Transcript
Speaker: Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound Critical Care 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: Acute severe elevations in blood pressure can cause significant morbidity due to organ injury.
Speaker: Furthermore, elevations in blood pressure are commonly seen in the hospital setting and are often mismanaged by clinicians.
Speaker: In today's episode of the podcast, we will discuss the latest evidence, the proper management, and potential pitfalls of acute severe hypertension.
Speaker: Our guest is Dr. Aldo Peixoto.
Speaker: Dr. Peixoto is a professor of medicine in the section of nephrology at the Yale University School of Medicine.
Speaker: He is also vice chair for quality and safety, Department of Internal Medicine, and clinical chief of the section of nephrology.
Speaker: His research interests include secondary and refractory forms of hypertension.
Speaker: He has published more than 100 peer-reviewed articles and book chapters in nephrology and hypertension, and is the author of a book on bedside diagnosis.
Speaker: He is an associate editor of Blood Pressure Monitoring and is on the editorial board of the American Journal of Nephrology and the Brazilian Journal of Nephrology.
Speaker: Dr. Peixoto is a recognized clinician, researcher, and medical educator.
Speaker: We are honored to have him as our guest.
Speaker: Aldo, welcome to Critical Matters.
Speaker: Thank you very much.
Speaker: It's a pleasure to be here, Sergio.
Speaker: So I think that we could maybe start by just if you could give us an overall introduction to acute severe hypertension in terms of is it frequent, what do we know about it today, and then maybe we can start diving into some of the definitions.
Speaker: Sure.
Speaker: So acute severe hypertension, which is the term that I chose to borrow from others to define both or to include both hypertensive emergencies and urgencies, and we can define them a little better in a second, is broadly described a blood pressure that's over a certain threshold, and the arbitrary threshold that's being used is 180 for systolic
Speaker: and either 110 or 120 for diastolic.
Speaker: This is very common.
Speaker: It's a very common cause of visits to emergency departments throughout the world.
Speaker: It's a very common cause for admissions, and it's a problem that is of interest to emergency physicians, critical care specialists,
Speaker: cardiologists, hospitalists.
Speaker: So I thought it was a very, always have thought of it as a very important topic to discuss.
Speaker: Absolutely.
Speaker: And I think it's one of those things, as we'll see, that even though we see frequently and we encounter a lot, often gets mismanaged in both directions, both over and under treatment.
Speaker: And I think that centralizing or focusing on some of the basic concepts that can guide our therapeutic conduct, I think, is always a good place.
Speaker: So could you give us, Aldo, maybe a little bit more precise definitions?
Speaker: And you did mention a little bit when you talked about the umbrella of hypertensive crisis and some numbers that, as you said, are arbitrary.
Speaker: But I think an important distinction really has to do with hypertensive emergency and everything else, or what some people call hypertensive urgency.
Speaker: How would you define these two?
Speaker: Very good.
Speaker: So if we start with a certain value, let's pick 180 over 120.
Speaker: And then the next step is really to define whether there is acute target organ damage.
Speaker: So if there is acute target organ injury, we call that an emergency.
Speaker: If there is no acute target organ damage, then it becomes an urgency.
Speaker: and so so it's important to define number one that the target organ injury is acute not chronic and obviously it needs to be an injury to an organ that's typically affected by hypertension and and that is the brain the heart the large vessels the kidneys the microvascular and one include would include the findings in the retina as part of this uh microvascular injury so
Speaker: If there is evidence of acute brain dysfunction, and whether that is due to an acute stroke, an acute intracerebral hemorrhage, or hypertensive encephalopathy, or if there's evidence of acute cardiac involvement, such as an acute coronary syndrome or acute decompensated heart failure, involvement of large vessels, and that's predominantly acute aortic dissection, acute renal involvement, so
Speaker: acute renal failure caused by severe hypertension.
Speaker: Chronic kidney disease can be caused by hypertension, but here it's important that it be recognized as an acute problem, which is typically part of microvascular involvement, which can be diagnosed either by the changes in the kidney that can happen acutely or by microangiopathic hemolytic anemia or by some of the findings in the retina, such as the acute
Speaker: retinopathy changes such as hemorrhages, exudates, and ultimately papilledema.
Speaker: So when these findings are present, findings of acute target organ damage exist, then we label those patients as having an emergency.
Speaker: And that has pretty significant implications to what we do with those patients.
Speaker: Those patients belong in the intensive care unit.
Speaker: They should not be managed on the floor.
Speaker: they should be treated promptly with IV drugs.
Speaker: And, you know, you're going to select the drugs according to the specific indications.
Speaker: You're going to lower the blood pressure following a pattern.
Speaker: I think we'll get to that later in our conversation.
Speaker: But what's important is that those patients be at a high level of monitoring, that they be treated with IV drugs.
Speaker: Most of them should have
Speaker: an arterial line to monitor their blood pressure.
Speaker: And this is a very select group of patients that really require aggressive therapy.
Speaker: In the absence of acute target organ damage, then that's when we can actually do harm by over-treatment.
Speaker: And in those patients, the approach to therapy is different and should focus
Speaker: on the if the patients have symptoms related to the blood pressure, let's say patients have a headache, patients have a let's say epistaxis, something that's that's acutely bothering them, we might want to try to control their blood pressure a little faster just to make them feel better.
Speaker: But the the ultimate goal is really to adjust longer acting medications,
Speaker: So, and obviously through oral therapy, not intravenous therapy.
Speaker: And those patients very often don't belong in the emergency room, don't belong in the hospital, but they need to receive intensive outpatient therapy.
Speaker: And I think that this is an important paradigm that is not followed that frequently.
Speaker: And that's a point that I always think is important to make.
Speaker: Absolutely, and I think that one question I have regarding the term of hypertensive urgency, I know that I've always found the construct useful, especially in explaining to others, but also in terms of my therapeutic approach.
Speaker: But I do know that lately it has become or fallen in disfavor, and some people really just say, focus on the emergencies.
Speaker: Everything else is just hypertension.
Speaker: Any comments on that, Aldo?
Speaker: I think that that's the big push for that is because if you hear urgency, it still has an urgent tone to it, right?
Speaker: And what ends up happening is that people think that those patients should be sent from the office to the emergency room, should be brought in from the emergency room.
Speaker: into the hospital, from the emergency room into the hospital, sometimes even into a step-down or ICU unit.
Speaker: And that's why the name has, the term has been, it has been proposed that they, that it not be used because those patients really should be treated as outpatients in a fairly aggressive way, but still as outpatients.
Speaker: And with that, I fully agree.
Speaker: Whether changing terminology will help in moving that agenda forward and changing the paradigm, that's arguable.
Speaker: I decided in writing recently about this, I decided to maintain the term urgency just because it's easier to drive the discussion, not because of one thing or another.
Speaker: I would not oppose that.
Speaker: eliminate this focus on emergencies and eliminating the term urgency and just defining the fact that if someone has a blood pressure that is at that kind of level, that the management in the outpatient setting should be done in a fairly intensive way.
Speaker: Absolutely.
Speaker: And I think that it's just important also to be coherent with our treatments.
Speaker: And I think that one of the pitfalls I often see is not recognizing
Speaker: that somebody has acute organ damage and not implementing the appropriate therapies.
Speaker: And then the other extreme is over treating people who don't have acute organ damage and be putting them at risk for damage from our treatment.
Speaker: So you talked about the two elements that define the hypertensive emergency, which are an elevation in blood pressure and the presence of acute organ damage.
Speaker: Could you talk a little bit more, Aldo, about proper measurement of blood pressure?
Speaker: which I think, I mean, is the first step, obviously, in terms of trying to figure out if somebody's hypertensive.
Speaker: I think that that is a major issue because at very high blood pressure levels, and when you start seeing systolics above the 180 range and diastolics above 100 to 110, the
Speaker: validating protocols that are used to validate most oscillometric devices that we use in most hospitals, emergency rooms and offices, those protocols don't hold as well because it's hard to find people that walk around with blood pressures of 220 over 120 in the ambulatory setting to participate in the study.
Speaker: So the validation protocols of the algorithms for these oscillometric devices hold very well in the range of systolic pressures between 90 to about 180, and especially 160.
Speaker: They hold well for diastolics in the 60 to 100, 105 range, but really lose accuracy afterwards.
Speaker: In the ICU population, post-operative population, this has been relatively well studied.
Speaker: And we know that when you get to systolic blood, to blood pressures in the range of what we call acute severe hypertension, there tends to be an underestimation of the intra-arterial pressure by these oscillometric devices.
Speaker: So you may be, and that the average underestimation may be as high as 50 over 30.
Speaker: So this is a significant problem.
Speaker: And then on the lower end of the pressure range, there is an overestimation of blood pressure, not of this magnitude, but still present.
Speaker: So bottom line, the same way as critical care specialists very often resort to putting an A-line to monitor someone who's on pressers,
Speaker: to make sure that they are guiding the blood pressure, the use of vasopressor agents well in the low pressure range, the same holds here.
Speaker: And if you're going to be using intravenous agents, you should have a very precise measurement of blood pressure.
Speaker: And therefore, these patients who have hypertensive emergencies, who get admitted to the ICU, in whom acute target organ damage exists,
Speaker: those patients deserve an A-line for more precise blood pressure measurement and treatment titration.
Speaker: And this lack of performance at extremes
Speaker: is not solved when you use a manual mercury string on a manometer if you're an old school person.
Speaker: Unfortunately not.
Speaker: Yes.
Speaker: Obviously, we don't even have mercury manometers, but it was a problem with mercury.
Speaker: It is a problem with aneroids.
Speaker: The accuracy of these devices and the use of a sculptatory technique doesn't improve that
Speaker: difference and that bias that's observed when compared to intra-arterial.
Speaker: So there's not only a problem in validating algorithms with oscillometric devices, but also an accuracy measurement when using auscultatory methods.
Speaker: Excellent.
Speaker: I think this is an important point because the presence, again, of acute organ damage is what should be dictating
Speaker: whether we bring somebody to the ICU, we use IV, we are more precise with our measurements, and identifying that, as we'll talk a little bit later, is really the key to this discussion.
Speaker: In terms of pathophysiology, Aldo, what causes acute severe hypertension?
Speaker: So, it can be caused by just about anything that causes hypertension.
Speaker: So, when we talk about pathophysiology specifically, that would be too broad a discussion.
Speaker: You know, you can have
Speaker: in the setting of acute microvascular injury, for example, pressure-induced injury, and the term that we used to use very often of malignant hypertension.
Speaker: So these patients, the acute injury to the renal microvascular drives a lot of this, and there's a very extensive activation of the renal angiotensin system.
Speaker: And in other situations, the mechanisms are going to be predominantly adrenergic,
Speaker: So, for example, acute presentations in pheochromocytoma would be a great example of that.
Speaker: So I prefer to look at it less from a pathophysiologic mechanism specifically.
Speaker: But I think in a clinical discussion, what's more valuable is to review what typical causes exist.
Speaker: And one thing is very obvious.
Speaker: the majority of patients who present with acute severe hypertension have a diagnosis of hypertension.
Speaker: That number is 80 to 90, sometimes even higher, 90% of cases.
Speaker: So these are people who already have a known diagnosis of hypertension and then present typically in a setting of not having taken medications.
Speaker: This is consistent across many observational studies
Speaker: And in different countries, this is not a United States problem.
Speaker: This happens around the world.
Speaker: So in someone who has, who comes in with this and gives you a history of not taking medications regularly, you know, ran out of medications, someone stopped meds and started a new treatment that's not exactly right, you're going to pick most cases just by this technology.
Speaker: And there really isn't, you should not be running to try to make a diagnosis of a secondary cause immediately in these patients.
Speaker: You might have to get back to it in case they are indeed resistant to therapy.
Speaker: But just the very fact that they presented with acute severe hypertension doesn't mean that you need to go look for secondary causes.
Speaker: any of the typical secondary causes, and we could go down the list of renal parenchyma, renal vascular, adrenal cortical, so primary aldosteronism in its various presentations, adrenal medullary, so especially the rare cases of pheochromocytoma, so on and so forth.
Speaker: We could go down the list of secondary causes of hypertension.
Speaker: Those need to be thought about
Speaker: when people present with acute severe hypertension without having a previous history of hypertension.
Speaker: In those cases, I would argue your threshold to rule out secondary causes should be much lower.
Speaker: But in those that already have a history of hypertension and who report decreased adherence, and people are often very candid in telling you that, in those patients you should probably focus first on management
Speaker: And then if they become resistant, just as you would do in anybody with resistant hypertension in the ambulatory setting, you would then trigger the evaluation of secondary hypertension.
Speaker: Does that answer your question?
Speaker: Absolutely, absolutely.
Speaker: And in terms of other precipitants that could also cause severe elevations in blood pressure that wouldn't be secondary or wouldn't be lack of taking medications,
Speaker: Can you mention some that we should think about at least when we see the patients in the ED or for the first time?
Speaker: Yes.
Speaker: Yes.
Speaker: So the most important ones are related to in patients who have salt-sensitive hypertension.
Speaker: Sometimes you have the combination of increased salt intake.
Speaker: So you start with not as well-controlled blood pressure that is salt-sensitive.
Speaker: So, for example, in African-Americans, in patients with underlying kidney disease, in patients who are older,
Speaker: And then you add to that an acute salt load, and often with another common precipitant, drugs are common precipitants, and then another class of drugs that can further enhance salt sensitivity, which are non-steroidals.
Speaker: So you could have that kind of perfect storm.
Speaker: You already start at a higher pressure.
Speaker: You eat a large salt load and take some NSAID for whatever reason.
Speaker: That's that often precipitate.
Speaker: The drugs that can be looked at as secondary causes are also very important, especially sympathomimetic drugs, so very important to think about them.
Speaker: And sometimes patients may be triggered on this one when they go on high-dose steroids, especially, again, if they are salt-sensitive and already poorly controlled to begin with.
Speaker: So thinking of medications is very important, and in salt-sensitive patients,
Speaker: A high sodium load is also something that very often throws patients into an episode of acute severe hypertension.
Speaker: Excellent.
Speaker: And Aldo, I think from a perspective of what causes organ damage, really, obviously, there's a lot that we don't fully understand, but a lot of it centers around two, I think, important aspects.
Speaker: One is out of regulation, and the other one has to do with
Speaker: endothelial injury, right?
Speaker: Can we talk a little bit about auto-regulation curves and how you view them from your perspective and ultimately how I think they have implication for the way we approach these patients?
Speaker: Sure.
Speaker: So I think that if we, so the best way we should probably just define auto-regulation first, which is the ability of a, so there are changes in arteriolar tone
Speaker: to modulate perfusion of an organ.
Speaker: So with vasodilatation in the low blood pressure ranges so that all the organ perfusion can be enhanced and vasoconstriction on the high end ranges to prevent pressure induced tissue injury.
Speaker: So the organs with this has significant importance in the setting of acute severe hypertension are
Speaker: Primarily, well, let's say three.
Speaker: The brain is by far the most important because of the concern about symptoms and injury related to the brain on both ends.
Speaker: So if blood pressure goes too low, obviously cerebral hyperperfusion, and that would be a complication of therapy.
Speaker: And if blood pressure goes too high and supersedes the autoregulation on the high end,
Speaker: then the symptoms associated with severe hypertension, such as cerebral edema causing hypertensive encephalopathy, focal cerebral edema causing, for example, posterior reversible encephalopathy, and obviously hypertension-associated strokes.
Speaker: In the kidney, that loss of autoregulation is also important because
Speaker: some of the microvascular injury that occurs in the kidney will then drive the process of malignant hypertension and acute kidney injury related to high blood pressure.
Speaker: The vasculature itself doesn't have an autoregulatory process because blood is flowing.
Speaker: And the microvascular injury, the extent of
Speaker: not only endothelial, but also injury to the wall happens by a variety of mechanisms.
Speaker: But during the exposure to very high blood pressure, you have extensive injury to the vascular wall.
Speaker: And in the part related to the endothelium, you have this process in the microvascular church that then
Speaker: is one of the mechanisms of generating a microangiopathic hemolytic anemia in which pressure-induced injury to the endothelium leads to microvascular injury, and these patients develop microangiopathic anemia with thrombocytopenia in a way that's classic and just the same as you would see with other mechanisms of endothelial injury, and this one just happens to be a pressure-induced injury.
Speaker: So this defines the importance of autoregulatory curves in mediating the complications in the brain, in the kidney, the endothelial injury for developing the MAHA-type presentation.
Speaker: And then the last one that's worth remembering is the heart, just because, especially in patients with acute coronary syndromes, that we need to be very cautious of what the diastolic blood pressure is doing.
Speaker: That doesn't really have to do much with auto regulation, but just has to do more with patterns of myocardial perfusion pressure and the concerns with excessive reduction of diastolic pressure in patients with acute coronary syndromes.
Speaker: So the next important concept to understand is that when we talk about treatment,
Speaker: understanding the autoregulatory curves to the brain, I think that the most important to understand, and it's also the best studied, is essential to define where we can go in terms of treatment.
Speaker: We need to remember that patients with chronic hypertension shift their autoregulatory curves to the right.
Speaker: So that affords them greater protection against very high pressures.
Speaker: but puts them at risk of cerebral hypoperfusion at blood pressures that wouldn't be too concerning for most of us.
Speaker: And so usually we don't worry about mean arterial pressures of 85 causing problems to anybody.
Speaker: But in a hypertensive with a very rightward shifted autoregulatory curve, that might be already
Speaker: in a range where they may have cerebral hyperperfusion.
Speaker: And then one last comment, Sergio, that I think might be worth making is that in patients who have an acute de novo hypertension, who were previously very normal tensive, they may develop significant brain cerebral edema
Speaker: related to pressures that are not as high as we would usually worry about.
Speaker: So those are people who can have a hypertensive emergency with a blood pressure that's less than 180 over 110 or over 120.
Speaker: Classic examples of that would be preeclampsia, eclampsia.
Speaker: Younger patients, especially kids with
Speaker: with acute glomerulonephritis and pheochromocytoma crisis.
Speaker: So these are important exceptions to just, you know, there are some people who are very fixated on a number.
Speaker: And, you know, don't sit on a young preeclampic woman who maybe two weeks ago had never seen a blood pressure above whatever, 100 over 65, who now has a blood pressure of, you know,
Speaker: 165 over 120 and you're not worried because the, or let's say 165 over 110, and you're not worried because it doesn't pass muster or doesn't cross the thresholds of the binary criteria that people develop.
Speaker: So I think that those are some of the important points that I wanted to make about auto regulation.
Speaker: And I think just to emphasize, it's very important
Speaker: to think about the numbers in the right context because I think it's very easy for a clinician to anchor their decision-making to an objective number.
Speaker: And like you said, in a young preeclamptic patient, maybe not be too concerned because, oh, it's only 160 over 110.
Speaker: Yet for that patient, that rapid increase has exceeded their ability to auto-regulate and is causing acute organ damage.
Speaker: And the converse, I guess, is also true is you see 180 over 110 in somebody who is chronically hypertensive, not taking their medications,
Speaker: And we've jumped to bring that down.
Speaker: And by doing that, we can cause more harm.
Speaker: So really focusing more on what it means for that patient and the presence or absence of acute organ damage.
Speaker: I think that's really where the auto-regulation curves and understanding them really come to play.
Speaker: Absolutely.
Speaker: So let's talk about therapeutic management.
Speaker: And really, obviously, there's multiple ways you could approach this.
Speaker: But based on the conversation that we've had so far, Aldo, it really seems that a sentinel decision point in terms of intervening from an intensivist perspective with an IV drug aggressively in an ICU centers around the presence of acute organ damage.
Speaker: Could you tell us how you approach a patient with severe acute hypertension in determining do they have organ damages from a very practical standpoint?
Speaker: Yeah.
Speaker: So, obviously, the main one is to look for symptoms, right?
Speaker: So, someone who has obvious findings, let's say obvious clinical symptoms to suggest a stroke, whether ischemic or hemorrhagic, visual changes to suggest press, chest pain to suggest an acute coronary syndrome or a dissection, shortness of breath to suggest
Speaker: acute decompensated heart failure.
Speaker: And in the basic labs that one would get, if there is acute renal failure and you would suspect that this is, and you have reason to suspect that that's new, so those would be, or let's say a new microangiopathic hemolytic anemia that wasn't present previously.
Speaker: So those are pretty obvious.
Speaker: The ones that the tougher distinction is in the absence of symptoms, right?
Speaker: Because the quality of laboratory tests and diagnostic tests to identify findings and the value, the sensitivity, and especially the specificity of these findings is difficult to interpret.
Speaker: So I use an approach that leaves room for discussion.
Speaker: But let's be pragmatic.
Speaker: So for example, if the screening neurological exam is negative and a fundoscopic exam, which I still do, I really do, is normal.
Speaker: I don't pursue anything further in terms of brain evaluation.
Speaker: In the heart, if the patient has a normal clinical exam and does not have shortness of breath, I very often don't even do a chest X-ray.
Speaker: In the ER, everybody's gonna get a chest X-ray.
Speaker: I do not know how to do echoes, so I don't carry a butterfly in my pocket.
Speaker: And if I did, I might take a look at the heart, although there are no data to show that that makes any difference.
Speaker: Same thing as doing BNPs.
Speaker: If the patient doesn't have symptoms suggestive of heart failure, a BNP has no value.
Speaker: The issue of doing troponins or not, I do an EKG on everybody, but without real certainty that that's of any value.
Speaker: If in the emergency room,
Speaker: patients get a troponin, and I'm very reassured if a troponin is normal.
Speaker: If a troponin is mildly abnormal, it not necessarily means that the patient has an acute coronary syndrome.
Speaker: It may be just a evidence of chronic injury, and that's a point of contention.
Speaker: Most patients that I end up seeing, either if I'm
Speaker: If it's in the hospital and I'm attending on the medical service or if it's someone that I go to the ED to see in the emergency room, those patients will have a troponin.
Speaker: But there's certainly room for contention there.
Speaker: In the presence of symptoms, then obviously we will guide the diagnostic evaluation based on
Speaker: as I discussed briefly before, on whatever you find.
Speaker: And then the modality, typically, of imaging will be guided by the symptoms.
Speaker: In the kidney, it's worth mentioning that if there is acute kidney injury, the likelihood, then the distinction that needs to be made is, is this a primary renal disease that's causing the hypertension?
Speaker: Or is this the hypertension causing kidney injury as part of the malignant hypertension syndrome, if you will?
Speaker: And that is not always, you know, very often it's a difficult diagnosis that you can only sort out by a kidney biopsy.
Speaker: Because even if you see a lot of red cells in the sediment, a lot of proteinuria, it could still be a malignant hypertension causing renal failure.
Speaker: rather than the other way around.
Speaker: So that is very often a difficult one to do without a kidney biopsy.
Speaker: And for microangiopathic hemolytic anemia, typically it would follow the typical work of MAHA.
Speaker: And I don't think I have ever seen someone present with severe hypertension with only MAHA.
Speaker: They usually have something else, typically renal failure,
Speaker: along with it, I've never seen someone present just with, let's say, hemolytic anemia and thrombocytopenia and nothing else as part of their presentation of severe hypertension, hypertension emergency.
Speaker: So that's my usual approach to diagnosis.
Speaker: What do you do?
Speaker: I want to, well, I take a similar approach.
Speaker: I think it's, well, I can tell you what you do that I don't do is a fundoscopic exam and that's shame on me, but I wanted to talk about that.
Speaker: So the two things that you mentioned that I wanted to dive a little bit more into are the fundoscopic exam and you talked about the butterfly.
Speaker: So on the butterfly, what I wanted to ask you before we go to detail in the fundoscopic exam is that more and more clinicians, especially in the ED and the ICU are proficient with ultrasound, are carrying ultrasound.
Speaker: And it's not something that I have done regularly, but I have seen studies suggesting that measuring the width of the optic nerve is a good correlate of ICP, increased intracranial pressure, or papilledema.
Speaker: Have you seen any of that?
Speaker: Could that be like the millennial fundoscopic exam?
Speaker: Any thoughts on that, Aldo?
Speaker: So I do not know the specific paper or papers that you're referring to in terms of optic nerve width.
Speaker: I have not read any such paper.
Speaker: There is a very good amount of knowledge of studies looking at arteriolar diameter.
Speaker: And as a measure of chronic hypertensive injury so as a pretty good correlate for hypertensive vascular injury, but that's all in the realm of chronic hypertension.
Speaker: I'm not aware of of anything in the acute hypertension injury, but it just means that I haven't seen those papers the the value that I see of endoscopy is that if you do not see
Speaker: uh exudates hemorrhages it gives you a a sense that the microvascular is holding on to that blood pressure pretty well and and i i i feel reassured about that uh on the other hand if someone who's asymptomatic and i'm looking at their fundus and i see exudates i see hemorrhages i may even see a little bit of papilledema
Speaker: that that's someone that I'm going to be very worried about.
Speaker: And fortunately, we see those very, very infrequently.
Speaker: There's a there's a device and I have no conflict of interest on this.
Speaker: There's a device that you can attach to your phone and that takes excellent pictures of the fundus.
Speaker: I do not have that device, but I've seen it being used.
Speaker: It provides really great pictures.
Speaker: And it has the advantage that you can share the pictures.
Speaker: Not only you get a good view of the fundus, but you can just, if you have an ophthalmologist that you can just send the images to, you'd have an extra layer of reassurance that what you looked at is exactly what you're thinking about.
Speaker: So most of all, what I do is with the ophthalmoscopes that I have in the room,
Speaker: rather than this, and this provides something that's useful.
Speaker: I just haven't spent the money to buy one for me.
Speaker: So, and I think it's important because obviously photoscopic examination is a lost art, and I think that people use it less and less.
Speaker: I mean, I would be surprised to find a resident or a fellow carrying an ophthalmoscope in his lab coat today.
Speaker: I would be very surprised if I find that.
Speaker: It's more likely that they have a butterfly like you mentioned.
Speaker: But clearly, the presence of severe grade three or grade four retinopathy, it's a red alarm.
Speaker: It's a signal that something needs to be done, that this patient is at high risk.
Speaker: And I think, like you said, the absence or presence is something that is very, very valuable in maybe directing therapy in some of these patients.
Speaker: And I think it's something that we should probably encourage people to think about, especially in the setting of the ED, which they should have a fundoscope that we could utilize to look at this.
Speaker: And I will definitely investigate more on that phone device, which sounds very, very intriguing, not something that I know much about.
Speaker: Now, you did mention retinopathy.
Speaker: The other thing that you mentioned, which I think constitutes with retinopathy, the too often forgotten acute organ damage,
Speaker: is the microangiopathic hemolytic anemia.
Speaker: And this is something I think a lot of times people tend to forget about and not think about, but clearly also, I mean, in some situations, it could be, I mean, an indicator that something requires immediate treatment.
Speaker: Could you comment a little bit more about how you differentiate microangiopathic hemolytic anemia from hypertension, from other syndromes that I'm sure you'd get called for, HUS or other symptoms,
Speaker: associated with this phenomenon?
Speaker: Yeah, so there will be, you know, HUS is a bad one to pick, right, because hypertension so often complicates HUS.
Speaker: Renal failure is uniformly a part of the presentation.
Speaker: So that makes it very hard.
Speaker: And that's going to be similar to the issue of what you do with, you know, a primary glomerulonephritis versus renal failure related to malignant hypertension.
Speaker: So in that one, it may be that your answer is going to come from control of blood pressure and cessation of the microangiopathy.
Speaker: So improvement in platelet counts and improvement in hemoglobin as you control the blood pressure better.
Speaker: The evaluation is the typical one of how you'd approach a patient with a
Speaker: microangiopathy with a hemolytic with suspicion of a hemolytic anemia so after the screen is positive you know whatever LDH is high heptoglobin is low platelets are low looking at a peripheral smear and then if there is because if you end up with someone who's encephalopathic with or without some LFT abnormalities and by the way you can see there are rare reports of hepatitis in the setting of a
Speaker: of hypercellular injury, let's call it hypercellular injury in the setting of malignant hypertension.
Speaker: So in those patients, you might end up even having to send an ADAMS-13 as part of the evaluation of a possible TTP syndrome.
Speaker: And so that evaluation is one that's going to depend on the severity of the process, how quickly you have to make a decision about the diagnosis,
Speaker: very often involving a hematologist so you can have a good input about what the peripheral smear looks like and if there's anything else that we may be missing.
Speaker: And then usually as you have these results coming back in, you can get an ADAMS 13 level pretty quickly.
Speaker: We as nephrologists are looking at the urine sediment
Speaker: the hematologist is giving a perspective from theirs.
Speaker: And in the meantime, the blood pressure is coming down, and then we can identify if this is part of the hypertensive emergency syndrome or if there's something else that's driving the process.
Speaker: In pregnancy, obviously, the issue is a little different.
Speaker: And fortunately, the delivery usually takes care of these things.
Speaker: And I think that you had asked, I mean, what would I, what do I approach it?
Speaker: And I think that the approach is, like I said, is very similar.
Speaker: And to be honest, although what I find is that I think is an important point is that a lot of times I will evaluate these patients in the ED.
Speaker: And more often than not, everything that I need has been ordered already as part of the routine workup.
Speaker: So it's really just, I mean, using those basic things to very quickly
Speaker: in a systematic way, eliminate the evidence of organ failure or presence, and that ultimately decides where the patient needs to go and what we need to do.
Speaker: The one thing that I wanted to get your thoughts on, and actually this is probably the highlight of my career as a fellow in terms of consultations, was recognizing in a patient that they were about to start an IV drip that he had a big prostate.
Speaker: and had a very, very large bladder.
Speaker: And my suggestion in a very tongue-in-cheek way to the ED attending was instead of the nicotapine, I would put a Foley in.
Speaker: And that took care of the blood pressure.
Speaker: Any comments on things that we need to make sure that we eliminate before we start treating the blood pressure?
Speaker: Yes.
Speaker: So, in your, so enlargement of the, you know, a full bladder.
Speaker: full undrained bladder is a cause of hypertension in anybody it will be a very it's a cause of severe hypertension in patients who have dysautonomia especially patients with autonomic dysreflexia due to spinal cord you know high spinal cord injuries so in those you're gonna see blood pressures that are truly phenomenal with just a an undrained bladder or
Speaker: or sometimes just with constipation.
Speaker: It's amazing the impact.
Speaker: But a large bladder can drive very high blood pressures on just about anybody, especially if you have pain.
Speaker: So the corollary to that is that severe pain from anything, since in patients, especially patients who already have a diagnosis of hypertension, the adrenergic surge related to that can very often cause very high
Speaker: blood pressures.
Speaker: So treat pain first before you reach to the, you know, let's say intravenous drugs to manage the hypertension.
Speaker: The same thing is true for shortness of breath.
Speaker: So in decompensated heart failure, sometimes it's not the hypertension that's driving the heart failure.
Speaker: It's the heart failure and then the adrenergic surge related to the hypoxia
Speaker: that's driving the blood pressure.
Speaker: And sometimes just control of volume promptly brings the blood pressure down.
Speaker: Obviously, fortunately, the treatment ends up being the same.
Speaker: So you can take both.
Speaker: But don't be surprised if just correction of resolution of pulmonary edema is enough to control the blood pressure and the hypertension doesn't remain for very long.
Speaker: Excellent.
Speaker: So if we determine that the patient has evidence of acute organ damage, as you mentioned earlier, these are patients that require aggressive treatment with IV drugs, likely benefit from an A-line and definitely should be treated in monitor settings like an ICU.
Speaker: How do you know how much to lower the blood pressure?
Speaker: How do you think about the target mean arterial pressure, Aldo?
Speaker: So there's a couple of things that you need to take into account for that.
Speaker: The first one is you're going to use pathophysiologic principles.
Speaker: You're going to use some lessons from the autoregulatory curves and what we've known from experiments in humans looking at this and make decisions about what is safe based on the autoregulatory curve.
Speaker: So that's the first point.
Speaker: The second point is specific to the individual conditions.
Speaker: Many of these specific recommendations are opinion-based.
Speaker: They are not based on trial data.
Speaker: The only, so we have okay data in the setting of ischemic stroke and reasonable data in the setting of intracerebral hemorrhage.
Speaker: For everything else, the decisions are largely driven by, you know,
Speaker: presumed pathophysiology and clinical observations.
Speaker: So let's go maybe one by one, if you will, of the major clinical sense.
Speaker: Absolutely.
Speaker: So, for example, for patients who have diffused microvascular damage, or as used to be called malignant hypertension, and patients who have hypertensive encephalopathy,
Speaker: So severe hypertension with microvascular injury and or a hypertensive encephalopathy.
Speaker: Those patients, you bring the blood pressure down and you respect the autoregulatory curve.
Speaker: So what are some principles?
Speaker: So that would be sort of the most generic reduction.
Speaker: So you can bring the blood pressure down by about 25% or so in the first
Speaker: hour.
Speaker: It's generally safe.
Speaker: If you do not bring the blood pressure down by more than 30% or so, you rarely get to the inflection point on the lower end of the auto-regulatory curve.
Speaker: Since we're not looking at graphics, let me tell you exactly what I'm meaning.
Speaker: So if you bring the blood pressure, as you bring the blood pressure down, there will be a point where
Speaker: where the auto regulation is lost.
Speaker: And at that time, cerebral perfusion will fall fairly abruptly.
Speaker: How abruptly it falls has a very large inter-individual variation.
Speaker: So you cannot predict what that is.
Speaker: But that point of an abrupt decrease rarely occurs
Speaker: at levels that are less than about 25 or so, 30% of reduction from where the blood pressure was at the time you started treating.
Speaker: So that's what gives you that cushion of safely bringing the blood pressure down by about 25%.
Speaker: That's where the golden number of 25% reduction of either systolic or menial pressure comes from.
Speaker: So that you can do within the first hour.
Speaker: It's probably okay.
Speaker: Some people want to be a little more conservative and bring it down within two hours.
Speaker: I think that in most patients, bringing it down in one hour is good enough and safe enough.
Speaker: So you bring that and then over the ensuing two to six hours or so, you try to bring the blood pressure to about
Speaker: let's say 160 over 100 or thereabouts.
Speaker: And most of the hypotensive events will occur in those first six hours.
Speaker: So at that time, you just play with the IV drugs.
Speaker: And if the patient does well in those first six hours, and definitely if you want to be conservative the first six to 12 hours, then that is the time you start adding oral drugs.
Speaker: so you don't have to stay given intravenous drugs for too long.
Speaker: And as the oral drugs, the long-acting oral drugs start acting, then you're able to wean the antihypertensives down.
Speaker: And your goal would be to reach your target blood pressure, whatever the target blood pressure is, arguably getting the patient down to the hopefully 140 over 90 range
Speaker: by the 48, 72 hour mark.
Speaker: So that would be sort of the most generic approach.
Speaker: But then you have the specific other situations.
Speaker: So as I told you, in stroke, we have more data.
Speaker: So there's a little bit of a better way to, you know, guidance to this.
Speaker: And in, for example, in hemorrhagic stroke,
Speaker: If the blood pressure is in the 150 to 220 range, there is no general agreement, by the way.
Speaker: Not even when I talk to our stroke neurologists, they don't agree among each other.
Speaker: They sometimes think that I'm too aggressive.
Speaker: They have told me that I am at times.
Speaker: And I'll tell you what I've written as a general statement that I got general agreement.
Speaker: is that if the blood pressure starts, systolic starts in the 150 to 220, bring it down to about 140 to 150.
Speaker: And you can do that fairly safely within the first hour.
Speaker: And that's particularly true for patients who do not have a history of hypertension.
Speaker: You don't want to delay it too much for people who do not have known hypertension.
Speaker: And in those who have, for example, an AVM or an aneurysm, because you want to control them well.
Speaker: In patients who have a very large hematoma or who have otherwise evidence of increased intracranial pressure, then you might want to be a little more conservative because those patients will be at risk of ischemia in the perihemorrhage area.
Speaker: So there is a formal recommendation that the systolic blood pressure should not come down below 140 because in those patients there were worse outcomes in one of the two large trials.
Speaker: So in the ATTACH-2 trial, there was harm in bringing the blood pressure below 140.
Speaker: So for cerebral hemorrhage, there is relatively good guidance on this.
Speaker: For ischemic stroke, then it varies according to whether the patient's gonna get thrombolytic therapy or not.
Speaker: If the patient's eligible for thrombolytic therapy, then the reduction would be to less than 185 over 110 before they can get the thrombolytics, and then it's kept at less than 180 over 105, at least for the first day.
Speaker: And if thrombolytic therapy is not gonna be used, then it's a little more liberal.
Speaker: And as long as the blood pressure is less than 220 over 120, then no intervention happens for the first two, three days.
Speaker: And that's largely because of concerns of excessive blood pressure reduction and extension of infarct because of the sensitive, the poor auto-regulation of the peri-infarct penumbra or the infarct penumbra.
Speaker: And then...
Speaker: A very important thing with stroke, with ischemic stroke, is that these people often have other complications.
Speaker: So they may come in also with heart failure or they may have an acute coronary syndrome.
Speaker: So if there is other target organ injury, then the management of the other target organ damage injury will also be factored here.
Speaker: So there may be patients with stroke
Speaker: that may have to be treated more aggressively because they have heart failure or because they have an acute coronary syndrome.
Speaker: Then for the three last well-defined syndromes would be in acute coronary syndromes, there is a suggestion.
Speaker: There are no strong data to back this up to decrease the systolics to less than 140, and you can do that within one hour.
Speaker: Just got to be careful with keeping the diastolic above 60 to not worsen coronary perfusion.
Speaker: In heart failure, the general agreement is to bring the systolic down to less than 140.
Speaker: Also do that promptly within one hour.
Speaker: Again, no data to back that up.
Speaker: And then finally, the often nightmares of aortic dissection.
Speaker: in which the goal is to both decrease the systolic blood pressure promptly, right?
Speaker: You bring it down to less than 120, so it's both prompt and aggressive, but also not forgetting to decrease the heart rate to limit the amount of aortic injury, so promptly also decreasing the heart rate to less than 60.
Speaker: So those are the general principles.
Speaker: And for every one of these,
Speaker: you will start oral therapy somewhere after that 12-hour period or so so that it allows you to titrate the oral medications off as the patients progress.
Speaker: And I think that's a very important point that I often see people misunderstand.
Speaker: The idea of starting is you obviously are very aggressive up front.
Speaker: You stabilize them.
Speaker: But the idea of starting the oral medications in that 6 to 12-hour window is so that you can effectively wean them off the drip in 24 to 36 hours.
Speaker: It doesn't mean that you're going to stop the drip at 12 hours or at 6 hours.
Speaker: And I think that's an often, I think, source of confusion.
Speaker: I see people basically control for 24 hours, and then they start, and then they wonder why the patient's still in the ICU.
Speaker: That's correct.
Speaker: So we talked about when to initiate aggressive treatment, which is the presence of organ failure and how to identify that.
Speaker: We talked about the targets based on our understanding of auto-regulation and the available evidence, which you mentioned is very lacking in general, but only available for some syndromes.
Speaker: Let's talk about drugs, Aldo.
Speaker: And I know that there's not a lot of good studies that show that one drug is superior to another, if any.
Speaker: Some studies have paired
Speaker: drugs head-to-head, but just in terms of titration.
Speaker: But how do you think about drugs and what are your general recommendations?
Speaker: So as you said, there are no, there are very limited data in terms of outcomes.
Speaker: We know we have very good control with calcium channel blockers, especially nicardipine and clavidipine.
Speaker: Those are excellent drugs.
Speaker: I had never used clavidipine until about a month ago, and then we've had a shortage in the cardipine.
Speaker: I used clavidipine in three patients in the last month, so that was a curiosity.
Speaker: And it's a very convenient drug.
Speaker: It's short-acting.
Speaker: I like short-acting drugs because it gives me flexibility to control the blood pressure.
Speaker: So...
Speaker: And these are drugs that have excellent control in clinical trials.
Speaker: Libetolol also has done fairly well in clinical trials.
Speaker: It has the advantage that you can both use bolus and drips.
Speaker: So it's a convenient drug to use.
Speaker: It's well-tolerated.
Speaker: And those are the workhorses, right?
Speaker: Nucardipine, libetolol.
Speaker: As I said, I didn't have any personal experience
Speaker: With clavidipine, our anesthesiologists use quite a bit, but in the CCU and ICU, clavidipine wasn't used very much.
Speaker: Esmolol is an important drug as part of the management of this section.
Speaker: Nitroglycerin, very important in the management of patients with acute coronary syndromes and heart failure.
Speaker: And these are the workhorses.
Speaker: I used a lot of nitride in the past.
Speaker: Nipride has become, obviously, there are the risks of toxicity in patients with prolonged infusions, patients with kidney disease, patients with liver disease.
Speaker: But also, it has become tremendously, almost prohibitively expensive.
Speaker: So nitroprosite has not been used very often, at least in our institution, for several years.
Speaker: So these are really the workhorses.
Speaker: The decision of which one to use will be guided primarily by the pattern of injuries.
Speaker: So if you have, you know, diffuse microvascular injury or hypertensive encephalopathy, most people can be managed well with either labetalol or necartipine.
Speaker: Nipride is an alternative.
Speaker: For hypertensive encephalopathy, it's the same.
Speaker: For patients with intracerebral hemorrhage or acute stroke, the same.
Speaker: Our neurointensivists really prefer nicardipine, so most patients end up being managed with nicardipine first.
Speaker: And then the acute coronary syndromes are largely with nitroglycerin, and obviously they end up getting a beta blocker along with the nitroglycerin.
Speaker: For heart failure, they get diuretics along with the nitroglycerin.
Speaker: And for dissection, most patients get
Speaker: a combination of Esmolol and Nicaridapine or Esmolol and Nipride.
Speaker: So those are really driven by the underlying process and personal preferences.
Speaker: And one comment that I really think is important to make is that aside from heart failure, hydralazine really should be, or
Speaker: aside from heart failure and pregnancy.
Speaker: Hydralazine really should not be used.
Speaker: It's a drug that gives us unpredictable responses, sometimes excessive.
Speaker: It really should not be used in patients with hypertensive encephalopathy and patients with stroke.
Speaker: But I would argue that aside from heart failure, especially heart failure with reduced ejection fraction, and
Speaker: in pregnancy that we should eliminate intravenous hydralazine.
Speaker: I really feel strongly about that.
Speaker: And it's probably the most commonly used, and I would say most commonly overused, antihypertensive in our hospital.
Speaker: Absolutely.
Speaker: And I think that even when you look at pregnancy in terms of safety and in terms of what we're trying to achieve from the blood pressure perspective, it really offers no advantage over something like nicardipine.
Speaker: So in terms of the patients in my ICU, I would always favor using something like nicardipine over hydralisine, which, like you mentioned, is unpredictable, has a long half-life, and is probably not a good drug to use from the risk of lowering the blood pressure too much.
Speaker: And I think that's ultimately what we're trying to avoid in these patients.
Speaker: And I think you mentioned clavidipine, and just for the listeners, obviously, clavidipine is a shorter-acting calcium channel blocker.
Speaker: Like you said, it's very, very prevalent.
Speaker: in the operating room.
Speaker: Most of the initial studies were done in intra-op and post-op patients.
Speaker: And I think that the reality is it's probably not as prevalent in a lot of our ICUs just because of a cost issue compared to nicardipine.
Speaker: But I do think that as that eventually might change, a lot of our listeners might have that available as well.
Speaker: And because it's shorter acting, it might allow for more precise titration or more rapid titration,
Speaker: even though there's no proven outcome benefit, might be beneficial from just a practice standpoint.
Speaker: So I think that as we're closing, Aldo, are there any special clinical situations that we didn't talk about?
Speaker: Maybe something that's not as common or a zebra or something in particular that you want to mention?
Speaker: Yeah, so, you know, so for example, patients who come in with cocaine intoxication avoid beta blockers.
Speaker: I would probably even avoid libetalol.
Speaker: You have other options.
Speaker: And if you think that the cocaine is part of the hypertensive emergency, you should probably avoid libetalol and certainly avoid beta blockers that do not have an alpha blocking activity.
Speaker: So, you know,
Speaker: That's one.
Speaker: The second one is, you know, let's not get into the pregnancy management.
Speaker: That's a completely different disease.
Speaker: And for those patients, you know, the rapidity of management is important.
Speaker: The delivery is important.
Speaker: Everybody should get magsulfate, et cetera, et cetera.
Speaker: So it's a different kettle of fish.
Speaker: And, you know, the rare zebra ones, there will be patients that you might see
Speaker: with who have, you know, a few chromocytoma crisis.
Speaker: You know, it's a rare disease.
Speaker: It's a disease you don't want to miss.
Speaker: And those patients are really best managed with fentolamine, right?
Speaker: And so the rapid initiation of fentolamine
Speaker: And then as soon as the blood pressure is better controlled, then add in a beta blocker, but only after they are well alpha blocked.
Speaker: Fortunately, most of those patients are diagnosed in the outpatient setting, but you definitely don't want to miss that.
Speaker: So those would be acute ketocollamine excess, whether due to feel or cocaine, and then pregnancy are probably the special clinical situations worth mentioning.
Speaker: Let me ask you one zebra that stuck with me and I've never encountered it in clinical practice, but I did encounter it in my medicine boards many, many, many, many years ago.
Speaker: And that's the scleroderma hypertensive crisis.
Speaker: Is IV ACE inhibitors still the drug of choice or is that just something that is long forgotten?
Speaker: No, it is not long forgotten.
Speaker: The treatment of choice, you just, you've got to be gutsy to make the diagnosis, right?
Speaker: The key thing there is making the diagnosis.
Speaker: And the treatment is, because it's the kind of patient who comes in with severe hypertension, acute renal failure, and the drug you go for is exactly the drug that you avoid most of the times.
Speaker: And that's for the rapid reduction of blood pressure, if the patient has, especially if there is extra renal involvement,
Speaker: you will need to use something else that you have greater control.
Speaker: So you will need to use nicardipine.
Speaker: You will need to use maybe the last one I saw, which was many years ago, we actually used nipride.
Speaker: But you need to start an ACE inhibitor at the same time.
Speaker: But it would not be a good idea to use IV enalaprolat as your only drug because you don't have that much control with enalaprolat.
Speaker: And this is someone that if they are taking PO,
Speaker: the drug of choice is actually Captopril because there might be an added advantage of the sulfhydro components of Captopril.
Speaker: So that is something still argued.
Speaker: There's not a ton of data on that.
Speaker: But people with scleroderma renal crisis are usually treated not only with ACE inhibitors, but specifically with Captopril.
Speaker: So the best approach would be to use a drug that you can titrate more carefully for the blood pressure reduction.
Speaker: And then at the very same time, start an ACE inhibitor.
Speaker: And whether you want to use inalaprolat immediately or just throw captopril at them, that in my mind doesn't make as much of a difference.
Speaker: You're using that to treat the renal crisis, but rely on something that's more potent and more easily titratable to treat the blood pressure.
Speaker: Does that make sense?
Speaker: It does.
Speaker: I haven't encountered one of these patients, but it's always nice to review some of these severs that stuck with us from our internal medicine training.
Speaker: But I think this has been a wonderful conversation, although I think there's a lot of obviously of very valid pearls, very actionable items for our clinicians who are listening to the podcast to take to the bedside.
Speaker: And I want to respect your time.
Speaker: I could continue talking about this for a long time, but I know that we want to be respectful of your time.
Speaker: So
Speaker: In closing, what we usually do in the podcast is... Sergio, excuse me.
Speaker: Can I make one comment?
Speaker: We didn't talk about hypertensive urgencies.
Speaker: And the one comment I want to make, because this is something that happens so often in the hospital, and not only in the wards, but also in the step-down units and in the ICUs, is the aggressive treatment of just plain hypertensive urgencies.
Speaker: And that's something that we should avoid altogether.
Speaker: eliminate IV therapy.
Speaker: So people who just because their blood pressure is now 200 over 120, the answer to that is not to give IV hydralazine or IV libitolol or whatever drug you choose.
Speaker: The choice for that is to adjust the long-acting drugs.
Speaker: And if the patient's symptomatic, there's a few and you want to see a little faster control, probably oral clonidine or oral libitolol are your best friends.
Speaker: So stick with those drugs only if you need to control symptoms or you want to calm people up so that people are not too excited for several hours.
Speaker: Adjust the long-acting drugs.
Speaker: Do not use IV drugs because we're going to cause more harm than good by doing that.
Speaker: So I just wanted to make sure that we didn't finish our conversation without that comment.
Speaker: Absolutely, and I'm happy you brought that up because I did have it in my notes, and it is true.
Speaker: one of the most frequent calls that our clinicians get is from a nurse for somebody who has a very elevated blood pressure.
Speaker: And it's almost like the knee jerk reaction is to give them something IV and we're really treating the nurse, but we're at risk of harming the patient.
Speaker: So I think that making that distinction, if there is or no organ damage and in those who are not, I agree with you a hundred percent, Alden, I'm happy that you made that point because I do think that this is a common occurrence in hospitals
Speaker: And then you go and look at the patient and they're asymptomatic, have no acute organ damage, and there's really no need to initiate, I mean, aggressive therapy that could just be harmful.
Speaker: So that's a great point, I mean, in terms of that distinction.
Speaker: Thank you for making that.
Speaker: So as I was saying, in terms of closing, we'd like to finish the podcast by tapping into the wisdom of our guests and asking a couple of questions that are unrelated to the topic that we were discussing clinically.
Speaker: Would that be okay?
Speaker: That would be okay.
Speaker: So the first question relates to books, Aldo, and I was wondering is what books have influenced you the most or what books have you most often gifted to others?
Speaker: So I thought of two books.
Speaker: One that really had a big impact on me about maybe 20 years ago or so is called Blindness by José Saramago.
Speaker: He's a Portuguese writer.
Speaker: I'm Brazilian so I speak Portuguese and I could read his work in Portuguese and he was a Nobel Prize winner in Sometime in the 90s for literature and he's a wonderful writer and this book is is a Real interesting story about the development of an it's acute blindness as an epidemic of
Speaker: and how the sudden development of blindness just brings the worst in society and how good people can suddenly be heavily changed by the fears that come along by that.
Speaker: And it's told in a wonderful way.
Speaker: It's really a wonderful book
Speaker: that makes us think about how fragile our stability is.
Speaker: And that's Blindness by Saramago.
Speaker: The second one is really a satire that it's called Portuguese Irregular Verbs, and it has nothing to do with Portuguese, by the way.
Speaker: And Portuguese Irregular Verbs by Alexander McCall Smith, who is a Scottish lawyer, and he's a satirist.
Speaker: And this is a short book, it's about 130 pages.
Speaker: And it's a satire about three professors who are romance, and one of them, the main character is a romance philologist.
Speaker: And it goes into this importance that we give to ourselves for things that are really meaningless.
Speaker: And I see that in academia very often.
Speaker: We think we are really relevant people.
Speaker: And obviously there are many of us who are.
Speaker: There are many people who are Nobel laureates and who have really changed the way life as it is.
Speaker: But there are so many of us who we are good people and we go through life.
Speaker: But sometimes we get so caught up in the little worlds that we live in and we lose sight of how, you know, there are so many more important things in life than that little world and that little expertise.
Speaker: And it's a wonderful read and it's so funny.
Speaker: I think it's a really worthwhile read.
Speaker: And I just don't gift it to my friends.
Speaker: because I don't want them to think that I think their work is irrelevant.
Speaker: You're giving them a message.
Speaker: So I definitely have not read that book, and I will look it up.
Speaker: Blindness, obviously, is a classic.
Speaker: And like you mentioned, Saramago is a Nobel laureate.
Speaker: But I think it also speaks, obviously, blindness.
Speaker: I mean, a way of looking at it is that we all have blind spots and that these blind spots also sometimes bring the worst out of us.
Speaker: And that I think that obviously he does it in a beautiful narrative.
Speaker: And I think both we will link to the show notes.
Speaker: And I will definitely look for Portuguese irregular verbs.
Speaker: I'm intrigued now, but I do like... It's a funny, interesting read.
Speaker: Absolutely.
Speaker: I love that.
Speaker: So the second question, Aldo, has to do with something you believe to be true in medicine or in life that most other people don't believe to be true or act as if it's not true.
Speaker: So I'm going to tell you one in medicine.
Speaker: And I don't know that most people believe it or not.
Speaker: I'll tell you that I believe, even though I can't explain, is that I think that patients often, that there is such a thing as death by giving up or letting go.
Speaker: In other words, a patient who has no reason to die, no reason to die today, but many reasons to die in a week or two,
Speaker: And you come by, you have a discussion about an end of life.
Speaker: We're going to withhold dialysis.
Speaker: We're going to withdraw dialysis.
Speaker: Obviously, that's the world I live in.
Speaker: But, you know, everything else is stable.
Speaker: The potassium is fine.
Speaker: The acid-base balance is fine.
Speaker: There's absolutely no reason for the patient to die.
Speaker: And we have that discussion at 4 o'clock in the afternoon.
Speaker: And I come by to round the next morning and the patient died.
Speaker: I cannot count how many times I've seen this.
Speaker: And so...
Speaker: this belief I do have that there's something that keeps you holding on to life and that letting go brings death more promptly for reasons that I cannot explain as a fairly intelligent physician.
Speaker: And it's very interesting, Aldo.
Speaker: I mean, obviously, in the world of the ICU, you always assume that you go from one extreme to the other.
Speaker: It's like a pendulum, right?
Speaker: And on one hand, obviously, there are patients in whom these discussions of goals of care are very appropriate, very meaningful.
Speaker: But as you move forward, I think studies have shown in different contexts, they haven't explained the reason, but this whole idea of a self-fulfilling prophecy.
Speaker: The more you talk to people about not doing this, not doing that, the more people die or the rapidly they die.
Speaker: And it might be touching on one of the observations that you make, and it might be something inherently
Speaker: in the patient that also, I mean, drives or helps accelerate that, which I think is obviously very, very interesting.
Speaker: But I think that that's a very interesting point.
Speaker: And I think it's something that I always grapple with because you go almost from one extreme to the other and really trying to find the balance is, I think, one of the big challenges in medicine and in life in general.
Speaker: So my last question is, what would you want every listener to the podcast to know?
Speaker: Could be a quote of fact.
Speaker: Yeah.
Speaker: So that is most know.
Speaker: Sometimes they forget.
Speaker: I think it's a very important one.
Speaker: There is no intelligent discussion about acid-base balance without a blood gas.
Speaker: So why am I bringing that up?
Speaker: Because periodically I get asked to comment, hey, Aldo, can you come by and comment on this urine and ion gap
Speaker: for this patient.
Speaker: And what's the type of RTA with this urine and ion gap result and the bicarbonate of 16?
Speaker: And I asked for the blood gases and we don't have it.
Speaker: And it's a patient with a pH of whatever, 747 because of a respiratory elk.
Speaker: So I cannot count how often I see this still coming from intensive care physicians.
Speaker: So whenever you want to discuss acid-base, I love talking about acid-base balance, but we can never have an intelligent discussion without blood gases.
Speaker: I love it.
Speaker: And I think it's a great point.
Speaker: Perfect place to stop.
Speaker: And maybe we'll have you back to talk about acid-base, and I'll have a blood gas if we do that.
Speaker: That's great.
Speaker: It was a pleasure talking to you, Serge.
Speaker: Thank you so much for your time, Aldo.
Speaker: I really appreciate it.
Speaker: And I sincerely hope to have you back on the podcast soon.
Speaker: You bet.
Speaker: You have a good day.
Speaker: Thank you for listening to Critical Matters, a sound critical care podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound Critical Care is transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
