So, we're going to end up with something that is not complicated, which, again, like my two talks ago, is something that most of you do on a daily basis. And I don't suspect there'll be a lot new here. I am going to go over a couple of new studies, and that is to talk about shock. And again, likely, this is part of your daily practice. And shock is defined by inadequate oxygen delivery to the tissues, unfortunately, outside of research. So, unless you put an orthogonal polygraph underneath somebody's tongue or in the groin you're not going to be able to diagnose shock at the tissue level. So, you're going to have to look at the end organs, confusion, capillary refill, as was used in the Andromeda II trial, and urine output. And the biggest issue that you have with shock patients is the imbalance between oxygen delivery and oxygen consumption. You know that when you have a patient with shock you've got to follow the ABCDEs and just make sure that if they're hypotensive that they can protect their airway. You always have the challenge in the peri-intubation period that stuff that you do likely will further drop their blood pressure. Sometimes you need to give a little bit of pushes of things to raise the blood pressure. And in really sick patients, especially those with end-stage lung disease, that half of your metabolic demands can end up going to the diaphragm. So, you want to, if you've got an imbalance between oxygen delivery and oxygen consumption, reducing oxygen consumption can help. In patients who don't have decompensated heart failure, I say this for my co-moderator who is a cardiologist, you generally want to give fluids to them, except again, and our hospital gets an awful lot of people with decompensated heart failure. You obviously wouldn't want to give them lots of fluids. We use now some directed methods, either following capillary refill, like the Andromeda shock trial did, or looking at your favorite method of looking to see whether or not somebody has a dynamic response to giving additional volume. And you want to decrease oxygen demands if you need so, and follow whatever works best for you in your practice. We know that goal-directed therapy doesn't improve outcomes in septic shock, but following goals is something that we all do clinically. And there are four types of shock, cardiogenic, obstructive, hypovolemic, and distributive. By far, distributive shock is the most prevalent by a factor of 10. And I've probably put in, and you may guess by my hairstyle that I've been in practice for a little while, I've probably put in about 1,000 Swann-Gans catheters, 10 of them have been in the last decade. Everybody knows how to put them together. Again, for people with decompensated heart failure, they often need them to get listed for transplantation. Sammy has probably put in a lot more in the last couple of years, but it's a useful construct. I worry, and so I'm going to, it would be awfully nice, we know that Swanns don't improve patient outcomes. I did a lot of them. Now I use a lot of ultrasound. It would be really, really nice to prove that it helps patients, even though we all do that. I worry a little bit that we feel good when we use it. I'm not 100% sure that patients will do better. There's not a huge amount of evidence, but most of us do this. In fact, I just bought for our critical care consult team, I just bought a couple of portable ones so that when they went around the hospital, they don't have to find the big one to use. The rest of the team is very excited about that. I don't think I need to go over in great detail the differences and the types of shock, either by echo or by PA catheters. Distributive shock is the only one with the increased cardiac output. So usually, it doesn't take a lot of brain power to distinguish between the types of shock. Occasionally, it does if you have no history, but somebody who is post-op and is tachycardic hypotensive tachypneic febrile and has bad findings on the abdominal CT is probably in distributive shock from sepsis. Again, it's the most common form of shock. It is occasionally, you'll see somebody with neurogenic shock or anaphylactic shock. We probably see about 10 cases a year of anaphylactic shock. Some of them get a little bit better in the emergency room and don't come to us. I talked earlier today about how you need to give some fluids. You probably don't need to use a Costco-sized dose of fluids in all patients. And you want to treat the infection, culture them, get source control. For anaphylactic shock, you need to stop the offending agent. I say this, I've had a couple of times where I'll go home for an evening and one of my trainees will reinstitute a medication that caused a problem because the blood pressure goes high. It was a blood pressure medicine and come back in the morning and you're back in the same problem. We all give epinephrine emergently, but the mainstay of treatment are really the antihistamines. Most people give steroids, whether or not they work, it's hard to say, but everybody gives them. And if necessary, you give some bronchodilators. For neurogenic shock, you've got to maintain an airway, give vasoconstrictors and inotropic support. Again, many people will give steroids here. It depends a lot on the institution that you're in. And the dose of steroids also varies, but most people will give them. We've talked a couple of times about the SOAP2 trial. This is the, it's now 15 years old. There was a numerical but not statistical decrease in mortality with the use of norepinephrine compared with dopamine for every, it was a pragmatic trial, so they included all forms of shock, but in cardiogenic shock, there was increased mortality with dopamine. And so it's probably not a good drug to give in cardiogenic shock, and dopamine caused a lot more dysrhythmias. It's been a few years since, also since there's been new data on vasopressin in the VAST trial. It was no worse, and maybe there was a subgroup that did better. And roughly eight or nine years ago, the VANISH trial compared in a factorial design, giving vasopressin alone, norepinephrine alone, plus or minus steroids, and there was no difference in outcomes between the groups. I am not going to talk about angiotensin 2 here. You can use it. It raises blood pressure. Whether it's good for patients is unknown at this point. Steve talked a little bit about steroids and septic shock. There's a lot of early data suggesting that you rev up your steroid production if you're really sick, and if you don't rev it up, then you're maximally stimulated. You won't do well, but following this response didn't help patients in several large trials. Steve also mentioned the ADRENAL trial, the largest steroid trial ever done. No difference in 90-day survival, but patients who are on hydrocortisone came off the vasopressors. They came off the vent faster. I should briefly mention Jalali Anand's study, mostly because it took 10 years to do, and it was conflated with giving activated protein C. Whether or not to give fludricortisone is an unclear... It's a controversial item. There have been a couple of cohort studies published in the last year based on national databases and local databases that have suggested if you get fludricortisone in addition to hydrocortisone that there's a mortality benefit. They're cohort studies. They're not a randomized controlled trial. I give it when I think of it, but again, it's not great data, and it's reasonable to do. You're unlikely to harm a patient by giving them an oral medicine when they're in shock. They may or may not absorb it. So you've got another case here in somebody who's diabetic, obese, hypertensive. She's hypotensive, bradycardic, and his EKG changes. Typically, most people, even who aren't in medicine, if their EKG changes and they have this, will say this patient has cardiogenic shock. Steve has talked a lot about the treatment of post-MI cardiogenic shock, and there are lots of things you need to worry about. You want to stabilize the patient. One of the things that is pretty clear when you do that is that reperfusion is key. You want to stabilize the patient, open up an artery if it needs to be opened up. And there's been a lot of older studies suggesting that there's a mortality benefit. This is the shock trial, which is now more than, I guess, 25 years old, showing that if you revascularize somebody in cardiogenic shock, that there's a six-month mortality benefit. And even though there's no mortality benefit that's statistically significant at 30 days, a 9% absolute risk reduction in mortality is probably something that most of your patients would raise their hands and say, yes, please. Our interventional cardiologists have lots of really neat toys that they really, really like using. And until a couple months ago, this was all based, their rapid use of them was all based on the fact that they had really neat toys and they liked using them. None of the earlier trials, putting in balloon pumps, putting people on VA ECMO for cardiogenic shock, none of them showed a mortality benefit. I should mention in the ECLS shock trial, they took people who had, many of them had already undergone a cardiac arrest. And you might imagine that people who have already arrested are probably not a great, that they're pretty sick and doing lots of stuff to help them, may or may not help them. So earlier this year, the danger shock trial was published. It took them 10 years to complete it. It started out all in Denmark, which is what the D comes for. Then they added Germany and then they added England to that. It was published earlier this year. There was a mortality benefit to post-MI cardiogenic shock that is roughly about 10%. So a real mortality benefit. There also are severe complications, renal replacement therapy, limb ischemia, bleeding. The number needed to harm is six for everyone you treat. So you're likely going to save somebody's life, but you probably need to warn them that there are some complications of putting this in. Sammy, did I get anything wrong? I'm not a cardiologist. The cost of renal replacement therapy is 40% of your life, compared to 20% in the control arm, which is huge. And then this device costs a lot of money. But at least now there's, and the one thing that the investigators said pretty clearly is that nobody got enrolled there if they'd already had a cardiac arrest, right? So they may have picked a better patient population. You want to pick people who are really sick, but perhaps not too sick, if you will. Not too hot, not too cold, just right, if you will. You want to get people who are at high risk of dying, and these folks are, but probably not, again, whether or not to do it in somebody who's already arrested may not be the right patient population. There are lots of forms of obstructive shock. You've heard earlier about giving lytics for people who have intermediate and high-risk pulmonary embolism. Steve talked a little bit about patients who have cancer and develop pericardial tamponade. You want to fix whatever the problem is. So shock is a disease state that you want to appropriately treat by, again, making sure that their airway, their breathing, their circulation is okay. Treat the underlying disorder. And if you walk into your hospital and you are not a freestanding cardiac place that doesn't take any other type of problems, the most common, the most likely thing that you'll see when you find a shock patient is that it's distributive shock from sepsis. And Sammy, is there any, from the cardiology stuff, is there anything you want to add that I got spectacularly wrong or even slightly wrong? No. Okay. But I personally think that any patient in shock should get a, in addition to history and physical, should get a ultrasound because I think it's an extension of the physical exam. I don't think there will be ever a randomized trial looking at this, but it could help differentiate between different types of shock. And I think also in, I should have that. So just to repeat, just to repeat this for the benefit of the virtual people, I was just saying that I think in addition to the history and the physical examination, I think one of the first line things to do is to do an ultrasound of at least the heart and the lungs only because I feel like the ultrasound is like an extension of the physical exam. There will never be a randomized control trial looking at this, but it just seems like it adds a lot of information. And to me, what seems like it's becoming more common in our patients is mixed shock because sepsis could lead to cardiogenic shock or cardiogenic shock could lead to SERS and distributed shock or obstructive shock could lead to something else. And those are the ones that require a lot more thought about them and how to manage them. And I feel like at least in my patient population, I've been seeing that in about 25, 30% of patients, patients with combined shock. So congratulations. You have successfully made it to the end of the course. Hey. Did you have a question, sir? Yeah. This blue pump has been like mainstay for so long. Why do you suppose it didn't meet the end point? How much time do you have? Okay. So just in general for all cardiogenic shock patients, there's a lot of arguments about how these trials are performed. There was an old trial called IAB shock, which showed some benefit. This is a subset of the original shock trial. Then another one came out in 2012 called the IAB shock two study, which showed no benefit to routine use of balloon pumps in patients that come in cardiogenic shock. A lot of cardiologists got in arguments about this because the balloon pump was put in after the cardiac catheterization and PCI was performed, and it was performed also placed in patients who didn't need it anyway. Nonetheless, I think that most people in the cardiac cath lab and the cardiac ICU environment do not routinely place these devices in all patients that come in cardiogenic shock. They use their judgment to determine whether they need to have a device or not. Two things. If you're thinking about using a mechanical circulatory support device for a patient who comes in with cardiogenic shock, a PA line is helpful because it gives you objective data that a patient's not doing well or doing well. There's no randomized trial looking at the value of routine use of PA catheters, but there is two that are in progress right now. And then the other thing is that maybe having a multidisciplinary team discuss whether a patient should be appropriate for mechanical circulatory support device also helps improve outcomes. This is only for cardiogenic shock, not for sepsis, obstructive, or any other type of shock. I should mention that one of the reasons we set up a critical care consult service is while 80% of it is trying to get people out of the emergency room, roughly 20% is for somebody who, on a floor, when somebody gets transferred in from the outside, that nobody knows what's going on, that they can come there when their blood pressure is 60 over 40 and decide whether or not you need to call the ECMO team or cardiac surgeon and an advanced heart failure patient or just give them some antibiotics. And as Sammy mentioned, in 45 seconds, a Sono can help narrow down whether or not you need to get five people up in the middle of the night or whether you can just call the nurse and ask them to start a therapy.

shock management

cardiogenic shock

distributive shock

sepsis treatment

vasopressors

ultrasound diagnosis