SCCM Resource Library-Why Arresting in the Perioperative Period Has Better Outcomes: Anesthesia ACLS (includes complex cases)

Video Transcription

Welcome to Why Arresting in the Perioperative Period Has Better Outcomes, Anesthesia ACLS. My name is Mark Nunley and I'll be your moderator for this session.  The field of anesthesiology has generated discussions around the causes of mortality and generated also significant progress in the reduction of mortality, but the problem  is more complicated than it might seem. Dr. Cates, in 1978, during the Crawford Long Lecture, discussed the fact that anesthesia  mortality is the confluence of several factors, patient factors, medication reactions, various  interventions, and even random chance interplay to generate the results that we see we need to track and we need to improve upon.  However, as he pointed out all that time ago, much more needed to be done to understand these interactions.  Much more fortunately has been done, and in recent years, we have published increasing information about why arrest in the perioperative setting is different, interventions should  be different, and indeed outcomes can be different. This panel today will discuss all of that.  We'll be talking about the epidemiology and history of anesthesia ACLS, the role of the surgeon in perioperative cardiac arrest, and discrepancies in medication administration.  I'm pleased to announce our three panelists, Talia Ben-Jacob is an assistant professor at Cooper University Hospital, John Chovanes is a trauma surgeon and the director of military  affairs also at Cooper University Hospital, and Kayla Nichols is a clinical pharmacy specialist at Emory University, and they'll each be tackling their respective topics.  Our goals today will be to talk about the epidemiology and etiology of arrest in the perioperative period, talk about some rare and complex cases, discuss the management  of shock, discuss the role of the surgeon, and compare anesthesia advanced cardiac life support with the American Heart Association algorithms.  It's my pleasure to introduce our first panelist, Dr. Ben-Jacob. Hi, everyone. Good afternoon. Today we're going to be talking about why arresting in the perioperative period has  better outcomes, also known as anesthesia ACLS. My name is Talia Ben-Jacob. I'm the division chief of critical care medicine in the Department of Anesthesiology at Cooper  University Hospital, where I'm also an assistant professor of anesthesiology. Today I'm going to be talking about the epidemiology and history of anesthesia ACLS.  Before we begin, I just needed to disclose that I received a one-time honorarium from the American Society of Anesthesiologists for chairing the revision of the anesthesia  ACLS CME activity. I also currently receive a quarterly stipend from UpToDate for an article on perioperative cardiac arrest.  So anesthesia ACLS, similar to regular ACLS, was developed as an extension of BLS, also known as basic life support.  BLS is the foundation of all life support, and that's essentially using CPR. ACLS, in the general population, focuses on common causes of arrest and incorporates cardioversion,  medications, and defibrillation. It manages patients who experience sudden cardiac arrest in the community.  This data and success rate was extrapolated for use for patients in the hospital and the perioperative period.  Being that the original research was not done with regards to patients in the perioperative  period, multiple studies and literature review was performed concerning cardiac arrest and  other crises surrounding the perioperative period to determine how ACLS can be extrapolated,  whether new ACLS guidelines specific to the perioperative period would need to be created. And so this talk will discuss the updated clinical perspective.  So after all that research was done, it was determined that anesthesia ACLS is needed because cardiac arrest in the perioperative period is different.  Cardiac arrest in the perioperative period is almost always witnessed. The precipitating causes are usually known. There's actually increased survivorship.  So it turns out the survivorship rate of perioperative cardiac arrest is 30% to 80% when compared to just 10% in the regular population.  Our patients that arrest in the perioperative period usually have better neurologic outcomes. Usually the causes are reversible.  The response is timelier because the physicians that are taking care of these patients are right at the bedside as the arrest occurs.  It's a focused resuscitation because usually the cause is known. The past medical history of the patient is known because the care providers are currently in the room with them.  And differently, whereas ventricular fibrillation is the most common outside hospital arrest, asystole is the most common arrest in anesthesia ACLS.  Another reason for the creation of ACLS is because it's very rare. The incidence of perioperative cardiac arrest is 5.6 per 10,000 cases.  There's also a lack of awareness, difficulty in recognition of crisis, delays to treat, and failure to rescue.  There's been a lot of survey studies with regards to perioperative cardiac arrest in the perioperative period among anesthesiologists.  And it was noted that sometimes it was very difficult to determine whether or not a patient was actually arrested as these patients are usually sedated.  They're under general anesthesia so you can't monitor their mental status. Their respirations are controlled by the ventilator.  The surgical positions also make it difficult to assess your patient on a regular basis  and large portions of the body are covered. So the failure to rescue is based on a hindsight evaluation.  In addition, multiple times a small doses of pressers are given during the perioperative period due to hypotension from general anesthesia.  Because of the treatment, it often delays the notification that the patient is actually in arrest.  So many famous cardiac anesthesiologists came together and they created measures, corrective  measures for monitoring patients in shock that lead to perioperative arrest in the perioperative period.  And they came up with guidelines that basically and algorithms to help manage this in order to ensure that there was no failure to rescue or delayed recognition.  And it's always important to note that whenever you undergo a crisis, the first thing to do  is always to recognize the crisis, call for help immediately, and then begin your resuscitation period.  We'll talk a little bit more about the algorithm and the directions for anesthesia ACLS a little bit later.  What's important to note is that a lot of the causes of perioperative arrest are very different from arrests either outside the hospital or inside the hospital.  Most importantly is recognition of perioperative bradycardia. Usually perioperative bradycardia can due to vagal responses due to surgical manipulation,  whether it's in carotid endarterectomies or the ocular reflex, vagotonic anesthetics, sympatholysis from anesthetic agents, beta blockers, and neuroaxial anesthesia.  Neuroaxial anesthesia, especially in elevated epidurals or high spinals, can cause suppression of cardiac accelerator fibers from T1 to T4.  A lot of the causes that we discuss in their management and their unique management will be discussed by Dr. Nichols in her discussion with regards to pharmacotherapy and ACLS.  Other causes of perioperative arrest include transfusion reaction, anaphylactic reaction,  hypoxia, but hypoxia can often rather be related to an intrinsic lung disease, may be related  to difficult airway or trouble, difficulty intubating in the operating room and desaturation, auto-peep on the ventilator, and bronchospasm.  In addition, there are multiple anesthetic conditions that can cause perioperative cardiac arrest, such as an overdose of medications related to anesthesia or pain management,  neuroaxial blockade. We talked about the blockade for the T1 to T4 fibers that suppress cardiac activity,  but also high spinals, which are elevated, can paralyze the diaphragm as well as the cardiac fibers, local anesthetic toxicity, for which guavacaine can be injected into  blood vessels and inadvertent regional blockade, as well as malignant hyperthermia.  There's also cardiac etiology related to causes to cardiac arrest, such as air embolism from  central line insertion or air embolism for beach chair position, for shoulder replacement, or even in sitting craniotomies.  Tension pneumothorax should always be on the differential, pacemaker failures, electroconvulsive  therapy can cause an arrest with cardiology in combination with anesthesia, prolonged  QT syndrome, and then other causes also include hypovolemia, whether it's simply being dehydrated  from being NPO and having a very large bowel prep, and also with regards to hemorrhage and trauma.  Hemorrhage and trauma with regards to communication and intraoperative causes and surgical causes  will be discussed by Dr. Chivanis later in this talk, because really, just like an ACLS and cardiac arrest intraoperatively and at the hospital, these are all team sports and  require communication among all the multiple disciplines and faculty.  Here's the main algorithm with regards to anesthesia ACLS. Most of the smaller algorithms that individually treat many of the causes that we discussed  earlier will be discussed by Dr. Nichols in depth in her talk, but what's important to realize is that the anesthesia ACLS algorithm differs significantly from the regular ACLS  algorithm. Important things to highlight would be that we often give calcium in the operating room because hyperkalemia presents differently in the operating room.  Many of our patients are end-stage renal disease, on dialysis, or have an AKI, and giving one gram of calcium often does not hurt. We also have vasopressin on our algorithm.  Vasopressin was removed from the standard algorithm of ACLS because it was done to simplify the algorithm, because once again, ACLS is done in the field by laypeople, so it's much  easier to remember to push one milligram of epi every three to five minutes rather than to add an extra medication.  What's also notable on our algorithm is that we have a lower dose of epinephrine listed.  This lower dose of epinephrine reflects anesthetic practice, and also it reflects the increasing  evidence that epinephrine is harmful in arrest states, especially including local anesthetic toxicity.  Story data suggests that harmful epinephrine-induced reductions in microvascular blood flow during  and after CPR may offset the beneficial epinephrine-induced increase in arterial blood pressure during CPR.  There was no benefit of adrenaline in survival to discharge or neurologic outcomes. Among patients with cardiac arrest requiring vasopressors, combined vasopressin, epinephrine,  and steroids, which we also include in our algorithm during CPR, had better survival  and better neurologic outcomes compared to those who did not receive steroids or an epinephrine-vasopressin combination.  Those still remain on our algorithm, especially because of the link to improved survival and favorable neurological status.  Just like regular ACLS, it's important to realize who will most likely survive and not survive, and we found that the lowest survivorship are in the elderly, those with higher ASA  status, and the ASA ranks their status from one to six, with one being healthy and six  essentially being an organ donor, and obviously, the higher your ASA status is, the more unhealthy  you are at baseline, and so therefore, it would make sense that those who are unhealthy at baseline who suffer cardiac arrest would have less reserve and be less likely to survive.  In addition, emergency procedures, whether it's abdominal perforations, abscessy drainage,  have decreased survival, in addition to infections, and then not surprisingly, nights and weekends,  so if you arrest in the operating room on a night or weekend, you actually also risk not being able to survive, and that's mostly due to the fact that on nights and weekends,  either you're most likely undergoing an emergency procedure, it's not a scheduled case, and in addition to the fact that there's less help around.  So if you do suffer, so if your patient does suffer cardiac arrest in the operating room, it's very important also to realize when you need to escalate care.  Ideally, you undergo anesthesia, ACLS, hopefully there's responses, but the stability of the patient needs to be obtained, so ideally, if stability can't be obtained, even with  ROSC, TEE or point-of-care ultrasound is readily available in the operating room and should be performed, whether for diagnoses, for line insertions, or even to guide treatment  management of the patient, and it's very helpful to see if perhaps, you know, if your patient's  failing levophed and vasopressin, that perhaps they need an inotrope by being able to do an intraoperative ultrasound.  Also, like CVP insertion for help with transfusion, if it's hypovolemia, or for vasopressor infusion,  but it's important to note that invasive monitors should not delay supportive care. So if you have the choice between either putting an arterial line in or getting your central  line in to give blood, you put your central line in to give blood first, and then you worry about your arterial line afterwards.  And then finally, depending on the cause of the arrest, if it's intraoperative MI versus, you know, hemorrhage or sepsis, you know, escalate care either by getting the patient  in ICU bed, having cardiology come to the bedside to take the patient straight to the cath lab.  But obviously, patients should not be transported through the halls prior to stabilization.  And then on a side note, and this is something that anesthesiologists, in my personal opinion, need to work on a little bit. It's about decision-making.  You know, patients come to the OR, and obviously, we always assume that if you're having a surgical procedure that we're going to be aggressive about your care.  We're even intervening and pushing small boluses of pressures prior to cardiac arrest just to try to prevent that, to keep the patient stable.  And so shared decision-making really needs to occur prior to the OR, especially when caring for these, like, sick AS, you know, the elevated ASA patients.  The patient's wishes and family wishes regarding heroic measures need to be discussed prior to the operating room, oftentimes because we do know that the majority of our causes  are reversible and that we can easily treat them and that we have everything readily available.  We try to suspend DNRs, DNIs, especially if a surgeon is going to work on a 16-hour case to save a patient.  He doesn't want to find out that when his patient doesn't come off the vent immediately after the operating room that there may come for care because they can't get extubated.  But this is hard, and these are big medical, these are big ethical, medical ethical issues, and the ASA has guidelines with regards to these, but that's where shared decision-making  comes in between yourself, the surgeon, and the rest of the team. And I always tell the story about I had a 90-year-old patient who fell out of a nursing  home, and she was DNR, DNI, and the family was electing to have her TIB-FIB fracture fixed but refused to revoke the DNR, DNI because they felt that if it was her time, it was  her time. However, they knew that if she survived, her quality of life would be severely impaired without her TIB-FIB fracture.  And so you guide your anesthetic plan based on that, but you have to respect the family wishes and not suspend the DNR, DNI, because clearly it was well thought out and they knew  what they had wanted for the patient. So in summary, cardiac arrest in the perioperative period is rare.  It usually arises from unique causes that are not necessarily, that do not necessarily occur on the hospital floor or in the community.  Anesthesia ACLS is usually managed by a team familiar with the patient and their history as well as their procedural course.  And anesthesia ACLS allows the medical team to intervene in a directive, effective, and timely manner.  Here's just some suggested further reading, and I just really like this cartoon, but we'll take questions at the end after all the presentations are completed.  Thank you for listening, and I appreciate and thank you, SCCM, for giving me this opportunity to speak.  Hello. My name is John Chivanis. I'm a trauma surgeon, acute care surgeon, and surgical intensivist at Cooper University Healthcare in Camden, New Jersey.  I'm also a colonel in the United States Army Reserve Medical Corps. Thank you for this opportunity to present to you this interesting topic, and thank you  for this opportunity to go to the society and to speak with such a distinguished group of panelists.  My portion of this large topic, perioperative cardiac arrest, will focus on the role of the surgeon, what I see as the surgeon does in this situation. I have no disclosures.  Objectives, there's a few, define what an interoperative cardiac arrest is. Also, this is a difficult timeframe to clearly define.  With damage control surgery, that is truncated operations, when does the operative phase begin? Beginning of the scalpel, sometimes the patient can be open for hours or days.  We're also going to review some key areas of failure, including, of course, improvements, communication, situational awareness.  This can get difficult when you're in the one, in the middle of the battle with the beast, that being death. What are some of the common causes?  What are the things we can do to mitigate those causes? How is this different than the typical cardiac arrest, in hospital, out of hospital?  The events of cardiac arrest that ACLS traditionally was designed to handle. These viewpoints are solely mine.  These do not represent those of Cooper University Health Care, nor the Department of Defense, nor the Society of Critical Medicine, nor other panelists. These are my viewpoints.  Let's start with context. The topic of severe injury, sudden cardiac arrest, or cardiac arrest, where it occurs  in the operating room, must be viewed in the overall picture of context. This is a 24-year-old patient, a male brought up directly from the trauma bay.  That's our trauma admitting area, separate from the emergency department, where seriously wounded come.  Is it in the battlefield setting, such as in Kandahar, or in Afghanistan proper? Is it an already critically injured or ill patient that you're prepared to expect worsening  condition? Or is this totally a surprise? Is this an elective outpatient laparoscopic cholecystectomy at a freestanding surgery center?  What is the context? What is your patient's overall condition from the beginning? And to frame this within context is, I think, an essence of this whole discussion.  The perioperative period can be quite large and lengthy. It can start from admission through the actual incision, anesthesia, the awakening from anesthesia,  over in PACU, the ICU and the wards, up to 30 days out, sometimes even 90, depending on how you measure it.  But for the portion of my portion of the panel, we're going to speak about the operative or interoperative phase, traditionally thought of as when the initial incision is made to  closure. But remember, with damage control surgery, the operations can be truncated and have multiple operations.  So if a patient didn't go into cardiac arrest in the OR after a very complex case where there are multi-cavities open and they're going back to the trauma intensive care unit  or the surgical or medical ICU for continued resuscitation, that could still be considered if they're open, the operative phase. Also, where are we on interoperative cardiac arrest?  It's a unique occurrence, but where are you in this occurring? A critically ill patient, where is the patient at the beginning of the case? Is this later on in the case?  Is this out on the floor where the patient's situation has changed, so therefore the differential has changed with them?  The interoperative cardiac arrest is a different animal, so to speak, than the traditional in-hospital cardiac arrest or out-of-hospital cardiac arrest.  Think of your pre-hospital system, CPR, time to CPR, the chain of survival for out-of-hospital, which still exists in a hospital, but the idea where the monitor, it's a more medical  event, the patient is down, someone witnesses them or don't, you put them on the monitor and you see those rhythms, that's a different type of situation than the operating room  where their patient and the caregivers, the surgeon, anesthesia, and other trained caregivers are observing everything that's going on, and they're not even more so than the ICU,  where there may be one nurse caring for two, three, four patients, so it's a different, the essence of this talk, I think, is this is a different type of situation, and therefore  needs different perspective, training, and abilities. Cardiac arrest versus sufficient cardiac activity. It's all from one's view, one's perspective, there's many things in life.  As the surgeon in an abdomen, when anesthesia says, I've lost pulses, sometimes all you have to do is look at the central tendon and you can see rhythm, a nice cardiac rhythm,  it might be pumping away at 120 or 150, 160, it may be too fast to allow for diastole to fill or there may be not enough volume in the pump, so maybe it's pulseless electrical  activity or in the old days, electromechanical disassociation, PEA and EMD, however, you may not feel the pulses, but they may be beating.  Now, when do you decide, do I do a CPR, is my blood pressure below 40, pulse rate? But the point is, is sometimes, from my perspective as a surgeon, I can quickly see, or we may  be in the chest and looking down at the heart, and anesthesia could just look over the curtain and see, oh, there is a heartbeat.  And I think that it's important to say, what perspective are you viewing that cardiac arrest? And although it's still maybe not generating a pulse, it may be organized, maybe CPR is  the last thing you want to do or shock the patient, maybe they just need a lot of volume. So what viewpoint of the curtain are you looking at?  And this is the essence of the advantage of when you're in an operating room, a surgeon  is seeing something different than the anesthesiologist at times, and it requires a magic of communication,  a steady hand, and quickly discussing, hey, I don't have pulses, hey, I'm looking at a heartbeat. And that's a key part, as noted in the objectives of this type of situation.  My colleagues do a wonderful job of clearly delineating the H's and T's of cardiac arrest, severe brain acardia.  And of course, as a surgeon, I focus more so on what I can help, and hemorrhages being  one of the leading causes of interoperative death, of course, hypoxemia. And then we can intervene to a certain extent on that hemorrhage, right?  We can somewhat stop the bleeding, somewhat, and allow time for there to be some repletion of that lost volume, repletion with blood, of course. Also, could this be a tamponade?  Is this a type of tension physiology or a tamponade, both compression?  I can relieve, we perform a urgent thoracotomy to relieve the tamponade, or is this a patient that we can do a, would be better served with doing a sternal window?  And with the benefit of ultrasound, bedside ultrasound, we can now view things that up  until 10 years ago, you had to use different techniques to figure out, could this be tamponade? But now a bedside ultrasound and someone who knows how to read it, more important,  can quickly help you diagnose tamponade, surgical intervention, or tension pneumothorax. Tension pneumothorax can be intervened with before the chest tube, a 14 or 18 gauge extra  long IV catheter. The reason it's extra long is it has to be matched appropriately to the patient.  We've learned in the wars that you have to take a three-inch gelco or a IV catheter. It's appropriate for a young, healthy patient who may have, or even a middle-aged patient  who may have some pectoralis bulk and a inch and a quarter, inch and a half IV catheter is not going to make its way through the chest wall. But you need a longer catheter.  To use that longer catheter on a elderly catechetic patient, you're not going to, you're going to go through the chest cavity potentially and go into the posterior chest.  So a tension pneumothorax can be treated initially with a needle, mid-clavicular space,  approximately two inner spaces, downward, inferior, and then touching the rib and going over it, advancing the catheter and withdrawing the needle.  So those are some things that as surgeons we can intervene or certain things that other caregivers you can decompress a chest, certainly put in a chest tube if you're trained.  And those top four are something we can immediately intervene on. Then you start getting into things like thrombus, embolized DVT, or toxins, more medical causes  that can be treated with medication or interventions away from surgery or procedure, something maybe you would see more in the traditional ICU after the case or in the PACU.  Of course, we started with the word context. And what is the context of the situation and what is your diagnosis? It must be rapid.  You can't say it's a cardiac event, a 28-year-old does not have a cardiac event if they're shot four times.  Eventually they die of cardiac arrest, but it's all those things that led up to it. So your differential must be rapid, narrow, and appropriate.  If you hear hoofbeats, think horses, not zebras. Are there significant hemorrhage? What is the definition of significant? What is significant?  You can think of a hierarchy of bleeding, a one to four scale. I like to use the vibe scale, one to four, one is minor, four severe. Think of audible hemorrhage.  Is the bleeding so severe and are you repleting? Are you repleting with whole blood, which is the ideal, gone are the days that we replace  blood with crystalloid, or at least one to one, one mixture?  There's a lot of data, the MATTERS trial and other studies that clearly show that trying to replicate the whole blood that is lost with one red blood cell, one FMP, one platelet,  one to six on the platelet six pack is a more appropriate, more effective resuscitation strategy in someone who is severely hemorrhaging.  Remember, hemoglobin hematocrit do not reflect real-time hemorrhage. If you want to upset a seasoned trauma surgeon, lean over the curtain and tell them the hemoglobin  is this, why their arms are up to the elbows in blood. The hemoglobin is a delayed response, no one really knows the refractory period between  accurate hemoglobin level and what the true blood loss is. So interoperative, don't let your eyes, trust your eyes, don't let the lab study take you astray.  If you see a lot of blood and that's difficult to diagnose, what one person may think is  a little blood, another person may think is a lot of blood, but if you have someone hypotensive,  cardiac activity is failing, see a significant amount of blood, then you know you have to replace blood. Is it non-hemorrhage?  We spoke about the compartment syndromes earlier, that there needs to be other interventions if it's more of a cardiac in nature, and that diagnosis has to be fairly rapidly done,  especially in the operating room. When you replete a large amount of blood, don't forget what used to be called the bloody  vicious spiral of death or the lethal triad, think of now as the diamond of death. A study from Ricky Ditzel, who is a special forces medic, look at this writing a paper  in J Trauma regarding, now don't forget when you replete the blood, recall that that blood that's banked has a citrate which will bind the calcium and deplete calcium.  In general, a rule of thumb I found to be effective is for every three units of blood, we give one amp of calcium. That's just my perspective.  Damage control surgery, this was a phrase coined by Dr. Schwab and Dr. Rotundo from the University of Pennsylvania that looked at rapidly truncating operations from folks  from the liver surgeries from the 80s, where they looked at severe blood loss as their time to shorten operations, stop the severe hemorrhage, stop bowel spillage, and allow  the patient to be resuscitated in the ICU, the intensive care unit, and come back and do the next step of the operation later, the closure, more definitive repairs, stop bleeding  and spillage. Damage control surgery and its sister would be damage control resuscitation, resuscitating  to a lower blood pressure, allowing time for the surgeons to stop the hemorrhage. And this phrase was coined from the Navy, where the Navy, if a ship was severely damaged,  wouldn't try to do everything at sea to get that ship to be totally seaworthy. Get enough completed on that ship to get it back to one dry dock, to a dock, and then  a little more, and a bigger dock, a bigger dry dock for definitive repair. And this damage control surgery, properly used, cannot be used cavalierly every time,  but at certain settings is a way to help resuscitate the patient. But now you've extended the interoperative period to 12, 24, or more hours.  Component therapy we spoke about, fresh, whole blood we have in the trauma bay at Cooper. We are part of a handful of centers five years ago. Others seem to be getting whole blood.  Warm whole blood is the ideal. Think of the walking blood bank, where we found in the wars, you take blood from soldiers,  suck it quickly, and get it into the severely wounded with excellent outcomes. A poor surrogate, but the only thing we have is either banked whole blood, or, which is  much better, or a component therapy, basically mixing, taking one PRBC, FFP, a little bit of platelet, a little bit of cryo perhaps, and allowing that to act as the surrogate  to loss of blood, especially large or significant blood loss in the operating room. So certainly gone are the need to dump in liters of crystalloid.  It has been well proven now that liters and liters of crystalloid dilute, cause acidosis, cause many other complicating factors. The supernormal concept was bunk.  As in any battle, preparation is the key, and this is our timeout. We have this in each hour, and that key blue timeout in the center clearly delineates roles  and look at anticipated blood loss. Are you prepared? Are you expecting blood loss? Are you prepared?  Do you need to have a trauma pack, a cooler of extra blood, or is this something you're not expecting?  But that open communication with anyone being able to voice concerns allows the team, a true team, to start to communicate, and if the pressure gets turned up, and this operation  goes from a standard, no such thing as standard, but an elective organized case, already there is, at least you know who everyone is, at least you said, well, I'm anticipating this  is going to occur. Also what are your resources?  Do you know how to call for help? Are you someone moonlighting in a hospital, but you really don't know who to call, and  who's the reliable person to call, rather than an overhead page where a bunch of people rush into the OR from all over the hospital, really don't understand what's going on.  Maybe this is appropriate to have an OR focused rapid response team, or a handful of highly  skilled technicians, or at least technicians and surgeons and doctors and nurses who understand the OR.  On the other side, you see our trauma pack, and this is equipment preparation. In our trauma room, look how we have this, always ready for additional, that extra calcium,  the epi, the bicarb, for those difficult, complex, hemorrhagic patients, or severe hemorrhage patients. Part of failing to rescue is failing to recognize.  There's nothing better than a trusted colleague, an excellent nurse or anesthesiologist whispering  in my ear, this or that, or communicating to the team, or getting my attention, this is occurring, letting me know that I'm missing the bigger picture, and my situational awareness  is becoming too tunnel visioned, too focused, which sometimes is good. Some incredible anastomosis being done by our CT surgeons, you need that focus, however,  if there's a greater failure occurring, you may need to break that focus, and knowing that you can safely do that, and do that judiciously, is an important skill.  Likewise, I need to listen to you when you do that, and that's probably a key part of situational awareness and teamwork.  Is someone identifying me listening, or the anesthesiologist listening, and us then together discussing a rapid plan, and moving forward, a steady hand, now's not the time to yell  or get all hysteronic, which is unusual that people occur that way, start behaving that way. We're supposed to be pros, we need to act that way.  Before you take the check, check the patient's pulse, check your own. Is this the time to initiate, truncate the operation, damage control?  Certainly easier to do in the emergency or urgent setting, difficult to do in the elective setting, but it is a tool to call upon if needed.  Once again, to reiterate, in a study of many of my, of the panelists, and many of the papers I've included in the reference, hemorrhage is a leading cause of death in the operating  room. Do you have blood readily available? Do you have the ability to access massive transfusion, or just augment your blood supply quickly?  This refrigerator is in our trauma bay, we also have blood packs, a three pack, a porter pack to kind of go up to the OR with three units of whole blood, in addition to having  it right here in our trauma bay. That is something that we need to use, work across to the entire country.  So teamwork, and that's the port of that communication, right? The share victory, share defeat, I love the phrase, orphan, an orphan, failure is an orphan,  and success has many parents. Well, I think that if things go well, we share the success, and once again, recall hemorrhage,  someone telling you that hemorrhage is occurring, or you know it, or did you look under the  curtain if there's multiple gunshot wounds, did one of your teammates say, hey, look under the curtain, bleeding now has increased from that femoral wound that we thought was minor  now that we have a blood pressure. So that team helping to communicate, think of the cause as a surgeon, we can help turn  things around, or you can say, I don't know, and we'll help you figure that out. Is any employee interested in receiving the COVID vaccine, and if so, we're taking walk-ins  in the... I have my COVID vaccine.  Again, if any employee is interested in receiving the first dose of the COVID vaccine, we are taking walk-ins in the conference center until 7 p.m. today. Thank you.  Drive down to Camden. Let's look at opportunities to improve. One thing that I found was interesting of this paper was the concept of the checklist,  the exemplar, the ideal model, and to use the aviation analog in high stakes, low frequency setting of which many times this will be, a quick, very short, very succinct checklist  may help guide all to say, are we missing something? Could a circuit be unplugged? Is there active hemorrhage? A quick checklist may help in this confusing setting.  Here's a list of some of my references, and some great information from the other panelists are here, some great insights.  Thank you for this opportunity to the society, for the audience. It's a true honor to speak, and I look forward to hearing comments. Thank you. Hello. My name is Kayla Nichols.  I am a clinical pharmacy specialist at Emory University Hospital in Atlanta, Georgia, in the CVICU.  Today I'm going to talk to you about anesthesia advanced cardiac life support, which I'll colloquially refer to as AACLS.  Mostly I'll be highlighting discrepancies in medication administration in the AACLS algorithms in comparison to ACLS. I have no financial disclosures to reveal. As Drs.  Nunnally, Ben-Jacob, and Chauvinas have alluded to, the goal in any perioperative arrest is  to prevent the patient from sliding into cardiac arrest, which is not unique to the O.R., but  the O.R. has the uniqueness that other in-hospital ACLS, in comparison to other in-hospital ACLS,  because it's almost always witnessed and frequently anticipated by the anesthesia providers, who  also have a lot of medical information about the patient prior to going into the surgery that's definitely not provided to many of our code leaders in other areas.  This is allowing for a focused and timely response, targeting the most likely causes of cardiac arrest in the perioperative setting, and this is frequently unique to that area.  Since causes of arrest in the O.R. can be boiled down to anesthetic conditions such as hypoxia, auto-PEEP, bronchospasm, or cardiac etiologies, the focus of the guidelines and  the guidelines itself tends to be on the cardiopulmonary interactions since anesthesia excels really  at respiratory, and you see here I have my anesthesia gold star indicating that most of what we'll be talking about is with the cardiopulmonary, cardiovascular etiologies  with regards to the guidelines. So as you will remember, the focus is really going to be on the four things that really affect cardiac output.  So we're going to look at preload, afterload, contractility, and heart rate. It's important to note that cardiac arrest within the O.R. is not as common as one may think.  Data from the National Anesthesia Clinical Outcomes Registry has an incidence of 5.6 arrests per 10,000 cases, so a 0.056% incidence, which is lower than estimates previously.  One of the first things that the anesthesia ACLS algorithm is going to emphasize prior to doing anything is to check and make sure that the monitors and leads are all attached  correctly. Other things that make this really difficult as far as identifying a patient who is going  to go into pre-arrest is that hypotension and bradycardia to the 40s is very common in the O.R. setting.  Lastly, I want to address that there is a lot of difficulty in monitoring certain patient populations satisfactorily.  This includes vasculopaths, hypothermic patients, morbidly obese patients, and even burn patients.  When I as a pharmacist think about ACLS, I think about epinephrine as the medication backbone of ACLS.  I use this slide to emphasize that as we're sliding into a patient who's becoming unstable, anesthesia is routinely pushing titrated boluses of vasoactive agents.  This includes phenylephrine, usually 100 mics per cc, epinephrine and norepinephrine. Our standard is usually 16 mics per cc, although this can vary by institution, and vasopressin  as well. Vasopressin is frequently used in anesthesia, and you can see here our little anesthesia  gold star loves vasopressin, and so they love to bolus from 0.5 to 2 units per dose, especially in catecholamine-resistant vasoplegia or in situations where catecholamines seem to  be exacerbating this issue. Anesthesia also tends to pull the trigger on steroids as a patient is sliding into cardiac  arrest, and the guidelines actually recommend hydrocortisone at 50 mg plus or minus NG or OG fludrocortisone in a patient who is in need of rescue, and the fludrocortisone dose  being 50 micrograms like we've seen in previous studies. As anesthesia is going down this route, we should also be establishing invasive monitoring  to rule out reasons for decompensation, and we'll discuss some of these reasons next. So the most common cause of hypotension in the OR is hypovolemia, as you might imagine,  and this is preload, right? So going back to our cardiac output, you know, are things that augment cardiac output and  help with cardiac output, but one of the difficulties is, you know, how do you determine if a patient is going to be volume responsive?  So they will frequently utilize systolic pressure variation or pulse pressure variation to assess if a patient will become, is volume responsive.  As you can imagine, other ways to assess volume responsiveness in the OR, such as a passive leg raise, have obvious complications.  Systolic pressure variation is the difference between maximal and minimal systolic pressure over one mechanical breath.  Pulse pressure variation looks at the maximum and minimum pulse pressure variation over one mechanical breath, and these are indicators of patient responsiveness to volume, but not  necessarily specific to volume. Other things that could be in the differential diagnosis for systolic pressure variation  include large tidal volumes, greater than 8 cc per kilo, higher lung compliance, like patients who have emphysema, and low chest wall compliance, such as a patient with third  degree burns on the chest. When we have a patient who is becoming unstable, one of the first things anesthesia will do  is one, get an echo and assess the heart function, and then we'll use that and apply it to a couple algorithms that we'll talk about shortly.  And then we'll use the SPV and the PPV to assess the patient's need for preload optimization. So we're in the OR, we're reviewing a patient who is decompensating.  This algorithm is highlighting that if a patient is hypertensive, you can see that the first decision box on this is if the patient is hypertensive or not.  And the first thing that is, if the patient is hypertensive and decompensating, we need to decrease afterload.  And there's a plethora of agents listed there, such as clavidipine, nicardipine, nitroprusside, etc.  If the patient is hypotensive, we're going to want to get a TEE to assess the patient's heart function.  This will help us decide whether this is left ventricular failure or right ventricular failure. A failing left ventricle is best supported by decreasing the afterload, which we kind  of discussed at the beginning of this prior to even assessing their heart status, or positive inotropy. And again, that's the focus of this.  So you'll see at the top if the patient is hypotensive, we're going to decrease hypertensive, we will decrease afterload.  If they're hypotensive, we're going to check their CBP, their systolic pressure variation or pulse pressure variation and give volume or blood as necessary.  And then if the patient still hasn't adequately filled LV, but they have poor contractility, we're going to start some positive inotropy with dobutamine and epinephrine.  If the patient is still vasoplegic at this point, you see that we will administer some vasoactive agents, vasopressin here with our anesthesia gold star seems to be the top choice  in the algorithm as well. I tell my pharmacy residents that conceptually the right ventricle is just the left ventricle on the other side.  And so conceptually, our goals in the setting of right ventricular failure are going to be similar.  We're still going to want to, after we address the volume status, we're going to target it positive inotropy, they're going to target a positive inotropy.  And I say that after we have evaluated the patient's volume status, we tend to use CBP in the setting of assessing right ventricular volume status, since it's right there.  Then we're going to target the positive inotropy if our echo tells us the RV contractility is poor.  And then after this, we're going to use pulmonary vasodilators, such as milrinone in combination with vasopressin, again, represented with my little anesthesia gold star or inhaled  vasodilators such as nitric oxide. We perform all of these actions with the hope that we do not evolve into a CPR scenario.  But if that were to happen, our AACLS algorithm is similar to the ACLS algorithm with shockable algorithm and a non-shockable algorithm.  The most common identifying method of identifying cardiac arrest in the OR is N-tidal CO2. You'll see that there are two big medication differences in the AACLS algorithm.  These boil down to the interchangeability of vasopressin in 40 units with epinephrine 1 milligram as our bolus of choice in the setting of our backbone of AACLS, as well  as the addition of a gram of calcium if the rhythm is ventricular tachycardia. Next I'm going to talk about some of the unique scenarios that happen in the OR.  Anaphylaxis is always on the differential in any kind of arrest, but while it's rare even in the OR, it is high on the differential as there are many common causes for anaphylaxis  listed here for you. These patients will present as you would expect with bronchospasm and acute onset hypotension,  and our goal is to remove the offending agent and secure the airway and then administer epinephrine.  Anesthesia routinely administers epinephrine intravenously in this setting unless they don't have IV access.  You'll notice the dose of epinephrine IV is lower than the intramuscular dose at 100 to 300 micrograms, and again anesthesia loves to give vasopressin and glucagon in the setting  of a non-responder to the epinephrine, and this is usually due to beta blockade prior or during surgery.  And then of course this patient will get the antihistamine combo and steroids. Peripheral nerve block is going to carry the highest risk for LAST, and there's a wide  range of neurobiological and cardiovascular symptoms. If we suspect LAST, we're going to remove the offending agent, and then we're going to dose intralipid 20%.  Local anesthetic systematic toxicity, or LAST, is also always on the differential for anesthesia in comparison to normal ACLS.  Peripheral nerve block actually carries the highest risk for LAST, specifically with bupivacaine.  If LAST is suspected, we need to remove the offending agent and intubate if that's not already been done, and then we'll administer intralipid anesthesia.  This is unique to the anesthesia repertoire as again represented by Anesthesia Gold Star, and the intralipid dose is 1.5 cc per kilo as a bolus, and then we'll continue 0.25 cc  per kilo per hour as a continuous infusion. If the patient does not respond to this, we can re-bolus and double the infusion dose.  Our goal, again, is to prevent the patient from decompensating into cardiac arrest, but if that were to occur, we actually have documented great neurological recovery after LAST, as  long as CPR is continued for at least 60 minutes. CPR duration will have to last a long time, but there's great neurological recovery documented afterwards.  Malignant hyperthermia is considered a once-in-a-career event due to the rarity, but with that being  said it should be considered especially in men and young patients who are presenting with muscle hypermetabolism, hyperpyrexia, acidosis, and cardiac arrest.  The indication for the medication to treat this is sodium dantrolene. We're going to give 2.5 mg per kilogram as a bolus and repeat these boluses for symptoms  like discussed previously, the hyperpyrexia, hypermetabolism, etc. The relative max is 10 mg per kilogram, but the guidelines say you could even go to a  max of 30 mg per kilogram for the setting. Again, we're going to want to cool these patients, and we're going to want to treat hyperkalemia,  which I'll discuss shortly, and I also just wanted to bring to your attention that there is a malignant hyperthermia hotline, again, because of the rarity of this, if you suspect  or are concerned that you need to treat it, you're welcome to give it a call if you can't remember what we talked about today.  Lastly, just touching on hyperkalemia management, the AACLS guidelines do, the cocktail of drugs is exactly as you would expect.  We see calcium for EPG changes, dextro D50 followed by insulin at 10 units, understanding that we might want to renally adjust that if indicated, and high-dose albuterol.  Note that it is a 10 mg dose, which is four times the normal 2.5 mg. The AACLS guidelines also provide dosing recommendations for sodium polystyrene and Lasix for potassium  wasting, and they're similar to what we would do in the out-of-OR setting. So in conclusion, perioperative causes of cardiac arrest are often anticipated and frequently  have targeted causes as a result. This is frequently related to the many unique causes for unstable situations that are targeted  with these unique medication variances that we discussed today. Thank you for watching, and I hope you enjoyed.

Video Summary

The video transcript discusses the topic of arresting in the perioperative period and its outcomes. It highlights the complexity of anesthesia mortality, which involves various factors such as patient characteristics, medication reactions, and interventions. The panelists in the video provide insights into the epidemiology and history of anesthesia ACLS (Advanced Cardiac Life Support) and the role of the surgeon in managing perioperative cardiac arrest. They also discuss the discrepancies in medication administration between anesthesia ACLS and traditional ACLS. The focus of anesthesia ACLS is on the cardiopulmonary interactions and the maintenance of cardiac output by addressing preload, afterload, contractility, and heart rate. The panelists emphasize the importance of early recognition of cardiac arrest and prompt intervention to improve outcomes. They also discuss unique scenarios such as anaphylaxis, local anesthetic systemic toxicity, and malignant hyperthermia, highlighting the specific treatment approaches for these conditions. Overall, the video aims to provide a better understanding of the factors influencing arrest in the perioperative period and the tailored interventions for better outcomes.

Asset Subtitle

Resuscitation, Procedures, 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

Describe differences in etiology, epidemiology, and management of cardiac arrest in the perioperative period
Identify rare and complex prearrest circulatory crises that require immediate response in the preoperative setting
Manage various forms of shock that may devolve into cardiac arrest
Discuss the role of the surgeon during cardiac arrest in the operating room and perioperative period
Compare the anesthesia advanced cardiac life support algorithm to the American Hospital Association algorithm and discuss the differences in medication choices

Epidemiology and History of Anesthesia ACLS
Talia K. Ben-Jacob

The Role of the Surgeon in Perioperative Cardiac Arrest
John Chovanes

Discrepancies in Medication Administration
Kayla A. Nichols

Meta Tag

Content Type Presentation

Knowledge Area Resuscitation

Knowledge Area Procedures

Knowledge Level Intermediate

Knowledge Level Advanced

Membership Level Select

Tag Surgery

Tag Cardiac Arrest

Tag Cardiothoracic Critical Care

Year 2021

Keywords

arresting

perioperative period

outcomes

anesthesia mortality

medication reactions

interventions

cardiopulmonary interactions

early recognition

tailored interventions

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