Hi, everyone. We'll go ahead and get started. Thank you for being here. Today, we're going to hear from Dr. Bill Brady. Dr. Brady is a professor of emergency medicine and also a professor of clinical medicine in the Department of Medicine and serves as the David A. Harrison Distinguished Educator within the School of Medicine. He got his MD From the Medical College of Virginia. He went to do his internal medicine residency at MCV. And then he went and did an emergency medicine residency at the University of Wisconsin in Milwaukee and then was a chief resident in emergency medicine there. He then came to UVA in 1994 and since that time has proven to be a great educator, both in the Department of Medicine and the Department of Emergency Medicine. And today, he's going to give us a talk on cardiac arrest care in 2019. So join me in welcoming Dr. Brady. [APPLAUSE] Thank you, sir. [APPLAUSE] Well, good afternoon, everyone. Thanks for making time to attend. This is actually a interesting website. The address is right there to take a look, if you have more interest in learning about the history of resuscitation. And it puts things in perspective. Some of these things are a little questionable and outright funny in some ways. And just remember, in 500 years, there's going to be a picture of one of us doing something that the audience is going to laugh at. So everything's relative. So we're going to talk about cardiac arrest resuscitation. When we discuss a lot of the data, much of it comes from the out-of-hospital setting. There's not, unfortunately, as much investigation occurring in the emergency department setting, in the inpatient setting, whether it be acute or critical care. There are studies and we will quote them when possible. But fortunately or unfortunately, depending on your perspective, much of the data comes from out-of-hospital medicine. Cardiac arrest in the out-of-hospital setting is similar, but it's not the same animal as in the hospital. And we'll talk more about that. So for those of us in the room that have been doing this for a while, a lot has changed over the last decade, regarding cardiac arrest management. First and foremost, basic is awesome. The impact of basic interventions has significant, significant, significant value. We need to focus on basic interventions, even when we are advanced life support providers with many complex interventions available to us. So what does that mean?-- chest compressions and early defibrillation for shockable rhythms. Advanced interventions are important, meaning airway insertion, medication administration, et cetera. But the impact of those is positive in a modest fashion compared to the basic interventions-- is positive in a massive fashion. And many times, we forget about the basics, particularly chest compressions. And they are so vitally important. I'll mention that in just a bit. Early provision of this basic care, whether it's out-of-hospital or in the hospital is very, very key-- very, very key. Less importance, as I've said, for the advanced life support interventions-- invasive airwaves and medications. Less importance doesn't mean no importance. It is still an important intervention and still has value in certain resuscitation scenarios-- but less important than many of us older folks in the room were taught 10, 15, 20 years ago. If anyone took ACLS 20, 25 years ago-- a lot of emphasis on airway, a lot of emphasis on medication. And if you've taken ACLS in the last five years or so-- significantly less emphasis on those interventions. Tailored approach to care-- in the old days, meaning 5, 10 years ago, when someone experienced a cardiac arrest, it was ABC, ABC, ABC, pretty much regardless of the patient, maybe with a little bit of fine-tuning. And we see that that is quite different now. So a tailored approach to certain scenarios is very important. And then once, hopefully, you resuscitate the patient, the significance in value of a comprehensive post-resuscitation management strategy is incredibly important, not just a targeted temperature management, not just PCI, but basic critical care. So you should do five things when you're taking care of a cardiac arrest patient, whether this is in the out-of-hospital setting and you come across them as a volunteer health care provider willing to intervene or you're in the hospital managing a patient. Enable systems of response, whether it's in your community or you're in the hospital that provide people with the tools and the mindset to intervene before you, the expert resuscitator, arrives. Because the patient is going to be saved in the first couple minutes of the resuscitation. That's true in the hospital. That's true out of the hospital. Perform awesome chest compressions, high-quality with minimal interruption. Apply defibrillation as soon as possible for pulseless V-tach and ventricular fibrillation, using some sort of device-- an AED off the wall in a public access setting, an AED in a clinic or other medical environment, or a more advanced device, the monitor defibrillator. Defibrillate these rhythms as soon as you possibly can. Provide an appropriate airway and administer bolus-dose medications as appropriate, without interrupting the basic interventions of chest compression and defibrillation of shockable rhythms. And deliver comprehensive post-resuscitation care. Those are the five key areas that we need to focus on in resuscitation of cardiac arrest in today's world. Now, all cardiac arrests are not created equally. Different locations have different types of patients with different causes and different needs and slightly different priorities of resuscitation. The out-of-hospital setting is somewhat similar to the emergency department. The emergency department is somewhat similar to the ambulatory patient and somewhat similar to the inpatient. But there are differences, as you go from out-of-hospital to in-hospital cardiac arrest. Certain things are the same, in terms of treatment interventions. But there are differences. In general, we see more shockable cardiac arrest rhythms in the out-of-hospital setting. In a very general sense, it's estimated that about 70% of people with out-of-hospital cardiac arrests have a cardiac cause of cardiac arrest, compared to inpatient. Depending on the acuity, the complexity, and your patient population, that can drop to somewhere 40% to 50%. In those patients that have non-cardiac-based cardiac arrest, we tend to see more PEA and asystole as your initial rhythm. So we do talk about cardiogenic and non-cardiogenic cardiac arrest. A cardiogenic cardiac arrest as a cardiac arrest that has a primary cardiac cause of the cardiac arrest. In the out-of-hospital setting, this is about 3/4 of patients. In our setting, it's probably about 45% of patients in the inpatient setting. The emergency department is somewhere between that 45% to 70%. So it's sort of a transition from out-of-hospital to in-hospital. These events usually occur suddenly. And the patient has minimal hypoxia, minimal waste product accumulation, isn't particularly acidotic and still has a lot of energy reserve on board when you begin resuscitation. And when you contrast that with a non-cardiogenic cardiac arrest, which is a cardiac arrest caused by something other than a primary cardiac event-- overdose, trauma, stroke, sepsis, et cetera, et cetera, et cetera-- these patients have a much more gradual decompensations. They become increasingly hypoxic, increasingly acidotic, accumulate waste products, use up all their ATP. So when they do arrest, they are even more ill than the cardiogenic cardiac arrest. And that's where some of the treatment priorities come into play. In a cardiogenic cardiac arrest, in the first 4, 6, 8 minutes, your focus is going to be on awesome compressions and defibrillation of shockable rhythms. In a non-cardiogenic cardiac arrest, you're going to be thinking about those two priorities. But there is more value in an early placement of an invasive airway and, likely, more value with your code meds, particularly epinephrine and intravenous fluids. In general, again, we tend to see more pulseless VT and VF in cardiogenic arrest. And a non-cardiogenic arrest-- more PEA and asystole-- general statements. Cardiogenic is not synonymous with VT, VF. And non-cardiogenic is not synonymous with asystole and PEA, although there are pretty significant parallels there that we need to pay attention to. And again, just showing that the spectrum of cardiac arrest location-based occurrence does change the patient profile-- in the pre-hospital setting, the majority of these patients are cardiogenic. In the hospital setting, the minority of these patients are cardiogenic. And again-- different treatment priorities, different types of patients. All right-- on the third floor. Many of you spend a lot of your time on the third floor. You've got a 54-year-old guy with ischemic cardiomyopathy admitted a couple days ago with community-acquired pneumonia. He was relatively hypoxic, a little hypertensive. But he's gotten markedly better and is actually getting, probably, close to discharge. But unfortunately, he's found unresponsive by nursing. So let's talk about pre-arrival care. This is true in the out-of-hospital setting. This is true in the hospital. Why am I mentioning out-of-hospital to you? As physicians and other advanced care providers, we all have a massive responsibility to enable these systems of response. I don't care how fancy your EMS system is. I don't care if your police carry AEDs. I don't care if you have the best ever most awesome resuscitation program in the hospital. If we're not getting care to the patient's side before EMS arrives, the likelihood of meaningful survival begins to drop way Off. So if we can get the mindset in the community that early care-- pre-arrival care, pre-arrival of EMS care-- compressions and defibrillation with an AED-- we can save many more lives. And as advanced health care providers, we need to be aware of that and we need to promote that, whether that's just, yeah, we should do that all the way through to including helping to educate in CPR education, advocating for AEDs in your church, in your gym, in the shopping mall-- wherever-- very, very important stuff. So survival curve-- in general-- and this is a "well, duh" statement-- the earlier we provide care, the better chance of survival. If we look in the out-of-hospital setting, average response time in the urban-suburban area of our community is about 8 and 1/2 minutes. If we wait on care to initiate at 8 and 1/2 to 9 minutes, survival is less than 10%, about 8%-ish. On the other hand, if we can enlist the public, we can push survival upwards of high 30% if not 40%. And the same thing is true by supporting nursing and non-LIP staff to recognize the problem, call for assistance, initiate compressions, and put an AED on. The same thing must happen in the hospital. The American Heart Association supports that. Everyone supports that. And it is literally black and white, in terms of how much we can increase survival. Pre-arrival care-- a lot of this is pre-hospital. But again, the idea can be translated into the hospital environment. Hands-only CPR, automatic external defibrillators, dispatcher instructions, crowdsourcing-- with the smartphones that we all carry, and some of us have two and three, there are a number of different apps-- one is called Pulse Point-- that if you register and a cardiac arrest occurs within 0.8 miles of your geo-sync location at any given time in a public area, you'll receive a warning with a suggested route. And it'll also show you the location of publicly-placed AEDs. That's being used in many communities. We're negotiating now with the attorneys for the 911 center to try to get this going here. In general, it brings people to the victim's side much more rapidly than EMS. These patients get CPR way more frequently. They are defibrillated by AEDs very more often. And they have a better survival rate. That data set is young. It's new. It's expanding. But it is quite interesting. And then very new-- of course, everybody is using drones for everything. You can get your Keurig pods delivered from Amazon overnight by an AED. We can also send an AED to your home. In northern Europe, particularly the Netherlands, they have a very advanced DMS system. They are looking at trial programs of dispatching AEDs from their 911 center to the location of cardiac arrest. So let's wait and see how that works. Major impact-- incredibly important. Here's a graph of survival relative to time of intervention in patients in the out-of-hospital setting. And we look at people on the left that actually have bystander care versus people on the right-- no bystander care. And in general, we can almost double the number of survivors at 10 minutes by providing high-quality chest compressions and defibrillation of those people that can be shocked with a public access device. We're not talking about fancy airways. We're not talking about intravenous access. We're not talking about medications. We're talking about pushing on the chest and connecting the AED to the patient-- very, very, very important. Take home points regarding pre-arrival care-- most definitely improves neuro-intact survival. It also increases the number of patients that have a shockable rhythm, VT or VF, when EMS arrives. Many of the VT, VF patients that initially develop those rhythms degenerate into a PEA or an asystole by the time EMS arrives. And the outcome from those rhythms is even more dismal than VT, VF. So by providing bystander care, even adequate chest compressions, it increases the number of patients with VT, VF when the team arrives, whether that be EMS or the code team in the hospital. It mitigates the impact of longer team response times. And we, as physicians, whether you're a medical director for an EMS agency or you work in resuscitation in the hospital, if you are an advanced health care provider in your community, whether that be hospital or outside the hospital, we have to support these interventions. This is what's going to save lives. There's no magic medicine. There's no magic intervention or tool or whatever that's coming down the pike. The thing that is going to save people's lives is early basic care-- very important for us to support this. Back to our patient-- the code team is called. Chest compressions are started by nursing, nursing staff. AED is placed. Shock is advised. Defibrillation occurs by the AED. They resume compressions. And we're waiting for the code team to arrive. Chest compressions-- extremely important. Heart Association for the Adult Victim of Cardiac Arrest recommends a rate of 100 to 120. I've done the math. Apparently, an average is 110. Depth of about 2.2 inches-- and allow for appropriate recoil. Those three features describe what awesome, high-quality, chest compressions are. I should add another point-- minimize interruptions. Interruptions are really bad, OK? Here's a graphic showing a patient undergoing chest compressions. Each one of those dotted lines is a single manual chest compression. The graph actually shows the blood pressure measured as a result of these compressions. The first thing to notice is, once you start chest compressions, you don't automatically develop a perfusion pressure. You have to sequentially provide continuous compressions to actually reach the best possible perfusion pressure. In general, it's about 40 to 45 seconds of continuous high-quality compressions to actually reach a perfusion pressure that's best possible in that setting. Each time you stop, perfusion drops to 0. No blood flow to the brain, the heart, et cetera. And then you resume again. So in this particular scenario, we reach an adequate perfusion pressure here. And then we stop for whatever reason there. And then the build up, again, to adequate perfusion is going to take about 40 seconds. So that patient's brain, that patient's heart, that patient's body isn't receiving perfusion of any significance or minimal significance for however long you stop plus 40 seconds. And you don't have to have too many of those interruptions to produce a patient that has irreversible anoxic brain injury. If you resuscitate that patient, I don't know if that does anyone any good. This is what we need to strive for. We do need to interrupt compressions in today's world for certain appropriate interventions. But when we do, it needs to be minimal. And we need to be very stingy of our time off the chest. This graphic just demonstrates initiating compressions with near continuous. We need to minimize compression interruption. The Heart Association and other investigators are just using a metric called chest compression fraction. Which-- advanced math here-- compression time divided by total resuscitation time. In general, the higher the chest compression fraction, the better the perfusion. The better the perfusion, the better chance of survival with neuro intact status. The American Heart Association is suggesting at least 0.6 or 60% or higher. I personally believe we should strive for 0.8 or 80% or higher. I mean, 0.6-- 60%-- that's slightly more than half the time of a resuscitation when somebody is pulseless. We should be pushing on the chest the vast majority of that time-- the vast majority of that time. A couple sobering facts-- in the first 6 to 8 minutes of a cardiac arrest resuscitation, each 10-second period of no compression negatively impacts survival by up to 5%. And what I've already mentioned to you-- it takes about 40 to 45 seconds to reach the best possible perfusion once you re-initiate chest compressions. So once you start pushing on the chest, you automatically don't have awesome perfusion. It takes almost a minute to reach an adequate or near adequate level of perfusion. A quick mentioned about mechanical CPR devices-- they are out there. They've been out there. I remember, as a medicine intern, watching the Thumper work in the emergency department with Joe Arnado. So they have been around for 30-plus years. They are gaining more and more penetration into the market. And oddly, you would think that these devices would produce very, very good results. They don't get tired. They don't get distracted. They don't want to do a fun procedure. When you turn them on, they do awesome compressions that you programmed them to do. And when you pause them, they will stop. And they will continue until they run out of juice or air. You can have electrically-driven devices, battery, or plug into the wall. And many of the devices have dual power source, where you can actually drive it with a gas cylinder, like oxygen, just to increase their ability to be used in many settings. So the literature itself-- lots of retrospective studies, a couple smaller prospective. So the data is mixed. But the American Heart Association does recommend them. Guidelines 2015 speaks to the austere environment. Out-of-hospital setting, where you don't have a lot of resource-- like, Madison County-- I'm the medical director for a couple EMS agencies, including Madison County. And they may manage cardiac arrest patients with two or three providers which, compared to the Cecil B. DeMille crowd and some of our resuscitations-- that's quite austere. Smaller hospital with limited personnel-- if anyone's ever worked in a small hospital as a resident-- I moonlit full-time. Don't tell my residency director that. But I worked in a hospital that had an ER nurse and a nursing supervisor. So when a cardiac arrest occurred, it was me, the two nurses, and maybe we could scrounge up somebody from the lobby to do chest compressions. So in those types of austere environments, these devices are potentially helpful. The Heart Association also recommends them as a bridge to ECMO, which people refer to as ECPR or ECLS. So stay tuned for that. We'll see more information on that, probably, in the next three to five years. Back to our patient-- code team initiates care. You have arrived. You are managing the case. Chest compressions continue. Monitor's in place. You note, at the next pause, that ventricular fibrillation is present. You defibrillate the patient a second time. You get right back on the chest and resume compressions. You think about epinephrine. And somebody says, should we intubate him? The code meds-- so first of all, what are the code meds? Epinephrine, amiodarone, lidocaine-- there's not too many of them left-- maybe sodium bicarb, maybe calcium, maybe magnesium. Those are the code meds. And before we get into the code meds-- just a quick refresher on the modified Rankin scale. This is used as one of the primary endpoints to assess neurologic status in survivors of cardiac arrest. 0 is great, no sequelae. Somebody has cardiac arrest. You intervene. You fix them. And they are exactly the same as they were pre-arrest. 1-- no significant disability, pretty much able to get back to their life. 2-- slight disability, able to maintain ADLs, but can't go back to work or school or whatever the way they were pre-arrest. 3-- moderate, isn't going back to their normal life, and does require assistance. 4-- moderately severely disabled. 5-- severely disabled. And 6 is dead, which means not alive. Many of the studies I'm going to show you use, as an end point for neurologic outcome, 0 through 3. I'd suggest to you that we want 0 through 2. So when you read these studies-- unfortunately, we've got to read more than the conclusion sentence of the abstract to fully understand what they're talking about. And I'm guilty of reading, like, the last sentence of the conclusion in the abstract. So epinephrine-- this is the 2015 AHA guidelines for cardiac arrest management. They messed up my colors. Basically, the recommendation is standard dose epi-- 1 to 10,000. 1 milligram every 3 to 5 minutes during your cardiac arrest may be reasonable-- may be reasonable-- interesting phraseology-- for patients with cardiac arrest. And that's a class 2B recommendation. A quote from the discussion that follows-- saying, early administration may improve ROSC and neurologic outcomes. Later administration may decrease both. So again, for the gray-haired people in the room, including me, it wasn't too long ago we were doing high-dose epinephrine, where you'd have to get, like, 15 code carts out there and large gallon jugs of epinephrine into the room. And we thought that was the way to go. And now the pendulum has gone way over there where, maybe, a little bit to no epinephrine is the way to proceed. So nothing is constant. So a couple quick papers on epinephrine and cardiac arrest-- out-of-hospital-- UK London Ambulance Service looking at out-of-hospital cardiac arrests. 8,000 patients, roughly split between standard cardiac epi, 1 milligram every 3 to 5 minutes, IV or IO, compared to same administration route-- a placebo-- large, double-blind, placebo-controlled trial. Their outcomes were survival with their neuro status at discharge and at three months-- so pretty good outcomes. And again, just as a quick aside-- outcome-- we got a pulse back is great. But many people that are initially resuscitated wherever don't go on to live. Or if they do, they don't go on to live with an intact brain. So when you look at outcomes and studies, you want to look at studies that look at survival with intact neurologic status-- important. So return to spontaneous circulation and EMS transport. We see it happen way more often in epi compared to placebo. Looking at 30-day survival-- way more often in epi than placebo. But then when we look at favorable neurologic outcome, look at the Rankin upper left-- 0 through 3 more often occurred in the epi group. But when we then look at Rankin 0 to 2 which, remember, is what we're aiming for-- less often in a significant sense. And unfortunately, when we look at the neurologically near devastated to devastated patients, we see that that occurred more often in the epinephrine group. So this study is similar to other papers and probably replicates our experiences that, yes, it does help us resuscitate people. But we're resuscitating people that are very, very compromised in a neurologic sense. Second paper-- does giving epi before the second shock help or hinder resuscitation? So here we're dealing with shockable rhythms, pulseless VT or VF. About 3,000 patients with shockable rhythms. 1,500 of them got epi within 2 minutes. This is an inpatient study. Get With The Guidelines is the American Heart Association in-hospital-based cardiac arrest registry. And basically cut off the bottom there. We see that later epinephrine in the shockable rhythms was better in terms of resuscitation, getting a pulse back, survival, and appropriate neurologic status across the board. Take home message for this in a shockable rhythm is, wait for the second or third shock before giving epi. So we're going to start to see some changes in our recommendations about epinephrine. And then last paper about epi-- does the timing of epi make a difference in both shockable and non-shockable rhythms? 9,000 patients-- outcomes were found in non-shockable rhythms, worsened ROSC and 1-month survival if epinephrine was delayed beyond 2 to 4 to 6 minutes. And the worsened outcome increased as you had increasing delay. For shockable rhythms, no significant impact. So take-home message from this paper is, in non-shockable rhythms, let's give epinephrine early. So this is an example of some very minor tailoring of our approach that can have significant impact. Take-home points for epinephrine-- epinephrine does increase survival. But it does not increase the proportion of patients with an intact or near-intact neurologic status. Early use in non-shockable rhythms-- early, as in the first 2 to 4 minutes. Later use, if any, in shockable rhythms. The role of epi in cardiac arrest is unclear, yet again. Stay tuned. Antiarrhythmic agents, which largely in cardiac arrest were focused on amiodarone-- again, AHA Guidelines 2015. Their recommendation basically says that amiodarone may be considered in these rhythms. Lidocaine may be considering as an alternative. And we don't recommend magnesium. And I've added-- in all patients. I personally believe, in certain subsets of patients, mag sulfate might be a reasonable intervention. A quotation from the discussion-- "no antiarrhythmic has yet been shown to increase survival or neurologic outcome after cardiac arrest due to pulseless VT or VF." This is probably the best study to-date. And again, I apologize for the color change here. This is a large out-of-hospital study published in the New England Journal. 3,000 patients over 10 sites-- 10 pre-hospital large communities. Patients had VT or VF and got one or more shocks and epinephrine-- so relatively standard resuscitation. When we look at amiodarone compared to lidocaine compared to placebo, the resuscitation rates were marginally higher with amiodarone than lidocaine and significantly higher than placebo. And then when we look at outcome. And again-- modified Rankin of 3 or less. Remember, 3 has some significant degree of disability. And that patient isn't going to return to his or her pre-arrest lifestyle. We see the same sort of trend. But the differences have shrunk somewhat. This paper got a lot of press in many different areas of medicine-- lots of letters to the editor. The authors responded. And they noted, again, in data that wasn't initially published, that there was a 5% improvement of amiodarone over placebo if the cardiac arrest was witnessed. In other words, it happened right in front of the paramedics. And a almost 22% absolute increase in amiodarone versus placebo, if witnessed and they gave the drug near immediately, which is a very small subset of patients. So stay tuned. Have I changed my practice, based on this paper? No. I'm still giving amiodarone. I try to give it earlier. But I know it is not the intervention that's going to make or break this patient's outcome. Systematic review and meta analysis-- out-of-hospital cardiac arrests from 1940 to 2016. That's a long time. And yet, they only found 10 studies to include in their analysis. Amiodarone did improve survival to hospital admission. But it did not change ultimate 30-day and 180-day survival. And it didn't have any impact on neurologic outcome. So like epinephrine, at the present time, there is no clear benefit of amiodarone versus lidocaine. Minimal evidence for amiodarone in witnessed arrest, given immediately. Late in VT, VF-- not clear if either drug has really any benefit. And again, probably most of us that do resuscitation have seen personally that medications have a marginal ultimate effect on patients-- not necessarily wrong, but a small positive impact, not a large positive impact. So factor that into your care of patients. All right-- third shock is delivered. Chest compressions continue. We give amiodarone, 150 milligrams, IV push. And somebody's saying, should we intubate him? We're going to talk about electrical therapy first. Coming soon to a hospital near you, quite literally next month, the entire health system is going to switch over to the Zoll Monitor defibrillator. For most of us in the room, we're going to have the R series. This is just a quick picture of it. It's a standard monitor. It cardioverts. It defibrillates. It paces, will monitor end-tidal CO2, and provides very excellent CPR feedback regarding chest compression rate, depth, recoil time, et cetera, et cetera. There will be a very robust education plan that will involve-- sorry-- a CBL. And then the opportunity that we strongly urge all of you to attend-- a session just for training purposes. If you're comfortable with the Philips or Physio Medtronics device, then you can pretty easily switch over. But I still would suggest that you get a little instruction on it. Sam Oliver is actually part of the decision team on this. So your department is very much represented across the board. So I can answer questions about that at the end, if that's OK. Quick paper that looks at the impact of chest compression interruption-- so look at the rhythm. Charge the device. And deliver a shock. The best way to do it and the way I do it is the circled way at the bottom. You're going along. You shock the patient once or you haven't shocked the patient once. And you're doing compressions and some other interventions. You're coming up through your 2-minute period and maybe about 1 minute and 45 seconds. Let's go ahead and charge the device. Let's go ahead and charge it and get it ready for the next defibrillation. Stop compressions. Look at the rhythm. Look for signs of life. If it's a shockable rhythm, deliver the charge and get right back on the chest. If you do that, that only takes 4 seconds, as opposed to compression, compression, compression. Stop. Oop-- we got to shock that. Let's go ahead and resume compressions for a couple of seconds while we charge. And let's stop again and shock him. First of all, that second period of compressions is just for show. It's not going to do anything. It's a good aerobic workout for the compressor. But it's not helping the patient. Because remember, it takes 40-ish seconds to get forward flow in a substantial way. And it significantly delays. Remember, all the machines-- the machines we have now, the machines we're going to have in October-- you can dump the charge. And the machines will also be configured to automatically dump the charge after some time frame that we're still working on. So I would strongly urge you to have your machine charged and ready to go so, when you stop compressions, you can look at the rhythm, look at the patient-- should I shock this patient? If so, push the button and resume compressions immediately. It makes a big difference. Think about changing pad positions. Remember, it's the direction of energy, the vector of energy. Typically, we're going to do base and apex on the front. If your patient isn't responding to the first two or three shocks, think about going AP. just altering the direction of current delivery can make a difference-- important. And of course-- the double sequential fibrillation for persistent VT, VF. This is a patient from earlier this year, an 18-year-old male with a tox issue. Cardiac arrest over on the corner at midnight-- got lots of shocks before he got here, lots of CPR. He arrived. And the attending caring forum said, I'm not going to let this 18-year-old die without trying this, that, and the other. So connected two defibrillators and said, go. Shocked him. And gosh darn it-- produced a perfusing rhythm. And the guy walked out of the hospital neuro intact, believe it or not. So interesting-- the cardiologists have been doing this for years in the EP lab, treating recalcitrant a-fib-- it's kind of redundant. I guess a-fib's recalcitrant no matter what-- but treating a-fib and selected other dysrhythmias. And they've been doing it for a long time. It's relatively new into the resuscitation world, but not a whole lot of data. Here's the largest study to-date-- 45 patients, again from London-- London Ambulance Service. This is a retrospective study. They compared the 45 patients to 175 that got typical one-device defibrillation and really had results that were not particularly helpful. Standard defibrillation versus double-sequential or double-defibrillation-- no significant difference in resuscitation rates, hospital resusced arrival, or being discharged alive. So not a lot of black and white data. We actually did a quick literature review that we published on that one case. And it's interesting looking at all the published case reports and smaller retrospective series. In general, double-sequential defibrillation in cardiac arrest is done very late in the arrest event, on average, after 5.5 shocks and 28.5 minutes of resuscitation. In most patients-- I don't care what you do at 28.5 minutes-- that person probably isn't going to have a neuro intact survival-- so don't know yet. This is an interesting paper. This actually looks at four different instances of double-sequential fibrillation using Zoll and physio-control machines. All four were done with AP, so AP pads and base and apex pads. 1/4-- so 25% of the defibrillators were found to be dysfunctional afterwards. We've talked to Zoll and asked them. And they point out that this would violate the warranty. So be really careful about that if you do it. I can't recommend it at this point, because the data is so sparse. But if you do do it, both machines need to go back to clinical engineering for a check to make sure you didn't fry the innards, OK? So take-home points on defibrillation-- as soon as possible, with minimal compression interruptions. But if you're in V-tach, V-fib, defibrillation is going to be what saves you, not the drugs, intubation-- none of that. What's going to save you is defibrillation. Consider altering your direction of energy by changing pad location if the patient hasn't responded to the first one or two shocks. Dual sequential or double-sequential defibrillation-- don't really know. Don't really know. Let's wait and see. If you do do it, make sure clinical engineering looks at both machines as soon as possible before they're returned to service. And now-- yes, the airway. For whoever wanted to intubate the patient, you can look and say, hey, go ahead and intubate. We're not going to spend a whole lot of time on this, because you aren't primary intubators most of the time. But I do want to mention it for completeness. So there is a difference. and this is definitely one of the areas where we want to tailor our approach. Cardiogenic cardiac arrest-- remember, sudden. They usually have some degree of oxygen reserve and not particularly acidotic for the first 2, 4, 6 minutes. Non-cardiogenic-- likely hypoxic, likely acidotic, likely pretty doggone sick before they cardiac arrest. Invasive airway is probably more important in the non-cardiogenic arrest early on, compared to the cardiogenic arrest. This is a very old animal study that looked at simulated cardiac arrest. Up top is your cardiogenic cardiac arrest. VF was induced in dogs. They did compression-only CPR for 7 minutes and then measured blood gas and other parameters. Oxygen saturation-- 83%. pCO2-- 37 and not acidotic. PH is 7.4. This is a cardiogenic arrest after 7 minutes of compression only, compared to the non-cardiogenic eugenic cardiac arrest, where they clamped the ET tube. Once the animal arrested, they started the clock, did compression-only CPR, and measured parameters at 7 minutes. Pretty significant oxygen deficit-- very high pCO2 and markedly acidic. So this has been replicated in other models and is talked about in humans. This basically paints the picture that cardiogenic-- we've got a little bit of time before we think about the airway. Let's do compressions. Let's shock shockable rhythms. Non-cardiogenic-- let's go ahead and try to intubate them earlier. A large study of hospitalized patients-- 25,000 cardiac arrest patients. Mean time to airway placement-- about 6 minutes. No increase in return to spontaneous circulation. Minimal increase in survival at 24 hours. That wasn't sustained to discharge. so looking at early versus later airway, earlier airway didn't make a huge positive impact. Not a lot of data here. These two slides-- I won't go into them in any detail, because we're getting tight on time. It shows us that placing an invasive airway has a massive impact on chest compressions. The average interruption in one large study showed that the typical single interruption for an airway insertion was 47 seconds. And the total interruption during that resuscitation event for airway management was 220 seconds. We can't tolerate that. We can't tolerate that. We have to be very, very stingy with our time off the chest. Take-home points about airway management-- cardiogenic shockable rhythm-- let's do it later. Non-cardiogenic non-shockable rhythm-- let's do it earlier. You can do it at any time during the resuscitation, if your airway management person can perform the invasive airway during compressions and you don't interrupt delivery of defibrillation and this and that. Airway management isn't bad. It is bad when it interrupts the basic care. There's a pulse! We've got a pulse back. We're kind of at time now, aren't we? We need to stop at 1:00? OK-- so just very quickly-- post-resuscitation care. Basic critical care is important, oxygenation and ventilation. Many of these patients do need to be intubated, if they're comatose or significantly altered afterwards. Airway protection is important to reduce the impact of aspiration. Let's also work on perfusion. And remember, your blood pressure isn't necessarily a great marker for perfusion. Brain malperfusion continues to occur even with inadequate blood pressure. So we need to be very cautious and careful about perfusion issues. Let's maintain temperature, avoid hypothermia, and maybe promote low-grade hypothermia. And of course, treat the inciting event. I won't go into any more detail about that. I think we'll stop. The two things I was going to mention is targeted temperature management. Remember in the old days, 10 years ago, the temperature range for therapeutic hypothermia was 32 to 34 degrees? A fair amount of research has shown us that, probably, 35 to 36 is adequate and avoiding hypothermia is key. And then taking the patient to the Cath lab is in the purview of the cardiologist. Get the patient in front of a cardiologist if they have a STEMI or if they have a significantly abnormal ECG that you think could be cardiogenic in nature. Make sure the cardiologist is aware of the patient. Show him or her the electrocardiogram. Some of these patients do need to go to the Cath lab quickly, not all though. So I think I'll stop there. And if we have any questions-- thank you everyone. [APPLAUSE] Any questions? What if your [INAUDIBLE] any breath [INAUDIBLE]? Yeah-- I've done it twice, once on JPA when I was driving along and some guy runs off the road and delays my getting home. And gosh darn it, he had a cardiac arrest. And one time in Georgetown, walking down the middle of the intersection, some guy just goes down right in front of me. In both those cases, I did compression-only CPR, yelled for an AED, and only stopped when an AED was there. I would not blow in the mouth for a couple reasons. One-- it's gross. I've done that once as an early EMT. There is a valid concern about disease contagion in the world, particularly viral issues. And most importantly, when you compare compression-only CPR to traditional blow-in-the-mouth push-on-the-chest CPR, outcomes are pretty similar and, in some studies, a little better with compression-only CPR. So my answer is, I would not blow in the mouth unless I specifically knew this was an airway issue, like an obstructed airway or some other issue. The impact is pretty marginal at best. Push on the chest, 110 a minute, 2.2 inches, good recoil. And don't stop until you get so tired you can't do anything or somebody with a uniform is there to help. Wow-- was I that clear? [LAUGHTER] Probably not. Can you talk a little bit about the plan for the education for all the different providers in the hospital for the-- Sure. Sure, sure. So October 15, the new Emergency Department opens. We can't wait. So the Emergency Department is going to be outfitted with the new devices. And since many of you are invited down to hang out with us from time to time, you also need to be trained on it. Stay tuned for announcements. That will be a CBL. Whether that's going to be required by Jamie for the resident fellow group is yet to be determined. And the clinical staff office probably won't require it for the LAPs, but it'll be strongly encouraged. You'd hate to come up to a cardiac arrest event and ask for the owner's manual to try to figure out how to turn it on when you have your V-tach patient there dying in front of your eyes. So CBLs-- and then dining conference rooms through end of October, beginning of November. They'll be training sessions that will be tailored for different groups. And in certain select settings, we can certainly come to meetings-- faculty meetings, resident meetings-- and talk about it. But remember, part of the training and the dining conference room is going to be touching the machine and pushing the buttons. We're not going to train to the AED, because that's pretty simple to use and Joe and Jane Public and the world can use it. So we're not going to train to that. Although if anybody wants to talk about it, let me know. Look for announcements later next month. And we'll go live October 15. And then we'll outfit the rest of the hospital over the next, probably, 30 to 60 days. We've already received the first shipment of AEDs and R series devices. So they are here. And clinical engineering is checking with them. There is an X series monitor defibrillator that none of us will need to use. That's more pre-hospital and it has 12-lead capability, among all kinds of other things. So you need to worry about or focus on the R series. Any other questions? Yeah, I just want to find out-- if you know someone in the family has had a cardiac issue and a cardiac problem, do you try to train any of the family members? So good question-- everybody heard that? I believe the world should be trained in CPR. Don't not-- pardon my double negative-- perform compressions if you haven't been trained. There's kiosks in airports and this and that where you can go up and, in 60 seconds, be schooled on appropriate chest compressions. To answer your question specifically, yes, I think it's reasonable for peace of mind. And you may be able to assist the person should they develop a problem. But in studies looking at home CPR training, people that are trained in CPR are more likely to use it on somebody out in the community, which is still good, compared to the loved one who doesn't ever have a problem or has a problem when no one's there. And as a correlate to that, there is one large study that looks at high-risk cardiac patients once they're discharged-- so people with low EFs, people with arrhythmogenic syndromes, people that have had cardiac arrest. Putting an AED in the home oddly hasn't changed the outcome. That's one paper. One paper doesn't make the literature on the topic. I have an AED in my house, just because-- well-- whatever. [LAUGHTER] But the literature doesn't support it. But does that answer your question? Thanks so much, Dr. Brady. OK, thank you, everyone. [APPLAUSE] It was great.