Transcript Video Targeted Temperature Management 101: The Science of TTM for Nurses Sara Salen DNP, RN, NPD-BC, presents the role of Targeted Temperature Management (TTM) and the physiologic impact of TTM. Hello. My name is Rebecca Offner from B. D. Medical Affairs. I'd like to introduce to you Sarah Salin. Sarah is a critical care nurse who has worked in community settings, large tertiary settings. She's worked and the north of the US South and mid western areas. After being in critical care. She's advanced her education, receiving a master's in nursing degree specializing in education. And then she went on to get her PhD as a doctor of nursing practice. Sarah could be doing a lot of things but is driven to improve care of critically ill patients in acute care. Currently she is a nursing professional development specialist at the Medical University of south Carolina. Yes she's in the ICU like you and does not hesitate to roll up her sleeves in critical care. Sarah thank you for being with us and I turn it over to you. Hi my name is Sarah Saline. I've been a nurse for 13 years. My background is cardiac meds, surge cardiac critical care and nursing education. I am here today to talk to you about the targeted temperature management care, the nursing interventions, complications and how we, as nurses can strive to improve care of the targeted temperature management patient. I am a paid consultant of B. D. My disclosures are listed on this slide in front of you today. We would like to talk about targeted temperature management. How can a nurse recognize what the significance of this role is? What is the evidence based practice surrounding this therapy and the bedside management and troubleshooting of a targeted temperature management patient. We are here today to understand the purpose of T. T. M. And how is nurses? We can do bedside care better and improve our patients outcomes. So that way they wake up hopefully with neurologic intact Before it became targeted temperature management. It was called induced hypothermia and we really did induce hypothermia in these patients targeting temperatures of 32-34°.. Now, research has shown that targeting specific temperatures outside of those can also help improve patient care and patient outcomes. Therefore, the term is now targeted temperature management. One of the things that we're going to talk about first is the ischemic reaction in a patient who suffers a cardiac arrest. As we know, blood flow stops does not get to the brain causes an ischemic reaction in a patient whose post cardiac arrest. This is known as global ischemia. One of the things that can happen is injury will occur during ischemic reaction during the cardiac arrest. Another implication is post cardiac arrest and the ischemic reaction that happens in the post cardiac or the recovery phase of a patient. Part of the concern is this idea of re profusion injury. Once re profusion has occurred, euro damage is going to happen from ischemia. One of the problems is the timeline in which this ischemic reaction happens and the amount of damage that can occur following it. This can be up to 72 hours post ischemic re injury and that's a problem. What we need to know is nurses is how can we stop or slow this chain reaction of ischemic events or an ischemic cascade and how can we prevent further damage from happening initially after the injury, right after the injury and then delayed. Also known as secondary injury or re profusion injury. The ischemic cascade encompasses several different aspects that can lead to increased neuro damage. In our patients, we have extra gluten mate that starts to center around causing an excitatory neurotransmitter response. The increased risk of calcium can lead to muscle contractions that can lead to other complications. Further on the disruption of cellular membranes allows for fluid and electrolyte shifting, which can cause complications as well. The increase in free radical production is toxic to tissues and organs. We also have blood brain barrier dysfunction. What leads to increased intracranial pressure and cerebral oedema that a scheme make response that I talked to you about. Just a little bit of go happens in this form. This is a graphical representation of that. You have the ischemic injury that's happening during the event, which is the red graph all the way to your left. What you also see right after that is that early re profusion injury that happens post arrest in that post cardiac arrest face. But the other concern that we sometimes forget about is that delayed second injury that happens about 4 to 6 hours post Roscoe and as you can see last hours, two days, those things that we talked about in the ischemic cascade, such as the inflammatory reactions in that middle cardio dysfunction. What if there was a means or away or a therapy that we could do to block those things from happening and hopefully improve the patient's outcome. Hypothermia is one of those that we can use to block these ischemic reactions and improve patient neurological outcome. Neural protection is so important in our patients after re profusion. Even after we reap refused the brain cellular damage and death can still happen. This is why T. T. M. Is so important. It not only helps the metabolic recovery during the issue, but it also helps after re profusion, preventing that re profusion and delayed secondary injury. Let's talk a little bit about the evolution of T. T. M. In 2000 and 10. It was recommended that comatose patients post Roscoe get cooled to 32 to 34 degrees for about 12 to 24 hours in 2015, it was recommended that all adult patients who are comatose post Roscoe received T. T. M. And are cool to temperatures of 32-36° With a specific maintenance phase of 24 hours. These landmark studies were the foundational framing for historical and current global guidelines that we now use and are targeted temperature management practice. These are great resources for you to look up. Let's talk a little bit about the phases of therapy when it comes to a targeted temperature management for a post cardiac arrest patient. We have the time to initiation, which we're going to hyper focus on for a minute. That is the time it takes for us to achieve that initial start of targeted temperature management. That is so important. The sooner we act, the sooner we can help our patients and increase their outcomes for neurological recovery. Following that you have the induction phase, which is the act of getting the patient to that temperature of 32-36. As we mentioned in one of the previous sides, we're going to maintain that temperature for 24 hours. Once we're ready for rewarming, we're going to rewarm at a controlled rate of 0.25°C in our That usually takes around 16 hours or so for them to achieve normal, ther bia Normal for me is the act of bringing them back to 37° and maintaining that for a period of time anywhere from 24 to 72 hours. There was a study that came out that talked about 36 versus 33 Hypothermia does have some complications that can arise. So research went out to try and look and see do we really have to take them down 32-34°?? What we found out in that study was 36 did have some implications that we could use for patients who qualified for that temperature. Yeah. When we look at 33 versus 36, there are specific reasons why we would choose one temperature over another. Some of those things that we need to consider are how long the patient was down. We know the longer downtime that the patient has, the longer they've gone without profusion and maybe the enchants of a higher risk of re perfusion injury. So some of the things that can happen is we want to reduce that oxygen consumption, inhibit the free radical production. We want to preserve that blood brain barrier and minimize any cerebral oedema and increased intracranial pressure. A 33° temperature allows for these things to happen, as well as decreasing that metabolic demand. And the patient which again can cause electrolyte and fluid shifting In a patient with 36°.. There are some things to consider. First off, they're going to be very close to the shiver threshold and we're going to talk about shivering a little bit later on in this presentation. That's something to keep in mind. With 33°.. You're going to go through the shiver threshold and get past it were 36. You're going to hover around it. Consider the patient who may have had, who make present with Bradycardia 36 degree, maybe a better temperature to start them at to make sure that they can tolerate it. And that's one of the things is toleration of 33 versus 36. Some of the updates we've seen recently in T. T. M. Is that specific conditions of the patient may favor one selection of temperature over another. And we just talked about that. The american Heart Association does recommend specific temperatures such as 33 degrees for seizure patients with known history or a seizure that has happened that caused cardiac arrest Where 36 maybe better in patients who have recent gi bleeds or recent clotting issues allowing patients to warm up to 36 or above 36 degrees is inconsistent with any T. TM recommendations. This is the four phases of therapy for a patient who is going to be targeted for 36°.. If you look, you can see where that graph shows less steeping curvature, where you have induction and maintenance very close together and re warming of 0.5°C to normal hermia of 37. The control for this patient is going to be so much more important when it comes to shiver management and normal thermal management. Because of the fact that we're targeting 36. We talked about there was some research done of 33 versus 36 at particular hospitals. What they found when patients targeted 36° is that there was a lower compliance with the targeted temperature of 36. There was higher incidences of fever And there was also a trend to potentially worse outcomes for patients when targeting 36° and only 36°.. One study found that after T. TM. After that study of 33 versus 36 was published. That the average lowest temperature in a post cardiac arrest patient in the 1st 24 hours in the I. C. Was actually higher than it had been. This was also associated with an increased worsening outcomes in patients. This was not seen in any other T. TM. Trial. One of the things that used to be common practice was the fact of cooling a patient ahead of time and now we don't necessarily do that. We don't cool them ahead of time prior to getting to the hospital. There is increasing evidence that fever though fever after re profusion is incredibly damaging. So even though we may want to if they become federal we don't want to cool them ahead of time. There is ideas that fever can actually expedite neuro damage in our patients controlling the patients normal therm. Eah. Whether from post cardiac arrest or not is so vital to the patient's neurological outcome. So how do we prevent fever in our patients? Well, since we know fever is associated with worse outcomes and ischemic injury patient, we do have to try to prevent them. There are definitely methods that we can do to prevent fever. How aggressive we get is going to be the choice of your organization. Simple things that we can do, such as Tylenol cooling blankets, anything like that can really help prevent that fever. But you get to a point in which the fevers were factory and it's not responding to typical treatments. What if there was a way or a device or a therapy that we could use to control the patient's temperature, maintaining normal ther mia and increasing their potential of a positive patient outcome. One of the things that you're seeing here is the active intervention. When do we intervene? For T. T. M. And in patients who we intervene sooner rather than later? Had a chance of a higher survival rate and a better positive outcome. One of the things that they're looking for us door to target time or door to therapy time when the patient enters the organization or achieves raw ask, the sooner we intervene in our patients with T. T. M, the better chances they have of a positive patient outcome. If you remember earlier when we showed you the graph of when that delayed secondary injury happens, it's in that first four hours post Roscoe, it's extremely important that we try to intervene with T. T. M, well ahead of that four hour timeframe. The sooner the better. So as I mentioned a little bit ago, routine cold fluids or ivy cold sailing being infused into patients who've suffered cardiac arrest is no longer a recommendation for T. T. M. Management or post cardiac arrest management. We're going to talk a little bit about the effects of T. T. M. So there's a lot of things that happen with our patients when we begin to cool them. As we know when we get colder we start to have a lower blood pressure, heart rate, um cardiac output. So we got any mindful of our patient's vital signs monitoring for things like bradycardia, hypertension. Okay. E. K. G changes. Some of the E. K. G. Changes are listed there that you will see especially when your patient goes to 33 degree as their targeted temperature goal. With that being said when comparing any E. K. G. To a priory kg before cooling. Be mindful of these changes that your patient is not actively having any sort of issue. But be mindful that the fact that your patient maybe 33° and you may be experiencing some of those physiological effects of the cooling. This E. K. G is a representation of one of those changes, such as a J. Wave or Osborne wave. You see the arrow pointing in your V. Two lead where you see a little bit of elevation. S. T. Elevation typically would be concerned about this in a cardiac ICU world or any. I see the world, But with the patient is 33°,, this is considered a normal physiological effect. Another physiological sign that we need to watch for is bleeding. Now that doesn't mean they're going to automatically start bleeding. But what happens is they are at an increased risk of bleeding. So being mindful of their platelet count, What are we poking into their skin? Such as subcutaneous injections? This is not the time to do central line placements or any other surgical procedures when our patients are 33°.. Another key methodological issue is a decrease in our white blood cell count. This makes our patients more exposed to infections. So it's very important that we're mindful of all of the signs and symptoms of hospital acquired infections. Those things can be your E. T. To making sure that your patient does not have any sort of signs or symptoms. When you look at their sputum. When you're doing suctioning. Being mindful of their fully catheters and making sure that you're providing good fully care and being mindful of your central line for clap. See management, decreasing the risk of any sort of bloodline infection that can happen with the central line in your Reynolds. You're going to have increased diaries is from fluid and electrolyte shifting post cardiac arrest. It's very important that we're monitoring our patients electrolyte distribution, especially potassium With potassium. As our patient begins to get colder to 33°,, potassium is going to enter the cell leaving the bloodstream. This means your serum levels are going to be depleted. It's very important that we consider electrolyte replacement in the induction phase and the maintenance phase. When we get to re warming that potassium is going to begin to leak back out of the cells into the bloodstream. Therefore you would not want to replace any electrolytes during the re warming phase. Once you reach normal therm. Eah you can go back to your electrolyte replacements as your patients, potassium levels will be normalized. When we talk about gi motility, we're talking about a decrease in guia motility especially the colder we get. It's very important that we consider that when we're monitoring our patient's abdomen and abdominal sounds. One of the things to consider is an O. G. Tube or N. G. Tube for decompression. We'd like to minimize any and all aspiration risks when it comes to our patients. So when we talk about some systemic issues, we're talking about the decrease in oxygen consumption and CO two production. It's really important to be mindful of your patients ph and A B. G. Levels when managing your patient whose T. T. M. Lactic acidosis is a common complication. That can happen in post cardiac arrest patients being mindful of your lactate levels and having a protocol in place for interventions of will conduct its begin to increase is important and prohibiting the expansion of lactic acidosis. When we talk about endocrine, we're talking about a decrease in insulin secretion. This is going to lead to an increase of hyperglycemia in your patient. This can also lead to an increased risk of an infection with your patients. It's really important to have a protocol in place of how and when to monitor your patient's blood glucose levels and when to intervene in management of your patient's blood glucose levels. That increased risk of infection we talked about earlier also goes into play when a patient suffers post cardiac arrest. Typically they're emergent lee intubated, which puts them at risk of ventilator associated events such as pneumonia. It's important that you have a protocol in place that allows you to intervene with routine oral care, routine suctioning and monitoring of your patients speed and levels when caring for a patient is intubated. Mhm. Drug metabolisms can be prolonged in patients who are colder. We have a decrease in that profusion to the kidneys and the liver. So being mindful of when you have sedation drugs on and or paralytic sahn that they could take a little bit longer in your patient's bloodstream, which means even if you stop the drips, they could still linger in your patients system. We're going to talk a little bit more about how shivering impacts a Tt impatient and why it's so important to know. Good interventions in shiver management a little bit later, shivering is a natural effect. We all have experienced shivering every time we get cold, our body involuntarily says, hey, we need to shiver. We need to warm up. The problem in a. T. T. M. Patient is that we want them to be cold. So shaving is counterproductive in our TT M. Patients. So with that being said, it's really important that we understand what shivering is and how we can intervene. As a nurse at the bedside, let's talk a little bit more about the natural physiological response of shivering. So as soon as you reach 37.2, your body begins to visa dilate, You start to sweat, You start to try to release that excess heat that may be happening, Going just 2/10 below 37. We begin to viso constrict that's trying to keep the heat towards the core of our body. Once we get down to 35.8, we're looking at shivering. This is our body's natural way to say we have gone way below our normal therm. Eah and therefore we need to do something drastic to bring us back to normal thermal to in the way of shivering with shivering again, it is involuntary, this is an involuntary response in in order to generate heat for our patients, basil. Constriction begins to happen. We get that goose bump reaction that your skin's way of saying it is cold, The brain says, okay, I'm going to shiver, we're going to warm back up. The problem with shivering in a Tt M patient is that we're trying to go in the opposite direction, We're trying to cool them. So with shivering, some of the complications other than delayed reaching of our target goal is an increase in our metabolic rate and demand and an increase in our oxygen consumption. And this is going to lead to an increase in your CO two production as well. One of the things we have to be mindful of is what are those interventions in shiver management and how can we as nurses at the bedside prevent shiver from happening? One of the things that's a great tool is a shiver assessment score and you can see that here in front of you. The score is 0-30 means no shivering. That should be our focus. That should be our goal When you go to assess your patient for shivering. When you get to a shiver score of one, a lot of times it's not something you can see, but more so feel. I encourage you to go to your bed side of your tt impatient. Take your hand and put it just underneath their neck, towards the top of their chest. When you put your hand there, what you'll feel if your patient is shivering some fine tremors, This is indicative of a shiver. Score of one. Why is this important? The reason this is important because when you get to a shiver score of two or three, it's more physical. Its arms, its legs, it's the trunk. It's something you can see more blatantly at the bedside, but it's also harder to manage and get ahead of. That's why if you can go ahead and put your hand just below the bottom of their neck, assess for that and feel those fine tremors, you can intervene ahead of time before it escalates to a shiver score of two or three. The higher up the scale we get, the more aggressive our interventions need to be leading up to and including a paralytic. So what are those counter shivering warmers that we can use? So, those things include socks on hands on feet. Those things can happen. You can warm your room up a little bit in your patient's room, maybe close the door to prevent any cross breeze from happening. Um, some institutions have some warming air apparatuses that you could use. They trick the skin into thinking it's warm and the brain goes, oh, okay, we're warm. I can stop shivering now. But what happens is if you've used those counter warming measures and you're not seeing a reduction in your shiver score for your patient, you may need to consider increasing medications such as sedation and leading up to paralympics. So let's talk about each phase of therapy and what are those common complications that we could see and how we can intervene as nurses at the bedside so we can really improve our patient's outcome. Now, remember in the induction phase we're trying to get our patient cold. So the idea is that we're getting cold and we want to get there as fast as we can. So some of the interventions that we may need to do will help us reach that target goal as soon as possible, careful monitoring of that fluid and electrolyte balance. We want to prevent any sort of arrhythmias, cardiac arrhythmias happening with our patients. Again, glucose control is so important for our patients. Making sure we're assessing their glucose levels and that we're intervening with whatever your protocol states to intervene with monitoring for the hemo dynamic stability of our patients, including heart rate and blood pressure. We talked about electrolyte management specifically potassium as we tend to get cold in this phase, potassium is going to be driven into the cell depleting your serum or your blood levels. So electrolyte management protocols are so important during the induction phase. The biggest thing the biggest takeaway from the induction face is shiver management, shiver management is so important and the interventions of shiver management are even more important. Monitor and assess as your protocol states and intervene when necessary in that maintenance phase. This is the idea of maintaining that temperature of 33 to 36. So we're going to monitor for E. K. G. Changes depending on what therapy level. We go to 33 or 36. We talked about we may see those E. K. G. Changes At 33°.. We talked about the risk of bleeding with our patients. So being mindful if we have lines in or we have other things going into our patient in which bleeding could happen. Monitor for skin changes in your patient. If you're monitoring for 33° that they don't have any sort of skin issues. Of course you're always going to turn a position your patient regardless of what temperature you go to maintaining that fluid status, making sure that you're monitoring your eyes and those for your patient. What's coming in and what's going on is to not dehydrate your patient. That infection surveillance. We've talked about being mindful of those hospital acquired infections such as collapse Ekati and via and our patients. It's so important being mindful of that and drawing cultures. As your protocol states frequent electrolyte monitoring. We talked about potassium and being one of those electrolytes to monitor and having a good protocol in place of when to intervene or when to replace those electrolytes, avoiding hyperglycemia. Again, we talked about monitoring your patient's blood glucose levels and making sure that you're intervening with your protocols way of handling hyperglycemia in your patients as we begin to rewarm. The idea is a slow controlled rewarm. We don't want to rapidly rewarm these patients because we can lead to another secondary re profusion injury. Some of the things to be mindful though even with a slow controlled rewarm is hypoglycemia. The reaction now that the pancreas is starting to rewarm and start to increase its insulin production. That could lead to a potential hypoglycemic reaction with fluid and electrolyte shifting as we begin to rewarm, increased intracranial pressure is a potential side effect. So, being mindful of your patients neuro status, we did talk about that potassium shifting. So now it's going to leave the cells re enter the bloodstream. And now we're looking at hypercholesterolemia as a potential side effect. Again, we talked about that in the rewarming phase. We should not be replacing electrolytes because of this normal physiological effect vessel dilation. As we get warmer is going to happen, we have the sudden rush of vaso dilation, him. Oh dynamic stability is a common complication. Your patient can become hypertensive leading into cardiac arrest, that rapid electrolyte shifting, that rapid vessel dilation. Your patient can become hypertensive and tachycardic very quickly. In the rewarming phase, rearrest is typically what we see. If we see this, we need to intervene. So be mindful of your patients hemo dynamic stability, heart rate and heart rhythm. So the final phase of therapy is the normal thermal phase. The normal thermal phase is just as vital as any other phase of therapy in managing A. T. T. M. Patient. Two most important things with the normal thermal phase. The first thing is we want to prevent rebound hypothermia. We know fever can be detrimental to any patient but even more so intense. Chemical Euro patient, it's important that we prevent rebound hypothermia In our patients. In the normal hermia phase, fever has been associated with poor outcomes, especially in our TTN patients. The other thing that's important about the normal thermal face is the recalibration of the hypothalamus. The hypothalamus is the temperature control center of our brain. Now we have taken our patients to all different temperatures over the last couple of days. With this. With this treatment, it's important that we try to tell the brain again what is normal and maintaining normal ther mia to allow the brain to recalibrate to that 37 degree marker. You're a prognostication is the last phase that we will see in A. T. T. M. Patient? What happens in the neural prognostication phases where a neuro physician will assess your patient to determine the percentage of viability in a patient outcome. It's important that during this that there are no medications running through the patients. I've such as sedation or paralytic drugs. These medications have to be shut off in a period of time and allow for the clearance of those drugs out of the patient's system to give a true accurate assessment of your patients neuro prognostication. And this sometimes can take 2-3 days after you reach normal hermia. We've talked a lot about the science and the nursing interventions, the care management, the complications. We've talked about so much. I now open up the floor to any questions that you may have at this time. Do all the areas in your facility. Use the same protocol in our adult I see us. Yes, we use the same protocol. It is universal to all targeted temperature management patients for all of our adult ICUs. And then when does the clock start for the TT. M. Period at your facility? We are trying now to implement the door to therapy time. So our clock is going to start when the patient either achieves Rosky in hospital or enters the organization. Stores. That is when our T. T. M. Clock starts. When do you consider the beginning of the maintenance phase? The beginning of the maintenance phase is once they reach target goal. So whether that be 33 or 36 that is when the maintenance face begins. And you mentioned to expect bradycardia. How is that managed? I know sometimes it could be a nail biting experience. Is that does the patient have a heart block? Do they need a pacer or is it just T. T. M. So with bradycardia management it's important to not hyper focus on the bradycardia, but whether the patients tolerating it or not and by that, I mean they're mean arterial pressure. So with our protocol, the way to set up is bradycardia management. We do not intervene with bradycardia Unless the patient becomes hemo dynamically unstable. For us. That's a map of less than 65. So for us, the way we look at it as we have a level of interventions. The first level is to go ahead and start a Veysel active drip on our patient. That's the first step. The second step would be raising their temperature from 33 to 34 1°1 time only. After that we consult our farm D for any other medications that they may have in their arsenal that they could support our patient with The last event would be putting a pacer wire in. But that's going to be the last resort because in a 33° patient we don't want to be poking into their bloodstream. You know, you mentioned a lot about shivering. Is it really a concern? Especially if the patients at 36. I mean it's almost normal. Yeah, I would say with 36 degree, it's even more important. When we looked at the slides, we saw that 35.8 was where shiver begins. So when you consider what 36 is and that's where we're going to be maintaining. We're so close to that shiver threshold That your patient could end up shivering the entire time of maintenance. So I would say shiver management is more important in a 36° patient than a 33° patient. That's what our protocol Pushes for is for a paralytic to be on board for induction maintenance and rewarming of a 36° targeted patient. And how can seizure activity be observed in a patient that has neuromuscular blockade are always cautious. We don't want to miss that activity. Absolutely. So with all of our T. TM patients they automatically go on a continuous E. G. Monitor. The nurses are not necessarily trained how to read the EEG but they're trained to be mindful of the wave forms and the differences in those wave forms. We have what appears to be like a call like button on our egg machine where the nurses can look at and say hey this waveform looks different than it did earlier and they compress it and it will send a signal to our E. G. Texas, Take a look to see from their training if there's any sort of potential for seizure or seizure like activity, what is the most at risk point during Tt M during that whole process. When do you think the patient is at most risk? Honestly, I think it's all how we start. I think if we start 10 hours post rostock then we're going to have some complications and potential poor outcomes. Where if we start within that 1st 60 minutes we have the chance of having a very positive outcome for our patients. So it's hard to to pinpoint a certain spot. But I know that if we don't get the ball rolling in the right direction, it's hard for us to play ketchup in the end. And what about the rewarming, the dangers that you mentioned associated with rapid rewarming? Is that reality? Yes it is reality. Have actually witnessed it a couple of times in which the the way that the patient was re warmed escalated. Um For whatever reason. And the patient went into S. V. T. And ended up going into cardiac arrest in which we did have to code them. And then we started therapy you know all over again kind of at the beginning and when you have somebody who re warms too quickly all of those reactions that we talked about during that rewarming phase are escalated. So instead of it being a slow incline we basically just rushed them in. So it's really important that we have that slow controlled rewarm. And that is the American Heart Association is 0.25°C/h.. Um This is just kind of more of a practical point. We are so cautious about making sure our patients are well nourished. And um do your patients stay MPO during tt M. When does your facility consider a tube feet or trickle feedings? That's a great question. So they always start out NPL with an O. G. Tube for decompression and aspiration prevention. We have an automatic order for a nutrition consult and our nutritionist. We'll see them within the 1st 24 hours of that order being put in and then based on the individual assessment of the patient they'll determine whether feed is appropriate or not appropriate for these patients. Now we're talking very very slow feeds. We're talking 10 CCs an hour you know maximum because of that decrease in gi motility. So we're talking very minuscule amounts but it all depends on each individual patient. And we allow the physician team and the nutrition team to make that determination. What about dialysis? If you have dialysis there is a heater on the dialysis machine which one controls the patient's temperature. And how do you manage electrolytes during dialysis? So that is a great question. And my experience being in a C. V. I. C. U. Where I've managed a patient who's on T. T. M. In Pella T t mm paella cr R. T. And ECMO. I certainly understand this question and that is making sure that any machine that we have temperature regulations on that. We're mindful that T. T. M. Is going to trump that. So with our C. R. T. Machines we have them default to 36. And when a patient on T. T. M. There to shut the heater directly off and not even turn it on for our patients. And that is actually written in our protocol under kind of our miscellaneous guidelines is being mindful of what devices have heater apparatuses and making sure that we're following the T. T. M. Protocol. Despite what other interventions are happening with our patients. When it comes to electrolyte management typically are nephrologist. When they are concerned with a T. T. M. Patient, they give 0 to 2 maybe potassium. It's like a two K solution or zero K solution and allow us to replace them more through the serum than through dialysis. Once they're through the T. T. M. Therapy, then they'll go ahead and re evaluate and adjust the dialysis eight fluids as needed. And then I was also curious. You mentioned that these patients undergoing T TM are going to be viso constricted and I have to do regular blood sample sticks for glucose. But how am I going to milk that out of a physio? Constricted patient's finger. Yeah, that's that's a tough thing for nurses. Right. They get cold and then they clamp down. Right? So with these patients typically they have all kinds of lines including art lines. Central line. Our protocols built to draw the glucose is off the art line with a certain needless apparatus that we have that allows us to go ahead and pull the blood glucose from the art line so we prevent any sticking for our patient when it comes to blood glucose management. Are protocols also built in the sense that if they have to back to back glucose is of 1 80 or higher or one glucose over 200. We actually start an insulin drip at that point because it doesn't make any sense to keep poking their belly with insulin every hour if needed. So we end up switching it to an I. V. Solution. Thank you. I appreciate that. You're welcome. So the management of critically ill patients is all encompassing. And to manage the patient with T. T. M. Will require everything that you've learned about critical care and putting it all together with the intention of improving patient outcomes. Sarah thank you so much for being the lead on this session. This is really important information and you explained it in a very uh very clear way. Created by
