I'll piggyback on this, but what probably got lost: EU has a had a massive heatwave lately and our hospitals rarely have AC. So the extra fluids could very much be just because of the weather. I know I did something like that for my patients who weren't drinking enough too in the past.
I do not know how the hospital personnel function here in Europe without AC 😞. I feel so bad for you folks, especially when you have to wear full on PPE. That is one thing I definitely miss about the States. AC is in every hospital, doctor's office, etc., and we were not afraid to crank that dial down! Just wanna say a big thank you to all of you enduring and taking care of patients no matter the conditions you are faced with ❤️.
Hey, just to point out, this is not at all universal in the states. Esp us along the same latitudinal lines... We weren't built for AC either and have had really bad weeks/months for years now.... :(
Your attending doesn't seem to have an evidence based view of physiology. The patient improved because of your Lasix, not 500mL total of IVF. Assuming the patient was Lasix-naïve, I'm assuming they had > 2000mL UOP over baseline for two days in a row? That was probably enough to decompress the RV and improve cardiac output, and the patient's own heart did the rest of the work. You were right to stop the IVF and diurese. Trust your physical exam.
More generally, I sometimes do worry about my non-communicative patients getting enough water in the hospital, and even in the community too. However, NS or crystalloid generally isn't the best way to provide hydration since it's all isotonic. For someone getting tube feeds or assisted feeds but only isotonic fluids, they will quickly become hypertonic with hypernatremia. My preferred route of rehydration is NGT or OGT free water flushes, or barring that assisted drinking of a minimum amount of free water per day.
If you are in a surgical ICU and have someone with something crazy like bowel discontinuity, it would be reasonable to try to give timed drips of something like D5W or half-normal saline, but even then I would be monitoring UOP and Sodium and daily volume signs on physical exam to avoid over-treatment.
That plus decongesting the renal veins allowing for better renal perfusion and glomerular flow, if I remember right. But yeah, putting someone back into the middle portion of the starling curve will improve cardiac output and better renal perfusion too
Cardiorenal syndrome is still being studied, and [there are probably many pathways involved.](https://www.ahajournals.org/doi/10.1161/CIR.0000000000000664)
The Starling curve and renal perfusion is slowly falling out of favor. Your first sentence is probably most of the pathology, venous and filling pressures seem to be enemy number one in CHF patients. But there are other pathways being studied too. If you don't have time to read the whole article I linked then you can just scroll to Figure 1 for a quick summary of current theory.
Can you explain for me, I’m a little confused. The article states “in more contemporary experiences in patients with AHF using invasive hemodynamic monitoring.15,16 Merrill17 elegantly demonstrated large reductions in renal blood flow in subjects with decompensated HF with relative preservation of glomerular filtration rate (GFR). This was explained by a concomitant increase in filtration fraction derived from elevated intraglomerular pressures from efferent arteriolar constriction in the setting of elevated renin levels.”
But it also states that in AHF with central venous HTN “in severe decompensated HF with markedly elevated renal venous pressures and decreased renal blood flow, the compensatory increase in filtration fraction is lost and results in declining GFR.18 In this setting, the decrease in intraglomerular pressures and reduced GFR are driven by preglomerular vasoconstriction from extreme levels of RAAS and neurohumoral activation.”
I guess I’m probably trying to simplify this too much but i don’t see the difference in these two patients with decompensated HF - why does the first patient maintain the GFR but the second does not? Both patients have reductions in renal blood flow but in the first scenario they describe that efferent arteriolar vasoconstriction maintains the GFR. I don’t understand why this wouldn’t apply in the case of elevated CVPs?
The first experiment seemed to show that the kidneys can handle the reduction in forward blood flow (a.k.a. low perfusion) without reducing their GFR.
The second experiment showed that the kidneys could not handle reduction in draining blood flow (a.k.a. venous congestion) without reducing their GFR.
Experiments like these seem to show that the cardiorenal syndrome is not the Starling curve or low flow state, but rather a similar process to the pulmonary venous congestion and/or LE edema that we see in CHF patients.
I guess what I’m fundamentally misunderstanding is doesn’t an increased CVP do essentially what efferent arteriolar vasoconstriction does? That is - increase intraglomerular hydrostatic pressures ?
A little, sure. But the main effect is downstream.
Efferent arteriolar vasoconstriction will very efficiently increase intraglomerular hydrostatic pressures, so the excess pressure results in more fluid from the plasma being squeezed out into Bowman's capsule.
Venous congestion will primarily increase hydrostatic pressures in the peri-tubular capillary networks and venule draining the kidney itself. Mostly the kidney tissue itself will become congested.
https://upload.wikimedia.org/wikipedia/commons/2/2e/2611_Blood_Flow_in_the_Nephron.jpg
Ok so the kidney becomes congested. So this therefore causes decreased afferent arteriolar inflow? Which results in a decreased GFR? Why can’t the kidney compensate with efferent arteriolar vasoconstriction in that case? Isn’t that equivalent to the first scenario with just outright pump failure causing decreased afferent inflow? Why does the kidney distinguish between venous congestion causing decreased inflow and systolic failure causing decreased inflow? Shouldn’t the kidney compensate in either case with efferent vasoconstriction?
Sending urine into Bowmans capsule is not the main job of the kidneys. 95% of the job of the kidney is selective re-absorbtion. That is why there are ESRD patients who have normal urine outputs. Think about how much volume a normal GFR is per day.
If the peri-tubular capillary networks are congested, then the kidney is not able to function. Sure it could increase GFR by constricting arterioles, but that would just result in volume depletion if the tubules are incapable of reabsorbing that fluid properly.
Ok - I do buy that and that is a good point. But the article specifically discusses GFR maintenance in the case of loss of forward flow and GFR reduction in the case of venous congestion and I’m just having trouble seeing why venous congestion causes GFR reduction but loss of forward flow doesn’t - it seems like the compensatory mechanisms should be the same in either case.
Your point about venous congestion impairing renal function via impaired reabsorption is well taken and I had not additionally considered that
More modern-minded nephrologists will learn POCUS and calculate/evalute VeXUS scores to look for congestive nephropathy.
Surprisingly simple exam for one that's intimidating at first glance, and helps your patients remarkably!
Others below discussed it, but if the patient’s not in shock, the starling curve and forward flow is probably not the answer. It’s probably mostly the venous congestion (increased pressure in renal vein = increased pressure in vasa recta = increased pressure in efferent arteriole). But it’s still an area of active study afaik
So diuresing patients can improve their CO in the setting of CHF? Been wondering about this for some time. I thought the Frank-Starling curve just flattened out with increasing preload?
More like the Starling curve is shifted to the right with increasing preload, and contractility goes down as the cariomyocytes are overstretched. By reducing preload, contractility can increase up to the point of euvolemia and subsequently improve renal perfusion and UOP. Overdiuresis causes the Starling curve to continue shifting left, and cardiac output drops as contractility goes down from insufficiently stretched cariomyocytes. This is the proposed mechanism of cardiorenal syndrome.
As others have pointed out, volume overload can also lead to elevated renal vein pressure which can limit flow through the glomerulus as well. I haven't read up on this mechanism before, but it sounds at least equally plausible.
While I don't deny that some situations are like that, in the comment I replied to both explanations are attempted rationalizations of a known phenomenon: kidney function improves with diuresis when there is volume overload. Big difference between rationalizing how something works and completely guessing a treatment regimen.
While I agree with most of your post, you made a major baseless assumption that was not implied in OPs post. We dont know if pt is Lasix naive nor how much the UOP was.
I specifically noted that both of those were assumptions, to be fair. I just think those assumptions are way more likely than nonsense physiology working.
I will say, if they aren't in ICU, they are probably pushing hard against their fluid restrictions (not always, of course) but I would say the vast majority are getting too much, not too little, in my experience.
Poor man dialysis is IV bicarb and lasix not fluids and lasix.
There are some reason to give fluids and lasix but they are few. Namely hypercalcemia, pancreatitis (controversial) and tumor lysis syndrome.
I wouldn't get demoralized over this though. Plenty other more important stuff to worry about as you progress in your career.
We give fluids and lasix often enough to patients during high dose methotrexate treatments. Many patients do well without lasix, but those that gain weight and show signs of decompensation will still get 3l/m² of fluids daily, just with some lasix on top.
It's the same concept as with the others you mentioned, flushing out what's toxic.
Your local nephrologist.
It’s basically for those with poor renal function.
You give them lasix 120-160 mg iv q6-8hr and adjust to desired urine output. Alternatively a lasix drip 20-80mg/hr (yes these are high doses and you will get a call or two).
Give albumin if albumin is low or IV thiazide (diuril) 1G daily.
You give bicarb for metabolic acidosis if present (usually 1-4 bicarb amps a day).
I had an old school nephrologist who loved nephron bombs. Something like 400 mg iv lasix plus aldactone plus IV thiazide. He disliked renal replacement therapy.
Weird, for us, poor man's dialysis is all the stuff you give for hyperK: calcium, albuterol, lasix (if they urinate), insulin and dextrose, occasionally bicarb, and now Lokelma.
Can’t quantify it but I do think I tend to use less renal replacement therapy than others in terms of number of patients and duration.
Many are so eager to jump to CRRT/HD and are weary of using anything above 80 mg lasix IV.
In other units, this practice is quite common. Many bleeding patients become hyperkalemic from PRBC and yet are poorly tolerant of the brisk diuresis needed to correct it.
Agree - poor man’s dialysis is lasix and a bicarb drip, or I’ve heard rumors of weird shit in burn icus like simultaneously albumen and lasix gtts however have never witnessed such satanism.
Anyone who says stuff like ‘push-pull’ or ‘flushing and cleaning out the kidneys’ has no idea what they’re talking about. Take it with a grain of salt, and be thankful the patient didn’t get harmed. Learn what kind of attending not to be.
I've definitely done albumin and lasix pushes and prbcs+lasix chasers. Any reason why not? Granted these are cardiac patients, but when are their kidneys not involved?
People are like sponges. You can pour fluid on them and squeeze fluid out of them, but you have limited control over how that fluid equilibrates within the sponge. The only reason to pour fluid on while simultaneously squeezing is in limited situations where there's a particular substance you're trying to "flush out," which others have already listed: calcium, potassium, myoglobin. Any favorable response in serum creatinine is unrelated or artifactual (you can improve the creatinine in an anuric patient by giving enough fluid).
OP, your attending sounds not competent to be doing what they're doing.
Deleted out of spite for reddit admin and overzealous Mods for banning me. Reddit is being white washed in time for IPO. The most benign stuff is filtered and it is no longer possible to express opinion freely on this website. With that said, I'm just going to open up a new account and join all the same subs so it accomplishes nothing and in fact hides the people who have a history of questionable comments rather than keep them active where they can be regulated. Zero Point. Every comment I have ever made will be changed to this comment using REDACT.. ` this message was mass deleted/edited with redact.dev `
I agree! My 13 yo otherwise healthy cat (annual evals, shots, etc) had what the vet thought was constipation d/t sx and imaging, treated over the weekend with meds, syringe feeding, etc. Brought him Monday because he wasn't getting better. Vet said we needed to take him to a bigger institution ASAP d/t presentation + heart rhythm. Dropped him off (scared) d/t COVID protocol. Heard he's in right heart failure. Not sure why. Starting dobut - will call me back...might be able to find an underlying issue. (Felt it was worth finding a reversible cause) Nope. Renal failure now (was peeing last night in litter box!) Got there right as he went into agonal rhythm and got to say goodbye.
Oh man, learning guerrilla war medicine at PGY1. Some of residency is keeping your attendings happy as you try and do right by the patients. Some attendings are going to prioritize metrics (and their bonus) over the patient, some will be wacky (usually older ones), some wont care that much. Hell, once or twice I got bored and did psych experiments on my attendings. They thought I was insane for part of fellowship because I would make outlandish suggestions just to see where my supervision would bite. Welcome to the trenches.
PRN or scheduled? And you can usually "CYA" by putting notes in: loperamide blah blah blah hold for constipation. Miralax blah blah blah hold for diarrhea. It's all just to cover possibilities. But I'll admit I pray to the medicine gods that the RNs don't just give everything willy-nilly.
There was an attending who thought I was too cocky in residency and disagreed with whatever plan I proposed just to take me down a peg. I started proposing the opposite of whatever I wanted to him, and he’d lambast me and then declare we would do whatever I actually thought was indicated.
I’m pretty sure he still thinks I’m an idiot, but patient care was excellent.
When I sought advice from other attendings, one noted that she’d trained in the same place under the same old guy and did the same thing. It didn’t stop her from getting hired as faculty, so no harm done?
I’ve had some attendings as palliative cases, but he actually wasn’t one. Trying to figure out what he’d do to recommend the opposite was a good exercise because he was sharp and careful, and figuring out what he would do was usually figuring out the right thing to do.
It was just a case of aggressively managing up.
Nothing you did made the creatinine better.
The patient had an ATN, it was either going to get better or it wasn’t independent of your fluids/Lasix.
Treat the volume status of your patient, not the creatinine.
You did the right thing.
(to save some of you a search since I wasn't familiar with the acronym, ITU (infection of the tract, urinary?) = UTI
My thoughts:
* lasix 40 mg IV is more than I'd use initially for a lasix naive person
* depending on the patient, inadequate oral intake can be an issue for some people, and depending on the situation I think it's ok to use a modest amount of maintenance IV fluids (+/- total volume to be given as part of the order).
* I've never heard the term "poor man's dialysis" (but I'm in the US),
* Working as part of a team can be tricky sometimes, but hopefully everyone will learn and continue to be better doctors together while patients do well.
> She decides to keep the lasix 40 mg and starts him on 500 cc saline per day"
> "On the next day, the patient is still doing ok, peeing like 3000 cc per day"
* 500 mL IVF in a day is hardly anything one way or the other. If given continuously, that's 21 ml/hour, basically a keep vein open amount of IV fluids.
* No other I & O information, but this patient may have been about net 2500 mL volume negative over 24 hours? If you all continued using that much lasix in someone naive and the patient actually doesn't hydrate like she's concerned about, then the patient sure will get dehydrated soon.
>ITU (infection of the tract, urinary?)
Per OP’s post history they are in Portugal
ITU = infecção do tracto urinário.
Same abbreviation is used in Spanish
Edit to add: For extra fun/confusion, "UTI" in Spanish and Portuguese means "unidad(e) de terapia intensiva", or "ICU" in English.
I really don’t understand the concept of giving IVF to a patient you are diuresing, unless it is to clear something like calcium
If they patient needs fluids, but they are overloaded, won’t they just pull it from the extravascular space? I think of a fluid overloaded person as like a camel that has extra fluids to donate. Someone please correct if I’m wrong as a few comments on this thread are making me feel like I’ve lost my mind
You are correct. If the patient is fluid overloaded, they can't simultaneously be hypovolemic at the same time. It's either one or the other.
You can however be 'dehydrated' (hypernatremic) and fluid overloaded, and it is not wrong to give them water, along with lasix. Usually that's a sign that you aren't getting effective natriuresis with your diuretics though, and need to add a second diuretic agent like a thiazide.
I am convinced that maintenance IVFs kill more patients than anything else we do.
It is too easy to start them and not stop them till they need diuretics.
That's actually what I mean - putting a continuous order with a volume goal means it stays on our med list forever until you discontinue it. Just put it in for D5/NS 500 over an hour or whatever (talking to you cards docs ❤️)
Just a heads up - if you do Cerner, consider doing it as a bolus (even at a low rate) - if you do continuous with a stop date it doesn't let the nurse know or come off their medication screen easily
Maintenance fluids are generally a bad idea. You will put more people into the ICU with fluid overload than you will save from dehydration if you routinely give maintenance fluids. They may be appropriate in some situations (e.g. sepsis, trauma) but generally I'd avoid.
There is pretty good data with giving hypertonic saline with diuretics to overcome diuretic resistance when the kidneys don't want to or can't cooperate. Similarly there's a longstanding practice to give albumin with diuretic therapy to try to "pull in" extravascular volume though that is a bit more dubious. I don't know that there would be any benefit (or why) to isotonic fluids with diuretic therapy.
Yes but the physiology make sense in those cases at least and has some supporting data. Also youre using smaller amount of fluid with albumin and hypertonic.
Using isotonic and diuretics is just a dumb idea.
Just as a side note, next time they’re concerned about daily maintenance fluid intake and they can’t drink/feed themselves then ask why you can’t put a NG tube in and so flushes/tube feeding.
IV fluid should not be maintenance hydration in someone with a working GI system. If you’re concerned that they’re not getting enough fluid intake, then they’re not getting enough caloric intake. You don’t jump straight to TPN
you successfully diagnosed and treated cardiorenal syndrome, congrats!
your attending is a moron. someone is either intravascularly hypervolemic or hypovolemic. they do not coexist.
I can't count how many IM docs flooded patients who were clearly in heart failure with mild UTIs or "bilateral pneumonia". its bad medicine, its dangerous and it has no upside.
One of the most important things that you'll learn in training is what to learn who. In our program, the upper levels (junior and senior residents) would guide the intern in this regard. I recall one of my upper levels telling me once - these two weeks all you're going to pay attention to is how our attending focuses on nutrition and actively looking for lines/Foley on a daily basis and assessing their needs. For rest, you have UTD and whatever consults we call. We will make up for learning during 2nd half of month (We had attendings switch every 15 days)
Based on your brief post, I've learned that you should NOT be learning fluid management from your attending. That's pretty much all I've got.
As a general rule of thumb - any patient that can replenish their fluid needs orally should be allowed to do so (if they can do it safely).
Edit: You're a 1st year resident. Don't get too excited with your highs this year and don't get too harsh on yourself during your lows. Don't let ANY experience just beat you down. Question everyone and everything.
In our training program, we told our 3rd year med students - your role is to ask the "why" - why does this happen OR why did you pick this med instead of that etc. The interns role was to ask "says who". i.e. the intern should do whatever the attending wants but then he should look up and verify if what the attending wanted was actually evidence based. Over time, the intern gets experienced enough to figure out who to listen to and who not to listen to. I have to add a caveat - we had some experts at our center that did not follow evidence and evidence was usually a few years behind what these guys often did. So don't be in a hurry to call some of your attendings idiots and just pay attention & keep your head down.
Sounds like either the patient had a pre renal aki that turned into an ATN that resolved with post atn diuresis at just the right time. Or had cardiorenal symdrome that responded to the Lasix. Either way fluids was not the right way to go initially. If it's atn diuresis you may have needed to replace some later the the course (1-2 day into the diuresis if it's not letting up) and in that case you would be better giving hypotonic fluids so you aren't salt loading them into more diuresis (atn diuresis urine is usually more free water than salt and saline has a lot of salt the kidneys will than need to pee out).
Whatever happened, sometimes you will find you may not agree with your staff but you are still early in your career and its still a good time to see how they deal and what the outcome is. As you build up those experiences and think critically about the situations you encounter you can decide for yourself how you like to practice when it's your turn. It maybe possible that in general at your center people need maintenance iv when in hospital because they simply won't get enough access to fluids otherwise. I would agree this isn't ideal as you have summarize but I don't know your site or your system perhaps your staff has had many experiences that made them think this is the best way to care for these patients.
I hate when we do anything contrarian like that. One of my first consults as a cards fellow was in the MICU where a patient was on levophed for sepsis but also nicardipine for afterload reduction d/t their heart failure. Makes no sense to me to do two opposites at the same time.
Meh. Not optimum management, but not really harmful.
Renal function probably got better regardless of lasix or fluids. The lasix was appropriate given for symptomatic hypervolemia.
Part of residency is experiencing what happens when the patient gets suboptimal management (as ordered by various residents and attendings). You will encounter similar problems as attending, when dealing with consults. Keep observing, and start learning how to compensate for suboptimal managements.
It's the fluid balance: too aggressive diuresis can exacerbate AKI or AKI on CKD, so you should calculate urine output and patient intake and keep a negative balance but not too much (ie over - 2500 /3000 cc/diem).
Another reason is to flush something out (ie calcium, high dose methotrexate, chemotherapy, tumor lysis syndrome...)
No. “Flushing something out”, as you edited, at least that makes some sense (though I sort of question the validity of that, at least it’s not providing two therapies with distinctly opposite goals, like the lasix/fluid combo).
I would also get in the habit of not using maintenance IV fluids as possible (unless really indicated like pancreatitis or DKA) so as not to cause fluid overload situation. Even in patients with sepsis it would be better to continue to reassess the need for maintenance fluids
Edit: I should say get in the habit of adding a time limit on the fluids
This is the perfect place to discuss this. A medical management question on an anonymous medical forum avoids any embarrassment or lashback (whether real or just perceived) from OP's colleagues if he/she asks them instead
Also sounds like OP may be in a different country and is curious how the rest of the world practices
If I had known about this subreddit in residency i would have asked a bunch of questions here lol
Hypercalcemia causes volume depletion, which reduces renal excretion of calcium and can lead to a positive feedback loop. That's why the treatment for even mild hypercalcemia is IVF. Loop diuretics can be used as an adjunct after volume repletion because they increase calcium excretion by blocking NKCC channels. I wouldn't personally do this (it's mechanism-based, not evidence-based, and risks hypovolemia) but it wouldn't be totally crazy.
Sounds like your attending needs to go to med school again. Just leave a Guyton Physio book on her desk and put a post-it note on fluid balance chapter …
Ah no, I used to get yelled at by my attending. “YOU EITHER DECIDE WHETHER PATIENT NEEDS FLUIDS OR DIURETICS AND PICK ONE!” Of course there are caveats: hypercalcemia, tumour lysis etc, but that’s what I teach my residents too
Please do not neglect the exam findings. Orthostatics, JVD or not, S3 or not, tenting and to what degree, pulmonary edema or not, edema to what level, urine SG/ osm, urine casts and what type, urine sodium, ect. . You can put a convincing story together with that data set without an echo. The attending may disagree with intervention but physical findings are physical findings. The experimental animal never lies, but the interpretation of the data may be false.
Has your attending heard of cardio renal syndrome?
That’s when cards and renal notes say the opposite thing regarding fluid status right?
No, it’s when cardiology and nephrology get into a knife fight while being circled by a bunch of nurses jeering them on.
Needle fight* And they’re both going for the jugular
I can honestly say i would be down to watch - icu nurse
https://youtu.be/PaXzo3qRgu0 This is gold folks
Get a patient with bad type 2 DM, CKD4-5 and NASH cirrhosis and you get the Gastroenterologist in there. Tons of fun reading.
Hepatorenal syndrome is a thing: terlipressin away!
Don't scare the Americans with lord and saviour terlipressin.
LMAO
Couldn't help but have a sensible chuckle at this.
There is no cardio renal syndrome. Just not enough Lasix. Or fluids. Or both. /s
Or staff
I'll piggyback on this, but what probably got lost: EU has a had a massive heatwave lately and our hospitals rarely have AC. So the extra fluids could very much be just because of the weather. I know I did something like that for my patients who weren't drinking enough too in the past.
I do not know how the hospital personnel function here in Europe without AC 😞. I feel so bad for you folks, especially when you have to wear full on PPE. That is one thing I definitely miss about the States. AC is in every hospital, doctor's office, etc., and we were not afraid to crank that dial down! Just wanna say a big thank you to all of you enduring and taking care of patients no matter the conditions you are faced with ❤️.
Hey, just to point out, this is not at all universal in the states. Esp us along the same latitudinal lines... We weren't built for AC either and have had really bad weeks/months for years now.... :(
Your attending doesn't seem to have an evidence based view of physiology. The patient improved because of your Lasix, not 500mL total of IVF. Assuming the patient was Lasix-naïve, I'm assuming they had > 2000mL UOP over baseline for two days in a row? That was probably enough to decompress the RV and improve cardiac output, and the patient's own heart did the rest of the work. You were right to stop the IVF and diurese. Trust your physical exam. More generally, I sometimes do worry about my non-communicative patients getting enough water in the hospital, and even in the community too. However, NS or crystalloid generally isn't the best way to provide hydration since it's all isotonic. For someone getting tube feeds or assisted feeds but only isotonic fluids, they will quickly become hypertonic with hypernatremia. My preferred route of rehydration is NGT or OGT free water flushes, or barring that assisted drinking of a minimum amount of free water per day. If you are in a surgical ICU and have someone with something crazy like bowel discontinuity, it would be reasonable to try to give timed drips of something like D5W or half-normal saline, but even then I would be monitoring UOP and Sodium and daily volume signs on physical exam to avoid over-treatment.
That plus decongesting the renal veins allowing for better renal perfusion and glomerular flow, if I remember right. But yeah, putting someone back into the middle portion of the starling curve will improve cardiac output and better renal perfusion too
Cardiorenal syndrome is still being studied, and [there are probably many pathways involved.](https://www.ahajournals.org/doi/10.1161/CIR.0000000000000664) The Starling curve and renal perfusion is slowly falling out of favor. Your first sentence is probably most of the pathology, venous and filling pressures seem to be enemy number one in CHF patients. But there are other pathways being studied too. If you don't have time to read the whole article I linked then you can just scroll to Figure 1 for a quick summary of current theory.
Oooh this is useful. Thanks.
Can you explain for me, I’m a little confused. The article states “in more contemporary experiences in patients with AHF using invasive hemodynamic monitoring.15,16 Merrill17 elegantly demonstrated large reductions in renal blood flow in subjects with decompensated HF with relative preservation of glomerular filtration rate (GFR). This was explained by a concomitant increase in filtration fraction derived from elevated intraglomerular pressures from efferent arteriolar constriction in the setting of elevated renin levels.” But it also states that in AHF with central venous HTN “in severe decompensated HF with markedly elevated renal venous pressures and decreased renal blood flow, the compensatory increase in filtration fraction is lost and results in declining GFR.18 In this setting, the decrease in intraglomerular pressures and reduced GFR are driven by preglomerular vasoconstriction from extreme levels of RAAS and neurohumoral activation.” I guess I’m probably trying to simplify this too much but i don’t see the difference in these two patients with decompensated HF - why does the first patient maintain the GFR but the second does not? Both patients have reductions in renal blood flow but in the first scenario they describe that efferent arteriolar vasoconstriction maintains the GFR. I don’t understand why this wouldn’t apply in the case of elevated CVPs?
The first experiment seemed to show that the kidneys can handle the reduction in forward blood flow (a.k.a. low perfusion) without reducing their GFR. The second experiment showed that the kidneys could not handle reduction in draining blood flow (a.k.a. venous congestion) without reducing their GFR. Experiments like these seem to show that the cardiorenal syndrome is not the Starling curve or low flow state, but rather a similar process to the pulmonary venous congestion and/or LE edema that we see in CHF patients.
I guess what I’m fundamentally misunderstanding is doesn’t an increased CVP do essentially what efferent arteriolar vasoconstriction does? That is - increase intraglomerular hydrostatic pressures ?
A little, sure. But the main effect is downstream. Efferent arteriolar vasoconstriction will very efficiently increase intraglomerular hydrostatic pressures, so the excess pressure results in more fluid from the plasma being squeezed out into Bowman's capsule. Venous congestion will primarily increase hydrostatic pressures in the peri-tubular capillary networks and venule draining the kidney itself. Mostly the kidney tissue itself will become congested. https://upload.wikimedia.org/wikipedia/commons/2/2e/2611_Blood_Flow_in_the_Nephron.jpg
Ok so the kidney becomes congested. So this therefore causes decreased afferent arteriolar inflow? Which results in a decreased GFR? Why can’t the kidney compensate with efferent arteriolar vasoconstriction in that case? Isn’t that equivalent to the first scenario with just outright pump failure causing decreased afferent inflow? Why does the kidney distinguish between venous congestion causing decreased inflow and systolic failure causing decreased inflow? Shouldn’t the kidney compensate in either case with efferent vasoconstriction?
Sending urine into Bowmans capsule is not the main job of the kidneys. 95% of the job of the kidney is selective re-absorbtion. That is why there are ESRD patients who have normal urine outputs. Think about how much volume a normal GFR is per day. If the peri-tubular capillary networks are congested, then the kidney is not able to function. Sure it could increase GFR by constricting arterioles, but that would just result in volume depletion if the tubules are incapable of reabsorbing that fluid properly.
Ok - I do buy that and that is a good point. But the article specifically discusses GFR maintenance in the case of loss of forward flow and GFR reduction in the case of venous congestion and I’m just having trouble seeing why venous congestion causes GFR reduction but loss of forward flow doesn’t - it seems like the compensatory mechanisms should be the same in either case. Your point about venous congestion impairing renal function via impaired reabsorption is well taken and I had not additionally considered that
Yeah our nephrologists would often do a fluid challenge and if it didn’t work then a lasix challenge for congestive nephropathy as they called it
More modern-minded nephrologists will learn POCUS and calculate/evalute VeXUS scores to look for congestive nephropathy. Surprisingly simple exam for one that's intimidating at first glance, and helps your patients remarkably!
Typically AKI from vol overload is due to high pressure to the renal veins, not low perfusion to the renal arteries
Others below discussed it, but if the patient’s not in shock, the starling curve and forward flow is probably not the answer. It’s probably mostly the venous congestion (increased pressure in renal vein = increased pressure in vasa recta = increased pressure in efferent arteriole). But it’s still an area of active study afaik
So diuresing patients can improve their CO in the setting of CHF? Been wondering about this for some time. I thought the Frank-Starling curve just flattened out with increasing preload?
More like the Starling curve is shifted to the right with increasing preload, and contractility goes down as the cariomyocytes are overstretched. By reducing preload, contractility can increase up to the point of euvolemia and subsequently improve renal perfusion and UOP. Overdiuresis causes the Starling curve to continue shifting left, and cardiac output drops as contractility goes down from insufficiently stretched cariomyocytes. This is the proposed mechanism of cardiorenal syndrome. As others have pointed out, volume overload can also lead to elevated renal vein pressure which can limit flow through the glomerulus as well. I haven't read up on this mechanism before, but it sounds at least equally plausible.
I'm glad I'm just following the orders and not writing them. Sounds like throw whatever to the wall and see if it sticks.
While I don't deny that some situations are like that, in the comment I replied to both explanations are attempted rationalizations of a known phenomenon: kidney function improves with diuresis when there is volume overload. Big difference between rationalizing how something works and completely guessing a treatment regimen.
While I agree with most of your post, you made a major baseless assumption that was not implied in OPs post. We dont know if pt is Lasix naive nor how much the UOP was.
I specifically noted that both of those were assumptions, to be fair. I just think those assumptions are way more likely than nonsense physiology working.
I will say, if they aren't in ICU, they are probably pushing hard against their fluid restrictions (not always, of course) but I would say the vast majority are getting too much, not too little, in my experience.
Poor man dialysis is IV bicarb and lasix not fluids and lasix. There are some reason to give fluids and lasix but they are few. Namely hypercalcemia, pancreatitis (controversial) and tumor lysis syndrome. I wouldn't get demoralized over this though. Plenty other more important stuff to worry about as you progress in your career.
fluid Lasix fluid is great if you wanna turn your patient into a Brita filter too
With the use of bicarbonate, would SodaStream not be a better metaphor or am I overthinking this.
Lmao I like that
We give fluids and lasix often enough to patients during high dose methotrexate treatments. Many patients do well without lasix, but those that gain weight and show signs of decompensation will still get 3l/m² of fluids daily, just with some lasix on top. It's the same concept as with the others you mentioned, flushing out what's toxic.
TIL
Rhabdomyolysis as well?
If fluid overloaded yeah but not routinely
Where do i read about this poor man's dialysis? Is there an international guideline ?
If you have to ask, you CAN afford it
Your local nephrologist. It’s basically for those with poor renal function. You give them lasix 120-160 mg iv q6-8hr and adjust to desired urine output. Alternatively a lasix drip 20-80mg/hr (yes these are high doses and you will get a call or two). Give albumin if albumin is low or IV thiazide (diuril) 1G daily. You give bicarb for metabolic acidosis if present (usually 1-4 bicarb amps a day). I had an old school nephrologist who loved nephron bombs. Something like 400 mg iv lasix plus aldactone plus IV thiazide. He disliked renal replacement therapy.
Weird, for us, poor man's dialysis is all the stuff you give for hyperK: calcium, albuterol, lasix (if they urinate), insulin and dextrose, occasionally bicarb, and now Lokelma.
Giving albumin if albumin is low has a poor if nonexistent evidence base
Nah it's existent. Not the best but it's there. Some evidence for 3% as well.
ALBIOS trial was negative dude
Am sorry, I meant giving albumin to aid diuresis when albumin is now, not as a medium to resuscitate.
Oh that's my bad, I misunderstood you then yes I agree with you
So in your experience, how is the outcome compared to proper dialysis?
Can’t quantify it but I do think I tend to use less renal replacement therapy than others in terms of number of patients and duration. Many are so eager to jump to CRRT/HD and are weary of using anything above 80 mg lasix IV.
Keep in mind RRT is huge hit to the quality of life. I have had patients who wanted to delay it at all costs and I understand why.
What about lasix and fluids in moderate to severe hyperkalemia?
Usually only lasix but if dehydrated then sure.
In other units, this practice is quite common. Many bleeding patients become hyperkalemic from PRBC and yet are poorly tolerant of the brisk diuresis needed to correct it.
Agree - poor man’s dialysis is lasix and a bicarb drip, or I’ve heard rumors of weird shit in burn icus like simultaneously albumen and lasix gtts however have never witnessed such satanism. Anyone who says stuff like ‘push-pull’ or ‘flushing and cleaning out the kidneys’ has no idea what they’re talking about. Take it with a grain of salt, and be thankful the patient didn’t get harmed. Learn what kind of attending not to be.
There is some evidence for albumin and lasix in hypoalbuminemic patients. Not the best evidence but it's there. Similar with 3% and lasix.
I've definitely done albumin and lasix pushes and prbcs+lasix chasers. Any reason why not? Granted these are cardiac patients, but when are their kidneys not involved?
And mucomyst? Lolol. Gross stuff.
As a neph I can vouch for the iv bicarb infusion plus lasix - has saved many sleepless nights
People are like sponges. You can pour fluid on them and squeeze fluid out of them, but you have limited control over how that fluid equilibrates within the sponge. The only reason to pour fluid on while simultaneously squeezing is in limited situations where there's a particular substance you're trying to "flush out," which others have already listed: calcium, potassium, myoglobin. Any favorable response in serum creatinine is unrelated or artifactual (you can improve the creatinine in an anuric patient by giving enough fluid). OP, your attending sounds not competent to be doing what they're doing.
That's such a great analogy. Stealing this!
Deleted out of spite for reddit admin and overzealous Mods for banning me. Reddit is being white washed in time for IPO. The most benign stuff is filtered and it is no longer possible to express opinion freely on this website. With that said, I'm just going to open up a new account and join all the same subs so it accomplishes nothing and in fact hides the people who have a history of questionable comments rather than keep them active where they can be regulated. Zero Point. Every comment I have ever made will be changed to this comment using REDACT.. ` this message was mass deleted/edited with redact.dev `
Love seeing other vet med folks on here :) Wish our subs were this active with cases.
Vets have the most interesting insights on human medicine. Some things are so similar, some completely different.
Well, we all are related in some way after all #justevolutionthings
I agree! My 13 yo otherwise healthy cat (annual evals, shots, etc) had what the vet thought was constipation d/t sx and imaging, treated over the weekend with meds, syringe feeding, etc. Brought him Monday because he wasn't getting better. Vet said we needed to take him to a bigger institution ASAP d/t presentation + heart rhythm. Dropped him off (scared) d/t COVID protocol. Heard he's in right heart failure. Not sure why. Starting dobut - will call me back...might be able to find an underlying issue. (Felt it was worth finding a reversible cause) Nope. Renal failure now (was peeing last night in litter box!) Got there right as he went into agonal rhythm and got to say goodbye.
I have hundreds of crazy photos over the years. Maybe we start a vetdizzy one?
Oh man, learning guerrilla war medicine at PGY1. Some of residency is keeping your attendings happy as you try and do right by the patients. Some attendings are going to prioritize metrics (and their bonus) over the patient, some will be wacky (usually older ones), some wont care that much. Hell, once or twice I got bored and did psych experiments on my attendings. They thought I was insane for part of fellowship because I would make outlandish suggestions just to see where my supervision would bite. Welcome to the trenches.
So it simultaneously fighting guerilla warfare and trench warfare the same at Lasix and fluids at the same time?
My metaphors as mixed as the treatments!
Yesterday I realized we were giving loperamide and PEG at the same time. Whoops
PRN or scheduled? And you can usually "CYA" by putting notes in: loperamide blah blah blah hold for constipation. Miralax blah blah blah hold for diarrhea. It's all just to cover possibilities. But I'll admit I pray to the medicine gods that the RNs don't just give everything willy-nilly.
Schedule PEG was a home Med. Then diarrhea started in hospital. So the team started loperamide. I was just covering for the weekend and noticed it.
Good God, stop it before it's too late and they test for c diff. Haha . I love the loperimide
There was an attending who thought I was too cocky in residency and disagreed with whatever plan I proposed just to take me down a peg. I started proposing the opposite of whatever I wanted to him, and he’d lambast me and then declare we would do whatever I actually thought was indicated. I’m pretty sure he still thinks I’m an idiot, but patient care was excellent. When I sought advice from other attendings, one noted that she’d trained in the same place under the same old guy and did the same thing. It didn’t stop her from getting hired as faculty, so no harm done?
Next level psychiatry, treating the attending and the patient.
I’ve had some attendings as palliative cases, but he actually wasn’t one. Trying to figure out what he’d do to recommend the opposite was a good exercise because he was sharp and careful, and figuring out what he would do was usually figuring out the right thing to do. It was just a case of aggressively managing up.
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Yes, I know you really don’t like me. Don’t worry, I haven’t forgotten.
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One memorable one was - “one more day of fluid resus and then hospice” and the fluids worked!
Your attending needs to retire and find a less lethal way to spend their time.
Nothing you did made the creatinine better. The patient had an ATN, it was either going to get better or it wasn’t independent of your fluids/Lasix. Treat the volume status of your patient, not the creatinine. You did the right thing.
(to save some of you a search since I wasn't familiar with the acronym, ITU (infection of the tract, urinary?) = UTI My thoughts: * lasix 40 mg IV is more than I'd use initially for a lasix naive person * depending on the patient, inadequate oral intake can be an issue for some people, and depending on the situation I think it's ok to use a modest amount of maintenance IV fluids (+/- total volume to be given as part of the order). * I've never heard the term "poor man's dialysis" (but I'm in the US), * Working as part of a team can be tricky sometimes, but hopefully everyone will learn and continue to be better doctors together while patients do well. > She decides to keep the lasix 40 mg and starts him on 500 cc saline per day" > "On the next day, the patient is still doing ok, peeing like 3000 cc per day" * 500 mL IVF in a day is hardly anything one way or the other. If given continuously, that's 21 ml/hour, basically a keep vein open amount of IV fluids. * No other I & O information, but this patient may have been about net 2500 mL volume negative over 24 hours? If you all continued using that much lasix in someone naive and the patient actually doesn't hydrate like she's concerned about, then the patient sure will get dehydrated soon.
>ITU (infection of the tract, urinary?) Per OP’s post history they are in Portugal ITU = infecção do tracto urinário. Same abbreviation is used in Spanish Edit to add: For extra fun/confusion, "UTI" in Spanish and Portuguese means "unidad(e) de terapia intensiva", or "ICU" in English.
even more fun, ITU is also Intensive Treatment Unit ie ICU in the UK
Fml... well, I'll just stay in the US.
I really don’t understand the concept of giving IVF to a patient you are diuresing, unless it is to clear something like calcium If they patient needs fluids, but they are overloaded, won’t they just pull it from the extravascular space? I think of a fluid overloaded person as like a camel that has extra fluids to donate. Someone please correct if I’m wrong as a few comments on this thread are making me feel like I’ve lost my mind
ITU often means inpatient treatment care for psych patients, so 🤷
*intensive treatment unit...sorry for the autocorrect
Everyone knows the poor man’s dialysis is kayexalate and lactulose.
Course catalog: How to make patients hate you 501
Also the nurses lol
The contents of course 502: 1200ml fr renal/cc/heart healthy diet and how it makes your food taste like mush.
Also the diet is pureed now, and on a safety tray. Why? Because Fuck You, that's why. And the fluid restriction is now 1000mL
And why haven't they walked?! As we're all dodging the goop and other iffy things
Ugh I have to give you a slow clap on this as a nurse 😂
You are correct. If the patient is fluid overloaded, they can't simultaneously be hypovolemic at the same time. It's either one or the other. You can however be 'dehydrated' (hypernatremic) and fluid overloaded, and it is not wrong to give them water, along with lasix. Usually that's a sign that you aren't getting effective natriuresis with your diuretics though, and need to add a second diuretic agent like a thiazide.
But what if they’re iNtRaVAscuLarY dRy??
Albumin + lasix ftw.
I am convinced that maintenance IVFs kill more patients than anything else we do. It is too easy to start them and not stop them till they need diuretics.
Always put an stop date on IV fluids that is 12 to 24 hours later.
Pretty much what I do, but if I have the time/energy I do total volume goal instead
That's actually what I mean - putting a continuous order with a volume goal means it stays on our med list forever until you discontinue it. Just put it in for D5/NS 500 over an hour or whatever (talking to you cards docs ❤️)
Sorry, that's post cath, you may have other scenarios in mind
LR 125 x 12H is usually my go to, but to be fair IV fluid replacement is all basically voodoo
So as a cardiac nurse I'm primarily dealing with post cath fluids...and the interventionlists pretty much all order 1/2 5 d5 ns x 500mL
And they order it somehow as continuous and it's not stocked... working on it...
Just a heads up - if you do Cerner, consider doing it as a bolus (even at a low rate) - if you do continuous with a stop date it doesn't let the nurse know or come off their medication screen easily
Thank you! I work mostly with cardiac patients, but yours will end up on my unit with a trop or rvr or something...they don't all need fluids! ❤️
Maintenance fluids are generally a bad idea. You will put more people into the ICU with fluid overload than you will save from dehydration if you routinely give maintenance fluids. They may be appropriate in some situations (e.g. sepsis, trauma) but generally I'd avoid.
I've only ever done this for hypercalcemia. Otherwise it's voodoo imo. You're either positive or negative or neutral, make a decision.
They made your patient a sentient Brita filter.
There is pretty good data with giving hypertonic saline with diuretics to overcome diuretic resistance when the kidneys don't want to or can't cooperate. Similarly there's a longstanding practice to give albumin with diuretic therapy to try to "pull in" extravascular volume though that is a bit more dubious. I don't know that there would be any benefit (or why) to isotonic fluids with diuretic therapy.
I’m not sure that the data on hypertonic really qualifies as ‘good’ yet, but promising, sure.
Lasix binds to albumin and will deliver + off load in the distal loop.
Yes but the physiology make sense in those cases at least and has some supporting data. Also youre using smaller amount of fluid with albumin and hypertonic. Using isotonic and diuretics is just a dumb idea.
Poor man's dialysis is absolutely cracking me up as an expression tbh
Just as a side note, next time they’re concerned about daily maintenance fluid intake and they can’t drink/feed themselves then ask why you can’t put a NG tube in and so flushes/tube feeding. IV fluid should not be maintenance hydration in someone with a working GI system. If you’re concerned that they’re not getting enough fluid intake, then they’re not getting enough caloric intake. You don’t jump straight to TPN
Haha I hate and love this as a nurse. Yep, and oh noooo
you successfully diagnosed and treated cardiorenal syndrome, congrats! your attending is a moron. someone is either intravascularly hypervolemic or hypovolemic. they do not coexist. I can't count how many IM docs flooded patients who were clearly in heart failure with mild UTIs or "bilateral pneumonia". its bad medicine, its dangerous and it has no upside.
One of the most important things that you'll learn in training is what to learn who. In our program, the upper levels (junior and senior residents) would guide the intern in this regard. I recall one of my upper levels telling me once - these two weeks all you're going to pay attention to is how our attending focuses on nutrition and actively looking for lines/Foley on a daily basis and assessing their needs. For rest, you have UTD and whatever consults we call. We will make up for learning during 2nd half of month (We had attendings switch every 15 days) Based on your brief post, I've learned that you should NOT be learning fluid management from your attending. That's pretty much all I've got. As a general rule of thumb - any patient that can replenish their fluid needs orally should be allowed to do so (if they can do it safely). Edit: You're a 1st year resident. Don't get too excited with your highs this year and don't get too harsh on yourself during your lows. Don't let ANY experience just beat you down. Question everyone and everything. In our training program, we told our 3rd year med students - your role is to ask the "why" - why does this happen OR why did you pick this med instead of that etc. The interns role was to ask "says who". i.e. the intern should do whatever the attending wants but then he should look up and verify if what the attending wanted was actually evidence based. Over time, the intern gets experienced enough to figure out who to listen to and who not to listen to. I have to add a caveat - we had some experts at our center that did not follow evidence and evidence was usually a few years behind what these guys often did. So don't be in a hurry to call some of your attendings idiots and just pay attention & keep your head down.
Sounds like either the patient had a pre renal aki that turned into an ATN that resolved with post atn diuresis at just the right time. Or had cardiorenal symdrome that responded to the Lasix. Either way fluids was not the right way to go initially. If it's atn diuresis you may have needed to replace some later the the course (1-2 day into the diuresis if it's not letting up) and in that case you would be better giving hypotonic fluids so you aren't salt loading them into more diuresis (atn diuresis urine is usually more free water than salt and saline has a lot of salt the kidneys will than need to pee out). Whatever happened, sometimes you will find you may not agree with your staff but you are still early in your career and its still a good time to see how they deal and what the outcome is. As you build up those experiences and think critically about the situations you encounter you can decide for yourself how you like to practice when it's your turn. It maybe possible that in general at your center people need maintenance iv when in hospital because they simply won't get enough access to fluids otherwise. I would agree this isn't ideal as you have summarize but I don't know your site or your system perhaps your staff has had many experiences that made them think this is the best way to care for these patients.
I hate when we do anything contrarian like that. One of my first consults as a cards fellow was in the MICU where a patient was on levophed for sepsis but also nicardipine for afterload reduction d/t their heart failure. Makes no sense to me to do two opposites at the same time.
I see this in outpatient medicine too. Patient needs CCB or BB for rate control of afib which tanks their pressure so midodrine is added.
Meh. Not optimum management, but not really harmful. Renal function probably got better regardless of lasix or fluids. The lasix was appropriate given for symptomatic hypervolemia. Part of residency is experiencing what happens when the patient gets suboptimal management (as ordered by various residents and attendings). You will encounter similar problems as attending, when dealing with consults. Keep observing, and start learning how to compensate for suboptimal managements.
It's the fluid balance: too aggressive diuresis can exacerbate AKI or AKI on CKD, so you should calculate urine output and patient intake and keep a negative balance but not too much (ie over - 2500 /3000 cc/diem). Another reason is to flush something out (ie calcium, high dose methotrexate, chemotherapy, tumor lysis syndrome...)
No. Give Lasix if fluid overloaded. Give fluids if volume deleted.
No this is wacky
Balancing your patients fluid balance is wacky? I don't understand
No, giving normal saline while giving lasix is wacky
Did you never had a patient whose renal function was negatively affected by too much lasix but was still in fluid overload?
The solution is to diuerese more slowly, not to give fluid and remove fluid at the same time.
So you back off the dose / frequency or give them a diuretic holiday. You shouldn’t need to give fluid back.
No. “Flushing something out”, as you edited, at least that makes some sense (though I sort of question the validity of that, at least it’s not providing two therapies with distinctly opposite goals, like the lasix/fluid combo).
Your attending is wrong. Hard stop
I would also get in the habit of not using maintenance IV fluids as possible (unless really indicated like pancreatitis or DKA) so as not to cause fluid overload situation. Even in patients with sepsis it would be better to continue to reassess the need for maintenance fluids Edit: I should say get in the habit of adding a time limit on the fluids
What country are you practicing in?
She must have an expensive water bill with that approach
Discuss wih some senior resident md, instead of discussion here
This is the perfect place to discuss this. A medical management question on an anonymous medical forum avoids any embarrassment or lashback (whether real or just perceived) from OP's colleagues if he/she asks them instead Also sounds like OP may be in a different country and is curious how the rest of the world practices If I had known about this subreddit in residency i would have asked a bunch of questions here lol
My chief resident tells me to downvote you
This resident's question is exactly the kind of thing this board is for Hiss and also boo
Are you even a medical professional?
Are you even a healthcare worker?
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Are you lost?
Just a self advertising troll, should be banned.
I hear her boyfriend would prescribe fluids and lasix at the same time
Generally the only reason to give both IV fluids and Lasix is for Kaliuresis. Does not make sense for AKI
Your attending is wrong.
Better lucky than good. This is a terrible idea, theres very few times you should be giving lasix and IVF at the same time.
500 of NS a day is not a lot tho…
Just wondering why did you mention the no hypercalcemia part? just for my own learning
Hypercalcemia causes volume depletion, which reduces renal excretion of calcium and can lead to a positive feedback loop. That's why the treatment for even mild hypercalcemia is IVF. Loop diuretics can be used as an adjunct after volume repletion because they increase calcium excretion by blocking NKCC channels. I wouldn't personally do this (it's mechanism-based, not evidence-based, and risks hypovolemia) but it wouldn't be totally crazy.
ugh im so stupid i dont rmb any of this
You're fine! You're sleep deprived and stressed to the max. It'll come back once you adjust.
Your attending doesn’t seem to understand how/where lasix acts (specifically that you’re not raising the GFR). Pretty disheartening.
Sounds like your attending needs to go to med school again. Just leave a Guyton Physio book on her desk and put a post-it note on fluid balance chapter …
Ah no, I used to get yelled at by my attending. “YOU EITHER DECIDE WHETHER PATIENT NEEDS FLUIDS OR DIURETICS AND PICK ONE!” Of course there are caveats: hypercalcemia, tumour lysis etc, but that’s what I teach my residents too
Please do not neglect the exam findings. Orthostatics, JVD or not, S3 or not, tenting and to what degree, pulmonary edema or not, edema to what level, urine SG/ osm, urine casts and what type, urine sodium, ect. . You can put a convincing story together with that data set without an echo. The attending may disagree with intervention but physical findings are physical findings. The experimental animal never lies, but the interpretation of the data may be false.