Diuretic Resistance Cases

Core IM Podcast

Time Stamps

• 01:53 Case 1: Diuretic Resistance from Ascites and Intra-abdominal Hypertension
• 09:57 Case 2: Diuretic Resistance from Low Cardiac Output
• 26:34 Case 3: Diuretic Resistance from Inadequate Renal Perfusion Pressure

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Show Notes

Diuretic Resistance Reminders:

• What is diuretic resistance?
  • Failure to achieve therapeutically desired congestion relief despite using appropriate or escalating doses of diuretics.
• Consider… Is something else going on?
  • Think about blood flow first
    • Diuretics cannot work if they are not reaching the kidney!

Case 1: Diuretic Resistance from Ascites and Intra-abdominal Hypertension

• Case Summary:
  • 46F with hypertrophic cardiomyopathy with worsening SOB, edema, and abdominal girth and signs of volume overload. Objective otherwise:
    • AKI with Cr 1.0 -> 2.0 mg/dl and poor urine output
      • No response despite high doses of bumetanide and acetazolamide.
    • Urinalysis: mostly hyaline casts
    • Other Data:
      • Normal blood pressures
      • Tense distended abdomen
      • Warm extremities
      • Normal lactate
  • Bladder pressure measured ~30 mmHg so paracentesis was performed.
    • Urine output significantly improved
    • Creatinine normalized back to baseline
    • Bladder pressure dropped to 12 mmHg.
• What is intra-abdominal hypertension (IAH)?
  • Sustained intra-abdominal pressure > 12 mmHg
  • Abdominal compartment syndrome = IAH + end-organ dysfunction (generally when this pressure > 20 mmHg)
  • Under-recognized cause of acute kidney injury
    • IAH causes a significant drop in renal blood flow and GFR.
• When to consider IAH as the cause of diuretic resistance:
  • Patients who have cirrhosis or cardiac ascites and a tense abdomen on exam

Case 2: Diuretic Resistance from Low Cardiac Output

• Case Summary:
  • 48M with ischemic HFrEF (EF 15-20%) admitted for volume overload and “feeling unwell,” started on IV diuretics.
    • Quickly escalated to multiple high-dose agents with poor urine output
    • AKI with Cr 1.0 -> 2.0 mg/dl and rising BUN
    • Other Data:
      • BPs 90s/50s mmHg
      • Warm extremities
      • Elevated bilirubin
      • Lactate 2.5 mmol/L
  • Right heart catheterization obtained:
    • RA 18 mmHg, PA 32/22 mmHg, PCWP 25 mmHg
    • Low cardiac index (CI) 1.7 L/min/m2 by Fick
  • Given concern for cardiogenic shock, he was started on dobutamine
    • Significant improvement in urine output
    • Improvement in creatinine and other perfusion markers
• Memory trick for normal right heart catheterization numbers: Nickel-dime-quarter-dollar rule.
• Remember: Shock ≠ Hypotension
  • Sometimes known as “normotensive cardiogenic shock” in this patient population
    • Related to higher central pressures and lower perfusion pressure (more below)
• When to consider low cardiac output as the cause of diuretic resistance:
  • Patients who have multiple other signs of hypoperfusion
  • Can be tricky and easy to miss
    • Similar abnormalities (like elevated LFTs) can be seen in just congestion alone
    • Must have a high level of suspicion for low output to catch it!

Case 3: Diuretic Resistance from Inadequate Renal Perfusion Pressure

• Case Summary:
  • 44M with WHO group I pulmonary hypertension on treprostenil who was admitted for volume overload and “feeling unwell,” started on IV diuretics
    • Quickly escalated to multiple high-dose agents with still suboptimal urine output
    • Worsening AKI with Cr 1.2 -> 3.3 mg/dl
    • Other Data:
      • BPs 100s/50s mmHg
      • SpO2 mid-90s on 6L NC
      • Warm extremities
      • Skin flushing
  • Echocardiogram was obtained:
    • Normal LV function, dilated RV with decreased function, significant tricuspid regurgitation
  • Suspicion was for worsening right heart failure:
    • Vasopressin was started to target a mean arterial pressure (MAP) goal closer to 75
    • Urine output increased dramatically
    • Cr improved to near baseline
• What is perfusion pressure?
  • Blood pressure gradient through an organ
    • I.e. Difference in the blood pressure going into the kidney and the blood pressure leaving the kidney
    • Organ Perfusion Pressure = MAP – CVP (approximately)
      • *MAP is the mean arterial pressure
      • *CVP is the central venous pressure obtained on a right heart catheterization or estimated by JVP assessment
• Why does perfusion pressure matter?
  • The kidneys (and other organs) depend on an adequate perfusion pressure to maintain blood flow (and GFR).
    • Through autoregulatory mechanisms in the blood vessels
  • In general: Perfusion pressure above 60 mmHg is enough to maintain adequate GFR.
    • May be a difficult target in some cases of decompensated heart failure
      • Since the CVP can be quite high!
      • Target of 50 mmHg may be enough anecdotally
      • *May require vasopressors or inotropy
• Why was vasopressin used?
  • Preferred by some experts in patients with pulmonary hypertension
    • Theoretically causes less pulmonary vasoconstriction compared to other vasopressors
      • Only studied in animal models
• When to consider inadequate renal perfusion pressure as the cause of diuretic resistance:
  • Patients with borderline MAPs (near 65) and relatively preserved LV function
    • *Caution in patients with poor LV function
      • Vasopressors increase afterload which may be detrimental in these cases
      • Definitely worth a multidisciplinary discussion

Transcript

Dr. Nayan Arora: The reason I like some of these cases is to really nail home that without flow, it doesn’t matter what you’re doing with the diuretics, you have to fix flow, then focus on the diuresis.

Dr. Shreya Trivedi: Hi all. Welcome back to Core IM. This is Dr. Shreya Trivedi.

Dr. Andrew Ling: And this is Dr. Andrew Ling, an internal medicine resident at BIDMC.

Dr. Shreya Trivedi: And on our cardiorenal considerations episode, we discussed all that we have in our toolkit to manage cardiorenal syndrome.

Dr. Andrew Ling: Right, and we recognize in real life these cases can be so hard and wanted to cement things with practical application. So we challenged Dr. Nayan Arora to share a few challenging cases of diuretic resistance to solidify and add to our teachings from the cardiorenal episode.

Dr. Shreya Trivedi: And he did not disappoint! I think both Andrew and I left hearing the stories on managing tough diuretic resistance cases with just such an appreciation of the nuances that each patient brings, and I definitely felt that love of medicine and challenge of medicine that made me once want to be a doctor hearing these cases. So we just thought, yes, we have to make this into a bonus episode.

Dr. Andrew Ling: Definitely Shreya, and I’m really excited for us to just share this all with you guys. So here’s Dr. Nayan Arora, a nephrologist who attends a lot on the cardiorenal service at the University of Washington.

Dr. Nayan Arora: I’m going to preface these cases by letting people know that these are all real cases. They are older and I’ve changed a lot of the non-relevant information just to protect patient identity as much as possible. The other caveat here is that I’m a nephrologist. I’m not a pulmonologist. I’m not a cardiologist. I come in to try to help make people urinate and we’re not going to be addressing a lot of the underlying disorders that are driving some of the diuretic resistance. And so I understand that it’s a little bit artificial the way we do this and in real life there’s multiple teams that are involved taking care of these folks. But what we’re focusing on here is what our service is generally consulted for, which is the diuretic resistance piece of this.

Case 1

Dr. Nayan Arora: The first case is a 46-year-old female with hypertrophic cardiomyopathy. She has an additional medical history of atrial fibrillation. She was admitted to our cardiology service with volume overload, so she subjectively described shortness of breath, increasing lower extremity edema and increasing abdominal girth for the last two to three weeks while she was at home. Her home medications are torsemide 150 milligrams twice daily and spironolactone 50 milligrams daily. Those are the relevant diuretics. She’s also on metoprolol and warfarin for anticoagulation given her atrial fibrillation. When she was admitted, she had a creatinine of 1, which is her baseline. She was started on four milligrams of bumetanide three times a day. She had a suboptimal response based on urine output, and so at some point, was given Diamox 250 milligrams twice daily. At the time that we were consulted, she was urinating roughly 600 to 700 ccs a day in response to those diuretics. The primary reason for consult was diuretic resistance, but also an acute kidney injury as her creatinine had gone to 2 from that baseline of 1. Her other electrolytes, she had a sodium of 126, a potassium of 4.1, a chloride of 88, bicarbonate at 28 and a BUN of 78.

Her urine sediment was notable for predominantly hyaline casts with very few granular casts. Anytime we see a patient like this, the way we think about it, or at least I think about it in order, is flow comes first and then diuretics come next. So we’re always thinking in this situation, are the kidneys getting enough blood? So I can tell you that her MAP was in the 70s, her heart rate was in the 80s, and she was in atrial fibrillation at this time. Her respiratory rate was 18 and she was saturating 96% on two liters at the time of our evaluation. On examination, she had elevated neck veins, she had 2+ lower extremity edema, and she had significant ascites. And so again, when we think about flow, the question is her cardiac function good enough that she has appropriate cardiac output?

We don’t have invasive hemodynamics in this case, but for what it’s worth, she was warm, her lactate was normal in this situation, and her LFTs were elevated, but this was attributed to congestive hepatopathy. Blood pressure seems to be reasonable. The thought in this case was given her exam, we were concerned about intra-abdominal hypertension or even abdominal compartment syndrome given that you do have that acute kidney injury. And so the way we do it, which I’m guessing most centers do it – a Foley was placed, we measured a bladder pressure. In this case it was 30, which is extremely elevated. She underwent a paracentesis which got her bladder pressure down to 12, and her urine output went from that 600 to 700 ccs to 3.3 liters the next day, subsequently 4.2 liters, then close to 5 liters. We actually had to back off on her diuretics.

I think what this case illustrates is something that I think is under-recognized in many patients. There’s older data to show that even an intra-abdominal pressure greater than 8 leads to a decrease in renal blood flow. I think typically we think about intra-abdominal hypertension as an intra-abdominal pressure greater than 12, and this is one of our more extreme examples. And then just relieving that pressure, improving renal blood flow, she not only responded to the diuretics, but her acute kidney injury improved as well.

Dr. Shreya Trivedi: Was there something about her abdominal girth that you were like, that is what we should go through next. Were there any pointers?

Dr. Nayan Arora: Yeah, usually it’s going to be the person with a tense abdomen. You may have seen those people with cirrhosis that have so much ascites that their abdomen gets tense. It’s no longer soft. You could argue in this case, did we actually need the bladder pressure? You could just go ahead and do the paracentesis, right? If there’s a significant ascites, you could argue that just go straight to the paracentesis. And we could have done that. This was more maybe for our own education and knowledge is showing that difference, and we could actually show that, hey, bladder pressure went from super abnormal at 30 down to 12, and you could argue, Hey, maybe that’s not the appropriate technique given that the patient wasn’t paralyzed, et cetera. And we could have just gone straight to a paracentesis.

Dr. Shreya Trivedi: Two questions. Just to close out the story of her creatinine being 2 and her having AKI post-paracentesis. How did the creatinine trend?

Dr. Nayan Arora: Yeah, it came back down to baseline, so it came back to 1.

Dr. Shreya Trivedi: Yeah, so I guess if we were classifying it, it’s the intra-abdominal hypertension would decrease… like a pre-renal etiology.

Dr. Nayan Arora: That’s exactly right. Yeah, you’re just causing mass effect and decreasing blood flow. So intra-abdominal hypertension has this definition in terms of what your intra-abdominal pressure actually is, and then compartment syndrome would be that in combination with end organ dysfunction.

Dr. Shreya Trivedi: Awesome. And then I’m curious, how often when you’re consulted, if you can quantify often, do you find that the paracentesis is the key? Is this a common thing?

Dr. Nayan Arora: It’s not that common. We also have a hepatorenal service at our hospital, and I think they encounter it much more. And I think just like it’s under-recognized in heart failure, I think it’s probably more common in hepatorenal syndrome and potentially under-recognized in patients with cirrhosis. And so they, I know, see it a lot more. We have maybe a handful of cases I’ve seen over the last four to five years, so it’s not that common a cause.

Dr. Andrew Ling: I just had one question too, and before we had talked about when trying to figure out why this person has an AKI looking at the sediment to see if there’s nothing else. When you see something that has no blood, no protein, just hyaline casts – are the main things in your mind, hemodynamic things?

Dr. Nayan Arora: In my mind, that’s what it is. Yeah. So I don’t like the term pre-renal in those cases because I don’t know if I mentioned before, but sometimes that’s a trigger for pre-renal means we need to give fluid or give colloid or whatever it is. And so I think hemodynamic is again, just you have normal kidneys in a bad environment and so you’re trying to fix the environment around the kidneys.

Dr. Shreya Trivedi: That was great. I don’t know why for me, hyaline casts triggers to me like, oh, this person’s really dehydrated.

Dr. Nayan Arora: Yeah, because you can get it with true prerenal acute kidney injury. You can see hyaline casts, but the kidneys don’t distinguish between “I am volume depleted” versus “I have cardiorenal syndrome” versus “hepatorenal syndrome” versus “I have extrinsic compression on my blood vessels” like this with intra-abdominal hypertension. And so if you think about it from a kidney standpoint, they’re responding the same way in all of those situations, but the treatment of all those situations is going to be different.

Dr. Shreya Trivedi: Yeah, that’s great.

Case 2

Dr. Nayan Arora: Next case is a 48-year-old male with coronary artery disease and associated ischemic cardiomyopathy. He has a known ejection fraction of 15 to 20%. He showed up in the ER essentially saying he just wasn’t feeling well, wasn’t more specific than that. And upon arrival in the ER, he has a blood pressure of 97/52. He has a heart rate of 96, a respiratory rate of 18, and at the time of evaluation, he was saturating 99% on two liters. So he’s admitted to a cardiology service because of volume overload. And at the time of our consult, he was urinating 1 liter to 1.5 liters a day on a furosemide drip at 30 milligrams an hour. He was given acetazolamide 250 milligrams twice daily as well as chlorothiazide 500 milligrams every 8 hours. And when we consulted, he had a sodium of 129, a potassium of 4, a chloride of 89, a bicarbonate of 28, a BUN of 56 and a creatinine of 2. His baseline creatinine is historically 1.

He had an AST of 34, ALT of 35, AlkPhos of 233, and a bilirubin of 4.9. His lactate was 2.5 and on examination, he was sitting up in bed. He had jugular venous distension up to his mandible. His heart rate and rhythm was regular. He had a III/VI systolic murmur, 2+ pitting edema, and he was warm to the touch. So just going back to kind of how we normally approach things, is this a flow problem? Is this a medication problem? And so in this case, we asked for a right heart cath and his right atrial pressure was 18, so elevated from your normal of let’s say less than 8 or so. Pulmonary capillary wedge pressure was 25. His pulmonary artery pressure was 32/22. His cardiac index by Fick was 1.7.

Dr. Shreya Trivedi: You mentioned the cath numbers. For someone who hasn’t been in the ICU for a very long time, can you go through what the numbers were again and how they showed, you said reasonable flow and elevated congestion?

Dr. Nayan Arora: Yeah, so you have in this case a right atrial pressure of 19. So that’s going to be your right-sided pressure elevated from your normal of let’s say less than 8 or so. You have a pulmonary capillary wedge pressure of 25, which is going to be a surrogate for that left-sided congestion. So normally, a wedge pressure should be less than 12, and then the pulmonary artery pressures is a little bit more difficult to interpret in isolation because we need more numbers, but could be associated just with underlying pulmonary disease. They can be elevated here in the context of just volume excess.

Dr. Andrew Ling: I think for the general person, there’s the nickel dime and quarter rule for what are normal pressures.

Dr. Shreya Trivedi: Oh yes. Oh my gosh, I used to know this like years ago!

Dr. Nayan Arora: That’s right. And so you’re right, so that’s kind of the nickel dime, however we teach it. With the caveat that in chronic – so normally a wedge pressure should be less than 12, although if you look at the older data, people with chronic heart failure, a normal wedge may be as high as 20. And so, you have to kind of take that into consideration. And so the definition of cardiogenic shock is either a cardiac index less than 1.8 without vasopressors or inotropes or less than 2.2 if [00:20:00] you’re on therapy, although I don’t think anybody would use that in isolation. It would be, you have a poor cardiac index in conjunction with end-organ damage. So the definition, just like you can have shock with a normal blood pressure or low blood pressure without shock. Shock is a clinical diagnosis where you’re seeing end-organ damage.

Dr. Shreya Trivedi: Thank you for clarifying that. All these numbers, I once remembered at one point on a 28-hour call shift.

Dr. Nayan Arora: So when we’re looking at this – and look, we have the hindsight. You know, we have the opportunity to play Monday morning quarterback. We don’t have to be the primary people. But if you look at this, there were some subtle signs that this patient wasn’t perfusing appropriately. You have this acute kidney injury. Again, there’s many reasons for that. That doesn’t necessarily mean that this was a blood flow or a perfusion issue, but then you have a lactate, which you know, it’s going to be red when you open up your labs. It’s not super impressive, but it is slightly elevated. And then you go to your LFTs and you see certain things that you would look at, which is your AlkPhos is high, your bilirubin was close to 5. So this all fit with the fact that you have a low cardiac index, so he is not perfusing well, particularly again, when you take the clinical picture that you have these signs of hypoperfusion. Bottom line, the feeling was that we needed to improve his contractility in this case. And so he was started on dobutamine and actually in response that had over 5 liters of urine output and all his other parameters like lactate, these LFTs, creatinine all improved. And again, I mentioned that we’re kind of isolating this to diuretic resistance. Ultimately, this patient needed mechanical circulatory support and got an LVAD, but in the time being to kind of temporize this person, he responded to inotropic support.

Dr. Shreya Trivedi: Amazing. One thing to clarify, you said the bili being five. Is congestive hepatopathy – no, this is not for congestive hepa- you’re just saying the flow isn’t good, that the bili was elevated.

Dr. Nayan Arora: You can see elevations in bilirubin with congestive hepatopathy, but in this case, you had both probably, right? You do have pretty significant congestion based on those right heart cath parameters, but at the same time, you also had poor perfusion.

Dr. Shreya Trivedi: What about the case made you think that you needed a right heart cath?

Dr. Nayan Arora: Yeah, so in my mind, not being a cardiologist, not being as smart as them, maybe is I look at these kind of cases where I’m really struggling here, right? He’s on very high doses of appropriate diuretics. He’s not responding. So in my mind, especially as a nephrologist, we love our labs, we love information. I need more information. And I think I’ve mentioned previously and one of the cardiologists here have taught me that in heart failure you need hemodynamics. And in this case, I think that hemodynamic data was helpful because where else are we going to go here? Instead of throwing more and more treatments at him, let’s get the full picture.

Dr. Shreya Trivedi: I understand. And I think one teaching point is that him putting out 1 liter to 1.5 liter, oh, we’re actually diurese, and maybe they put out 600, but you can’t get ins and outs. I don’t know, should I up the dose, should I not? What is your threshold? Do you have a mental model for like, they’re on this much bumetanide or they’re on this much of a drip and this is how much I want them to respond.

Dr. Nayan Arora: So I like to see at least three liters of urine if I’m appropriately decongesting somebody. At our center, I think I mentioned we put a lot of stock into urine sodium levels and we use that to guide our threshold dose.

Dr. Shreya Trivedi: Yeah, yeah. Andrew, what questions do you have?

Dr. Andrew Ling: What was his initial blood pressure you said?

Dr. Nayan Arora: 97/52.

Dr. Andrew Ling: One thing I wanted to ask was, I guess even sometimes when people have reasonable sounding blood pressures like 100s/60, they can still get almost like an ischemic or low flow type of insult to the kidney. Is there some physiology of it that I’m not understanding?

Dr. Nayan Arora: Yeah, I think the point in general is that blood pressure in and of itself doesn’t equal perfusion. Let’s take hepatorenal syndrome as an example because that’s probably the most well-known example for most medicine folks where the treatment of hepatorenal syndrome is what? You increase their MAP by 10 mmHg almost irregardless of what their underlying blood pressure is. So even if you have a “normal blood pressure”, you’d look at it and say, okay, this person has a normal MAP. Let’s say it’s 65. But the point is that blood pressure is not enough to achieve appropriate perfusion and we have to increase it to match perfusion, right? You guys have seen this in so many parts of medicine that these numbers in isolation are just a guide and you have to correlate it clinically to… You know, you’re not going to treat anything in isolation like this.

Dr. Shreya Trivedi: Awesome.

Case 3

Dr. Nayan Arora: This is a 44-year-old male with WHO Group I pulmonary hypertension. He is admitted with volume overload and the consult for us, in this case, was acute kidney injury. The rest of his medical history is that he has type two diabetes as well as hypertension. He basically came in feeling poorly for two days. He said that his weight at home had gone up to 258 pounds where he says he feels good and targets a weight of 249 pounds. This was associated with worsening shortness of breath as well as increasing lower extremity edema. At home, he’s normally on sildenafil, ambrisentan and Remodulin. He also takes torsemide 150 milligrams twice daily as well as spironolactone a hundred milligrams daily. When he comes in, his temperature is 38 Celsius, heart rate is 118, respiratory rate is 22, and he is saturating 96% on six liters. His blood pressure, which I didn’t mention, is 104/50 or a MAP of 68.

On examination, he has this flushed kind of appearance. He’s tachycardic. He has 2+ lower extremity edema and an elevated jugular venous pressure. He’s also tachypneic and he has decreased breath sounds at both of his bases. He has an echocardiogram done, which shows normal LV function, a dilated right ventricle with decreased function and tricuspid regurgitation. At the time of our consultation, he’s on a bumetanide drip at two milligrams per hour. He’s getting chlorothiazide one gram twice daily. In response to that, he has a urine output of about 630 ccs and his urine sodium in this case was 11. When we see him, his labs show a sodium of 128, a potassium of 5.9, a chloride of 95, a bicarbonate of 25, a BUN of 26, and a creatinine of 3.3. And normally his creatinines are around 1.2.

And so just like with every other case flow and then diuretic management. So what we’re looking at here is somebody who has significant right heart failure. He is getting pretty large doses of at least two diuretics, and he has a pretty suboptimal response both by his urine output and his urine sodium. Irregardless of whatever his urine sodium was, this person needs some kind of intervention. And so this is one of those cases where we said, even though his MAP is normal – you would look at a MAP of 68 and say he has a normal MAP, his systolic pressure is 104 mmHg – we said, I think we need to start vasopressin and target a MAP closer to 75. And so that’s what was done. And he had a urine output increase to 3 liters and his urine sodium increased to 72 and ultimately his creatinine came down to 1.3. And so, I think we mentioned this in the previous recording where this whole concept of renal perfusion pressure, which is your MAP minus your CVP, I think becomes pretty important here. And it’s probably not something that’s discussed enough. We mentioned a little bit in HRS and how we extrapolate to CRS that your renal autoregulatory curve might be shifted a bit to the right where you need higher pressures to maintain normal renal blood flow.

And we like vasopressin in our center, and I know there’s differing opinions around the country about this because, at least in animal models, vasopressin appears to selectively vasoconstrict your efferent arteriole without having significant impact on your afferent arteriole. And when you’re in low flow states, you rely on efferent vasoconstriction to maintain GFR. So that’s one good thing about it. And of course, particularly in these cases, you don’t want to increase RV afterload. And so that’s another enticing prospect with vasopressin that we like. But again, a lot of this is just empirical. And so, the thought here is that you have a significantly elevated right atrial pressure and you need to increase that gradient by increasing your MAP. And at the same time, you’re using that to better perfuse your RV. And he responded in this case, and we’ve had a number of cases similar to this where they just need that vasoconstrictor therapy. And to be fair, you’re not as worried about increasing afterload because he has a normal LV. You’re going to be more hesitant in people who have struggling LVs. We don’t use this therapy quite as much in those folks because you don’t want to increase that LV afterload. In this case, you have a normal functioning left ventricle, so you’re not quite as concerned about that increase in mean arterial pressure.

Dr. Shreya Trivedi: I have two questions. One is – this will also just show how much I haven’t thought about ICU medicine in a while – but with our last case of the person who wasn’t having adequate urine output and the right heart cath also showing a lot of numbers that still showed congestion, we chose a contractility agent of dobutamine and here we’re choosing vasopressin. How do you think of the differences between reaching for milrinone versus dobutamine versus vasopressin versus I’m sure there’s other players?

Dr. Nayan Arora: Yeah, and potentially milrinone would’ve been a reasonable choice here, to be honest with its impact on pulmonary hemodynamics. And I’m not aware of data to guide one way or another. If you ask a pulmonary hypertension specialist, maybe they would say, maybe we would use milrinone. In this case, we use, I would argue more vasopressin and that’s been supported by our pulmonary hypertension experts. But I would love to hear from other pulmonary hypertension experts around the country to see would they have done this differently and would they have used something like milrinone instead? But you might be more hesitant with the acute kidney injury in terms of using something like milrinone. Are they going to get a lot more hypotensive with that, which may be counteractive to what you want to do? So this would be a great discussion to have with a pulmonary hypertension expert.

Dr. Shreya Trivedi: Oh, sounds good. No worries. I think I was just like, I vaguely remember like, oh, dobutamine versus milrinone. Maybe if you are worried about tachycardia with one.

Dr. Nayan Arora: Yeah, that’s right. So dobutamine is going to generally cause more tachycardia. milrinone you might get more hypotension, and particularly when you have reduced renal clearance, it might exacerbate hypotension.

Dr. Shreya Trivedi: I see, I see.

Dr. Andrew Ling: My experience with it too, at least when I was in the CCU recently, is milrinone takes longer to act and it’s a longer half-life. So in the acute setting, they use dobutamine more, but milrinone is more of a maintenance inotrope for someone.

Dr. Nayan Arora: So you could argue for any of those agents. I think there’s potentially reasons to select one over the other, but I’m not aware of any trials to say you want to use this over this over this.

Dr. Shreya Trivedi: Yeah. Okay.

Dr. Andrew Ling: I think this might also just be dependent on patients too, but is there a certain renal perfusion pressure that you usually target for? Or is it kind of like you have to just see?

Dr. Nayan Arora: Right. So if you look at the textbooks, they’re going to quote things like 60 to 65. You’re not going to get that, particularly in your patients with heart failure. And so traditionally we aim for around 50, but that’s not based on data. That’s just what has traditionally worked for us. And so we generally target 50. I’m going to reiterate that is not evidence-based, okay.

Dr. Andrew Ling: And that’s just a straight like MAP minus CVP.

Dr. Nayan Arora: MAP minus CVP, yep. And so I was just going to say for people interested, the underlying cause of this was actually high output heart failure from his Remodulin. And we got a right heart cath that showed that his cardiac index was actually 4.9, and that’s probably what was responsible for that flushing tachycardia. You could see a relative widening of his pulse pressure, right? He had a systolic of 104, a diastolic of 50, and his SVR was actually quite low on that cath. It was 555. Normal is kind of 900 to 1400 or so. And weaning him off Remodulin actually fixed the whole clinical picture.

Dr. Shreya Trivedi: Awesome. Let me try to summarize. So, these cases were all about flow and you did different things to improve the flow. First case being intra-abdominal hypertension and trying to relieve that so there was better renal perfusion. The second case being …

Dr. Nayan Arora: Low flow state with decompensated heart failure, needing inotropic support.

Dr. Shreya Trivedi: Exactly. And then last one, the teaching point is even if a MAP is normal, maybe for this person, they might need more renal perfusion to really give you the diuresis you’re looking for.

Dr. Nayan Arora: That’s right. I think that the thing I always try to highlight in all these things is people generally want to go straight to focusing on the diuretic management. But the reason I like some of these cases is to really nail home that without flow, it doesn’t matter what you’re doing with the diuretics. You have to fix flow, then focus on the diuresis. And to be fair, these cases are relatively extreme examples. This is not going to be important in over 90% of the patients that I think most folks in medicine see. You’re going to see the typical heart failure patient whose volume overloaded, and you just need to diurese them and that’s where in the previous recording we were talking about using various agents and having a diuretic protocol in your mind of how you want to approach that. But I think highlighting that if something’s not working, you need to step back and really think “Hey, what are my hemodynamics in this situation?”

Dr. Shreya Trivedi: I love that. So I think it’s a very refreshing, but actually this is what you need to be thinking about when you’re feeling like you’re coming up for straws. And on that note, that is a wrap for today’s episode, opinions are our own, and do not represent the opinions of any institutions. Thank you.

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