Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: Hypotension and shock are recognized complications post-cardiac surgery.
Speaker: Some patients may develop more severe shock refractory to fluids and catecholamines.
Speaker: In today's podcast episode, we will discuss vasoplegia after cardiac surgery.
Speaker: Our guest is Dr. Iqbal Ratnani, an intensivist who practices at the Debeki Heart and Vascular Center and the Center for Critical Care at Houston Methodist Hospital.
Speaker: Dr. Ratnani is an Associate Professor of Clinical Anesthesiology and Critical Care for the Department of Anesthesiology and Critical Care at Whale Cornell Medical College.
Speaker: In addition, Dr. Ratnani is a Director of Critical Care Education at the Center for Critical Care.
Speaker: A recognized clinician and educator, it is a true honor and pleasure to have him with us today.
Speaker: Iqbal, welcome to Critical Matters.
Speaker: Thank you very much.
Speaker: It's my pleasure.
Speaker: So today we're going to talk about basoplegia, which I think is a very interesting situation at the bedside.
Speaker: And we're going to focus mostly on basoplegia that occurs after cardiac surgery.
Speaker: But I wanted to start with maybe a broad definition of basoplegia, also known as the basoplegic syndrome.
Speaker: So...
Speaker: Sergio, I will say that vasoplasia in simple terms for the students and for clinicians is that it's the loss of vascular tone.
Speaker: Or in other words, when vessels cannot provide enough vasoconstriction in response to hemodynamics.
Speaker: That's a very simple, in simple words.
Speaker: But technically, if we talk about the best definition came out in 2018, and I think that that's the most precise and concise definition
Speaker: on vasoplegia or vasodilatory shock, this is a condition as a profound, uncontrollable vasodilatation due to persistently low systemic vascular resistance with normal or high cardiac index.
Speaker: So that's in total, but I still go when I try to teach students, I suggest it's a loss of vascular resistance or not an appropriate vascular tone.
Speaker: Now, I will just add one more line that if you look at the literature and that really sometime shocked me that after so many years with our failures and our trials and tribules and all this thing, vasoplasia, we haven't gone beyond the definition.
Speaker: We haven't talked about the categories or the types or refractory or even gradings.
Speaker: Vasoplasia can even have a grading.
Speaker: We have not done that.
Speaker: So we have only this definition available right now for vasoplegia or vasoplegic syndrome, as it's said, because it affects the whole body.
Speaker: And I think it's important what you mentioned, Iqbal, because technically if somebody is vasodilated and requires vasopressors to support them, they have vasoplegia in a situation like septic shock.
Speaker: But when we talk about vasoplegia with experienced clinicians, they're thinking of a particular subset of patients that
Speaker: that is more refractory, more difficult to manage, that has maybe a much more severe vasodilatory situation.
Speaker: And like you said, the lack of grading systems or clinical guides really make this a very broad concept.
Speaker: But we're going to be talking about those patients that have difficulties in terms of managing them post-cardiac surgery due to the vasodilation.
Speaker: What other conditions can vasoplegia occur in?
Speaker: Let me put it this way.
Speaker: If you talk to people who are not clinicians or who are not even doctors and on the outside, anaphylaxis is the best example of an outpatient in the population.
Speaker: But when you talk about inpatient, two, three major categories are sepsis and especially cardiac surgery.
Speaker: And some people, and it can be actually, we don't realize that it can be acute and chronic.
Speaker: And some people may have acute and chronic.
Speaker: We haven't talked about that.
Speaker: Probably we have to keep advancing this conversation like we talk about grading.
Speaker: So like in acute, when people have sepsis, they come and they have acute vasoplegia.
Speaker: Or people who get cardiac surgery, especially who get cap plus valve are more prone.
Speaker: These are the more pronounced.
Speaker: But in hemorrhaging shock, in surgery,
Speaker: And then we often don't recognize or we don't talk about it.
Speaker: Some people may have a chronic vasoplasia going on, like people who have cirrhosis.
Speaker: So if I have to put as a bad side for ICU people, I think sepsis and cardiac surgery.
Speaker: And if you have a patient who have a renal failure or cirrhosis, you have to be very vigilant about it.
Speaker: Excellent.
Speaker: And in terms of a very practical question as we start a deep dive in our clinical discussion, why should a bedside critical care clinician care about vasoplegia?
Speaker: You know what the reason is that simple as that, that it increased mortality.
Speaker: And this is an independent risk factors.
Speaker: Vesoplasia is independent of any other risk factor.
Speaker: It can increase mortality.
Speaker: And it was proven in 1998 article came out and it says that, and we have put in our reference that it can increase mortality up to independently 25%.
Speaker: And going forward, 25%.
Speaker: two decades in 2018, though the study was done for the LVET patient, but they found that those LVET patients who develop mesoplasia can have actually double the mortality in comparison to other LVET patients.
Speaker: So this is just the right writing on the wall that increased mortality.
Speaker: On top of that, every time we have a sick patient who goes on pressers, we know that it increased length of stay and sometimes they get acidotic.
Speaker: and they become tachypneic and we intubate them, so mechanical time.
Speaker: So the mortality, morbidity both goes remarkably up if we don't recognize vasoplegia early and if we don't treat it early.
Speaker: Perfect.
Speaker: In terms of, you mentioned LVAT patients.
Speaker: Could you tell me a little bit about what are some of the known predisposing factors for vasoplegia or risk factors for vasoplegia after cardiac surgery?
Speaker: Right.
Speaker: Unfortunately, the cardiac surgery patients are more prone to vasoplasia because they already carry the risk factors which are known for the vasoplasia.
Speaker: These are the patients who are before surgery, pre-cardiac surgery, maybe on AC inhibitor.
Speaker: which is very much used for the afterload reduction.
Speaker: If they have some sort of cardiomyopathy, and cardiologists have put them on AC inhibitors.
Speaker: And if they have some sort of cardiac failure, CHF, they may have some underlying renal insufficiency.
Speaker: That also makes them prone to go into that.
Speaker: Plus, on top of that, when they go for the surgery, if they have a...
Speaker: pump time outside of and studies have shown that once whenever the pump time goes more than 180 minutes it can increase because the blood is in contact with the pump pipes and all the cannulas which does not have endothelium so it can increase the chances of having vasoplasia
Speaker: So these are the these patients, unfortunately, and I talk about AC inhibitors and studies have shown that beta blocker can also cause going forward in post cardiac surgery can cause vasoplasia.
Speaker: So these patients are prime.
Speaker: to have vasoplegia with preoperative taking with the AC inhibitor, beta blocker.
Speaker: They may have some sort of renal insufficiency.
Speaker: They may go into a long pump time.
Speaker: And on top of that, if this cardiac surgery patients are getting dual surgery for valve and cap together, that by itself sometimes increase the pump time.
Speaker: And so they are very prone.
Speaker: And unfortunately, they are sitting at the perfect target to be vasoplegic.
Speaker: So in general, really, I mean, for our patients undergoing cardiac surgery, those that have more risk factors, which are, like you said, are more and more common in this population, are going to be at a higher risk.
Speaker: So it's important to be vigilant about these patients.
Speaker: Iqbal, could you give us a high-level overview of some relevant pathophysiology related to vasoplegia after cardiac surgery?
Speaker: You know what, this is an interesting question.
Speaker: And as soon as more I read about vasoplegia and I look into the pathophysiology, sometimes I question myself that vasoplegia after cardiac surgery, vasoplegia after sepsis, are they, vasoplegias are completely different.
Speaker: And if I look into their pathophysiology, it is so complex.
Speaker: Sometimes I question myself,
Speaker: that are these different diseases even and we are just using vasoplegia as a one umbrella term to cover all of them there may be a different pathophysiology for each different subset like cardiac surgery sepsis or even we talked about anaphylaxis and cirrhosis this
Speaker: This is the most complex pathophysiology of vasoplasia I can think of, of any other disease, because so many things are involved there.
Speaker: It is one thing which we need to understand that this is the pathophysiology coming from the endothelium of the vessel wall.
Speaker: And whenever there is a damage or any inflammation or any kind of insert to the endothelium wall that start the cascade.
Speaker: And one thing which I always try to tell students that every time when people talk about vasoplegia and they talk about the pathophysiology of vasoplegia, they always mention nitric oxide.
Speaker: But if you remember, and I always tell my students that always pay attention to the terminology, always pay attention to the nomenclature, the actual, and in the beginning with the nitric oxide, it was referred as an endothelial-drived relaxing factor.
Speaker: And if you pay attention to that nomenclature of nitric oxide, endothelial drive, and I'm repeating it because it's important, endothelial drive relaxing factor.
Speaker: So whenever there is an insert, nitric oxide level goes up.
Speaker: And as the name said, it increase, it relaxes the vessel.
Speaker: And
Speaker: The other important factor is that this nitric oxide diffuses into the neighboring smooth muscles and cause the vasodilatation.
Speaker: And with simultaneously, there are a lot of other things happening, platelet activation, leukotriene addition.
Speaker: And then we have vasopressin, arginine vasopressin activation.
Speaker: And these all end in potassium pump and calcium pump,
Speaker: All those get activated and this caused start having decreased SVR.
Speaker: That would be see that people start having dilatation of the vessel and that caused decreased SVR, decreased blood pressure and cardiac output goes up.
Speaker: And then when all this thing happened, pathophysiology does not stop there.
Speaker: there are, it became a cascade where interleukin-6 and interleukin-8 goes up and they cause the impaired LV function causing more problems.
Speaker: And that's how all this negative cascade just keep going on and on
Speaker: with the negative feedback and the cycle never stops.
Speaker: And that's why the vasoplegia is one of the disease which is hard to sometimes treat because once this cascade of inflammation goes on, it just create a cycle which you have to break when you are treating the patient.
Speaker: And as you mentioned, I think in particular with our cardiac surgery patients, exposure of the blood to the artificial circuits, the surgical trauma itself, organ ischemia, ischemia reperfusion injuries that are common in these surgeries can all lead to also release of endotoxin from the gut and from the vessel, which usually, I mean, exacerbates this problem.
Speaker: The other thing that I read, and I don't know, I mean, if you could comment, if this is something that has been studied, is
Speaker: that also there's a common practice of using CellSaver, which is giving blood back to the patient, and that blood might be hemolyzed, and that might also exacerbate this inflammatory cascade.
Speaker: Any thoughts on that?
Speaker: Indeed, indeed.
Speaker: And I should take the blame for it that we did not mention that in our article, which we should have.
Speaker: And I wish reviewers would have asked us to, but this is absolutely true.
Speaker: Whenever you use and hire the amount, the self-saver,
Speaker: higher the amount of cell saver, it can also.
Speaker: And that also tells you when the cell saver volume is higher, it means that patient has more bleeding during the cardiac surgery.
Speaker: And patient may have a hypotension or more pump time.
Speaker: And patient may have a blood transfusion.
Speaker: These all have created another stage with actual pathophysiology to cause the vasodilatation and vasoplegia in the cardiac surgery.
Speaker: Iqbal, this is, I think, a great overview to lead us down to what we really care about, which is management.
Speaker: What do we do at the bedside?
Speaker: And I think that part of the challenge with these patients is that it is not uncommon for patients to come out of the OR after cardiac surgery into the ICU and have hypotension, require either fluids, require a little bit of vasopressors, but not all of them in our mind are deemed as vasoplegic syndrome.
Speaker: So why don't we talk about the management and maybe we can start with ensuring adequate preload and cardiac output and then move on to how you would treat patients that become more and more difficult to treat despite that.
Speaker: Right.
Speaker: In cardiac surgery patient, one of the challenges is that they may have some kind of cardiomyopathy.
Speaker: So you have to be careful.
Speaker: And people, we did one review article on treatment of congestive heart failure.
Speaker: And as a treatment on the first number one, we put IV fluid.
Speaker: And one of the questions we got from the reviewer that if patient is in heart failure, how it can be, volume could be the treatment.
Speaker: But people don't realize that uvolemia, we target negative balance in congestive heart failure when people are volume overloaded.
Speaker: This patient may still be in the negative balance and may still need to travel towards uvolemia.
Speaker: So first thing we do is resuscitate with IV fluid, with the hemodynamic management, hemodynamic measurement.
Speaker: Now, people always think of hemodynamic measurement, and I know that you have spoke about maximalist and minimalist approach toward hemodynamic monitoring in the past.
Speaker: But I think a good clinician does not need a lot of tools to have a hemodynamic measurement knowing that it's uvolemia.
Speaker: Like a simple passive leg raising can tell you a lot of things.
Speaker: But if you have an A-line, which you usually have in the cardiac surgery patients, all this weaving of the A-line with drop of systolic blood pressure with inspiration and expiration will...
Speaker: tell you that patient is volume deficient.
Speaker: So first thing is definitely volume resuscitation.
Speaker: And once you assume that, or once you are satisfied that the enough volume has been given and still patient is hypotensive and SVR is low, if you have a swang and scatheter, pulmonary artery catheter in place, and if not, then if it's your clinical judgment, you know that enough volume is given, then you go towards the pressers.
Speaker: Now, talking about the pressers, we have a first line as norepinephrine, but we found that vasopressin sometimes works better or maybe in combination with norepinephrine works better.
Speaker: So our clinical approach is that start norepinephrine and if we don't see much response by five or six mice, we actually, especially in a cardiac surgery patient, we are quick to add vasopressin and norepinephrine
Speaker: and that's where we see the response many times and we have other pressers available too we have dopamine which is now almost going out of the practice but we have phenylephrine which we use many times so we have used all this traditional but in terms of dosing if we see
Speaker: norepinephrine is nothing doing up to five or seven mics we quickly add vasopressin now problem with vasopressin for us is that we have only one trial available vast trial which shows which was done with the dose of 0.03 and uh studies uh one study published in 2005 in intensive care medicine uh from europe showed that beyond 0.05 it can cause coronary ischemia misandry ischemia so with vasopressin you have to walk a very fine line
Speaker: uh when you are talking between evidence-based medicine and patient-based or personalized medicine we usually go up to 0.04 or many times i have to write order in the chart that no escalation beyond 0.04 without md approval but that's how we start our management that we go with this is the first line management we go with volume resuscitation and we see that still the blood pressure is low and
Speaker: we need to work towards the vasodilatation or vasoplegia.
Speaker: We go with norepinephrine and very low threshold to add vasopressin.
Speaker: And I think an important aspect that you mentioned earlier in the definition is that you would anticipate in these patients, if you have invasive monitoring, which is more common after cardiac surgery than some of our other patients, you would be able to document the low SVR and the high or normal cardiac index, right?
Speaker: Suggesting that volume is not the issue anymore, right?
Speaker: And the way I understand what you were saying about the catacolamines is you start with norepi, which I think most of us agree based on the available data should be first line for most situations, especially outside of cardiac surgery.
Speaker: But it sounds like in this particular case, early use of vasopressin, right?
Speaker: Adding that very quickly is a good idea.
Speaker: And that's what we should be thinking of.
Speaker: Right.
Speaker: And this is where the translation medicine and bench side to bedside.
Speaker: When we look into the pathophysiology earlier, we were talking and the increase and the vasopressin receptors, downgrading of vasopressin receptors in the endothelium that bring this practice of using vasopressin early in the course in comparison to other hypotension situation.
Speaker: So we have a low threshold for vasopressin and if nor epi and vaso is not working.
Speaker: And that's why I was talking that we haven't talked in our quest for the treatment for the vasoplegia.
Speaker: We haven't talked about the grading.
Speaker: We haven't talked about the types of vasoplegia, which we need to be now.
Speaker: We should have been done by this now.
Speaker: So if that doesn't work, then we go to the second line of treatment for the vasoplegia.
Speaker: And in terms of targets, I presume we use the usual targets of targeting a mean arterial pressure of 65 and above.
Speaker: Is that usually what you're looking at?
Speaker: you know what i'm glad sir you ask it just yesterday just yesterday we had a discussion about that and i was talking to ashish khanna he has done a lot of work and kind of an expert in uh blood pressure and then this is a this is and we uh this is the time that like we have optimum peep on ventilator
Speaker: We need to know that every patient has its own optimum MAP, mean arterial pressure.
Speaker: So personally, I believe that the era of targeting MAP of 65, we should stop thinking about it.
Speaker: Every patient, every clinician should establish, and that's what we were debating, are we ready to establish a model where every patient can have his own MAP?
Speaker: And there's one study right now in Australia and New Zealand going called REACT shock, which is working towards that to see that what could be the optimum map for each patient.
Speaker: And that's the hardest part, I think, in vasoplegia, that some patients may have their map very well.
Speaker: Some patients who are cirrhotic and living their life and establish their map around 55, 60 even,
Speaker: they may just need a MAP of 60 or 55.
Speaker: And some patients may need who are hypotensal of their life.
Speaker: They may need a MAP higher than 65.
Speaker: So it is actually more the perfusion of the organ which determines the MAP rather than one arbitrary number of 65 blanketing on the patients.
Speaker: Yeah, and I think that's a great point, Iqbal.
Speaker: I think we all like simplicity, and it's easy to say 65 and above.
Speaker: But you're right.
Speaker: I think as we develop more and more tools, we might be able to do it in a more sophisticated way.
Speaker: But that doesn't take away that we should, from a conceptual framework, think of or ask the question, what's the optimal MAP for my patient that I'm treating right now?
Speaker: And there are many surrogates that we can use to try to figure that out.
Speaker: And I think it just illustrates once again in medicine that having the right questions is really what drives better patient care.
Speaker: So I think that's a great point.
Speaker: So what happens when we are...
Speaker: done with conventional vasopressors such as catecholamines and vasopressin and we're still having trouble so we gave fluids we optimized that we gave catecholamines we gave vasopressin and what are some of the non-conventional vasopressors or therapies that have been proposed for the treatment of vasoplegic syndrome
Speaker: One of the, now has become for us in our institution, and I also go with that and favor that is the hydroxycobalamin, which is vitamin B12 in simple words.
Speaker: We give a bolus of 5,000 units right away there, and it's called cyanocid in pet site, as how it is supplied by the pharmacy and known as a brand name.
Speaker: So we use the word a lot, cyanocid, but it is hydroxycobalamin bolus.
Speaker: And we have seen that it has worked better for us just a few years ago and still in many institutions, the practice is to use the methylene blue.
Speaker: as a bolus and then as a drip but the thing is that over the last two three years i'm moving away from methylene blue for a reason and the reason is that many patients who are coming to the hospital for the elective surgery like a bypass surgery many times they are using a lot of antidepressant and ssris
Speaker: And at least I have encountered two for sure and third maybe with the serotonin syndrome because either it got missed or overrated and nobody thought about it and patient was given methylene blue.
Speaker: And we have seen severe cases of serotonin syndrome.
Speaker: Personally, I found the cyanokate is more effective and has less interaction with other medications.
Speaker: So if we persistently see that despite giving volume, despite giving two pressers, some of our patients who have some cardiac insufficiency, our NECDF folks have started epi, so they're already on three pressers, epi, vaso, nor epi, and still have a lower MAP, low SVR.
Speaker: then our first line, and I think that that's better than methylene blue, is cyanocid, hydroxycobalamin.
Speaker: And if that doesn't work, the chances of methylene blue working, it's low.
Speaker: And that's where you are encountering refractory vasoplegia.
Speaker: But people have used two doses of cyanocobalamin, and if that doesn't work, have tried as a methylene blue after that.
Speaker: now talking about uh when all this uh if cyanokate is not working methylene blue is not working we have another uh in our armor we have another drug which is called angiotensin 2. the trade name i don't know you allow us to use uh trade name here or not but it's called geopresa and i usually call it angiotensin 2. angiotensin 2 is well known
Speaker: for a long time and the reason I think it works also well in cardiac surgery patients though our study is done on the more on the septic patient because in the pathophysiology of vasoplegia there's a lot of role of renin angiotensin aldosterone cascade which we call it a ras cascade and that's why the ac inhibitor is also a risk factor for the post-cardiac surgery patients
Speaker: So angiotensin II, we have used it with success as a, when the even cyanocobalamin and when the methylene blue is not working.
Speaker: So we have used angiotensin II.
Speaker: Said all that, said all that, talking about all the treatment from IV resuscitation to talking about the angiotensin II, if you ask me what you need
Speaker: you need a lot of patience and time is actually the greatest healer of the vasoplegia that sounds very uh uh philosophical or but i think that you have to just uh stay on top of the things that when you keep perfusing the organs
Speaker: And as one of the anesthesiologists from Africa, I was visiting Africa, and he said that your best management could be a poor menswongens catheter, and poor menswongens catheter, he meant the urinary output.
Speaker: So as far as your organs are perfusing and you keep trying, eventually the vasoplasia takes a lot of time.
Speaker: That's a good point.
Speaker: And I think that with these non-catecholamine agents or let's say non-conventional, I just want to emphasize a couple of things that you said.
Speaker: First and foremost is that it's the hydroxycholamine that you go to first.
Speaker: It's five grams, I guess, infusion, right?
Speaker: And you might repeat it one time.
Speaker: So that's not titrated.
Speaker: It's a one-time dose trying to replenish it.
Speaker: or try to inhibit your granulocyclase and your endothelial nitric oxide production, right?
Speaker: So it's a one-time thing or two-time thing.
Speaker: The other thing you mentioned, Iqbal, that I think is super important is you mentioned angiotensin 2, which is approved for refractory shock.
Speaker: I mean, we can use it in this conversation, obviously, commercial names because there is no other angiotensin 2 right now.
Speaker: It's just, I mean, the commercial one available.
Speaker: A lot of our pharmacy colleagues have been a little bit shy with that just because of pricing, right?
Speaker: And I think it hasn't been shown to be any better than what we usually use.
Speaker: But when those conventional vasopressors are not working, this might be something that you use.
Speaker: And it's a angiotensin one agonist, which seems to be inhibited in basal plagic syndrome.
Speaker: So it makes it makes sense to try that.
Speaker: And that you I guess that that's a continuous infusion, right?
Speaker: You start, I believe, at 20 nanograms per kilogram per minute, and you infuse titrated to MAP, correct?
Speaker: Right.
Speaker: And then you can, if 20 is not working and you go to 40 and if 40 is not working, you can go to 80.
Speaker: Here, one thing I will say that one thing, and that was coming from the conversation yesterday with my colleagues, is that if people have to respond to angiotensin 2, you will see some response in the beginning.
Speaker: We go from 20 to 40, we go from 40 to 80, but if you are not seeing response at 20, the chances are that you might not see that response at 40 or 82, and that patient may be refractory to angiotensin and some other underlying pathophysiology is going on.
Speaker: So I start dreading myself when norepinephrine and vasopressin combination doesn't work for me.
Speaker: I know that I'm on a long haul for that and there is some different pathophysiologies there and I may be going a long course here.
Speaker: The other thing that I wanted to reemphasize was a little bit on the methylene blue in terms of just because I think a lot of people probably remember methylene blue associated to vasoplegia.
Speaker: And like you mentioned, Iqbal, the...
Speaker: The literature doesn't, we don't have any good studies to say, oh, this is what we should use, right?
Speaker: There's anecdotal reports.
Speaker: But what you mentioned, I think, is super important that often clinicians who don't use it frequently forget is that it is associated with real side effects, right?
Speaker: And that you mentioned the serotonin syndrome, which has been well described and with an increase in many of the outpatients, like psych medications, that it can be something we have to be very careful with.
Speaker: I also believe in people who have a 6GPD deficiency, it can cause severe hemolysis.
Speaker: That is something that we usually don't think about, right?
Speaker: And I think the other thing that people forget, which is a problem that you already mentioned with vasopressin, is that it can cause significant splatonic, vasoconstriction, and ischemia.
Speaker: And that can just add, I mean, problems to our patients.
Speaker: But when you do use methylene blue, how do you dose that?
Speaker: We usually give a bolus dose of 120 to 150 microgram, and then we just continue the drip.
Speaker: And I usually ask my pharmacy colleagues to help me out there.
Speaker: Now, other thing, which, as you mentioned, which we don't think about it, that many of our patients in our institution and many tertiary institutions, there's a lot of use of INO, intrinsic nitric oxide.
Speaker: for when patients having a RV failure or patient having a high pulmonary pressure.
Speaker: And when you use INO with methylene blue, it negates the effect of each other.
Speaker: So that's another thing people in tertiary care centers, the intensivists who are working in tertiary care centers, they have to be mindful that if INO is on board, you probably better avoid the methylene blue.
Speaker: Perfect.
Speaker: So we talked about conventional catecholamines after fluids optimization.
Speaker: We talked about non-conventional vasopressors, hydroxycholabalamin.
Speaker: Can you make some comments, other things that I know have been mentioned in the literature, and I just want to know your thoughts are hydrocortisone or corticosteroids and vitamin C, which seems to never go away.
Speaker: What are your thoughts and where do we stand on those today?
Speaker: That's true.
Speaker: And this is the treatment which I call adjuvant treatment or the simultaneous treatment while you are working with pressers and you are working with cyanocate and all this thing.
Speaker: Most of this patient when come out of the cardiac surgery, they have they have available the NG tube.
Speaker: So personally, if I see that I'm going towards refractory vasoplasia, I start midodrine.
Speaker: And steroid, you know that it's a topic where half of the intensivists are pro-steroid and sometimes you find people half are anti-steroid.
Speaker: And when you are managing post-surgical patients, especially post-cardiac surgery patients, you might not even have sometimes time to send a lot of labs.
Speaker: So in that kind of situation, I have used many times hydrocortisone and just only 50 to 8 hours.
Speaker: And if I know the patient has a renal failure, I have used Florine F also.
Speaker: So these are all simultaneous treatment.
Speaker: We don't know, truly speaking, they work or not.
Speaker: And because they are simultaneous and adgen treatment, we don't know the pressers are making it better.
Speaker: Our cyanocobalamin 5-gram bolus is making patient better.
Speaker: after immediate acute hours, passing 12 hours, passing eight hours, mid-ordrain and maybe hydrocortisone just for 24 or 48 hours, six doses of 50 milligram Q8 hours, it helps to sustain what we have achieved.
Speaker: So I use personally in my practice, if I have refractive vasoplasia, hydrocortisone, I have used mid-ordrain and if renal failure patient, I have added fluorine F, I have done that.
Speaker: As far as vitamin C, when it came out, there was a lot of waves and a lot of talk about it.
Speaker: I have seen a lot of blogs, both in favor and both against vitamin C. And we have mentioned in our article also about the vitamin C.
Speaker: But if you ask me that question, if you have asked me the question when we were preparing that article, I would say that, yeah, if nothing is working, use vitamin C. But after that, we have studies which have shown, and now it's pretty much settled the issue that vitamin C doesn't work.
Speaker: So I may have used one time or two times when it comes out and I was in a situation of refractive with the plagia, but I stopped using it and I will not advise.
Speaker: And we still, I will say that that's how our learning ramp is.
Speaker: That's first we get and we have been in critical care with this learning ramp so many times with so many things.
Speaker: I don't want to bring a lot of past stuff we have learned by our failures.
Speaker: But I will say that this is one of the thing which is we tried, we failed, and I will not go to worse.
Speaker: Personally, I don't think that I think with all these studies coming afterwards, the issue is centered that vitamin C doesn't help.
Speaker: And it's a large dose.
Speaker: It can cause more renal.
Speaker: It can cause actually harm.
Speaker: That's how I see it.
Speaker: I will not use it.
Speaker: Perfect.
Speaker: So I think that really very interesting discussion, Iqbal, you gave us a lot of good advice here.
Speaker: As we close, are there any pearls or pitfalls you want to make sure we reemphasize for our clinicians?
Speaker: One thing which I always tell people that don't treat numbers, treat the patient.
Speaker: You will have a swan-gan's catheter, which is itself maybe having a lot of artifact going on there.
Speaker: If somebody put the numbers on the monitor wrong, you may have wrong numbers there.
Speaker: So, numbers are there to help you.
Speaker: But seeing the patient, seeing that patient is clinically doing simple stuff, like patient is making urine, patient blood pressure looks better, those simple vitals.
Speaker: So, use your clinical judgment rather than going towards only one number.
Speaker: So, that's number one thing.
Speaker: Unfortunately, with the advent of the numbers, and we are getting more and more hooked to the computers,
Speaker: we are doing less and less physical exam.
Speaker: So frequently, especially in this subset of patients who are vasoplegic, going to the patient bedside, putting your hand on patient pulses on the periphery, on DP pulse radial, putting your hand on patient belly that is soft.
Speaker: looking into the listening to the heart sound looking into the heart rate all these things so more physical exam and treating patients that would be my simple advice but I think this goes a long way you did mention at the beginning and through our conversation Iqbal that obviously there's still a lot that we have not figured out with this particular clinical syndrome of
Speaker: basal plegia after cardiac surgery.
Speaker: Any comments on what you're excited about or any studies that are ongoing for the future or things that we really need to figure out?
Speaker: Right.
Speaker: So yesterday I was talking to one of my colleagues and they are interested asking us to join.
Speaker: It's called the REACT Shock Trial, which is based in Australia and New Zealand.
Speaker: And that's what they are trying to look into the optimum map.
Speaker: That's one I'm very excited about.
Speaker: And the second one, which going forward, I think we need to figure out either by studies or either by doing some lab work that
Speaker: I see that if I get a response to the presser early in the course, this vasoplegia is reversible.
Speaker: So we have to come up by this time working together, finding some grading of the vasoplegia, grade one, grade two.
Speaker: So it guides clinician like grade one if patient responds to low dose of pressers.
Speaker: and grade two if patient does not respond to presos but respond to cyanocobalamin or grade three or grade four where everything is refractory so we have to come up with some grading we can work with society of critical care medicine or other societies and but we need to work a lot more on that side but i'm very excited about the shock trial which may happen at australia and new zealand
Speaker: Perfect.
Speaker: Well, I think that this has been a very instructive conversation on a topic that maybe not all our listeners are super familiar with because they might not have the volumes that you manage at your institution.
Speaker: Iqbal, so I really appreciate you sharing your expertise.
Speaker: But as we close, we would like to ask you a couple of questions that are unrelated to the clinical topic.
Speaker: Would that be okay?
Speaker: Oh, absolutely.
Speaker: Excellent.
Speaker: So my first question relates to books.
Speaker: Is there a book that has influenced you significantly or books that you have gifted often to other people?
Speaker: You know what?
Speaker: One book which I advise all of my students who walk into the ICU and they ask me and many times I got this question from students which book they should read.
Speaker: So I give them two advice.
Speaker: One book which I consistently tell people to read and have it is Manual of ICU by Dr. Marino.
Speaker: That one book in the beginning of my career helped me.
Speaker: And it is very simply written and easy to understand critical care.
Speaker: But going forward, I have realized that now the way our medical literature has evolved
Speaker: manage the information rather than getting the information garbage in garbage out as they say so we have so much resources now available and everything is available on the our hand tip with our cell phone you can quickly google stuff you can quickly see things you can go to the up-to-date you can look into the pub match so learn the most important
Speaker: skill I think being a clinician for us to is to learn to manage the information that which informations are important which are relevant and unfortunately lot of since anyone can now publish there's a lot of junk going on inside our literature so to know that which information to target which to read and which not to read that's extremely important
Speaker: One book which lately I will say that I was reading and I was very much impressed.
Speaker: One thing which we don't pay attention is a concept called pathography.
Speaker: Pathography is a concept where you try to see the disease from the patient perspective.
Speaker: And lately we have seen a book coming out from Dr. Eli who has done a lot of work in delirium.
Speaker: He did deep down breaths.
Speaker: So thinking of disease from the patient perspective or the shock, the book Shock came out from one of our colleagues from
Speaker: Cincinnati she was in hemorrhaging shock and was admitted in ICU and she wrote a book about her experience so I think lately the concept of pathography and the books which depict the experience from patients perspective is really something giving me more passion about the patients
Speaker: Excellent.
Speaker: And we'll definitely link all these recommendations in the show notes.
Speaker: The second question is about, they say that the measure of intelligence is people who are able to change their mind when they're faced with new information.
Speaker: Could you share something that you changed your mind about over the last couple of years?
Speaker: I have done it.
Speaker: I have done it.
Speaker: When I started my career, I was very much sold out to the evidence-based medicine.
Speaker: But as I evolve and as I start, I learn two things.
Speaker: One is that it is
Speaker: very important to know on the bedside what to do and we spend last one hour talking about what to do when the vasoplagia happens.
Speaker: But I also am learning over the time that it is also very important as a clinician for us to know what not to do.
Speaker: And sometimes we do things just because we somebody said so and we can harm the patient.
Speaker: So that's number one lesson.
Speaker: Number two lesson is that your clinical judgment is extremely important.
Speaker: You have all the resources, you have all the numbers, and we are spoiled in United States and especially where I work in a medical center, we have a lot of resources, medication, everything on our hand tip available.
Speaker: But your clinical judgment should supersede
Speaker: and as you get experience and there is a word for it that's called factor of extra information being a physician you have with your experience of extra information which sometimes you can't explain so more and more work towards putting everything together patient your clinical judgment and your numbers just not go fit only one thing that what I am evolving
Speaker: And I think to your first comment that you made of doing things like that, that almost bias we have to do things and say, well, what do we have to lose?
Speaker: Well, you gave a perfect example with methylene blue.
Speaker: If you develop a certain ergic syndrome, you just made a bad problem worse, right?
Speaker: So you do have complications and doing things does have a price often for our patients, right?
Speaker: So I think that being a little bit more cautious and thinking about that is also very important.
Speaker: So I think those are excellent, excellent lessons for the audience.
Speaker: And to close our conversation, is there anything you would want every listener, every intensivist listening to know?
Speaker: Could be a quote, a fact, or just a thought.
Speaker: You know what, I always think of a quote from Carl Sagan, and he is a Cosmos person, and he has sent a beautiful thing, and I always think about when I'm on the bedside, that absence of evidence is not the evidence of absence.
Speaker: So that's a very profound quote that sometimes if we don't see anything, it doesn't mean that it's not there.
Speaker: And the most frustrating thing for a clinician is to not know that what he's dealing with.
Speaker: So being a clinician, my advice is that that continue to even sometimes we have we just think in our mind, I will just give a simple example that patient come with acidosis and patient is diabetic.
Speaker: And we just before seeing patients, sometimes we make up our mind that patient has a decay.
Speaker: It may not be a decay.
Speaker: It may be
Speaker: the preconceived notion or making judgment very quickly on the patient on the diagnosis.
Speaker: Continue the treatment, continue the management, but continue to look for something which you may be missing.
Speaker: So be on constant strive and one in this regard, I give one advice to all my students.
Speaker: We all have CV of success, but going home every day, driving back, also think that what you have not done right today, what you could have done better.
Speaker: So it is being a clinician, the best thing you can have is the satisfaction in your heart that you have the patient, you did something right.
Speaker: But it's also important to know that what you haven't done right, what you could have done better.
Speaker: And that's called CV of failure.
Speaker: So knowing your CV of failure is also important.
Speaker: Iqbal, I want to thank you for a wonderful conversation, for sharing your time and expertise.
Speaker: I think this is the perfect place to stop.
Speaker: I hope to have you back soon.
Speaker: Okay.
Speaker: Thank you, Sergio.
Speaker: It was a great pleasure talking about this topic, which is very near to my heart.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound's transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
