Well, thanks, Nancy, for a fantastic survey of shock. I think we have a few questions that will be coming in from the audience, but as we do that, I thought a great place to start would be with your pre-test question. And I was looking at the polling results and many of the scenarios were straightforward for the audience, but not all. So the ones that tripped the most people up were the first scenario, which was a patient who had high felling pressures, and I can just tell you the numbers. The blood pressure was 84 over 48, the CVP was 22, the PA pressure 52 over 34, wedge was 28, index was 2, and SVR was 1,200. So maybe start with that case and then I can give you the other one. Sure. So this is an example of a patient, you know, I would say these are the hemodynamics of a well-treated chronic heart failure patient who shows up in cardiogenic shock. This is clearly cardiogenic, low cardiac output, high felling pressures, but SVR is normal. It's not low like you'd see in distributive shock where there's a vasodilatory state. The patient has a normal SVR, and that's often the case in well-treated heart failure patients. So this is a patient who needs inotropes because the primary problem is the low cardiac output. So if you can't afterload reduce that patient more, you'll probably make them more hypotensive. And so the correct answer is this is pure cardiogenic, not a mixed shock picture because of the SVR being normal. Great. And then the other case that was complex for folks was case six, which was again a low blood pressure patient with a CVP of 24, a PA pressure of 52 over 34, a wedge of 10, a cardiac index of two, and an SVR of 2000. Comments about that case? Yeah. So this is a tricky one, but this is RV failure, right? So the wedge is normal, but the right side is clearly failing. And the key is that the SVR is very, very high. So that tells you cardiac output is low. The patient is vasoconstricting in response to the low cardiac output, but the low cardiac output is because of failure of the right side, not the left side. The left side is actually, you know, probably a little underfilled because of failure to move blood forward to the left side from the right. But this patient's going to be cold, modeled with elevated CVP, but not elevated wedge. Hard to treat, obviously, this patient, but probably most of us would start with sominotropes to support that failing right side, potentially move to right-sided mechanical circulatory support if the patient's otherwise salvageable. Perfect. Well, thanks for that. I think the other ones were relatively straightforward for the audience. More than 90% got the other ones correct, so we won't focus on those. We're waiting for questions from the audience. I think people are slowly filtering in and getting geared up for the day. I had one that I posted to the chat. One was, which is really, you know, you gave us a nice array of options for management of pressors and shock. How do you start and how do you select pressors for shock? And are there any to avoid in cardiogenic shock? Yeah, you know, there are some data, and I think for purposes of the boards, you're really going to be tested on the data. So there's one small randomized controlled trial comparing norepinephrine versus dopamine as initial choice, and the norepinephrine arm had improved outcomes. In that trial. So between those two agents, you want to choose norepinephrine. And then there's another larger trial actually comparing norepi to epi. And again, norepinephrine had better outcomes than patients randomized to norepinephrine. So I think for purposes of the boards, if you're choosing an initial vasoconstrictor in a shock patient, norepinephrine is the correct choice. I think a lot of people clinically like to use epinephrine, right? Because you might get some inotropy with your vasoconstriction with epi. But you have to remember anytime you're using an inotropic drug that it's energetically unfavorable for the heart. The heart has to use more ATP, and you may worsen sort of lactate production and things like that that are markers of poor outcome in shock. So the data for those drugs suggests that they tend to be harmful. And so the randomized control data we have suggests norepi has fewer adverse outcomes than epi. And that would be the right choice for the boards, although clinically we've all seen all of these drugs used. And as I mentioned in the talk, the important thing really is once you've stabilized the patient, attending to the problem at the level of the heart, because ultimately vasoconstrictors and fluids, which may be necessary for stabilization, are going to not be viable long term if the problem is truly cardiogenic. You need to get that patient on therapy that improves cardiac output, and those two agents typically don't do that. And is there, there are a couple of questions that have now come in. Any change in your answer for patients with dominant RB failure, for example, in the setting of mechanical circulatory support? Yeah, so RB failure, as we all know, is incredibly difficult clinically to manage, and there are no randomized controlled trial data. I think most of us do use inotropes. You know, in every large study that's done, there's a group of what they call HEF-PEF patients, or heart failure with normal EF, who are put on inotropes, and everybody says, why would you do that? And the reason is the RV. Those are RV failure patients. And just trying to get that RV to pump forward to the LV often requires inotropes, particularly if the patient's massively volume overloaded. To get that volume off in a reasonable time period, you have to get it over to the kidneys. So I think most of us would use inotropes. Milrinone has better pulmonary vasodilation than dobutamine. And so if the patient has systemic blood pressure that will tolerate milrinone, it's probably a better choice in RV failure. Right now, there is no dobutamine, so we're all using milrinone in patients. We wouldn't use it in any way. But, you know, sometimes patients just don't tolerate milrinone because of the systemic hypotension. You might counter that with norepi or tridobutamine in an RV failure patient. But it's really empiric, you know, and ultimately placing RV support devices to get a patient through who's otherwise got endpoints and isn't, you know, a palliative patient. That's great. Yeah, we've occasionally used inhaled lepiprostanol as another. Right, yeah, pure pulmonary vasodilators, if you have them available, might help, especially if the LV is really normal, right? You've got to make sure the LV is really normal in those patients. One additional question that came in through the chat before we move on to another topic is about phenylephrine and any role and where would you consider it, particularly in patients with cardiogenic shock? Yeah, I mean, people use phenylephrine. There are no randomized controlled trial data to guide its use, and so I think, again, for the boards, norepi is the right answer. You know, phenylephrine is typically added to norepi when things are really bad, and we know that, you know, days and minutes and dose over time of vasoconstrictors is a strong predictor of failure to recover and organ damage. So, you know, if you're reaching for multiple vasoconstrictors in a true cardiogenic shock patient, you're probably contributing to peripheral hypoperfusion, and you really need to think about what you can do at the level of the heart to provide perfusion to the rest of the body. And often, if you're reaching for phenyl or multiple vasoconstrictors in a cardiogenic shock patient, pure cardiogenic shock, you probably need to talk to your heart team about mechanical circulatory support. Now, in mixed shock, it may be different. If they've got a diffuse vasoplegic or vasodilated state, you may need multiple vasoconstrictors just to get SVR up to normal and start restoring organ perfusion and do things like correct acidosis, which may be damaging cardiac function. These are really complicated shock patients, you know, and I don't think this is going to be tested. You're going to have pretty straightforward shock scenarios on the board. And then two quick questions, and they're not that quick, but in order to get a few more in. One is really briefly your thoughts on when to use hemodynamic monitoring in shock, and then the second question was about steroids. Yeah, so I think increasingly in the, particularly in the heart failure world, we believe that hemodynamic monitoring is very helpful in intelligent use of vasoactive medications in the shock patient so that you're not harming the patient in terms of impairing peripheral perfusion, and you can really, if you understand the medications and how to use the hemodynamic monitoring, you can tailor the IV vasoactive medications to try and optimize the hemodynamics and you can do it relatively quickly. If you've got, you know, PA line in place, and all your IV vasoactive medications to be used, you want to try and get that patient to the closest as possible to normal hemodynamics. So if you're, if the patient is extremely vasoconstricted or extremely vasodilated, use your medications to get that SVR into the normal range and inotropes. Once your SVR is normal, to get cardiac output up if it's not responded to optimization of vascular tone. So I think that's really, you know, intelligent use of a PA catheter, as I tried to show at the end of the talk, can really improve outcomes in these patients, I believe, and when you don't know what's going on or the patient's going downhill, get that PA catheter in, it would be my advice. And then I think the last one was really any role for steroids. I know, mostly in the, but in, I guess, specifically here, we're talking about cardiogenic shock or- Right, not in cardiogenic shock. There's no data to show that steroids will improve outcomes. Of course, if you have a mixed shock patient in whom there's an inflammatory syndrome that might respond to steroids, otherwise, you know, I would talk to your critical care colleagues, or if you're critical care trained, great, and use steroids as appropriate for that shock state, but not for cardiogenic shock, no. Great. Well, I think we'll hold it there. There are a number of other questions that have come through, but I think we'll have to hold those for later in the day, and we'll move on to Joe Rogers talking about mechanical circulatory support in our first session on durable MCS devices and outcomes.

shock

cardiogenic shock

systemic vascular resistance

inotropes

right ventricular failure