Hi, thank you everyone, I'm glad to have this opportunity. My name is Tina Chen, so I have no disclosure. So one of the clinical questions I often have in the ICU taking care of patients with septic shock is, have I adequately resuscitated this patient? So in our study with volume chasers, we looked at patients with septic shock and we categorized these patients with having had compliance with surviving sepsis guideline in their resuscitation effort, receiving fluid and or vasopressor and with lactic clearance. And we saw that a good proportion of them still were in shock, meaning their blood pressure was below 60, map below 65 or remain on vasopressor. And this group of patient actually had higher mortality than they would if their shock resolved within the first three hours. Over the years with sepsis spam, comparing low versus blood pressure target, they didn't see a mortality benefit between high versus low target and other studies that's comparing these targets and using various dose of vasopressor to achieve these target did not show mortality benefit. In a systematic review looking at the 65 trials, sepsis spam as well as ovation, the overall mortality was not different when we target a higher and lower blood pressure target. Actually in this issue of critical care medicine, there is another systematic review including more at least six studies. So we know that resuscitation is a balancing act between micro and macro circulation. And we want to take into account of early versus late septic shock. Sepsis changes our oxygen delivery and oxygen consumption. I'm showing you a graph with a relationship between delivery and consumption. In a normal patient, there is a critical point at point B where below this level of oxygen delivery, our oxygen consumption would change. In a septic patient, that relationship is altered. In here, that point is at a much higher delivery point and the consumption also changes. So with that in mind, early goal-directed therapy built on this using CVP to guide our preload, MAP to start vasopressor, SVO2 to improve oxygen delivery with transfusion and inotropy support. And there was a significant mortality benefit in the early resuscitation of patients in septic shock. However, in the past nine years with ARISE process and PROMIS studies, we compare CVP, MAP, and CVO2 guided therapy with usual care that did not find a mortality benefit. So how do we really think about this? Reviewing the topic of micro and macro circulation, I just want to go over some of the auto-regulation issues. Right? So arteries bring flow and that's really the blood pressure generating part. We have small arteries and arterial that will change perfusion to the capillary and maintain a constant perfusion into an organ for perfusion. There is a range between 60 to 165 millimeter of mercury MAP where the auto-regulation will change flow into capillary to maintain a certain pressure in there. In sepsis, we know microcirculation can be changed. There's changes in microvascular density and perfusion and there's increased heterogeneity in the capillaries. In animal models, especially in sepsis, that there is micro and macro circulation discordant. And this I'm showing you an example of rabbits receiving LPS infusion. MAP changed after infusion by 90 minutes and in the microcirculation here, the changes were as early as 30 minutes. So there's a discordance about 60 minutes in this model. So other targets to consider for perfusion. We talked about MAP which is really a global sign of how someone's not doing well. We often use lactate, another global signs of perfusion, and CVO2 for oxygen delivery and cardiac output consideration. The other things that are starting to come into favor of how we should target perfusion would be the gap between carbon dioxide between arterial and venous side. Perfusion index which is more in favor now but much harder to do because we require infrared technology or microscopy. The other two things that's really much easier to perform will be capillary refill time as well as modeling time. And just reviewing some evidence of the clinical application of these other perfusion targets. So lactate clearance back in 2004 by Nguyen et al, they did show that lactate clearance by 10% has improved survival. And later in the phylo study show that presenting lactate of less than 2.5 had better survival. And this is sort of how a CCM surviving sepsis campaign came up with the cutoff of two for lactate. Capillary refill time is another method that we could assess perfusion and guide our therapy. So in this Andromeda shock study that compared capillary refill time, we're using slides on our index finger, pressing for 10 seconds and a refill time less than three is adequate and a refill time greater than three seconds would be inadequate. Using this to guide resuscitation protocol was similar in terms of outcome with lactate. But the fact that we could use capillary refill much easier than waiting for blood results to come back makes it a lot easier to operationalize. Sepsis span study also look at modeling time in their post hoc analysis. And this regardless of map target, patient had the same amount, there are groups of patient that would have same amount of modeling versus non modeling. They were looking at duration, they were not looking at how large the area of modeling time these patient had. So here comparing patients who had modeling versus no modeling, there was actually no mortality, the mortality was much higher in the group that had modeling. So and some I really just want to say that resuscitation is complicated, a single target is really not enough. Sepsis does affect both oxygen delivery and oxygen consumption and a hemodynamic discordance between micro and macro circulation really is a problem we need to solve. And lastly, the micro vascular based resuscitation using capillary refill time, lactate clearance or even modeling duration should be incorporated in our shock management. All right. Thank you.

septic shock

ICU

mortality rates

oxygen delivery

shock management