be a problem because it completely occludes the aorta when it’s inflated. So timing of the inflation and deflation of the balloon is very critical. Fortunately, the device does that very well, very, very well, such that most people nowadays have lost the nuance of timing because the machine is so automated it just does it well itself. But it’s using, it triggers off of the patient’s EKG rhythm to inflate and deflate. We look at the waveform and look at the arterial waveform to time when the balloon should inflate and deflate to assess it.

But the device is using the ECG trigger to determine when it’s systole and when it’s diastole based on the ECG signal. [INAUDIBLE] Good question. It used to be a big pain in the ass when a patient would go into atrial fib because their heart rate is so irregular. The devices now have this sophisticated algorithm that it recognizes that the patient has atrial fibrillation and it goes into this mode called auto R-wave deflate.

So no matter where it is in the inflation/deflation process, if it senses an R-wave it deflates the balloon. So it’s a very safe way of operating. It’s a default setting on the balloon pump now, auto R-wave deflate. Years ago, when I first started out as an ICU nurse you were screwed if your patient went into atrial fib. You could spend hours just timing the pump instead of just trying to deal with the arrhythmia because the balloon would be inflated during systole and all kinds of nasty stuff would happen. So very– again, I can tell you’re listening and understanding what I’m saying if you ask a question. This is the controls of the pump. And the pump that we use in the hospital is the one you take on transport. It’s probably about 200 pounds. Has some wheels on it. It’s very unstable in the back of an ambulance. It has to be secured because you wouldn’t want it sailing around in the back and of the ambulance. You would kill somebody. The balloon pump inflates and deflates in a sick patient one to one. So for every systole and diastole there’s an inflation and deflation of the balloon.

So I said that the balloon inflated during diastole and the balloon deflates just before the next systole. And that’s how it does the second part of what we said it does. It increases coronary artery perfusion and it decreases afterload. So if the balloon is stretching the aorta more than it would ordinarily be stretched, if I leave that stretched balloon inflated and a stretch there for a split second right before systole, when the left ventricle contracts and the aortic valve opens up there’s more space in that aorta for the end diastolic pressure. The diastolic pressure is lower so it takes less squeeze of the left ventricle to open up that aortic valve. So I lower my diastolic blood pressure. That’s the most difficult concept to understand. So you get the inflating during diastole, improving coronary circulation. The balloon stays inflated just before the next systole and it deflates.

And in that split second, it’s right when the aortic valves are opening up. That left ventricle is squeezing and the aortic valve opens up with less pressure from the left ventricle because there’s less pressure in the aorta at that time. There’s more space in there so it opens up. Yeah? [INAUDIBLE] It’s not really void, but yeah. It’s more space. It’s full of blood, but there’s less pressure there because there’s more room for that blood to be in. Yeah. Again, the difference that we’re talking about here and the difference in the diastolic blood pressures to having the balloon there or not there at that moment in time is we’re talking 5 millimeters of mercury.

It’s the difference between somebody’s diastolic blood pressure being 90 diastolic and 85 diastolic. Which doesn’t seem like a whole lot, but when your heart is in failure that little bit of lowering of diastolic blood pressure across the trajectory of time– hours and days– really takes away some of the workload that the left ventricle has to pump against. And it makes a difference when you can’t get oxygen to the coronary arteries because you’ve got coronary artery disease, it helps with decreasing myocardial oxygen demand. It improves circulation to the coronary arteries and decreases the workload of the heart by lowering afterload.

Everybody with me on that? So it’s indicated for cardiogenic shock, left ventricular failure. Those are the two most common things. Stunned myocardium, cardiac surgery probably next. The use of it in septic shock and drug-induced cardiac failure not so much. The company will tell you that, but in reality we’re not putting balloon pumps in people in cardiac failure as a result of septic shock. It’s not going to work really well and it’s not going to change the outcome.

So the balloon is rapidly inflated with helium and deflated with helium with each cardiac cycle. Timed off of the ECG signal is the most common way. So the patient will have your three or five lead EKG for your monitor and they’re going to have an additional five leads nowadays connected to the balloon pump so that the balloon pump can see the EKG waveform so that it can adequately time. The balloon also can pump time off of changes in the appearance of the arterial waveform. So for some reason if during your movement of the patient, the leads from the balloon pump pop off it’s not going to stop the balloon pump from pumping. The balloon pump will switch from ECG as the trigger to pressure as the trigger, the pressure waveform as the trigger. As soon as I hook the leads back up, it switches back to ECG as the trigger. [INAUDIBLE] No. It’s so amazing compared to– so can I guarantee that every hospital that you go to around the state is going to have the most state-of-the-art balloon pumping equipment? Probably not.

The most common kind of device is made by [? Mecet ?] and most everybody around here has that device. There are other devices that work a little bit differently and I can’t speak to exactly how they work, but around here it’s going to be a [? Mecet ?] balloon pump at a very sophisticated operating mode because that technology’s been around for 10 years. So I can’t imagine anyone working with a balloon pump that’s older than 10 years right now because they don’t work well that long. So yes, you would be OK around here. On flight, they will sometimes take that device. You can see it’s relatively portable looking. It’s heavy though. They could strap it on a helicopter. Flight actually has their own balloon pump and it’s not one of those [? Mecet ?] devices.

Or at least it wasn’t five years ago. I haven’t asked in awhile. It’s a different kind of device. And quite frankly, it’s not that sophisticated. At least, it wasn’t then. But it’s much lighter, smaller, much more appropriate for the inside of a helicopter. That is as much as another patient could weight. So weights and balances and all that kind of nonsense can be effective. It’s not nonsense. You know what I’m getting at.

Contraindications to a balloon pump or anybody that has a poorly-functioning aortic valve because the coronary artery perfusion is dependent on a functional aortic valve. If the aortic valve is prolapsing on itself, where is that bolus of blood going to go every time the balloon inflates? Back into the left ventricle. What is that going to do to the left ventricle if I keep blasting blood back to it? It’s going to put it into failure. So I can really hurt a patient with a balloon pump if I don’t know all of the nuances of who it can be used on and how timing works. So peripheral vascular disease, they’re at risk for injury to blood supply to their lower extremities. That’s a big risk factor for patients with terminal pulses. As a matter of fact, there’s actually a Doppler. You guys know what a Doppler is? For assessing pulses built right into the balloon pump so that you can frequently, every hour, check the distal pulse because it’s such a big deal because that catheter is so big.

Irreversible brain damage. We’re not going to put a balloon pump into somebody like that. Somebody with endstage heart disease that’s not a transplant candidate. We’re not going to put a balloon pump in them. That would be foolish. Anybody that has, obviously, a dissecting aortic or thoracic aneurysm. You probably don’t want to put a polyurethane balloon that’s going to inflate with 40 cc of balloon 100 times a minute in that dissecting aorta. So that is actually one of the complications that you’re always assessing a patient for who has a balloon pump because it can induce injury to the aorta, dissection of the aorta. So if a patient with a balloon pump suddenly complains of back pain, my brain immediately goes to, we need to get an x-ray and make sure this patient isn’t dissecting. Yeah? [INAUDIBLE] Not generally speaking. They can feel like it’s like somebody tapping your chest. It feels like that, but it’s not any discomfort or pain.

So discomfort, pain in the past, you have to think that this is what’s happening. And in the back of an ambulance or a helicopter, there’s not going to be much you’re going to do about it. But let them know at the receiving hospital what’s going on. The biggest side effects or complications, as we’ve said, are limb ischemia, bleeding at the insertion site. You have to remember when they are putting this in in the cath lab they give a lot of anticoagulants. And so now they are poking the femoral artery with all these anticoagulants on board so there tends to be a lot of oozing around the insertion site. So you have to watch for that. Thrombocytopenia not for you to worry about, but over time, over days, that balloon inflating and deflating, it damages platelets so it can make your platelet count go down.

A balloon leak or rupture happens. Particularly, if patients have calcified aortas. And it’s not usually something in the first 24 hours that will happen, but 2, 3, 4 days in. And the balloon doesn’t rupture like a party balloon. It gets a hole in it and the helium leaks out of it. So it’s not like there’s pieces of balloon circulating around the patient’s body. They’ve done lots of studies on that. When the balloons first came out, they were latex balloons and they would rupture and leak fragments of the balloon, but now they’re– I feel bad I didn’t bring it in. It is almost like thick Saran wrap. That’s what the balloon looks like. It’s clear, thick Saran wrap for lack of a better term. Infection, as you brought up; aortic dissection; and then compartment syndrome. Do you guys know what compartment syndrome is? You know about it from casts and things like that. But any time you have decreased circulation to an extremity you can get compartment syndrome. So that’s the other thing we’re always watching for by watching for our distal pulses, assessing for pain and paresthesias in that extremity, which would be indicative of poor blood supply, potentially compartment syndrome.

I have seen patients lose legs from having a balloon pump in. It is a risk factor. Obviously, the patient that has peripheral vascular disease, like a diabetic with a balloon pump in, actually, the highest rate of complications like that for balloon pumps are female diabetics with peripheral vascular disease. Small body habitus, small blood vessels that are peripherally damaged. And if you’re diabetic, you know you already have bad vasculature. So that is the patient population that has the highest risk. VADs. You’re going to have somebody come and talk to you about this. But VADs are the flip side of all this. VADs are now designed more for long-term use in patients. So patients can go home with a VAD. You don’t go home with a balloon pump, obviously.

That would be a little tough to take care of somebody at home where there’s that much at stake at any given time. I think there are a total of six VADs, five of which are used in the Milwaukee area– St. Luke’s, Froedtert– in the Chicago area at UW Hospital. So these patients now are trickling out into the communities. And I know someone’s going to come talk to you guys, I think, about that. Or you did already. They’re out there. They all rely on, basically, the same need for adequate volume status of the patient to work properly. Some of them are pulsatile, meaning they create a pulse. Some of them just create flow. So you could have a patient that’s wide awake and talking to you that you can’t feel a pulse on because it’s just providing forward flow of blood, not in a pulsatile fashion, like a heart contracting.

Some of the VADs contract. We used to think that that was very important. Now we know that it’s more about the flow. So most of the newer VADs just generate flow and no pulsatility. So it’s becoming more and more common that you would find a patient that you don’t feel a pulse on, but they’re awake and talking to you because this VAD is just continuously pushing blood around as opposed to pumping it around and circulating it around. Most of the VADs, as you learned, are for a bridge to transplant, although there are some that are used for patients that are in endstage life and go home and maybe get another year or two on this VAD to be at home with their family, but ultimately, the goal is that they’re going to die with this device in. So in summary, critical care paramedics probably not going to be establishing or inserting any of these devices or lines, but you’re going to be responsible for caring for patients that have them; understanding this idea of leveling, zeroing, transducers, knowing what a square waveform test is, knowing what the different waveforms look like, what you expect, knowing what the patient’s baseline is when you pick them up so that you know what to watch for and thinking about what you’re going to intervene with if the patient deteriorates.

And then understanding these concepts of how we can manipulate cardiac index via the heart rate contractility preload and afterload. All the various ways we can do that. And then understanding this difference between how much oxygen we deliver and how much oxygen is returned and determining how we’re taking care of patients. That’s like a minute summary of everything we talked about for the last 3 and 1/2 hours. What kind of questions do you have about that stuff? Yeah? [INAUDIBLE] Yup, it does. Stop the balloon from pumping and transport the patient. [INAUDIBLE] Yup. So everything that we were trying to gain with the balloon pump is now lost and we’re just going to have to deal with the patient until we can get them into a place where they can replace the balloon. And the balloon has to be– they can’t take the old one out and put a new one in through the same site.

It has to be placed in a different site. So it’s a big deal. It doesn’t happen that often, quite honestly. Most of the time, balloons never rupture. Yeah, so that’s the one thing that could happen to you on transport is that the pump could fail. Helium can run out. The device should always be plugged in in the back of the rig so that– around here, what are you going? A 20, 30 minute transport. Max. Live out in North Dakota or Wyoming, this becomes a bigger deal. The battery will last hours. A fully-charged battery will last hours. Helium. I would check the helium supply to make sure I had at least a half tank of helium. It uses a 40 mL bolus of helium for about two hours and then it cycles in a new bolus of helium in. So even if you turn the helium off, I have two hours worth of time with this balloon using the same.

So they’ve got this thing so well figured out. The one thing that can happen is pump failure. In a hospital, I go get another balloon pump, hook it up, and start pumping again. You’ve got about 15 minutes of the balloon being static in the body– not moving in the body– before clot starts to form on it. So after 15 minutes we say, no matter what, do not start reinflating that balloon again unless you manually inflate and deflate the balloon with a syringe and helium that you take or air that you take from the atmosphere. Put a stopcock on it and intermittently, once every couple of minutes, just inflate and deflate the balloon with 40 cc of air just to keep it moving while your waiting.

I’ve never done that. i teach it. I show people how to do it, but I’ve never done that. But I’ve never had a balloon pump fail on transport. And that’s the only time that you would do that. So the balloon has to keep moving. Otherwise, clot is going to form on it. And you have about 15 minutes of a static balloon before enough clots. And you can imagine what would happen if I had clot forming on there and then I inflated the balloon. I’ve got clot in my carotid arteries all over my body. It would be devastating. So it doesn’t happen.

The other thing that can happen is– so the catheter is this long and then there’s an extension tubing that goes to the helium pump on the balloon that’s about that long, about four feet long. The balloon pump can only have one of those extensions on it. It knows that that volume of helium that it needs is that extension tubing plus the volume of the balloon.

If I add another length of extension tubing on there, I decrease the amount of helium that gets to the balloon. So it’s not going to hurt the patient, but I’m not going to benefit the patient as much as if I fully inflated that balloon with each diastole. [INAUDIBLE] You can’t adjust it. No. It comes with that one length and that’s it. And I’ve seen that happen. Gotten patients from other hospitals where– not making fun. I know if you don’t know, you just do what you would ordinarily do for other things– where crews have added lengths of extension tubing, opened up other balloon pump kits at $450 a kit just to get the extension.

Big red flag if you’re having to open up other kits to get something out. Probably, you shouldn’t do that. And again, it didn’t harm the patient, but for that hour-long transport, two-hour long transport from– I don’t know. It was up somewhere up north. The patient wasn’t getting the full benefit of the balloon pump. It wasn’t hurting them, but it certainly wasn’t helping them. As opposed to not having the balloon inflate or deflate at all, and then that would be devastatingly harmful to a patient. As long as that thing is moving even a little bit, it’s enough to keep clot from forming on it. If I’d have brought one, you would have seen how easy it is to hook up that 60 cc syringe or 40 cc syringe or 30 cc syringe even with the air and just inflate, deflate really fast. You don’t have to worry about timing it or anything like that. You’re just trying to move the catheter. You do that once every two or three minutes, you’re good. It’s [INAUDIBLE]. Done. Hopefully, it’ll never happen for you. Yeah, it depends on where you work and what you see and– You’re just talking about devices? Devices.

Devices, yeah. There’s a total artificial heart, right? No one’s going home with a total artificial heart today, but it is a VAD. There’s probably three or four that people can actually can go home with these days. Maybe not even. Maybe just three. But the risk of heparinizing patients today is pretty high for heparin-induced thrombocytopenia. And the risk-benefit of heparinizing somebody on a balloon pump or not, it doesn’t– think again about who’s getting these. They’ve just been in the cath lab. They’ve just been heparinized. Or they just had cardiac surgery and they’re still anticoagulated from the surgery. They generally don’t need it because they’re already anticoagulated. If I had a completely normal– if you’re transporting a patient on a balloon pump, they’ve probably got [? RealPro ?] or something else running.

Just got loaded up with TPA. I’d worry about this balloon clotting in their body, causing a clot in their body. If I had a patient who was completely normal from a coagulation standpoint, we might think about anticoagulating. Once you develop that antibody to heparin– so the Swan. It’s heparin coated. You talked about having a catheter that has something on it. It has a heparin-based coating on it. That’s enough where if somebody ever had HIT, I’d put that in their body, they will get heparin-induced thrombocytopenia from that teeny, tiny, little bit of heparin that’s on that catheter. So we don’t like heparin. We use it a lot still to prevent DVTs and things like that, but as soon as a patient can be off of it, the better because of issues with it.

All right. Any other questions? Those are all good questions. Great. My work here is done..