ECMO therapy significantly alters medication pharmacokinetics through four key mechanisms: increased volume of distribution due to hemodilution, reduced protein binding in critically ill patients, altered clearance from renal and hepatic dysfunction, and drug sequestration by the extracorporeal circuit. These changes necessitate individualized sedation and analgesia strategies, with ELSO guidelines recommending deep initial sedation followed by gradual reduction based on patient response. Multimodal analgesia approaches and careful monitoring using scales like RASS are essential for optimal patient outcomes.
Deep Dive
Prerequisite Knowledge
- No data available.
Where to go next
- No data available.
Deep Dive
Cátedra café: Manejo de Sedación en EcmoAdded:
[music] Good afternoon everyone.
Welcome to this academic day and especially to the last session of the open lecture on pharmacology for nursing corresponding to the academic period 20261. Best regards. I remind you that my name is William Andrés Flor Muñoz and together with Professor Juan Manuel Dagua Fernández we will have the pleasure of accompanying you during this activity. For us, it is very satisfying to close this academic cycle counting once again on the participation of students, teachers, graduates and other professionals from the different health institutions who connect and help us to strengthen this valuable training space.
The chair continues to consolidate itself as an academic and outreach strategy led by the nursing program and the Yen research group, promoting critical analysis, disciplinary updating and discussion of topics of interest for nursing care, always from a scientific and humanized perspective.
We would like to remind you that these lectures are completely free, open to the entire academic community. Also, those who have participated in at least 90% of the scheduled sessions, remember that they will be able to access the corresponding certification for 2026. On this occasion, we are joined by nurse Ana María Giraldo Duque, who will develop the topic called sedation management in ECMO. Ana María is a nurse who graduated from the University of Santiago de Cali, sorry, she is a specialist in intensive care from the University of Valle and an etmologist. Ana María, it is a pleasure for us to have you with us this afternoon. Well, I think we can start your presentation now so as not to delay the talk any further. Okay, welcome back.
Thank you so much for joining us.
Ready. Okay, thank you very much. They can hear me well there.
Yes, ma'am, we can hear and see you perfectly.
Ready.
Well, it's a pleasure to participate in these educational activities that enrich both you and me, helping me to improve my path as a nurse and teacher.
Well, I have the pleasure of presenting to you a topic that I am very passionate about and that has been passionate about me for the last few years, and that is ECMO therapy. Uh, something very novel perhaps in our country, but which is trending internationally. Well, the topic I'm offering you today in this pharmacology lecture is urgency.
Uh, it's a challenge as nurses and as healthcare professionals to sedate patients in intensive care units. This is even more true when we are dealing with critically ill patients who are on ECMO therapy. In order to give you an introduction to analgesia in this type of patient, I'm going to talk to you about what the therapy is. Ready.
Okay, so what is an echo? Uh, in its acronym, as they say in English, it is extracorporeal membrane oxygenation, which is an extracorporeal membrane oxygenation. The ELSO, which is the entity that governs ECMO worldwide, reports that ECMO is a life support that provides ventricular assistance and oxygenation to all patients. Well, that they are critically ill, that they have pump failure, pulmonary failure. So, this therapy will provide assistance for a certain period, whether days or sometimes months, so that the organ can rest, recover, and we can define the final management of this type of patient.
What is the goal of this therapy?
Well, as such, the therapy does not cover the underlying illnesses of these patients. It is merely a support that provides life and oxygenation. While the crucial time that is in this therapy, the organs as such, as I was telling you, rest, heal, or we are waiting for the transplant of the lungs or the little heart, if necessary.
to quickly explain the components of the system, because it is very important to know them and why they have such a significant impact on patients when we are sedating them.
Um, if we have our sick patient, uh, we're going to connect him, let 's say, we have a patient with severe ARDS, then we're going to subject our patient to an ECMOVENOUS, uh, we must connect him to some cannulas to be able to extract and drain the blood, uh, depending on his size, body weight, age and all the flow that we want to provide him.
So, this will define the type of cannulas we are going to use.
After we have cannulated our patient, the centrifuge, through negative pressure, extracts all the blood we need, sends it to our machine, which is the console where we can control the flow and the revolutions we want to give. Uh, this sends it to the oxygenator or membrane where, by means of a mixer or blender and accompanied by a heater, we are going to give the blood temperature so that we can continue with the temperature that we need for our patient. And the mixer or blender, which will be the one that makes the mixture of fresh gases depending on the amount of oxygen we want to provide to our patient and whether or not we want to remove a certain amount of carbon dioxide from the blood, in order to regulate our patient.
The membrane is then compressed and directed back to a cannula to introduce the blood into our patient.
If it's an ECMO, I already know what we're doing, so there's going to be a classification. Well, it depends on the patient's needs, the pathologies, and how we want to approach it.
So, we have two main classifications: venous ecmo and venoarterial ecmo. Ecmorenovenous support is basically the support that will replace our lungs.
Okay, let's talk, for example, about peripheral cannulation. So, the blood will leave the femoral vein, it all leaves the venous system, our pump extracts it, it goes to the oxygenator, the blood is oxygenated and returns again, for example, to the subclavian vein or the jugular vein, depending on which vein is cannulated. And this would be the venous echo, like the configuration, in a very large and gloomy way speaking. And the veno- arterial ecmo configuration, as its name suggests, is extracted from the venous system. For example, if it's a peripheral ECMO, we bring it from the femoral vein, it goes to the pump. The pump in this type of ECMO is basically our heart, where we control the revolutions and the flow, which is basically the cardiac output that we are providing to our patient. It then goes to the oxygenator and re- enters, but this time it enters the arterial system to irrigate the entire body of our patient.
Okay, now getting down to business, having learned a great deal about what ECMO is and how the therapy works, I'm bringing you three articles in a collection that will help us understand why it's such a big challenge to anesthetize or sedate our patients when we have them in intensive care units.
This article, which basically talks about the anesthesias given to patients in surgery in general, aims to describe how the people who manage these patients cope when there is an emergency, when there is an absence of a perfusion team, such as the masters of the extraction area or a cardiovascular anesthesiologist.
We as ecology specialists need to know how we are going to manage these types of patients according to the sedation we are providing. So, this article brings us three very important things, and the first is that it informs us about the pharmacological changes that our patients experience when they are undergoing therapy. So, these four factors that I'm showing you on this slide are the volume of distribution, the binding of the drug to the protein itself, the clearance of the drugs, and the sequestration of the drugs by the circuit. There are four quite important factors that influence medications and which is why it is a challenge to be able to prescribe them. Why is distribution volume so important? Well, the effect of the drug decreases or increases according to this volume that is in the body at the intra- or extravascular level. Well, obviously there are many changes depending on this volume, so medications that are hydrophilic decrease their distribution if we have a patient with an alteration in the OLM.
Another important factor is the binding of drugs to proteins. Well, considering that medications bind to certain proteins to be transported, in critically ill patients, such as septic or polytrauma patients, the catabolism of all these proteins is severely affected. So, as a consequence of this, there is an increase in the free level of the drug in the bloodstream, and we can have toxic effects from these medications in our patients.
Another important factor is clarification. What do we mean by clarification at this moment?
[snort] In both patients who have intravenous or intraarterial administration, there is renal dysfunction and hepatic dysfunction, which means there is an alteration in the clearance of the waste products of these medications from the blood.
So, to avoid pharmacological failure in these patients, we have to be very attentive to their renal and hepatic function to avoid alterations in these organs mainly.
And the last factor, but no less important, is the hijacking of medications by the network.
What does this mean? The circuit is designed to be biocompatible with humans. It is made of polyvinylpentene, which is very biocompatible, but at the same time, because it is something outside our body, it increases and alters our inflammatory response, and generally all the products of the inflammatory chain adhere to it, including medications; that is, medications that are lipophilic generally have a certain affinity with this component of the circuit.
So, we're not always going to give the patient the exact dose, uh, in terms of sedation, and also if we 're talking about, for example, antibiotics. So, these are very important things to keep in mind.
What other important information does this article give us? Well, there are very important factors related to the therapy that cause pharmacological alterations that are purely expected. One of those is the curved cell of the circuit. Uh, there is an increase in the patient's blood volume, there is hemodilon, since if they are adult patients, when we are able to purge the circuit, we do it with saline solution, with Ringer's lactate. Well, in children it is done with blood, so there isn't as much of an increase in hemodilution. In contrast, a lot of hemodylon is seen in adult patients.
And as I already told you, the volume of distribution alters the medications that we are administering to our patients in echocardiography. Another factor inherent to the circuit, as I said, is kidnapping; the newer the circuit, the more kidnapping there is.
Therefore, the bioavailability of medications in our patients decreases. And others are the net factors of the patient, inflammatory load, hyperdynamic patients who are in multi-organ failure, so we have to put them into hemodialysis, hemofilter. All of this will alter the medications and their bioavailability in the blood of our patients.
This little picture I'm showing you here is really cool. Because?
Because it tells us about all the sedation or analgesic medications we can use in our patients, and according to the volume of distribution and the binding to its protein or the affinity it has and its level of whether it is lipophilic or hydrophilic, what can we do?
Um, one drug that we use a lot for ECMO patients is, for example, propofol, but sometimes, depending on the type of patient, their age, their illness or their history, we have to use extremely high doses.
So, as you can see, propofol has a high volume of distribution, which is about 60%, and has good protein binding, but since these patients are so hemodiluted, we obviously don't have a way to reach the patient directly and generate sedation in these patients, so we have to use other alternatives and we started using propofol accompanied by solar amines in some cases. If we have a patient who is already waking up and we want to see how they are waking up and their neurological state, then we start playing with propodexmedeto, with ketamine and never forget, obviously, apart from the sedatives, to use very good analgesia. Um, for example, fentanyl is unfortunately a drug that is highly hydrophilic, so it sticks too much to both the membrane and the circuit. So, sometimes we don't get very good doses of pain relief with this medication. So these are patients who are on multiple drugs, like ketamine, fentanyl, paracetamol, and countless others, but it's always like multimodal analgesia.
Well, another article I want to bring you is about medications in patients during extracorporeal membrane oxygenation. The truth is we continue, uh, as if building the evidence. Because? Because it's very, uh, how do I explain it? We are building the evidence day by day with our patients. There aren't yet very precise guidelines to define whether patients have to be treated this way or if there's an international protocol stating that all ECMO patients must be treated this way, right? They are very individualized and also everything depends on each center.
So, with this review, I'm bringing up two pretty important things, and it's also what I was explaining to you earlier: all the critically ill patients we have are affected by this; it absolutely changes everything.
These patients experience increased cardiac output, increased capillary permeability, and increased or decreased affinity for proteins.
So, all of this causes the concentrations of the drugs in plasma to decrease and decreases, sorry, increases the clearance, uh, as I was saying, the clearance of these drugs in the blood, it increases the volume of distribution. Because?
because these are patients who are constantly being given fluid loads, along with other very specific therapy-related things. So, drug sequestration, these are quite complex patients and there are many pharmacodynamic changes in these patients.
So they are daily challenges. Today the patient can be very calm and we need very small doses. The next day the patient was septic, tachycardic, and hyperdynamic. Therefore, all of this affects the pharmacodynamics and pharmacokinetics of our patient.
This little chart basically tells us what the effect of medications is on our patients in extracorporeal therapy, based mainly on whether they are hydrophilic or lipophilic.
Well, depending on the volume of distribution, the mode of clearance, whether it's renal or hepatic, the affinity for proteins, and also depending on the amount of time our patients are in therapy. The older our circuit is, the more often we have the availability of the medication, even if it's in the circuit and not our patient, and this can affect us, as I said initially, generating toxicity from certain medications.
Well, this is another article that I really liked, and it's about sedation and analgesia strategies in ECMO patients.
Just as we have sedation and analgesia strategies for patients in intensive care only, how do we initiate sedation depending on the type of patient we have? What sedative are we going to use? If a patient has liver disease, we're not going to be giving them propofol. So, we also do all these things on our ECMO patients. Uh, this article also talks a lot about the changes that ECMO induces in our medications, and they are all basically derived from three important things. One, the absorption of the drug or the sequestration of the drug by the circuit, the increase in the volume of distribution and the changes in clearance. In other words, all the articles talk about those basic things.
But then this little article raises three big questions for us. One of them is, how are analgesics and sedatives affected in our patients by the extracorporeal circulation membrane?
So, as you can see here, the pharmacokinetic characteristics of each analgesic and each sedative show whether they are highly hydrophilic or lipophilic, what their affinity is for proteins, and if we have a decrease in albumin and alpha-glycoprotein, which are where these medications adhere most, then the effect of these medications in the blood begins to decrease.
For example, fentanyl is a drug that we constantly use in our intubated patients, I think in 80-90% of cases.
Uh, and unfortunately due to the circumstances of the circuit we have losses between 67 and 97% in just the first 24 hours. Well, one might say, "No, well, that's a loss of medication," but no, I mean, these patients sometimes absolutely require neuromuscular relaxation, so they're given full doses of fentanyl, levothyroxine, propofol. Sometimes we've even had to use isoflurane, inhaled sedation, to be able to control our patients very well and achieve perfect sedation, without affecting the brain, and to have our patients in optimal condition to get the best results from both the sedation and the therapy. Because we have to work with the patient and our therapy; it's not all done individually. No, we have to see the patient and the machine as a whole.
So, it 's super important to see how these medications bind to proteins, how much sequestration we have of these medications, and what other options we have to help us generate very good pain relief in our patients.
Another question this article raises is, is there really an increase in the requirements for sedation and analgesia during the Oxygenation by, well, or by the use of the extracorporeal membrane?
The article tells us that many of our answers, which I think many of us must have, are simply based on perception. On many occasions, patients, simply because of their diagnosis, patients with SARS-CoV-2, COVID-19, or influenza A, become critically ill and experience hemodynamic and respiratory deterioration within hours. These are patients that one says, "No, I have to isolate them too much simply because of their diagnoses and in order to prone them." Patients who increase their respiratory drive, patients for whom we have to, in addition to everything else, increase sedation and use neuromuscular blockers to bring them to a top of zero and be able to pronate them. We have patients on protective ventilation, or we also have other patients whose ventilatory parameters are too high and who do n't tolerate it; the pressure in the airway has increased.
So, boss, what should we do to give it more? Um, another thing, things very specific to patients, we have very young patients who have a history of psychoactive substance use, so one says these are patients who have tolerances to certain medications, so I will have to increase the doses of the medications. Yes or no? Um, depending on the degree of response to these medications in our patients.
There are others who, with 3 cc of propofoel, are super asleep, and others who, despite having fentanyl, myasola, and gigantic doses, definitely begin to develop a tolerance, so we have to not increase the dose, but help or use other medications. So, basically, everything is perception; everything is what we think, but it's not reality. Actually, everything depends on the experience center that is handling the patients. Sometimes, if we don't achieve very good sedation, it's because we don't have clear sedation goals based on the neurological assessment tables we have in intensive care units like RAS, or because we have excessively sedated patients and don't have adequate monitoring, or it's simply insufficient.
So, all of this leads us to think, based on perception, that we have to use excessive doses or increase the sedation requirements in our patients. Everything depends on our experience and very good monitoring of patients in order to achieve the goals we want.
And as a final question, this article asks us what the analgesia strategy should be for a patient during ECMO therapy. We've been looking at both global and national perspectives, including reading the Red Book, which educates us about ECMO, and listening to colleagues from other institutions with extensive experience, such as the cardiology center in Bucaramanga, or colleagues who work at the Chavia Hospital in Bogotá. They don't have an established protocol; rather, everything is developed as we go along.
Elso simply advises us, she advises us that at the beginning of therapy we should have very deep, very sleepy patients to decrease oxygen consumption, so that we can quickly reach a stable point, stabilize the patient and begin to see results, but little by little, according to the patient's response, gradually decrease the dose of these medications so as not to overdose.
Uh, and also, well, everything is very individual according to each patient.
Uh, let's remember, shall we? All medications are for all patients, also depending on the objective we want as an intensive care unit, as intensivists, as nurses, because all the time we have to be guided by a goal, I don't want the patient at a certain level or I want the patient at zero, I want to start waking him up or I don't need him super asleep. So, it all depends on what we want, what we need, and it's very much geared towards that, to individualize each patient and manage the sensation accordingly.
This algorithm or this flowchart, and I really liked it a lot.
This study also provides us with this information, which is actually a bit old, but it's from 2017, if I'm not mistaken, actually this one is from 2022, but it's basically what we do. What does it tell us?
We have a patient with necrosis, he needs cecal analgesia, yes or no? Does he/she need deep sedation, yes or no? If it is a patient who does need deep sedation, then let's start with analgesia. What will we need? Well, our first- line medication, which although it's not very hydrophilic, sorry, it's very lipophilic, so obviously we still administer it, and then we help ourselves with morphine.
Uh, but then, how are we going to guide the administration of this medication? It is always using our analog pain scales, whether numerical or in many intensive care units. We also use the one that is very qualitative with the little faces from the bad happy to the saddest. And if we need deep sedation, then if we have a hemodynamically unstable patient, what are we going to use? Midazolam.
Because? Because propofol induces hypotension. So, it would be the second-line drug.
We also know that the bioavailability of this medication is not the best in our therapy. And failing that, if neither midazolam nor propofol works for us, then we can use other alternatives like isoflurane, which are inhaled sedatives, and the truth is, there is an experienced center that knows how to handle it. They have a reduction in resources and two sessions, which are truly excellent and very good, and with very good results also when evaluating neurological status.
Ready. We already have this patient in deep trouble and we also manage it through what means? From the biospectral review. In many highly experienced centers we use neurological monitoring, not only checking pupils or checking verbal motor response, but we also have electroencephalogram monitoring by means of BIS.
Well, to be honest, this has worked out great for us at our center. And we have patients that we've found to be effective simply with isufloran, without even adding anything else, and that has been enough.
[snort] Ready? We want to start waking our patient up and we need light sedation.
So, use, as I told you, multimodal analgesia and always evaluate our pain scales. And to begin reducing the ante, the best companion in these is dexmedomidine, which helps us to have conscious sedation and directly evaluate the neurological state and also helps us to see the hemodynamic state of our patient.
So, depending on how we want to see our patient, this algorithm tells us if there is clinical improvement, if not, if they are still unwell, then we would need to increase the sedation, if it is a difficult analgesia, then if it is a patient difficult to sedate and with analgesia, uh, it is no longer enough, for example, with opioids, if we have fentanyl, we have morphine, we are also helping with acetaminophen, uh, with ketamine, then we begin the use of opioid rotation, we start the use of methadone to also decrease the consumption of fentanyl and so little by little this algorithm tells us how we can use our medications in a very easy and simple way and all guided by goals and guided by, well, basically by goals. So if I want a ras of minus 1, well I wouldn't like it, but then a ras of zero, a ras of minus 1, patient with Eva of less than cu, this algorithm I really love, I recommend it when you have the opportunity and read the article. They're going to love this.
So, what conclusions can we draw?
Well, having these three articles, I made several conclusions, but they are what we have been talking about during this time and it is, what do we want with ceoalgesia in our ECMO patients? Basically, to achieve well-being and facilitate the adaptation of these patients to therapy. It's not easy to have a patient on a ventilator, with tubes attached. So, imagine having this patient who, besides having a tube in their mouth, has cannulas that look like PVC pipes; they have very high risks. So, it's about completely minimizing the consequences and adverse effects that these medications have on our patients and being able to bring them to a recovery in the best way possible.
We know that managing neuroanalgesia can be a challenge, especially in our patients who have pharmacokinetic and pharmacodynamic changes related to their disease, the therapy, and also depending on factors such as age, gender, and race. So, these are challenges we face every day, and the only thing we really do every day is learn.
The eo, as you can see, increases variables that cause us setbacks, because we can all go through them, we can all overcome them, and they are the drug sequestration, the volume of distribution, and also depending on the clearance of these medications, which, as I have already made quite clear, [snort] we must always individualize our patients, not only in my case, but at any moment in life that we are treating, children in PP, in any case, we always have to individualize them, not only in our therapy, but it is of utmost importance, since this makes us pay close attention to detail, especially in these critical patients, and we must be very careful in the use of analgesics in our patients.
And it is very clear to us that many prospective studies are needed, and this makes us as nurses want to go further, want to read, want to study, want to contribute something to those who remain or those who come after, even to our colleagues. So what remains is to continue generating information, capturing it, wanting to multiply it in these spaces, for example. [snort] And we are clear that ECMO is a pretty big impact on our patients, but also especially on the use of medications, due to the increase of all these factors and variables that impact both the dosage and the proper use of medications. I've seen doses that one would say, as they say colloquially in institutions, doses for horses, but unfortunately they stay in the circuit, so we don't have a target in our patients, but we have to do it very carefully and always seeing the effects we are generating in our patients. It is extremely important to always know the pharmacokinetics and pharmacodynamics of all the medications we are administering, especially when dealing with patients on multiple medications. In other words, besides the high levels of sedation, there are thousands of other medications that can cause interactions and either increase the severity of the illness or perhaps improve it.
Pharmacotherapy in these patients really needs to be optimized a lot in order to see the effectiveness and the outcome for all our patients on ECMO. And this is crucial, then, to see the best results, being redundant here. And well, we hope that in future advances the clinical application of the therapy will provide us with tools to improve the use of all drugs, both in critically ill patients and in patients we have, uh, and that at some point we can have a monitoring chart, a medication guide that doesn't make us so empirical, but that helps us do things better and better.
Well, thank you very much for your attention.
Hello.
Hello, boss. We are very attentive here, we are very focused on your presentation.
Thanks a lot.
With pleasure.
We have a few questions, William. I don't know if we have time to present.
Uh, yes, yes, Juan, of course. I'm having problems with my connection.
Thank you to the boss, thank you very much for your participation. Hey, look here, Juan, if we suddenly have any questions in the chat.
Yes, yes. Uh, I've received a question here internally and two more questions that we have here in the chat.
Okay.
Hey, can you hear me, boss? Yes, yes, I do listen to you. It's just that someone else is listening to me here. [laughs] Ah, well, boss, they're asking me here if, considering what you have in your clinical practice, uh, is there any difference in the response to sedation in different patients? They call me, they ask me very specifically if black patients, indigenous patients, or if there are any differences, and if they respond to the same medications and in the same timeframes.
Well, the truth is, as I said, these patients need to be treated very individually.
Patients, for example, of black race, are generally patients who suffer from hypertension and are difficult to manage. Sometimes they are either poorly sedated or they don't have good pain relief. The truth is, it all depends on the type of patients, and also on their medical history.
So, I can't classify them and say, "Black patients are easier to sedate, or maybe not, or Indigenous patients." The truth is, it all depends on the patient, and in many cases, as I mentioned, monitoring helps us a lot. For example, with patients, I want to set a specific sedation goal, and if it's an elderly person, elderly people generally fall asleep easily with very little sedation.
So, it's about working with that, doing a very good assessment, applying the scales, checking vital signs.
All of this allows us to say, "I can sedate this patient in this way." But it's all individualized; we can't generalize.
Okay, boss, thank you very much. Now, let's proceed with some questions we have here in the chat, boss. One of our teaching colleagues asks, "How does the EMCMO circuit affect the pharmacokinetics of sedative medications?"
Okay. So, with the three articles I brought to your collection, as I mentioned, we have three very important factors that affect the Pharmacokinetics of medications, and their bioavailability, are affected for three reasons. One, the clearance of these medications, because the kidneys and livers of our patients with, well, sometimes multiple organ failure, are affected. So, that 's one factor. Two, the volume of distribution. We have patients who are frequently resuscitated, so patients with hyperbolic, hemodiluted blood, and, on top of everything else, the affinity of these medications for protein binding decreases. So, these are medications that are free in the bloodstream, but we don't have very good bioavailability when it comes to exerting their intended effect on the body. So, that's another factor. And finally, the sequestration of the medication by the circulatory system.
Despite being a substance, well, something very bioavailable and, excuse me, biocompatible with the human body, it tends to adhere to the walls of the circulatory system and remains free in the system, but doesn't exert its intended effect on the patients.
Okay, perfect. Boss, another question I received here via internal message... One of our colleagues asks, "What has the experience been like, and how do you make the switch to wake patients in these cases, and even more so?" It's complex, especially when they have polypharmacy or multimodal sedation.
It's a challenge; we've had some very scary cases, and it all depends on the assessment. As mentioned, we have patients on multiple medications.
For example, we have patients on propofol, Mielan, fentanyl, and sometimes neuromuscular blocking agents.
So, we gradually reduce these medications. For example, we decrease the neuromuscular blocking agent, which is being monitored by all the electrodes, to see how relaxed the patient is. They've already started to move.
So, we have movement, we have one of our assessments, for example, a Glasgow Coma Scale score, and they have a motor response. So, right now, waking our patient up is the biggest challenge. How do we do it? We start reducing the medications they're taking. Much more asleep. And how do we know? At our institution where I work, we personally use biospectral monitoring a lot.
We have two types of monitors, and they show us, both through graphs and values, how sedated our patient is. Generally, the sedation goals using biospectral monitoring are for patients we want to have between 40 and 80, more or less. When it starts to go closer to 80, it's because the patient is much more awake, more superficial, so we start to reduce sedation according to the biospectral response. But also, when we see that our patient has opened their eyes, is ready, has started to obey commands, then we start to reduce sedation, we start Exmedo- Miidine. So when we start Exmedo-Miidine, we start to completely stop the other medications, but always accompanied by very good analgesia because it's not just about giving the patient pain relief. These are patients who are bedridden, have limitations in mobility, patients we've had a lot of For example, if they're relaxed, you can imagine the decrease in muscle strength these patients experience, which is crazy, but we're always monitoring them, assessing them, seeing what I'm getting. There's always a response.
So, if I decrease something, how did they respond? Did they respond well? Did they respond badly, did they wake up agitated?
Then they need sedation, okay?
So, let's call the psychiatrist, or if there's someone with enough experience at our institution, let's ask them to assess the situation. They need sedation. Obviously, the use of benzodiazepines increases delirium in our patients, but sometimes we do need benzodiazepines to help modulate the behavior of these patients. But that's how it is; it's all action and response.
Okay, boss, thank you very much. In that sense, our next question is: What sedation scale is recommended for ECMO patients, and what are its limitations?
For us, we always use the The RAS scale. Uh, and well, limitations.
Hm, sometimes we do have limitations with this scale, and it's because patients sometimes don't cooperate, but their response is very predictable.
Uh, patients who have a bad awakening, so we have to reinstate sedation. So, the patient we wanted to have at perhaps -1 is now back at -4 because they became agitated, and the risk for us is that they might need cannulation, we could have a catastrophe, and therefore the patient could die. So, of course, there are fears and anxieties, but it all depends on their response. Whether we have a good response or not, we are guided a lot by the RAS, also by the pain assessment scale, because these patients sometimes aren't even ill, but rather uncomfortable: "I have pain," "I have discomfort," " Help me with my leg." So, we discover these kinds of things as we observe them. We also analyze the patient's entire context, but generally we use the RAS.
Perfect. Okay, I'm going to read another question here in the chat, boss, that I find very interesting, okay?
How can nursing staff differentiate between pain, delirium, and agitation in critically ill patients on ventilators?
Okay.
There's another scale I haven't mentioned, but it's also very relevant to the patients we work with in intensive care, and it's the CAMICU scale. It helps us determine whether or not our patients have delirium. We have hyperactive delirium and hypoactive delirium. So, it's all about observing how our patients behave.
Sometimes we see a patient who's still and staring into space, unresponsive, unreactive, and we think, "No, they seem calm." But no, they're not calm. The patient is actually experiencing active delirium.
So that's when we start to identify it: my patient is in delirium. It's not that they're perhaps oversedated, but rather that they 're acting inappropriately. In other words, they're not themselves. We also have to rely heavily on... The family or those close to our patient in their daily life are also important to identify changes in these patients. So, we also have our crazy patient who wants to jump out of bed, who kicks, and we assess them: "Hello, how are you? Do you know where you are?" Then we start working with them. "Look, this happened to you, you're in the ICU, today is Tuesday, today is May 19th, I don't know what." We guide them to bring them back down to earth and help them understand where they are. It all depends on the patient's specific conditions. For example, a polytrauma patient with a frontal stab wound isn't necessarily facing forward. So it's very much about assessment, I think.
Boss, I find that question very interesting, and even more so your answer, especially understanding the patient's history or what makes them critically ill, because the management will depend on that. The management is very different.
Like Wilbert's question, pain management... Delirium, knowing whether opiates or benzodiazepines are being used, the interactions and side effects this can have in an ECMO patient, as you mentioned, with those significant impacts on the pharmacokinetics of the medications.
Thank you so much, boss.
The questions continue. I'm getting a question here in the chat: how viable do you consider the implementation of light sedation protocols in ECMO patients?
Well, it all depends on what we need. As I mentioned in one of our conclusions, ELSO tells us that at the beginning of therapy we need completely sedated patients to be able to reach our goals. Sometimes we have patients with biventricular failure, so these are patients who literally don't have a heart. We need them to consume the minimum amount of oxygen from their system so we can give them everything from here, from the therapy. So, it's a patient I need to keep still. For ventilation, protective ventilation, so I know they're consuming the minimum amount. I 'm also helping them with my membrane. Although at this moment it's an echocardiogram, look, what I'm doing is pumping. So I minimize the support requirements for this patient, but when the patient starts to contribute, the heart has rested enough, the heart rate and aortic valve opening are improving, then I say, look, this patient is much better, let's start reducing the support, and I also start a neurological assessment. What do I have? If I've had this patient so sedated for four days, let 's start seeing how they wake up, let's start reducing the sedation to see how they begin to respond, doing neurological assessments so I can say, "Okay, I have brain function, I have heart function, I have lung function, let's reduce it."
So it's all very much like that, I mean, it's like playing around, they're critical moments, but the truth is, you see it from the outside and you think, how cool to see how everything is working and that I can do it this way. But then at the beginning of therapy it's not so recommended because we want to give them all the support with the machine, for example, if it's a BA. But In patients we have on ECMO BBB, who are sometimes bridges to lung transplants, they can be in therapy for months. It's not a patient where I'm just going to give them analgesia for two months. So, I start reducing sedation while monitoring neurological aspects. Then that patient responds to me, obeys me, already knows what happened to them. We focus on what they have, what we're waiting for. We do n't have to wait. This machine is what keeps you alive. We see patients awake, walking with the ECMO, patients doing physical and respiratory therapy sitting in a reclining chair, but that's because these are centers with a lot of experience. You see patients, for example, in Bucaramanga, which is crazy, patients sitting on a stationary bike with the stents right next to them. So, it's not that we have patients completely in a coma for that long, because obviously what we want to give back to the world is a functional person. So, I would like, and I would love, for them to be able to do a Very superficial sedation, but sometimes it's not so good. Initially, according to Elso, then, we start with deep sedation and gradually decrease it according to the patient's needs and responses.
Perfect, boss.
I'm reminded of a phrase I heard this morning at a symposium: that as professionals we must have the knowledge, but the patients tell us what to do. Boss, I'm going to present the last question here due to time constraints. In the case of therapy, the recommendation would be dexmethomidine, for weaning from therapy, excuse me.
Okay. Uh, yes, usually and generally that's what we do with our patients. Uh, we have that great help, and that is that dexmethomidine has been, I mean, one of the best options when weaning or switching sedation, because our patients are calm, but conscious, and cooperative.
And they start to get agitated, so I'll raise it another two points, let's see, or I have it at one-four, because There are patients who have a crazy tolerance to these medications, and I have them on the maximum dose and they're still awake, whereas with another patient, I could have them on the minimum dose and they'd be completely exhausted. So, honestly, dexmetodine has been a great help in reducing pain in these patients.
Boss, with dexmetodine, you always have a couple of concerns: anxiety and hypotension. Yes, but in those situations, as the professor's question mentions, during weaning from therapy, and with the urgency, or rather the need to have the patient under control, the challenge is significant because on one hand, I have them under control, but on the other hand, how do I counteract the cardiac effects that dexmetodine can generate? It's one of the things, as you mentioned, how do we play this game—if we could use this term without [laughs] sounding cold? No, boss.
No, no, no. I mean, something that working at the USIA has taught me is humanity, and it's not a game.
Unfortunately, we tend to use words very casually, but no. It's like playing Jenga, you know, take this out, put that in, you know, you have to see, and the truth is there's a lot of multidisciplinary work involved because then the intensivist comes in, there's the nurse, there's the nursing assistant who tells me, "Boss, he's about to throw himself out of bed." Then the psychiatrist comes in and says, "No, come here, it's all medications, let's take this out and put this in." It's a combination of many, many, many people and many things that mesh together and work together.
Thank you very much, truly, a fascinating topic, and your way of presenting it makes it even more fascinating.
The impact of this presentation you're giving really translates into the films... The questions and the connection they generate among those of us here. Thank you so much, Professor William.
Thank you, Professor Juan Manuel.
Thank you, Ana María.
We invite all attendees once again to please fill out the attendance form using the link you'll find in the chat on YouTube. And before we conclude, we also want to express our gratitude to the Communications Management Center for their ongoing support in broadcasting and disseminating each of the lectures held during this academic period. As this is our last lecture, we also want to sincerely thank each and every person who was part of this process. Thank you for connecting, for participating, for asking your questions, and for helping us continue building knowledge around care and pharmacology, specifically in the area of nursing. We hope that each of these sessions has contributed not only to your academic training but also to your professional and personal growth. And finally, Juan Manuel, well, I think we have nothing more to add. I invite you to stay tuned for the next academic period, in which we will be opening a new cycle of open lectures, new topics, new speakers, new guests, and of course, this learning space that I believe we must continue to strengthen every day.
Thank you all so much for joining us this semester. We hope to see you again very soon. And Ana María, the presentation was spectacular.
Thank you so much.
We hope to have you here again.
Exactly. I wanted to invite you, Ana María.
We want to invite you to a new meeting next semester. Yes, I'll be here next semester. Okay, thank you very much.
Yes, ma'am. We'll see you around here then. Thank you very much. You're very kind. Goodbye. Goodbye.
Thank you so much.
[music]
Related Videos
3 Reasons Eating Meat Will Kill You?
Professor-Bart-Kay-Nutrition
1K views•2026-05-28
Group launches palliative care training campaign – May 29, 2026
cpac
593 views•2026-05-29
#shorts | First Guess of Brain Stroke? | Dr Manoj Vasireddy | Neurology | Sri Sri Holistic Hospitals
SriSriHolisticHospitals
103 views•2026-05-28
Whether you have chronic infections or mystery symptoms, Evvy’s Vaginal Health test can help you
evvybio
584 views•2026-06-01
🍉 Benefits of Watermelon During Pregnancy | Healthy Fruit for Mom & Baby #medicoabhijit #healthymum
medicoabhijit_br
1K views•2026-05-30
7 Sneaky Attacks on Women's Womb Health You Never See Coming
DrBobbyPrice
1K views•2026-05-29
#pregnancyafterloss leaves you feeling very scared and all i can go on is the information i have
Changedbygrief-TFMRMama
498 views•2026-05-31
Beyond Liver Disease: The Hidden Role of Protein in CLD Recovery | Dr. Karan Jain & Ms. Reshma Aleem
VoiceofHealthcare
420 views•2026-05-29











