SCCM Resource Library-Fifty Years of Resuscitation in Critical Care: Lessons for the Next Generation

Video Transcription

Welcome. Today I have the pleasure of moderating our session entitled 50 Years of Resuscitation  in Critical Care Lessons for the Next Generation. We're joined with a wonderful group of panelists  who are experts in this topic, and we look forward to hearing their concepts. My name is Enyo Ablardepi. I'm coming from Washington University in St. Louis. Our learning objectives  today are the following. We're going to review the approach to science in cardiac arrest, medical and trauma surgical resuscitation. We're going to describe what has worked and  what has not worked in transitioning to new ways of practice in resuscitation. We hope to inspire young physicians to make changes in resuscitation care in the future. And finally,  we'll analyze the advancement of resuscitation strategies for patients with severe traumatic  brain injury and significant injuries to other organ systems. No disclosures for our panelists and myself. Our panelists today come from a variety of fields with expertise in these  areas, first starting with Dr. Vinay Nadkarni, who is a professor at the University of Pennsylvania.  Then Dr. Samuel Tisherman, coming from University of Maryland. Then Dr. Shirley Chang, coming  from Duke University. And again, myself, coming from Washington University. Our agenda today is that after this introduction, we're going to hear from our panelists, starting with  the first topic, staying alive, the evolution of CPR and resuscitation. Then early goal  resuscitation, then and now. And then finally, initiation or initial resuscitation of patients with severe traumatic brain injury. We'll have some questions and discussion, so feel  free to please submit your questions and comments in the chat box. We'll make an attempt to address all of those during our discussion period. And with that, we'll get started from  our panelists. Well, welcome. It's really great to be with you on 50 years of resuscitation in critical care, to talk to you about staying alive,  the evolution of CPR and resuscitation. I have no relevant conflicts, although I have  some research grants and sit on some voluntary scientific advisory boards related to resuscitation.  But if you think with me, what are the facts? How do we get from anecdotes to studies to evidence, to guidelines, to practice, to actually saving lives? We've come a long  way on the shoulders of giants and really the founders of the Society of Critical Care Medicine were those people who were bold, meticulous, and began with the end in mind,  thinking about resuscitation. Peter Saffer and Max Harry Weil and William Shoemaker, all interested in goal-directed resuscitation related to cardiac arrest.  At the time that SCCM was beginning, we were just learning how to use the newly invented  tools of the trade led by people like Alfred Blalock and Vivian Thomas, who had done pioneering  vascular surgery, inventing tools and learning how to resuscitate with the first large cardiopulmonary  bypass machines. And here, a photo of the early pacemakers and the precursors of our advanced monitor defibrillators that have become public access defibrillation automated  AEDs currently. Let's take a moment to reflect and think about the tools, perhaps the most  important tools that we have, the hands to provide circulation through CPR and the preservation  of neurologic function. Because what we know, how they get translated to guidelines and medical standards, what we can teach, learn, and remember, and what we do creates almost  an Olympic ring chain of survival that oftentimes we get lost in translation. But with rigorous  audit evidence evaluation practice, and really reflecting and debriefing, we are able to double survival from in-hospital cardiac arrest with the modern critical care approach.  Where we started was with linemen who were, in our electrical companies, putting up high tension wires. They would get shocked and fibrillate, and they needed a mechanism in  order to address this fibrillation of the heart. Discovered in the lab during defibrillation  studies, modern CPR started with pressure on the chest from paddles that keen observation noted blood pressure changes and blood flow changes. And this was brought to the operating  room where early studies and reports of closed chest cardiac massage were successful. Guided  by goal-directed therapy, the arterial blood pressure from this early report in 1961. And then observed, studied, and monitored, and programs developed like this one by Peter  Saffer early in the game, where he was able to demonstrate that life-saving rescue breaths could be provided by laypersons with 17% oxygen exhaled air. That led to resuscitations  like this spectacular resuscitation, responding to the need. And then combining with others  to create mannequins and training tools that have led to modern day resuscitation. We have discovered that there are three phases of cardiac arrest. The electrical phase, then  the hemodynamic phase where perfusion is critical, and the metabolic phase where extracorporeal life support and adjuvant therapies may be critically important. But the key is that  we know that when no CPR and no defibrillation is provided, survival outcomes are very poor. When we simply add early effective CPR, we can double to quadruple survival. And when  early defibrillation is added, much better outcomes occur. And finally, when advanced cardiac life support with early goal-directed therapy in the post-resuscitative phase is  added, we can start to see miraculous recovery on 30 to 60% of the patients with good neurologic survival. We have learned over the years, the lessons learned, that the medications  are not as important as early effective circulation and attention to detail goal-directed therapies  for both the heart and brain. And we have studied and learned that the myocardial dysfunction, much like the sepsis syndrome, is present and can be supported in the first 24 hours  after cardiac arrest. And that some of the things that we thought were so great, like  100% oxygen, are sometimes harmful to the heart and to the brain. And the monitoring and titration of therapies to the electrical and physiologic condition of the brain is  perhaps one of the most important things that we can do in the post-arrest period. Therapeutic  hypothermia used as early as the 1960s has been refined to targeted temperature management  and the understanding of how and when and who to apply this to in a goal-directed fashion.  So that the tools of the critical care clinician at the bedside have become critically important  and advanced in both monitoring and therapeutic effect. Emergency preservation and resuscitation  from the bench to the bedside and beyond is here and with us. And using extracorporeal therapies in a goal-directed manner may, in fact, for selected populations, lead to miraculous  outcomes that are better and better. But technology, we know, cannot do it alone.  This technology, the automated external defibrillator, early in its conception shows that unless  we actually know how to use it, it doesn't make a difference. This clinician who was at the court side of a basketball player who dropped dead from ventricular fibrillation  and not been adequately trained and confident on using the advanced technology in his right hand so he carried the dead and dying player off in his left hand without applying the  life-saving tool because of the training and the implementation of the system of care that  was not in place. We now know that technology can help us after cardiac arrest with goal-directed  therapies targeted to temperature, cerebral perfusion, blood pressure, oxygen, control of seizures, and glucose. Our early efforts in 2002 through 2012 suggested that targeted  temperature management was indeed effective after cardiac arrest. And several trials showed  improvements over usual care. But more recently, studies showed equivalent outcomes when targeted  temperature management was preventing hyperthermia after cardiac arrest. And we know that the  control groups in these studies were not equivalent and therefore allowed fever or hyperthermia  to occur in the post-arrest period. We have learned and we are getting better at managing  this. Most recently, the Hyperion trial with targeted temperature management for non-shockable cardiac arrest rhythms suggested that if we controlled the temperature in both groups,  we could see an improved neurologic outcome in those that were cooled after cardiac arrest,  but there was no difference in mortality and no difference in adverse events, an improvement that had a meaning. So when we think about cardiac arrest and resuscitation science now,  we think about the patient and event and system factors that underlie the cause of arrest, how we can educate, use devices, drugs, and quality of the systems, and then measure not  only discharge survival, but quality of life in the long term. These are important outcomes. In order to achieve it, we must train the individual, train the team, and train the  environment. And in the near and far future, we are developing algorithms to continuously scroll through the electronic health record to improve the early recognition and early  response to prevent and treat cardiac arrest before and immediately as it happens. We still  have many questions about our cooling techniques, our depth and duration of cooling, and our  rewarming in particular. And we are developing adjuncts that are not man versus machine, but man and machine working together to improve the survival outcomes of our patients. We  are learning how to measure and adjust cerebral hemodynamics and electrophysiology so that  we can both improve the survival outcomes, but also understand when it is time to stop and when we have important markers, biomarkers and electrophysiologic markers that suggest  that good neurologic survival is not possible. And we are learning how better to prognosticate  and how to measure what really matters, the batteries of the cell, mitochondrial resuscitation  and how we can manipulate and provide cocktails that improve the function of these key organelles  that control the survival and recovery of muscle and brain. We are learning how to use  live capture and video analysis in order to get situational awareness for the teams and  also use simulation and real cardiac arrest debriefings in order to improve our team performance,  leadership and followership. And we are adopting advanced techniques in live capture video,  instant replay and debriefing and coaching techniques from our sports colleagues in order to better provide real time, immediate and after event reviews. We are learning how to  monitor both our patients and our providers using sports science and advanced wearable technology to know the stress level, the task load and the performance features of  our teams and to study and learn the performance and fatigue characteristics of our providers  as they provide resuscitation to our patients. We are learning to link human factors and  performance in a way that was never done before and that our forefathers never imagined could  be done. And with this advancement, we can learn to create virtual command centers to  support and monitor and train our teams at and near the point of care, similar to what  OnStar Online does for the cars or the NASA Command Center does for the space station.  And we are developing new techniques to deliver the life saving tools such as drone delivered  AEDs that will in fact support and eventually automatically improve the time critical response  for cardiac arrest. In the future, our targets are better surveillance, early detection,  rapid response, better team performance, improved monitoring and coaching, the evolution of  mechanical and extracorporeal supports and elegant post-resuscitative care with audit and  quality review. As we move these features forward, we are getting better and better at  simplifying and making these innovations low tech and employable for our patients.  In resource limited settings, but we are also learning from those settings how to make our care less expensive, less treacherous and more implementable. In fact, the American Heart  Association has created a new sixth link in recovery and added it to the chain of survival as  an important new link. And paying more attention to not just the short term outcomes, but what  leads to long term survival and survivorship of meaning. As we learn and discover new knowledge,  process it and translate it into training and performance and measure how it transfers to  improve quality of life and long term quality of survival, we are moving towards what our  forefathers imagined. Our formula for survival has evolved to be a product of medical science,  educational efficiency and local implementation, which is not only the key to survival, but  survivorship. As we move forward through 50 years of critical care medicine, we are  learning to save more lives together. The time is now. Thank you. And I hope you join me in  celebrating these 50 years. Greetings. I'm Sam Tisherman. I'm a surgical intensivist at the University of Maryland.  And today I'll be talking to you about early goal directed resuscitation, then and now. I have  nothing to disclose. So here's a case to begin the discussion. So a 56-year-old obese CEO is at a  party. He suffers a gunshot wound to the abdomen. The only surgeon around is a gynecologist who  repairs the injuries. And then the patient is taken to the home of the party host and treated with  broth, brandy, enema, strychnine, and dig. And then he dies a couple of days later from sepsis.  We might chuckle a little bit about this, but this is how our president McKinley was managed 100  years ago when he was shot and eventually died from sepsis. So I'll use this as an introduction to  talking about early goal directed therapy for both sepsis and trauma. What I'll focus on with sepsis is  hemodynamic stabilization and source control. And with trauma, I'll start with source control because  you really need to control bleeding before we can talk about hemodynamic stabilization. So let's  start with sepsis, hemodynamic stabilization. And one thing about the goal is if you don't know where  you're going, you might not get there. So said Yogi Berra. Now, back when I was a resident,  somebody came in with sepsis in the emergency department, with all due respect to my emergency  medicine colleagues, so many years ago, somebody would see the patient, order fluid, see another  patient, maybe get some cultures, go on coffee break, get some more fluid, go to lecture, start  dopamine, hand off to somebody else, start some antibiotics, and then eventually call the medical ICU.  And what happened 20 years ago is Manny Rivers and his group at Henry Ford really changed this  paradigm completely. And basically what Manny did was have a resident or fellow sit at the bedside and  fix the patient's physiology quickly. And there were goals for CBP, mean arterial pressure, and central  venous O2 saturation, but the main thing was fixing the hemodynamics quickly. And they found that this  improved mortality, both short-term and long-term. And I think it's really important to realize how much  this changed practice. As the CDC thing says here about getting ahead of sepsis, people started having  sepsis teams and sepsis alerts, and really the management of sepsis was completely changed. Which  brings me to some more recent studies looking at this whole process of early goal directed therapy. There's  the American trial, the process trial, there's a trial in Australia and Asia, the ARISE trial, and there's a  study in the U.K. called PROMIS. And all these studies basically show no difference between some sort of  early goal directed therapy and what was standard care. But if you notice, the mortality in these studies  is actually similar to Manure's treatment group. The key thing that people miss sometimes because they say,  oh, these studies didn't show that early goal directed therapy makes a difference, the thing is, every single  patient now at major institutions gets early goal directed therapy. So now we have bundles of care that have  been promoted by the surviving sepsis campaign, such as within three hours you need to give a bolus of  fluid for hypotension and high lactate, within six hours start vasopressors for tractory shock and reassess.  And now these bundles are being compacted into a one-hour bundle. The goals by Manure Rivers were central venous  O2, surviving sepsis campaigns pushed the idea of using lactate, more recently there's a study comparing  capillary refill with lactate and find no real difference in outcomes. Maybe something like looking at the  microcirculation would help, but you got to have some goal in mind with your early goal directed therapy.  So let's talk for a minute about source control. For infections, it's getting cultures and starting  antibiotics. And the timing is critical here. So this is an interesting study from the New York Department  of Health looking at timing of the three-hour bundle and the time to completion of it. And for every hour of  delay, there's an increase in mortality. Similarly, if there's a delay in giving the antibiotics, there's an  increase in mortality, no real difference in timing of the IV fluids. So timing is really critical here.  Now one thing that doesn't get much attention is surgical source control. If somebody has a problem that  needs to be trained, debrided, a device removed, or something resected, that would be surgical control. And  surviving sepsis only says that you should try to do this within 12 hours. And in my mind, as a surgeon,  surgical source control gets no respect. So it really is important to do this as early as you can.  Now let's shift gears to trauma and talk about source control. Again, kind of back to when I was a resident,  if somebody came in with trauma, we might give some crystalloid, maybe think of giving red cells, we'd call  surgery, call anesthesia, maybe give some fresh frozen plasma, check some labs, and eventually the patient  might get to the operating room. But this has really changed over the years, and now we do all these things  much faster, and we have trauma activation. So if you look at the time to the opening of the operating room,  this is one study looking at penetrating torso trauma, and really describing the golden 10 minutes.  So the patient gets to the operating room, within 10 minutes, they do significantly better than if you delay  longer than that. So really, the time to source control, if somebody's bleeding, is critical. Every minute counts.  Now we have some novel ways that we can try to get bleeding under control these days. We have the  Resuscitative Endovascular Balloon Occlusion of the Aorta, or REBOA, which can help decrease bleeding.  And this can even be taken out into the field, as demonstrated here by London's Air Ambulance Service doing this  in the field in London. Again, the sooner you can get control of bleeding, or at least decrease the bleeding,  the better the patients are going to do. Now what about hemodynamic stabilization? And this mainly is a  discussion about fluid and blood transfusions. So World War I, whole blood was given as pretty much standard.  This is still true for the most part of World War II, with some freeze-dried plasma being added.  And then Vietnam, there was still whole blood, but there was a significant increase in the use of  crystalloids for resuscitation, and component blood banking was becoming a thing in our own blood banks here.  So this led to what was commonly taught in the Advanced Trauma Life Support course for many years, of you give  crystalloids, and once you've given a couple liters, the patient still needs fluid, you can consider giving red blood  cells. And somewhere along the line, think about giving plasma, cryo, or platelets.  Now this approach is really very reactive, as opposed to proactive. We'll come back to this in a minute.  I do want to step back for a second and talk about what to do while the patient is still bleeding. So this is an  important question. While there's still a hole in an even blood vessel, what is the best fluid resuscitation  strategy to keep the victim alive until hemostasis can be achieved and to promote intact survival?  And this is another landmark study in the trauma history. This is a study done in Houston, now 30 years  ago. Patients with penetrating torso trauma that are hypotensive, and they got randomized to either immediate  fluid resuscitation or delayed fluid resuscitation. And what they found was that survival was actually  significantly improved with delayed resuscitation, which kind of makes sense. If the patient is still  bleeding, if you just give them more fluid, they're just going to bleed more. So again, the key thing is  source control. So what's the best fluid strategy after you've now controlled the hemorrhage? This is one  recent retrospective study that's very important here, looking at what blood products were given. And they  found that there's a decrease in six-hour mortality if there's an increase in ratio of plasma to red blood  cells, an increased ratio of platelets to red blood cells, an increased ratio of platelets to red blood cells. And basically, if that ratio is less than one to two,  compared to ratios of greater than one to one, there's a three to four times increase in mortality. This is the PROMPT trial,  which then led to the PROSPECTIVE proper trial, where in this study, with patients who expected to need massive transfusions, they were randomized to one to one to one,  or one to one to two plasma platelets to red cells.  Primary outcome was mortality. And what they found was actually not a significant change in mortality, either at 24 hours or 30 days, but there was a significant decrease in death  from exsanguination in that first day.  This too has changed practice. Here's the damage control resuscitation idea, which this now is called, and the Eastern Association for the Surgery of Trauma  guideline for severely injured trauma patients suggest that any institution should have a massive transfusion or damage control resuscitation protocol,  and they recommend targeting a high ratio of both plasma and platelets to red blood cells for resuscitation.  Now, I'm not gonna talk at length about whole blood, but I wanted to mention that this has really become a popular topic again in the trauma world.  Now, let's quote Phil Spinella here, who says, blood is for resuscitation, salt water is for cooking pasta. And also, Yur Stradninez,  who says that we should make whole blood great again.  So the current guidelines for endpoints, so we've talked about the endpoints for sepsis, what should the final endpoint be for trauma? Well, certainly in both cases,  just looking at heart rate, blood pressure, urine output are probably not enough. Now, trauma oral lactate and base deficit have been popular,  and they're certainly easy to look at too. With this guideline, we suggested consideration for focused ultrasound or the use of arterial pulse waveform analysis.  Both of these seem to be associated with detecting fluid responsiveness and preventing organ failure and complication and decreasing mortality. But this is not based on great data,  but it's clear you need to do something  beyond just looking at heart rate, blood pressure, urine output.  So I've been talking about these issues of hemodynamic resuscitation and rapid source control. And for trauma, certainly rapid source control is critical.  You gotta stop the bleeding before you can normalize the hemodynamics. With sepsis, you can do both more readily at the same time, but they're both quite important.  But this is really not a choice. And I'm going to quote Peter Safra here,  who's one of the founders of our society. And one of these comments that fits in with what's been called Peter's laws is when given a choice, take both.  And really these need to be done simultaneously with both emergency situations.  Now, another really important point was brought up by Ron Mayer during his gutter oration in 2013. Small early changes can lead to major frequently unpredictable differences  in outcome for better or worse. And this is kind of like the butterfly effect. If a butterfly is flittering in Beijing, this could theoretically cause a tornado in Kansas.  So it fits in with this concept that I've been discussing of hemodynamic resuscitation and source control. The more we can do quickly upfront,  the better the patients are going to do down the road.  Now, sepsis and trauma is certainly complicated. And there's been lots of research on the basic science and the pathways that occur during these emergency situations  of hemodynamic resuscitation. And these have led to novel therapies that have undergone many, many trials that most of the time have not really proven to have much benefit.  And I'll just point out that people are always looking for the single magic bullet that will totally change everything. There really is no single magic bullet, at least not yet.  But I'll throw out there that it's worth thinking about combination therapies that have multiple pathways, as well as more personalized medicine to really improve how we apply  the basic science that we've learned to the bedside.  Now, if you want to get interested in resuscitation research, it isn't necessarily easy, but it's fun and exciting and a great way to advance your career.  And so if you get into research and you think about a good question, do some lab work, maybe do some more lab work, hopefully then take some of the results from the lab  into clinical trials, perhaps more clinical trials, and eventually actually improve patient care.  The key thing with this is asking the right question and then sticking to it to get the answers and get the outcomes that you're trying to achieve.  If you're going to be a researcher, you want to think about being an agent of change. And an important point here is don't get stuck on dogma.  So some final thoughts from Peter's Laws.  Multiple projects lead to multiple successes.  Patience is a virtue, but persistence to the point of success is a blessing.  Bureaucracy is a challenge to be conquered with a righteous attitude, a tolerance for stupidity, and a bulldozer when necessary.  So if we look back at early goal-directed therapy from a hundred years ago,  and what was used to treat our president when he was shot, we can certainly see how we've come a long way since then with the therapies that we're now applying  and saving many, many lives that we couldn't have said and saved even 20, 30 years ago. What are we going to see for early goal-directed therapy in 2021-2020?  I don't know, but that's why we need more people in resuscitation research to really push the field further and see if we can save people that we still can't save.  But no matter what happens, I'm sure that'll involve some cool computer graphics.  Well, hopefully this was inspiring you to get into the resuscitation research field. There's lots to be done in sepsis and trauma.  And thank you very much for giving me the opportunity to speak to you today. Thank you for joining me for the initial resuscitation of patients with severe traumatic brain injury.  I'm Cheryl Lee Chang. I'm the Division Chief of Neurocritical Care at Duke University. And it is my pleasure to address you today regarding resuscitation in critical care  in the last 50 years. For my disclosures, I have no financial disclosures, but I am required to tell you that I am a current member  of the ABIM Critical Care Medicine Board Exam Committee, but I will not be disclosing any exam questions during my presentation to keep this exam confidential.  So our learning objectives, and you heard from some of my other colleagues that have addressed cardiac arrest and trauma resuscitation,  but I'm going to be talking about what has worked, what hasn't worked, and the practice of resuscitation regarding TBI. So that is my topic for today,  and hopefully inspiring you to make some changes in resuscitation for the future.  So when we look at resuscitation, especially regarding TBI, we actually know the scale weighs more heavily in what not to do rather than what to do.  So we know we shouldn't be wearing our helmet on upside down, that we shouldn't be doing dangerous things, including putting ourselves in harm's way  when people are doing target practice. What we really want to have are more guidelines and more medications that might help us in resuscitation,  and these are an area still for exploration and lots for you to do in the next 50 years. So for many years, we've codified what we've known in the 2007 guidelines for severe TBI,  and it took us nine more years to understand a little bit more. And you'll see in 2016, these guidelines for severe TBI came out as a fourth edition.  It added 102 articles to the body of evidence, but 27 of those were insufficient to support a change and 34 were sufficient but didn't support a change.  These are going to be considered living guidelines. You're not going to necessarily see a fifth edition and they're going to have ongoing revisions. So you'll want to stay tuned,  keeping up with the braintrauma.org and following what's going on in the literature as time goes on. Now, if you're interested in pediatrics,  there are these guidelines that came out in Pediatric Critical Care Medicine in 2019.  So when we talk about TBI resuscitation, we're going to be talking about understanding some of the barriers and then what we know more about preventing secondary injury,  making sure that we have adequate perfusion pressure and talking about what our targets are, what fluids should we be using, and then a little bit about hemostasis.  And then the holy grail that we still haven't found is neuroprotection. So we'll cover that a little bit and some of the lessons learned and how we're going to move forward.  One of the largest barriers in managing TBI and indeed a lot of diseases that we approach are the heterogeneity of injury. So this workshop with the National Institute  of Neurologic Disorders and Stroke, supported by the Brain Injury Association, the Defense and Veterans Brain Injury Center and the National Institute of Disability  and Rehabilitation Research identified, they came together and identified the fact that there are different patho-anatomical lesions that we have to deal with  and all may be somewhat different in their pathophysiology. So you can imagine the mechanism of injury with a epidural hematoma is different from the severe injury  that occurs with the amount of velocity it takes to create a subdural hematoma in patients. Contusions are going to be different than the subarachnoid that we know  does have worse in outcome in these patients. We have the DAI patients and then the diffuse swelling and all are going to be different  in what type of pathophysiology we're dealing with, the severity, and of course, we're dealing with different patients with different plasticity, different ages,  different comorbidity. So this is part of the problem of what we're trying to address a common solution to, but maybe something different. And as I've talked about,  there's different patho-anatomical sequelae depending on the overlap that's occurring in your patients. So it is really hard to try and find solutions  to how to best treat our patients in resuscitation. So some of the things we do know in secondary brain injury comes from the traumatic coma database for many years ago  that we know that just a single episode of dropping your systolic less than 90 is going to cause significant hypoperfusion to increase morbidity, double mortality,  and hypoxemia defined as a PaO2 of less than 60 is going to increase your poor outcome to 71% from 28% and increase mortality to 50% from 14.3. We know that also harmful mediators  such as reperfusion injury, inflammation, and then seizures, which may cause excitation, more bad neurotransmitters, and then electrolyte changes like hyponatremia,  hyperglycemia can all be a problem for these patients.  So we talked about trauma resuscitation. It is these overlapping, these Venn diagram that you have are penetrating thoracal abdominal injury or blunt injury.  And then for TBI, blunt or penetrating injury as well. The literature, which I'm not going to go in through to for my brief time that I have with you,  is we know with penetrating injury, restrictive crystalloids initially targeted to a much lower systolic blood pressure just until operative control of the bleeding occurs  and blood products are available. And you know, there's a whole body of literature regarding that. And blunt injury, not a lot of large trials looking at liberal versus restrictive,  but we know that you can liberalize the blood pressure a little higher to 80 to 90. The question is, what do we do for TBI?  So we do know, and just going all the way back to looking at your autoregulation is that as our blood pressure goes up, we autoregulate to vasoconstrict  to keep our cerebral blood flow the same. And when we overcome those mechanisms, we're going to have edema. And when blood pressure is too low, we're going to have ischemia.  Now this autoregulation is happening in the parts of the brain that are good,  but when you have injury to the brain with contusions or hemorrhage, you're going to have defective autoregulation. So the higher the blood pressure,  you're going to have edema and more hemorrhage. And then the lower the blood pressure, you're going to have ischemia. So we have to balance that.  Now also cerebral perfusion pressure, which you're aware is the mean arterial pressure minus ICP are numbers that also have been looked at  in the literature trying to find out what is optimal. So we don't have a lot of time to go through  all these studies, but just so that you are aware that these are in the guidelines, if you want to go back to Carney's, the fourth edition  and look at all the different studies they looked at for creating the threshold guidelines that we have. And distill it here. And first, just talking about the PAO2,  which I'd mentioned earlier, those haven't changed. There's not enough literature to make any difference here as far as making sure a PAO2 is greater than 60  and we're setting greater than 90. For the systolic blood pressure, which was easier to remember back in 2007 until 2016 was greater than 90, but based on all the literature  that I showed you in that one slide that they've made it even more difficult to remember, but the systolic blood pressure should be greater than 100  for ages 50 to 69, but at the extremes of age, so between 15 and 49 or greater than 70, the goal is greater or equal than 110 to decrease the mortality. So how do you remember this?  And I was trying to figure out, well, what's the best way if you remember a smile? So at the extremes, you want the 110 and at the lower between 50 to 69,  you want the greater than 100.  So for the cerebral perfusion pressure, just talking about the threshold changes, it used to be 50 to 70. They've changed it upward to 60 to 70  dependent on whether you have intact autoregulation. And then before they were saying, based on some of the work done  by Claudia Robertson was showing that if the cerebral perfusion pressure was too high, especially using fluids and pressors, there was ARDS.  Now they're saying that you need to avoid it to avoid aggressive attempts to keep the CPP greater than 70. It might be considered, but based on cerebral oxygenation,  we may need to be higher. There's a trial coming out called the BOOST-3 trial that hopefully we'll know more about this. So just these are our guidelines  that we're talking about just to distill it again, that now we have a little bit of answer to that. Now, just briefly, just mentioned that norepinephrine,  as many of our critical care diseases, we're talking about using norepinephrine for TBI patients as well. I just want to mention with adequate perfusion  for ventilation strategies that with PaCO2, remember we're vasoconstricting to make room for the brain with the ICP to get the ICP down with the cerebral blood volume down,  but it causes significant vasoconstriction based on a lot of studies. So recommendations are, and this is again trying to keep good perfusion in the brain.  We don't want to have prolonged prophylactic hyperventilation less than 25. It can be a temporizing measure, but really want to avoid it, especially in that first 24 hours  where we're trying to keep perfusion and blood flow better. So with the fluids, what should we be using? We know that colloidal suspension of blood is the best.  Studies are, and I'll show you briefly about albumin. We know that the synthetic colloids have problems with AKA and coagulopathy and anaphylaxis.  And crystalloids, they're mostly compared to hypertonic saline, not comparing the usual crystalloid, just remembering the different sodium contents of these,  but I'll just briefly talk about the hypertonic saline. We know with the albumin study, the SAFE trial, which you're probably very familiar with, in 2007,  that study showed that with 460 patients, GCS of less than 13, so moderate to severe, that outcome at 28 days to 24 months or two years, most of those patients, as you can imagine,  died within those 28 days. You could see that the probability of survival was less with albumin, so therefore we don't use albumin at 24 months.  Again, higher rate of mortality with albumin versus saline and for severe TBI even more so, 41 versus 22%, so statistically significant,  probably because albumin may be third spacing across the brain, causing more edema, we're not sure.  So when we talk about saline and hypertonic saline, pre-hospital, this study by Cooper with 229 patients using 7.5% saline versus lactated ringers  and as you would imagine, the sodium did go higher from the 141 with LR to 149. There wasn't a difference in survival to hospital discharge.  The six-month extended Glasgow outcome scale or favorable outcomes using other measures was not statistically significant. So hypertonic saline, prophylactically also,  just like albumin, is not felt to be helpful. This study with over 1,000 patients using the 7.5%  versus the 7.5 with dextran or normal saline was stopped due to fertility with no difference in the 28 survival. So hypertonic saline prophylactically  has not been shown to be helpful in our patients and just showing you if you're interested in referring to this 2019 meta-analysis showing hypertonic saline versus crystalloid  and just in the forest plot just showing you, again, not statistically significant for relative risk of mortality. For crystalloid also, for good clinical outcome,  hypertonic saline, not helpful as a prophylaxis. And then if you also look at not just crystalloids but you pull it out and look at normal saline  or LR by itself, again, not statistically significant for relative risk of mortality. So just to mention that for a number of interventions,  as you had imagined, using hypertonic saline was helpful, seemed to have a trend towards decreased IC length of stay  and that was managing ICP. So we've covered that, just mentioning hemostasis and then in our last few minutes of neuroprotection is that TXA is the CRASH-3 trial  for trying to prevent more injury and decreasing more hemorrhage. We know in the patients that were not severe, so these are patients with GCS of greater than nine or 12,  that one gram of TXA over 10 minutes within three hours followed with the one gram over eight hours given again within three hours was helpful to patients.  This is showing that with GCS that are mild to moderate, those are the patients that benefited. Those that were severe were not. Those with bilateral reactive pupils  also tended to do better, but in those patients that were not reactive, one had not reacted was not very helpful. So this is showing that for every 20 minute delay,  you're going to have decreased effectiveness and these again, mild to moderate and with severe, we don't give it at all in these subset of patients. So my last few minutes,  I'm just going to mention neuroprotection because these are where we're hoping the future will lie, but have not found anything yet. There's excitotoxicity that happens  after the initial impact or injury, there's depolarizations, inflammation, apoptosis that occurs days later. And we know that something like hyperthermia  can accelerate neuronal injury in many different ways of increasing free radicals, what bring barrier breakdown, inflammation.  And studies have shown in this first trial with Don Marion seem to hasten neurologic recovery and just showing that here, that empiric hypothermia after TBI,  all the different studies have so far been negative. So the current guidelines for neuroprotection with hypothermia show that it is not recommended to improve outcomes.  So what's next? The phase three trials with progesterone studies have taught us a lot. And this is what I want to finish up with is that there's been 100% failure  for neuroprotective medications in clinical trials. So progesterone would look like a clear win in all the preclinical work that was done  in brain and spinal cord contusion injuries, nerve injuries, reducing inflammation, glutamate or excitotoxicity, edema, apoptosis and enhancing recovery.  So it all seemed like this would be helpful in repairing the damaged brain. Multiple studies, 300 preclinical trials, male and female look promising.  We did two phase two trials using a vehicle of intralipid or a different oil, but the PROTECT-3 trial came out, a double-blinded, two-arm study was stopped for fertility,  looking at mortality and that good outcome. The SYNAPSE trial, 180 centers done across North and South America, Asia and Europe, completed enrollment of over a thousand patients  but no difference as well. So the INTREPID trial, just mentioning that that is another synthetic analog that is working to improve outcomes after injury  by inflammation, improving synaptic function, was in a study in different outcomes and also was a negative trial. So I just, the last two slides talking about  what's hampering us from finding good resuscitative medications. One is the heterogeneity we talked about, different patients have different plasticity or comorbidities.  We may lack biomarkers or other markers to identify baseline severity. And then the question is, do we have the wrong doses? There's preclinical trials that showed  U-shaped dose response occur, so maybe too high was used, people clear differently, depending also on gender, and then a duration of treatment, timing in the window.  And then are we not doing these trials, being able to execute them more homogeneously across centers? How about rehab and are we picking the right early end points?  And then lack the later end points may be a problem. We should maybe be looking at more detailed neuropsychological outcomes. So the ability to control animals  in the preclinical work has been helpful, but humans don't have that same homogenous injury. So these seem to be our biggest problems  and maybe our solutions are preclinical animal trials that should be designed to mimic human injury. Also, they find that negative trials  are not reported as much as positive trials. Maybe looking at specific injuries, we need to maybe pick a subset of patients based on biomarkers or other findings,  and then developing better physiologic or predictive biomarkers that are gonna help us enroll the right patients into these trials and look at maybe even their inflammation,  and then define reliable functional outcome measures that are gonna allow us to localize and quantify the injury over time. And finally, harmonizing how we're conducting  the trials and data collection. So we need to look at the research centers, how they're managing patients and addressing data entry errors.  So in conclusion, all these trials I have not failed. I've just found 10,000 ways that won't work and we know Thomas Edison has been successful eventually in his work.  Albert Einstein, a person who never made a mistake, never tried anything new. And this one, if at first you don't succeed, try two more times so your failure  is statistically significant. So thank you very much for joining me today and I hope you enjoy our 50th anniversary of Critical Care Congress  for the Society of Critical Care Medicine. Thank you.  All right, thank you for that awesome lecture. That was a great review of just the advances, where we've been, lessons learned, and future possibilities for resuscitation in CPR,  in trauma and sepsis, and in TBIs. We have some wonderful questions from some of our audience. Feel free to keep posting questions there. We'll use the time that we have live  to answer some of those, and any additional questions will be answered if you just check back on your site. So one of the questions here being asked  is about commenting on the role of optimizing human factors in the conduct of resuscitation. For example, the AHA's Resuscitation Quality Improvement Program,  as a good step in that domain, or is it only a half measure?  Well, I know I can speak a little to that. So along the way, a lot of the programs have focused on the skills of resuscitation. So chest compression depth, and rate,  and ventilation rate, et cetera.  But where we're really moving is to understand the choreography of resuscitation. I think we've seen this a lot in the COVID era, where our masses of resuscitation response  have been honed down for PPE reasons. And the elegant choreography that improves the movement around the bed, getting the right procedure to the right patient  at the right time, and the communication issues, particularly with PPE in place, have sort of come to the fore. So there's now an increasing focus  on doing the few simple things that we know work, like getting circulation going, chest compressions, getting defibrillation to the right patient,  getting ventilation and oxygenation to the right patient, and doing that in a timely manner through communication and training.  And a lot of that has now moved to just-in-time training for smaller teams, that sort of touch base or huddle to work together.  Sam, are you seeing the same thing?  Yeah, I would agree. I was gonna point out that in the trauma world, we've kind of done more of this traditionally because we record trauma resuscitations  because they kind of happen in one place with one team, as opposed to cardiac arrest teams that can be much more random. And so the work that you're talking about,  I think is really critical to kind of figure out how to make those sort of ad hoc teams work well together. Everybody needs to know what their roles are.  And the more we can practice, you know, insight to simulation practice, that kind of thing where you practice before you have a resuscitation is really gonna be critical.  And from the TBI standpoint, I think unfortunately lag behind our cardiac and trauma colleagues in the fact that it isn't as well algorithmed,  you know, that there's different type of monitors that can be put in. There's, you know, the timing's not really clear, the treatment choices of what we use first.  So those are, we're still lagging that and there's a lot of human factor and trying to create algorithms and try to standardize them and then even study them.  And it is the variability, as I was mentioning in my lecture of, you know, how we perform resuscitation, why some of these trials may be failing  is because there is so much variability despite attempts to create algorithms, there's always that human factor.  And then, you know, I think another thing to emphasize is that a lot of the standardization, like the first five minutes is very protocolized and sort of the same across the board.  But these clinical protocols that Shirley's mentioning, we don't wanna take the thought out of the treatment that we still have to personalize  into those special resuscitation circumstances around the patient. So standardization of approach doesn't necessarily mean standardization of treatment,  or the same treatment for every patient.  Yeah, I think that's a great point. And another question to sort of get you guys, all of you, your thoughts on is that, you know, this research,  some of the data that you've been presenting to us is wonderful, but we know that practice lags behind research. And so what are some of the big and upcoming aspects  of resuscitation practice improvements? Where do you think those are headed next? What are some of those big picture practice improvements?  And we'll start with Dr. Tisherman.  Thanks. EPR, Sam.  I think one thing that, as we've kind of already a little bit talked about, the human factors issue, I think more interprofessional training and looking at the human side  is gonna have a lot of impact. Cause as we've all kind of touched on, you know, a lot of the drugs or individual therapies kind of come and go. There's a great excitement  because of a big trial that comes out and we try something and then you find out some more data a few years later, eh, you know, activated protein C didn't really do anything.  And then it's off the market. So I think a lot of the basic stuff is really the key. And that's where we can, no matter where you are, you can make a difference by, you know,  hitting the mark early on those first few minutes of getting the team together and doing what needs to be done. And some of this other stuff, I don't know where the future will be,  you know, maybe precision medicine or whatever. It's gonna be a while though. And, you know, as I've kind of said, fixing the patient's physiology as fast as possible  is probably the most important thing. And it's gonna probably stay the most important thing for a long time. And from the neurologic standpoint,  I mean, one of the big practice issues that we fight is the nihilism that comes in sometimes with dealing with bad TBI patients and trying to figure out, again,  which of the patients that are gonna benefit from our treatments and not, you know, throw the baby out with the bathwater. There might be certain subsets that we aren't studying.  So actually the practice improvement is still gonna rely on a lot of research, at least in the TBI area, and trying to understand, you know, which patients are gonna benefit.  And then also not, you know, finding better ways to parse out which patients were really, should be creating or having prognostication for it  and others that we really know that we don't know. And I think we're learning more that we don't know a whole lot about how these patients are gonna do.  And so that's where our research has to go into improved practice, because we need to make sure we're not withdrawing too soon on these patients.  Yeah, I really agree. I think that the goal-directed approach is really not gonna go away, that it's just gonna be that we're gonna be better  at defining the specific goals for the specific patient that probably will involve stratification of what we do based on biomarkers, electrophysiologic markers and genomics perhaps.  And also I think that some of what we're learning about the resuscitation will start to penetrate the prevention of a lot of these events  in that as we get better at sort of recognizing  and deploying to resuscitate, we also will be getting better and better at learning at those precipitating factors that are leading up to the resuscitation  that we can intervene on early. I think Sam touched on this a little bit about the quotation he had about really trying to identify things that one could do early  that then would prevent the cascade of the subsequent need for resuscitation.  Yeah, I think that future lens of like where it goes and I think the punchline being that the basics are still the basics and it seems like even over time,  those basics, those processes true to the physiology of the problem really is where our focus remains and should be.  I had a question again for- We shouldn't be nihilist though, right? We shouldn't be nihilist if we look at over the last 50 years if we even look at over the last 10 years  if we even look at over the last 10 years for cardiac arrest, for trauma and for neurocritical care, we've seen great advances and improvements  just by doing the few things that we know work and work well. And we haven't seen this steady upstream of survival and good outcomes. So we shouldn't really be nihilist  even though we don't have all the answers. Right, so do what we know works and do it well and learn how to do it well. And so there is space in the tent, if you will,  for those who want to discover newer advances that kind of send us in the future with machine and all those sorts of optimizations,  but then also doing from an implementation standpoint, doing what we know the literature is very clear works and doing that well. Yeah, it's not all magic bullets.  A lot of it is just hard drudgery to get the few things that we know work to work better. Yeah, there's a few more questions here in the chat that are, I think, very specific,  but I think from the bigger picture question, final question to the group and all these questions that are being posted, we will address those.  So again, check back on your site for them. So keep them coming, the questions as you watch the videos or rewatch the videos, because it was quite excellent.  Final thoughts from the panelists about sort of pearls and tips and mistakes to avoid,  especially if you're at an institution where there are challenges to doing what we know works well.  We have just a few seconds to kind of get thoughts from somebody who has something coordinated.  I think Sam had the best slide about just being persistent.  I don't remember the exact quote, Sam, if you can quote it, but I think that was very good. Sometimes you just need to keep working at things and not take no for an answer  and work with your team and get everybody on board. Sometimes we do have to make change, work with our administrators and everybody that are part of it and including everybody.  Yeah, that's a key thing is getting all the stakeholders on board from the beginning. Otherwise you're going to get pushed back. Yeah, well, that was awesome.  This has been so very helpful. Thank you guys so much for your time, your expertise, your research and your contribution as we try to advance science or resuscitation  in those three areas.  Thank you. Thank you all for attending. Thanks everybody.  ♪♪♪

Video Summary

In this session entitled "50 Years of Resuscitation in Critical Care: Lessons for the Next Generation," the panelists discuss the evolution of CPR and resuscitation over the past 50 years. They focus on three areas: cardiac arrest, trauma, and traumatic brain injury. The panelists highlight important lessons learned and advancements in resuscitation strategies. They emphasize the importance of early, effective CPR and defibrillation in improving survival rates for cardiac arrest patients. They also discuss the role of goal-directed resuscitation in trauma patients, specifically the importance of source control and hemodynamic stabilization. In the context of traumatic brain injury, the panelists discuss the challenges of resuscitation due to the heterogeneity of injuries and the need for personalized treatment approaches. They highlight the importance of optimizing perfusion pressure and the use of fluids in resuscitation. The panelists also address the ongoing search for neuroprotective therapies and the need for further research in this area. Overall, the panelists stress the importance of continued research, collaboration, and adherence to evidence-based guidelines in improving resuscitation care for the next generation.

Asset Subtitle

Resuscitation, Trauma, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives

Review the approach to science in cardiac arrest, medical, and trauma surgical resuscitation
Describe what has worked and what has not worked in transitioning to new ways of practice in resuscitation
Inspire young physicians to make changes in resuscitation care in the future
Analyze the advancement of resuscitation strategies for patients with concomitant severe traumatic brain injury and significant injuries to other organ systems

Staying Alive: The Evolution of CPR and Resuscitation
Vinay M. Nadkarni

Early Goal Resuscitation: Then and Now
Samuel A. Tisherman

Initial Resuscitation of Patients with Severe Traumatic Brain Injury
Cherylee Chang

Meta Tag

Content Type Presentation

Knowledge Area Resuscitation

Knowledge Area Trauma

Knowledge Level Intermediate

Knowledge Level Advanced

Membership Level Select

Tag Cardiac Arrest

Tag Traumatic Brain Injury TBI

Year 2021

Keywords

CPR evolution

resuscitation advancements

cardiac arrest

trauma

traumatic brain injury

early CPR

defibrillation

goal-directed resuscitation

source control

hemodynamic stabilization

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