I actually will present for her because she submitted full complement of slides. I don't see my University of Vermont people here, but she actually did her training over there and then she came to Hopkins, did dual fellowship in cardiac anesthesia and critical care and she's now practicing medical cardiac ICU and cardiac surgical ICU at Maine Medical Center. And that's going to be stumped intensivists, sepsis cases, trying to talk about a few more cases to illustrate pitfalls and actually advantages of doing serial exams. So then you had no disclosures and again this is a reminder about markers of fluid intolerance and sepsis resuscitation using ultrasound guided assessment, then talk about how phenotypes, the ones that Anubis mentioned in his first presentation, that it can change during serial evaluations, thus the value of following up on your patient in the ICU and recognize how chronic RV dysfunction plays a role in adjusting treatment, maybe with some bonus at the end. All right, so this is a 75 kilo 68 year old patient, has lots of chronic illnesses, coronary artery disease, hypertension, poorly controlled diabetes, so metabolic syndrome and vascular path like how we would commonly call them vascular peripheral arterial disease, had all fem pop bypass in the past and presents of course with sepsis because sepsis is the main theme here, so fever, leukocytosis, lactate is 4.6, so septic shock, gangrene of the right foot is the source of infection, taken to the OR for debridement, arrived on norepinephrine, received two liters of fluid intraoperatively, lactate is down, blood pressure seems to be more normal but still on vasoactive and a resident orders another liter of crystalloid to help clear lactate and win of norepinephrine, I mean that's something new, correct? No, it happens all the time, so instead of actually just proceeding with the order like well how about taking a look at that patient and that's what they saw, that's a subcostal view for just a reminder, the problem here with this particular view is that you cannot see the left ventricle really well, you see the heart is slow, so that's one of the situations when you ask well just because I don't have full information let me look elsewhere, right, so in this case going to the apical foot chamber and all of a sudden you see that the ventricular function is at least moderately reduced, right, I mean with the more typical apical ballooning here, maybe consistent with a stress cardiomyopathy and bradykariac, right, so probably not enough delivery to where the flow is supposed to go, so that ultrasound, kariac ultrasound changed the management and the fluid was held, vasoactive medications were continued, they gave a low dose epinephrine at the time and then reviewed the ultrasound when the changes further happened, so that's again the value of repeat, right, so deliver intervention and follow up on that, that patient did better, so in case two it's called seems fairly normal, alright, I don't know, 82 year old, it's already a bad starting point for many patients, with prior mitral valve replacement, heart failure with preserved ejection fraction and bladder cancer, received partial cystectomy and has chronic suprapubic catheter, now comes to the emergency department, again with fever, altered mental status which are common signs of sepsis in older adults, family says he was complaining of flank pain for three days prior to arrival and assessment in the emergency department, he was intubated for airway protection, given one liter of crystalloid and started norepinephrine and still low blood pressure, and of course they followed all the sepsis resuscitation, obtained cultures, started broad spectrum antibiotics, and that's initial ultrasound at the time of arrival to ICU, nothing profoundly, remember it was called seems relatively normal, right, so it does seem relatively normal except that RV looks a little bit big, I will ask for Sarah's opinion because she was talking about RV so much, yeah, it looks a little bit big, right, Yeah, so, seems fairly normal. Let's go back to the original statement of this case, right? But some concerning signs. Maybe we have to pay attention and reexamine the patient as the resuscitation continues. Oops, can you go back? Sorry. And that's what they saw in the other views, AVC view and shore access view. So they decide, you know, fluid is great. So instead of giving like one liter, which was initially given, they proceed and give another two and a half liters. And unfortunately, norepinephrine doubled. So it's a correlation. The more fluid, the more norepinephrine this patient needed. And that was the time of assessment with another sort of ultrasound exam. So this time around, they saw this. I told you. So Sarah, what did they see? The LV looks underfilled, the heart rate is pretty slow. And I'll give you more views, how about that? So, right, just for those who cannot hear, right, to summarize, it's a central volume overload, right, we're just being consistent with all the presenters, and Morad, when he talked really nicely about the organ congestion, right, all we can state right now is just looking that there is high feeling pressure at the central compartment, right, as well as the RV seems to be more volume loaded than anything else. And they do this, and they see a lot of tricuspid regurgitation, and the apical food chamber looks completely consistent with what Sarah was concerned about, even on the first exam. So compare how it was before and after, right, and that's after two and a half liters, maybe two and a half liters too much, right? So change in phenotypes, so phenotypes have changed, and maybe it was too much too fast, and the increased pulmonary vascular resistance can occur, actually, in sepsis, and can be also additional confounder why the right ventricle doesn't like it, and impaired intraventricular dependence, so that changed the management for this patient. So promoting forward flow, right, maintain optimal preload, so not too much, not too little, stop volume in this patient, decrease PVR, improve hypoxemia, hypercapnia, work with the acidosis, minimize PEEP, or actually I should say optimize PEEP, and inotropic support is needed, so that we're able to sort of stabilize this patient ultimately to take volume off. This is interesting, right, don't see that every day. So something not for every day, 72-year-old, idiopathic pulmonary hypertension, and paroxysmal atrial fibrillation, not on any anticoagulation, severe abdominal pain, secondary to acute mesenteric ischemia, to the operating room for emergent laparotomy and partial bowel resection, comes to ICU intubated on norepinephrine and vasopressin. Lactate elevated, so septic shock, blood gas you can see below. That's how the heart looks. Oh, Nibirus, what phenotype is that? Right ventricle hypertrophy, and now we have septal shift during syphilis for the LV, so pulmonary hypertension. Yeah, and on top of it, left ventricle may look also thick, right, but it's hard to evaluate when the heart, the septum is pushed, and see IVC completely dilated here. This is just a few other views, right? You'll see how thick the right ventricular wall is in this patient. This is the view, by the way, between the apical and the subcostal. It's not the most typical view. In this patient, you have right ventricular hypertrophy from pulmonary hypertension, and all it illustrates is a vicious cycle, basically. If RV decompensates, volume of filling increases, worsens left ventricular compliance with the septal shift, and decreases LV preload, decreases RV perfusion, and everyone, instead of a vicious cycle, it becomes a vicious spiral, and vicious spiral down, actually. The worse the RV, the worse it ultimately becomes, and the person can develop cardiac arrest, and on top of that, you add extra pressure load at the pulmonary hypertension or pulmonary vasculature level. The important things, maintain RV perfusion pressure. Very tiny, small fluid boluses can consider sometimes. Again, remember all the other exams we talked about today? Anatropic support, pulmonary vasodilators, optimized tissue perfusion markers. We talked about value of serial exams. We talked about impact of chronic disease, and that's how this patient looked after a little bit more resuscitation, and the last one is a bonus, right? And that's why I think it was called one for the road, and then we can bring all the speakers to the table and answer all the questions that you may still have. Forty-five-year-old, has history of tetralogy of flow repair, a long time ago, 43 years ago, right? Complicated pulmonary insufficiency at the time, right? And pulmonary hypertension, second degree AV blocks, has permanent pacemaker. Now, he has polysubstance abuse, so admitted to ICU for respiratory failure, intubated, febrile with leukocytosis, again, it's part of the sepsis series, and now we'll know, we just take the ultrasound machine and go evaluate the patient, and what do we see here? I guess, what phenotype? Let's start with that. That's biventricular systolic dysfunction. So, biventricular systolic dysfunction, okay, with increased volume loading. And that's how it looks in the apical 404 chamber. So, giant atria representing acute and chronic issue. Look at in this corner, there's something also there. I guess it's a scientific term, right, of Goomba, right? Okay. Oops, one slide back. And that Goomba can be even more so seen here, right? That's a little bit further tilt in the parasternal long axis view to open up the RVOT. And you can see the severe pulmonary valve insufficiency. So now you start asking what phenotype, right? We already talked about that. And the questions are very typical, right? I mean, are we giving fluid, no fluid, are we doing pressers, no pressers, are we doing inotropes, no inotropes, or we phone a friend? Yeah, phoning a friend is always a good thing when you have a group practice. These are, say, the point here that you're, despite the complexity of diagnostic information that you are collecting, you're ultimately trying to package it in a way so that you can answer relatively straightforward clinical questions. Are you giving fluid, you're taking fluid off, you're stopping fluid, right? So fluid, pressers, inotropes, any additional interventions. If it's a rhythm problem, you give, consider antiarrhythmics. Okay. And I will ask all our speakers to join us. Thank you.

sepsis management

ultrasound-guided assessment

fluid resuscitation

right ventricular dysfunction

patient phenotypes