Let's get salty part 3

First I recall time served on the inpatient Cardiology service in residency. Then we review the evidence for salt and fluid restriction in acute and chronic heart failure. 

 Aliti GB, Rabelo ER, Clausell N, Rohde LE, Biolo A, Beck-da-Silva L. Aggressive fluid and sodium restriction in acute decompensated heart failure: a randomized clinical trial. JAMA Intern Med. 2013 Jun 24;173(12):1058-64. 

Herrmann JJ, Brunner-La Rocca HP, Baltussen LEHJM, Beckers-Wesche F, Bekkers SCAM, Bellersen L, van Eck JWM, Hassing HC, Jaarsma T, Linssen GCM, Pisters R, Sanders-van Wijk S, Verdijk MHI, Handoko ML, van der Meer P, Verbrugge FH, Januzzi JL Jr, Bayés-Genís A, Nieuwlaat R, Rodwell L, Gommans DHF, van Kimmenade RRJ. Liberal fluid intake versus fluid restriction in chronic heart failure: a randomized clinical trial. Nat Med. 2025 Jun;31(6):2062-2068. 

Hsu SM, Lin YH, Lin YC, Liu SJ, Liu CJ, Hung CL, Wang TJ. Fluid intake impact on heart failure: Systematic review and meta-analysis with trial sequential analysis. J Formos Med Assoc. 2025 Jul;124(7):650-659. 

Mullens W, Damman K, Dhont S, Banerjee D, Bayes-Genis A, Cannata A, Chioncel O, Cikes M, Ezekowitz J, Flammer AJ, Martens P, Mebazaa A, Mentz RJ, Miró Ò, Moura B, Nunez J, Ter Maaten JM, Testani J, van Kimmenade R, Verbrugge FH, Metra M, Rosano GMC, Filippatos G. Dietary sodium and fluid intake in heart failure. A clinical consensus statement of the Heart Failure Association of the ESC. Eur J Heart Fail. 2024 Apr;26(4):730-741. 

Urban S, Fułek M, Błaziak M, Fułek K, Iwanek G, Jura M, Grzesiak M, Szymański O, Stańczykiewicz B, Ptaszkowski K, Zymlinski R, Ponikowski P, Biegus J. Role of dietary sodium restriction in chronic heart failure: systematic review and meta-analysis. Clin Res Cardiol. 2024 Sep;113(9):1331-1342. 

Transcript

SPEAKER_00 0:14

Hello again, friends! This episode is late coming out because work has been crazy. And my son and I just got back from a trip to Paris. I can sum that vacation up in three short words. Hot as shit. It was in the 90s and relatively humid every day, and France hasn't caught on to air conditioning yet. Now I know what it's like to live inside a teenage boy's ball sack for two weeks. Basically, I started sweating the minute I got off the airplane and didn't stop until I got back on the airplane to go home. On the bright side, I sweat so much that I only had to pee like three times the whole trip, so I largely avoided the need to find clean public toilets. It was not my first trip to Paris. I love Paris when it's 20 degrees cooler. We saw all the art, ate all the food, smelled all the body odor, but that's a story for another time. Today I'm going to start off by talking a little about cardiology. Specifically, one of the cardiology rotations I did in residency. Twice. Because after my intern year, someone in a position of authority finally came to their senses and realized this particular required inpatient cardiology rotation would be better as an R2 rotation, and that having interns do it was feeding us to the wolves. So I did it as an intern where I was absolutely wolf food, and then I did it again as an R2, and fortunately loved it. Most of the time. This was the so-called regular cardiology service at the big academic medical center where I trained. We took care of a little bit of everything. Heart failure, arrhythmias of all flavors and colors, adult congenital heart disease, valvular disease, including folks coming for TAVER or fancy new mitral valve procedures. I think the only folks we didn't take were those with ACS or who were needing LVAT or transplant. And because this was often the place where all the patients were sent when their local hospitals couldn't handle it, and I hadn't done a ton of cardiology in medical school, I developed a very skewed impression of heart disease in general. Catastrophic presentations became the norm. At least 50% of our service was heart failure exacerbations, almost exclusively half-ref. I don't think anyone had an EF greater than 20, and mostly it was single digits. To me, 30% was shruggable. Everyone was on the same regimen. Preload reduction with isosorbide dinitrate twice daily, afterload reduction with hydralizine, TID, loop diuretics until you break their kidneys, plus minus metolazone. If systolic pressures were above 90, they were too high. You hadn't done your job unless the patient was near syncopizing when sitting upright. Low salt diet, fluid restriction depended. One attending would come on and proclaim one liter fluid restriction for everyone, and we would diligently place the orders. Then a week later, the next attending would come on, fluid restriction is crap, and everyone would diligently take off the fluid restriction. The patients hated the fluid restriction and would threaten to leave. One guy would go into the bathroom, lock the door, and drink out of the faucet where no one could see him. I bought about 20 different kinds of chewing gum and let the patients take their pick when the fluid restriction would start. Great rapport builder. We had a fair number of patients with toxin-induced cardiomyopathy, most of them young, some of them still using meth. I remember one patient in particular who'd been doing real well and then had a bad week of partying and showed up in tears because his balls were the size of large cantaloupes and he couldn't sit. He had to lie down in the back seat spread eagle while his friend drove him in. He admitted that his legs and gut had started to swell a few days prior, but that it took his balls ballooning to make him finally seek medical care. Then we'll ignore a lot of things going wrong, but not their junk. Speaking of which, I didn't have a ton of experience with folie catheters before being on this service either. I was a nurse at an ALF before medical school, but it was all female residents except one and no folies. One of our heart failure patients, he had a foly in and his penis started to dissect down the middle, like the folio filleted wide open. And because of my lack of experience, I again thought, oh, this is something that commonly happens. And for the next six months at least, I was terrified of having a foly put in any of my patients until I confirmed with a urologist that this is not something that usually happens. And now I see folies every day and can confirm I have never come across this again. The patients with adult congenital heart disease were all in their 20s and had just graduated from the Pete's hospital. One memorable, sweet and innocent appearing young woman had quite the mouth on her, which I can respect, but oh my goodness, the attitude. I remember her complaining to me about what a CU next Tuesday her nurse was. Okay, so I swear a lot, a lot, but there's just something about C U N T that I find particularly vulgar. And I don't even remember exactly why we were treating her in the hospital, but one night her boyfriend came to visit, and one of the nurses found them having sex, and I just remember being terrified and wondering if her heart was in good enough condition for sexual activity and looking back at her EKG and Echo and trying to figure out how I was going to explain to the attending in the morning that this girl had died on my watch. I don't remember exactly what happened, but I'm sure she didn't die because I'd have remembered that. One of my favorite patients was a 90-something-year-old with, pardon for saying this, the nicest breasts I have ever seen, because she had been on estrogen for 40 years. As such, all of her coronary vessels were completely blocked. She was with us after PCI for a STEMI, now with new heart failure, and was still intubated when we went to see her for transfer over to our service. Intubated, but alert and listening, because when we started talking about how she needed to come off the estrogen after the MI, she pounded on the bed and then raised her hand, looked directly at us, and waggled her finger back and forth in vigorous dissent. I was on the service the first time in November of my intern year. There were no seniors on the service, just the cardiology fellows who'd mostly gone to outside residencies and who also had no idea how to admit or discharge patients in our system, blind leading the stupid, as they say. And some of the cardiology attendings had no patience for our lack of experience, which was probably fair but nonetheless painful. One particular attending you could just tell thought we were stupid and didn't want to be there, so we didn't want to be there, and we had no doubt every morning that we were going to gloriously disappoint her. Toward the end of her stint with my particular group, I recall we were walking down the hall into another wing, and I was the one pushing the computer workstation, and I was exhausted and just not paying attention, and I ran her over, propelling her forward and knocking off both of her shoes. We all froze. Everyone was mortified, and no one said anything. The attending just paused and stood there for a moment, real still, with her back to us, probably fuming and deciding if she was going to punch me now or later. Then she slowly bent over, put her shoes back on, and continued walking, never looking back. One of the nicest attendings I worked with had this annoying quirk of stopping to thoroughly examine every single patient we rounded on while the rest of the team would just stand there and behold the majestic mastery of a thorough heart exam by a learned cardiologist. Heart sounds thoroughly ascultated at all four sites, JVP precisely measured, pulses checked against the heartbeat for delay, peripheral edema, a solid five minutes per patient. We learned so much from that by osmosis. When you have 30 to 40 patients on service, you could be rounding until 2 p.m. Another attending, a prolific researcher and innovator who was slightly less patient, would stop rounding at 11 regardless of hood you'd gotten through or not. It was refreshing. Then we just card flipped the rest with the fellow. One of my most memorable moments in residency came when that attending and the fellow were seeing a frail older man on the service who was wandering through his room confused. The patient turned away from us and his bare butt was poking out the back of his gown and he had some fresh poop smeared over the back of his leg. Wouldn't you know when I put on some gloves and grabbed the wipes off his bedside, the attending and fellow got right in there with me and we all cleaned the poo off his backside together. It was sweet, really. You can never have too many publications to wipe a butt. Probably the most nerve-wracking part of the surface was being the overnight intern, because you could get called about patients all night long for things you had no idea what to do about. The teletech would call at least once an hour to let you know a patient had non-sustained VTAC. Should I be concerned about that? I had no idea. I would ask the attending the following day if NSVT is something I needed to worry about. Possibly, they would say, and then walk away. I never had any idea what to do, so I would always check electrolytes, mostly because that's what the other residents were doing, and replete to a goal of two and four. I have no idea if it made any difference. I drew a lot of unnecessary labs, probably. And chest pain. The nurses called all the time about chest pain. Some of these patients had chronic, probably cardiac, chest pain, and there wasn't anything we could do to fix it. But you draw a troponin and get an EKG and stare at the EKG and then see the patient. They're usually sleeping by now, and so you have to wake them up, and so they are annoyed, and you ask them if they have chest pain, and they just look at you like you are crazy and then tell you the only pain they have is you. And you get called about hypotension, because someone with a systolic pressure in the 90s while awake and stimulated drops into the 70s or 80s while asleep. But you are afraid if you stop the Bumex drip or hold the hydralizine, you will get yelled at in the morning. So you do nothing. And then when the patient syncopizes, you get yelled at for not holding the hydralizine. So the next time you do hold the hydrolosine and the patient doesn't syncopise, but their systolic pressure in the morning is in the low hundreds, and then you get yelled at for trying to kill them with afterload. But that rotation was part of the reason I continue to love cardiology so much, and why I considered becoming a geriatric cardiologist. I didn't though, obviously. I became a cynic instead. But now, on to the evidence-based medicine.

Some things about sodium, water, and volume regulation in heart failure

SPEAKER_00 9:46

Okay, so I'm just going to be completely honest with everyone right off the bat. Sodium is confusing. Water is confusing. And as if sodium and water weren't confusing enough in the setting of hyponatremia, just wait until we talk about our two friends in the context of heart failure, which is where we are venturing today. Sorry, not sorry. I know what you are thinking. Sodium and water are bad in heart failure, right? Well, not entirely. Cardiologists have been known to get a little up in their feelings about salt and fluid intake, and I'm here to argue that some, if not most of it, is probably unwarranted. There may even be utility in intentionally flooding, okay, not flooding, just priming, the vasculature with hypertonic saline and acute heart failure exacerbation. But I'm getting ahead of myself. Let's first review a few things about how the body manages sodium and water. The GI tract has evolved to be very efficient at absorbing nearly all available sodium and water that enters the gut. This is an evolutionary adaptation to scarcity that is now only really helpful if you are lost in the desert or kidnapped and locked in a dirty basement for days. I wrote a song about this once. The kidneys then have the job of figuring out how much sodium and water to dump to maintain homeostasis. Dump more when too much is coming in, dump less when intake is reduced. This is largely regulated by a part of the nephron called the juxtaglomerular apparatus, or JG apparatus for short, which isn't actually that short. The JG apparatus responds by regulating renal blood flow and secreting renin to activate the dreaded renin angiotensin aldosterone system. Too little salt and volume flowing through the system, RAS is activated to reabsorb sodium and water. Too much, and RAS is turned off. As with regulation of ADH secretion in the brain, it doesn't matter how much total salt and water is actually in the system, just how much the JG apparatus senses. Now let's touch on volume regulation and heart failure. Before I was a doctor, I could not figure out why heart failure was called heart failure. Patients are still able to pump blood through the vessels, so the heart hasn't failed completely. But now I understand the problem is it does so with elevated filling pressures. So there is a backup of fluid on the venous side of the system, or congestion, and in turn higher venous pressures. This higher venous pressure makes the excess fluid leak out into the periphery, the abdomen, the lungs. At a certain point, we call this an exacerbation. To prevent and treat this, we need to reduce the amount of fluid volume in the system. How? Well, loop diuretics. That is the mainstay of treatment. But there are a few other things that many cardiologists seem to think are super important to management, and that is salt and fluid intake. All the salt and fluid that a patient takes in has to go somewhere, and if we are purposefully trying to get them to dump more salt and water, why add an excess to the mix? Seems reasonable on its face. You can imagine that having too little volume and or too little salt flowing by the JG apparatus might be counterproductive in heart failure as it causes RAS activation and thus sodium and water retention. So there is a theoretical argument to be made that salt and fluid restriction might actually be harmful, but is

Fluid restriction in heart failure

SPEAKER_00 12:57

it? Let's first talk about fluid restriction. You have heard me rant before about how much I hate fluid restriction. Why? Well, it increases thirst in the same way that starvation leads to binge eating and just overall makes a lot of patients miserable. But we find ourselves doing it all the time in heart failure anyway. What does the evidence tell us about the utility of this barbaric practice? Well, it doesn't tell us anything amazing, but there are two studies we can extract a few juicy morsels from. The first was a systematic review and meta-analysis published in 2025: Fluid Intake Impact on Heart Failure, Systematic Review and Meta-analysis with Trial Sequential Analysis. This study was fine, I guess. They used Prisma guidelines and a Cochrane quality assessment. They included only randomized controlled trials that compared liberal versus restricted fluid intake in adults with heart failure, PEF, ref, and everything in between. They found nine studies, each with 12 to 205 patients, most with 30 to 60, a total of 961. The studies overall were high to moderate quality, though in the aggregate, in my opinion, there was just too much heterogeneity to make the meta-analysis super useful, although looking at the individual results of the various studies in one place was super handy. One problem was the definitions of liberal versus restricted fluid intake across the studies. Typically the restricted patients were allowed 1 to 1.5 liters, and liberal wasn't necessarily any particular amount. However, one study considered 2 liters to be restricted, while another study considered 2 liters to be liberal. That led to a weird crossover of intervention and control conditions. They did try to compensate for this by doing a sensitivity analysis, excluding the 2 liters as liberal study, but for other reasons. What is a sensitivity analysis, you ask? This is where you change up the variables to account for an anticipated source of bias. Like, if you have a bunch of missing data, you might do an analysis where you presume that data is extreme one way and then the other to see if it would change your results. If not, it probably doesn't matter that it's missing. An example would be if you were trying to test whether taking a statin reduces risk of death, but you are missing the endpoint in 25% of the patients. You could analyze the data with the assumption that everyone with missing results died, and then again with the assumption that everyone with missing results lived. If your results don't change in either of those scenarios, then your results stand even though the data are missing. In this case, they repeated the analysis without the data from the study with the outlier definition of liberal fluid intake. Spoiler, it didn't matter, but there were other issues. The review also blended together studies with stable chronic heart failure and those with acute decompensated heart failure, and they are quite different situations. Active management of volume overload is a bit different than maintaining euvlimia in a stable patient. In the acute setting, the kidneys are congested and often responding to diuretics a little differently, the heart is too far to the right on the starling curve, things are just screwy. So the impact of increased fluid intake on fluid dynamics might vary in these different situations. Three of the nine studies were in patients with acute heart failure, and thus the follow-up time for those studies was shorter, two to four days, while the follow-up time for the rest of the studies was eight to twenty four days. Weird to group those together, no? Problems aside, what were the results of the study? Well, there was no difference in the amount of diuretics used or mortality, whether on liberal versus restricted fluid intake. The study may not have been adequately powered to detect mortality, to be fair. There was a statistically significant reduction in weight in the fluid restricted group compared to the liberal group, but that really didn't seem to apply to the three studies in acute heart failure where we care more about weight change. Meta-analysis shenanigans aside, only one of the individual studies showed a benefit of fluid restriction, and they were also messing with sodium intake, so hard to parse out what was what. Okay, so what does this tell us? Maybe that aggressive fluid restriction is not so helpful, but the evidence is just so thin that it's hard to say. In the discussion, they mentioned some intense anticipation for the results of the Fresh Up Study, which has since been published and everyone likely has since deflated. The Fresh Up Study was a randomized trial assessing 1.5 liters fluid restriction versus liberal intake for three months and outpatients with chronic heart failure. It did not include folks with CKD4 or worse or pre-existing hyponeatremia less than 130, but it was otherwise pretty inclusive. The primary outcome was quality of life, as assessed by the Kansas City Cardiomyopathy Questionnaire overall summary score. This is a health status tool for patients with heart failure. And I love patient-oriented outcomes because we like to torture patients with our ministrations and some other things like mortality and lab values don't matter when you are being tortured. The secondary outcomes were mostly heart failure-associated safety concerns like did patients need more diuretics or hospital care if we let them drink ad lib. So the study was pretty well designed. They recruited enough patients and about 94% completed the three-month follow-up. 87% were New York Heart Association Class 2, so not the most severe heart failure patients. What were the results? Well, there was no difference in the quality of life measure at three months. Thirst distress was statistically significantly lower in the liberal group, but I don't know if that's reliable. They just had people rate how thirsty they were on a scale of 1 to 10. I feel like when people tell me I can't drink anything, my thirst is immediately a 10, and when they say drink whatever you want, I'm a two or a three, even though nothing has changed physiologically. So I'm not really giving that outcome much weight. A big caveat of the study was that the mean fluid intake was only measured for the first week in the liberal group. Then we don't know how much fluid they were consuming. The investigators didn't want to have the liberal group track their intake because they thought it would negatively impact quality of life. During the first week, the mean fluid intake in the liberal group was only 1.75 liters, compared to 1.5 liters in the restricted group. I suspect that 250 cc's per day really wouldn't make that much of a difference. We don't know if they maintained that intake though, or if they actually went bonkers and ridiculously escalated their fluid intake in subsequent weeks after they didn't have to track it anymore. People eat less when they track what they eat. Same might be true for beverages. So we're not really sure how much fluid intake we were comparing per se, just that one group was tracking and the other wasn't. Nonetheless, there was no difference in quality of life after three months. There was also no difference in the safety outcomes, which means their heart failure status was equivalent. No difference in diuretics or hospital care. So ultimately, more evidence that we really shouldn't give a crap. I guess if we have to sum up the data on fluid restriction in one word or one sound, it would be meh. The mediocre evidence we have seems to suggest it doesn't matter in either acute or chronic heart failure, although we don't know what would happen if you went completely nuts and drank in excess of 3 to 4 liters per day, which hasn't been and never will be tested in a controlled setting. It does seem that drinking less, though, is not at all helpful, possibly because you have a counterproductive upregulation of RAS. Hard to say at what volume of fluid intake that would happen, though. Probably it differs among patients. Similar to how much diuretic each patient needs varies. In my practice, I will probably continue to fluid restrict at 2 liters in the acute setting, so my eyes and nose look pretty unsatisfying, which is a horrible reason, but I'm just being honest.

Sodium restriction in heart failure

SPEAKER_00 20:20

Okay, now what about salt restriction? Well, like I said before, pretty much all of the sodium that enters the GI tract is reabsorbed. Blood sodium levels start to increase about a half hour after oral ingestion, with water passively following, of course. Such a submissive. The important thing here is that ingested sodium does affect blood sodium and blood volume, at least in the short term. And excess sodium and water absorption sounds bad, right? Well, sodium intake is not that big of a deal on healthy folks with well-functioning kidneys. You just pee it out eventually. Sure, you might get a little bloated after a Chinese takeout marathon, but the body gets itself straight soon thereafter. In patients with stable heart failure, the renal hemodynamic and neuroendocrine responses to sodium intakes seem to parallel those in healthy individuals. It has been studied. We don't know if this is the case in acute heart failure, though, possibly not. But that doesn't mean we should shun sodium entirely because if you are consuming a profoundly low sodium diet, presumably the JG apparatus will turn on you and ubregulate RAS as a self-preservation move. So some dietary sodium intake is helpful. Another issue with very low sodium diets is that they are associated with poor intake of other nutrients and not getting enough calories, and they are very difficult to adhere to. But what is the amount of sodium that is too much or too little in heart failure? That is the question. When looking at the evidence, we again need to differentiate acute from chronic heart failure, and wait for it. We actually don't have any randomized control trials of sodium restriction and isolation and acute decompensated heart failure. A few of them have looked at combined sodium and water restriction, though. The most Notable of which was a trial by Aliti et al. in 2013 published in JAMA Internal Medicine. This study included adults hospitalized with Hefraf exacerbation, without severe renal disease, cardiogenic shock, or other prevailing comorbidities, like you couldn't have a touch of heart failure on top of your severe sepsis from pneumonia, for example. The intervention group was restricted to 800 cc's of fluid and 800 milligrams of sodium per day. So punitive. The control group were able to consume up to 2.5 liters of water and 3 to 5 grams of sodium in the diet per day. The primary outcome was weight loss and clinical stability at day 3 as defined by the clinical congestion score and cessation of diuretics. I had to look up this clinical congestion score. It is, I quote, a bedside tool used to quantify the severity of volume overload in patients, primarily heart or renal failure. It's actually pretty helpful. It looks at JVP, orthopnea, peripheral edema, and crackles in the lungs. So all the things. I feel like JVP is too subjective though. There have been a lot of patients for whom two different cardiologists have told me two very different JVP measures like five minutes apart. This was in residency where all the cardiologists were super smart and high achieving. I still try to assess the JVP in every patient I treat with heart failure, but much of the time it is an uneducated guess. So not even hypothesis forming caliber. I'm digressing. Back to the study. They recruited 75 patients with only four loss to follow up. They basically met their recruitment goal, though, they anticipated being able to detect a difference in weight loss of 2 kilograms within three days, which seemed ambitious and which they were not able to do. The mean age of the patients was 60 and the mean EF was 26%. The results? Well, there was no difference in weight loss or clinical congestion between groups. I suspect they at least overestimated what the effect would be, so possibly the study was underpowered. Thirst was worse in the intervention group, but folks weren't blinded to how much fluid they were getting, and I already explained why I think a Likert scale to assess thirst is stupid. Strangely, they also looked at outcomes 30 days out, and there was a significant difference in congestion score at that point, and it was higher in the intervention group. So those on restriction did worse? Well, they didn't correct for multiple statistical tests, so it might have been a false positive, the so-called type 1 error. I also wonder if it was a rebound effect whereby salt and water deprivation while inpatient led to overuse after discharge. It's also possible that the clinicians underestimated how much diuretic the patients in the intervention group would need at home because the salt and water deprivation didn't mimic their home conditions. In any case, salt and water restriction and acute heart failure was pointless and ultimately may have been counterproductive in the long run. The only other relevant study we can reference with respect to sodium intake and acute heart failure is the Osprey trial. This was not a trial of sodium restriction, it was actually a trial of sodium loading, where patients were given an additional 6 mg of sodium daily in the form of salt tabs on top of liberal sodium intake to see if it would improve response to diuretics. We'll talk more about the principle behind this and additional studies of IV hypertonic saline in the next episode, but the long and short is that a dramatic increase in dietary sodium over several days didn't do much. I'll concede that the patients in this study were also on very high doses of diuretics, which may have counteracted the sodium loading, but I think more than anything it affirms that extreme sodium deprivation is probably not necessary, although you may need to jack up the furosomide. Okay, what about sodium and chronic heart failure? We do have more evidence in this setting. There have been several systematic reviews and meta-analyses published on the topic. The most recent was published in Clinical Research and Cardiology in 2024. I had never heard of this journal, which always makes me a little suspect right from the start. But in any case, this review included interventional and observational studies looking at outcomes of sodium restriction in adult patients with chronic heart failure. They excluded studies with mixed intervention, so none of those sodium plus fluid restriction designs, and they also excluded those with inpatient interventions only. They looked at a number of possible endpoints, all-cause cardiovascular or heart failure-related mortality, hospitalization or ED visits, and heart failure decompensation. They included nine articles with around 2,200 participants. The follow-up time ranged from 12 weeks to three years with a mean follow-up of 15 months. Six studies included all types of heart failure, and three included reduced EF only. I wasn't so much interested in the observational studies. You know my opinion about observational studies. The randomized controlled trials compared a sodium-restricted diet of 1.5 to 2 grams, depending on the trial, to more liberal salt intake, which was either around 3 grams, so not that liberal, or just some advice to restrict sodium, which translated into only about 2 grams in some of the studies. They reported that the randomized control trials were good to moderate quality, so fine. And what amazing things did we glean from their results? The analyses showed that brace yourselves, there was basically no benefit of sodium restriction for any of the outcomes. There are some important things to point out here as well. First, the liberal sodium group wasn't particularly liberal at 2 to 3 grams. And like with the fluid restriction trials, one study's definition of restricted was another study's definition of liberal. And there are certainly a lot of unanswered questions, like is 2 grams better than 4 grams, or how about 6 grams? The evidence just shows us that extra low isn't better than low. The studies also aren't able to tell us if sodium restriction matters based on the type of heart failure you have. It's been suggested that sodium is more damaging in hef PEF than hef ref, but we just don't know. Interestingly, the review did show that study year was a significant confounder. So possibly with better GDMT in more recent times, sodium restriction is less important than it was in the past. Okay, so I should mention that there have been several additional systematic reviews and meta-analyses on sodium restriction and heart failure. The most prestigious, as it were, was published in circulation in 2022. But I had even more issues with this study. It included trials in the acute setting, but all restricted both sodium and water. And it also included trials that restricted both in the chronic setting. They did do a sensitivity analysis to account for this, but I just didn't see the point of including them in the first place. Notably, their results didn't differ much from the 2024 review. In one analysis, they showed that sodium restriction of less than 2 grams per day might actually be associated with a higher risk of mortality or hospitalization, though this was a trend and not statistically significant, so I'm not sure why they even mentioned it. Man, I hate it when studies say there was a trend towards significance, because that is not a thing and is in direct contradiction to every principle of sound statistical analysis ever conceived. The p-value is the point at which the outcome is considered to be not from chance alone. Calling anything with a p-value that is higher than the preset threshold relevant, usually 0.05, implies significance in the absence of evidence and is unethical. Just saying. So, despite the crap evidence we have, the esteemed societies of the world have put out guidelines with their recommendations for salt and fluid restriction. The ACC AHA guidelines on heart failure management published in 2022 barely mention sodium. They give a low-grade, poorly supported suggestion that you might restrict to two or three grams per day. Regarding fluid restriction, they admit to having no idea if it is worthwhile, which is one of the first times the ACC AHA has admitted to not knowing something, so either they have absolutely no clue whatsoever or they just don't care. The European Society for Cardiology has more specific recommendations and in fact put out a full clinical consensus statement specifically addressing fluid and sodium intake in patients with heart failure. It seemed reasonable, so I'll give you the details. They take the approach of moderation. In chronic heart failure, try to keep the fluid intake normal and guided by thirst. They define normal intake as 1.5 to 2.5 liters per day. Sodium intake should be less than 5 grams, or adhere to what is quote unquote normal as well, which they consider 1.5 to 4 grams per day. With all the processed garbage Americans eat, I thought it must be more, so I looked it up and Google swears that the average American eats 3.3 grams per day, which is just another reason why AI is suspect because not the Americans I know, my patients eat nothing but TV dinners all day and sometimes drink V8 with soy sauce poured in. Back to the consensus statement though. In acute heart failure, they say there isn't great evidence one way or another for salt or fluid restriction. That may be the case, but I refuse to believe that extreme sustained salt loading isn't harmful, even if it might be keeping Russ placated. I once took care of a cirrhotic patient in the hospital with rapidly reaccumulating ascites after a para whose windowsill was stacked high with cans of Pringles and bottles of Gatorade because that's all he would eat or drink. His fluid status improved after we negotiated a 48-hour stay on the junk food. You know what they say though, 100 anecdotes does not a randomized control trial me. I digress though. At the end of the day, we just don't know what to do in the acute setting, and anyone who claims to know is a liar. I'm going to shoot for non-punitive moderation of both sodium and water and hope for the best. That brings us to the end of this delayed episode. I hope it was worth the wait. If it wasn't, oh well, this content is free. Sorry, not sorry. See you next time. Thank you.