Practical Management of Heart Failure (25 May 2026)

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Dr Marilena Giannoudi (MG): Hello everyone and welcome to another episode of Clinical Conversations, brought to you by the Royal College of Physicians of Edinburgh Trainee and Members Committee. My name is Doctor Marilena Giannoudi, and I am on the T&MC. And today I'm delighted to be joined by Doctor Sam McClure, who is a consultant cardiologist in Sunderland. He himself described that he was a little unusual. So, I'm using the adjective on my own as he is an interventional cardiologist, but also the clinical lead for heart failure. And today we will be discussing all things heart failure. So, Doctor McClure, welcome. Thank you for joining me.

Dr Sam McClure (SM): Thanks very much for the invite, Marlena, and hopefully get along easily with learning a little bit about heart failure today.

MG: I hope so too. I'm sure we will. I guess the best place to start is defining or classifying what heart failure with reduced ejection fraction actually is, and how can we classify it?

SM: Well, this is almost a never-ending question. How things are defined, and the classifications seem to change every few years. But fundamentally, the classical heart failure that I think we all think about with reduced ejection fraction, it more or less practically relies on a diagnosis made by an echocardiogram. These days, that's the most readily accessible means of assessing heart function and making a final decision about things. Obviously, as I'm sure we'll be speaking about later on, obviously, a great number of heart failure patients, probably about half, actually don't have reduced ejection fraction, the preserved ejection fraction group. When you first encounter the patient, the priority is probably just to treat heart failure, treat with a diuretic. But then the more precise targeting of treatment, it really evolves from the use of some sort of imaging. And usually that will be with echocardiography.

MG: And I know that you mentioned different classifications and they have been changing over time. At the moment, how should we be technically classifying heart failure with reduced ejection fraction with regards to its severity?

SM: Well, really because the evidence for the rather better forms of heart failure, the patients who have only slightly reduced heart function because the evidence in favour of some of the four pillars of heart failure treatment is a little bit less robust in that group. The European Society of Cardiology decided in their last guidance to talk about that group of patients as having mildly reduced ejection fraction. Now, personally and in practice, I think it's quite difficult to perhaps deny those patients treatments that we think should modify their clinical course. So when the ejection fraction is reduced, even if it's quite modestly reduced, I think you'll find that most people tend to try to apply the four pillars of heart failure treatment that we use for patients with reduced ejection fraction with left ventricular systolic dysfunction, as we've also called it.

MG: And just because we've got a wide range of listeners as an audience, what are the cut offs that we should be using when giving either heart failure with mildly reduced ejection fraction or reduced ejection fraction?

SM: Well, I think the key quotes in ejection fraction of forty-five to fifty five percent as being mildly reduced. And obviously beyond that, they're saying that's proper heart failure with reduced ejection fraction. I think the differences are quite subtle, but the firm evidence it's true in that mildly reduced group is perhaps not quite so strong for some of the four pillars. The evidence is pretty strong in that mildly reduced ejection fraction, for instance, to use Sglt2 inhibitors, but perhaps not so strong for Ace inhibitors and beta blockers that we would use in the more severely reduced ejection fractions.

MG: And what I'll do for all of our listeners, I'll make sure that the link to those guidelines is on the podcast footnotes for everyone to have a read in their own time. And I know you've briefly mentioned treatment with regards to what medications we should be using, but do you mind just going over that in a bit more detail? Because you said once we have someone with heart failure, we just need to treat them. And you mentioned diuretics, and I know that sometimes as more junior members of the team, even just knowing what dose to start on can sometimes be mind boggling. So, in your experience, how do you think we should approach these patients?

SM: Well, I think probably first of all, we think about four pillars of heart failure treatment these days. And I think that we're going through an era where people are very conscious of the need to introduce these disease modifying treatments. And, you know, that's great that we've got to that stage and that people are focused on that. But really, when you first encounter a patient, be it in the outpatient clinic or be it in the emergency room or on a medical ward, if the patient has clinical heart failure, the one treatment beyond all others that is likely to make a difference to them in the short term is the prescription of a loop diuretic. And we'd want to get that on board. And again, I'd also just point out that if a patient is ending up in a hospital setting, and I would imagine most of the listeners to this will be people practicing in hospitals. It basically means that they probably have either not responded to oral diuretics, or they've really come in a lot sicker than we think we can probably handle with oral diuretics. Very often when the patients admitted, in most cases, when the patient is admitted, the main reason for the admission is for them to have access to intravenous diuretics and people to manage that initially will then be able to classify the patients. We'll investigate them a little bit further with an echocardiogram, and that allows us to decide whether they need four pillars or whether, if they turn out to have preserved ejection fraction, if we maybe have less options available for them. But right across the spectrum, it's the use of diuretics and diuretic. Naive patients on a smaller dose of a diuretic might be appropriate, for instance, fifty milligrams of intravenous frusemide to see if that makes a difference in patients who've been diuretics for a while, they may have a little bit more diuretic resistance. And if they've been on oral diuretics as an outpatient, you're probably going to need to start with a larger dose, maybe one hundred milligrams, and really just titrate to response. And during the inpatient stay, we'll look at that response both with what level of diuresis they achieve with the patient's daily weight being measured. These sorts of techniques to just see how the patient is responding.

MG: So, in terms of looking for response, you'd be doing daily weights. How important do you think daily user needs are as well as looking at urinary sodium in assessing for effective diuresis?

SM: Yeah. I mean there have obviously been studies looking at the use of urinary sodium. And I think seeing that you're managing to make the patient diaries and produce lots of sodium does seem to be a very good idea and would probably, if it was widely easy to do, would probably be a very good way of monitoring the patients checking renal function. Personally, if I have a patient on IV diuretics as an inpatient, I prefer them to have their renal function checked on a daily basis. I think it's difficult to continue with intravenous diuretics and often adding in other nephrotoxic drugs as well, to not be monitoring daily using these. The occasional patient, of course, will have big variations in their potassium level, which would be a concern in a patient who's already, by definition, a little bit unstable. From the cardiac point of view. It's very, very important to monitor potassium levels, monitor renal function with daily checks of the renal function.

MG: And can I ask what is the role for metolazone in these patients where we're really struggling with diuresis in the inpatient setting? Because I've never quite got my head around it, and I can't quite grasp in which kind of patients we should be doing. And after what time span should we be trying Metolazone.

SM: I think in the real world, that's probably a complex interaction between the patient's well-being and that of the hospital setting in which the patient is being cared for. I think if we're not seeing a good response to intravenous loop diuretics within the first couple of days, we would then certainly think about adding in metolazone as well, particularly in the patients who are really grossly fluid overloaded. But drugs like Metolazone, one of the concepts that came up in the recent talk that gave to the Royal College was the concept of sequential nephron blockade. I think it's a concept that's used in renal medicine as well as heart failure medicine, and it's just adding in different drugs to produce more and more reduction of sodium and water reabsorption within the kidney. So, loop diuretics usually first, you might then use a thiazide diuretic with often use an MRA as well. And just blocking more and more of the nephron and reducing the sodium and water reabsorption. So, in my own practice, you know, within sort of maybe about three days of admission, if the patient's not really losing weight significantly, I would be considering adding Metallism. And I think we all think about metallism. But just bear in mind that other thiazides are also available. Or thiazide like diuretics are also available. So Bendroflumethiazide. Just as a little trick and a little concern to be aware of is that obviously, many patients may be treated with thiazides as outpatients for hypertension. For instance, if they develop heart failure, you need to be very careful about that. If you're adding an intravenous diuretic, when the patient is admitted, you can very rapidly cause a major change in renal function or in electrolytes. If you start prescribing loop diuretics to someone who is still prescribed that, say, bendroflumethiazide when they're admitted. So there needs to be great caution. Ideally, I would normally stop the outpatient thiazide diuretic while the patient is on the intravenous diuretics just to see how things go with loop diuretics on their own to start with.

MG: And if we take it just one step further, still carrying on diuretics, when the time comes for the patient to come off the IV diuretics. Do you have a preference for amide versus bumetanide. And I've seen a lot of, you know, chopping and changing between flutamide and bumetanide in the outpatient setting. Is there really a role for this or actually, if one isn't working, it's probably that the patient isn't on the right dose as opposed to let's just keep swapping between them.

SM: I think there's a lot of truth in what you're suggesting there, but there is some evidence that bumetanide may be a little bit more available and may be a little bit more potent. Obviously, we normally regard roughly forty milligrams of furosemide as being roughly equivalent to one milligram of bumetanide, but it is variable. I personally, if I feel that the patient has, let's say, a lot of ascites or a lot of congestion of the abdomen, I will tend to use bumetanide perhaps a little bit more readily, but that's just a very personal thing. I think you were sort of alluding to how long to go with the diuretics, and a lot of that has to be adjusted to the clinical situation that you might be in my service. We're very fortunate in that we've got a good set up to review the patients early after discharge, usually within at least a couple of weeks, if not earlier. And it means that you can continue the intravenous diuretics up until the point of discharge, and then switch them on to your best guess of oral diuretic at that point, but with the reassurance that someone's going to see that patient early to make sure they're on enough diuretic, and also make sure that their renal function hasn't suffered too much early after the discharge.

MG: Mhm. And do you think should be referred to a heart failure service or a heart failure clinic? Because I think we're seeing a lot of people with, you know, swollen legs. Of course, let's make sure it's not heart failure. And actually, a thorough clinical examination usually hasn't been done. And this patient has got swollen legs for lots of different reasons, of which heart failure is not one.

SM: Well, again, a good question. And as I sit and triage all the referrals at the moment into our suspected heart failure service, this is a question that often comes to mind. Nice guidance is, of course, to make use of N-terminal pro-bnp levels, and the guidance has been revised a little bit over the years, but they've more or less stuck with the same thresholds. So, an N-terminal Pro-bnp over four hundred would justify an echo and a clinical assessment within six weeks, and the BNP over two thousand. We're meant to try to see those patients within two weeks. I actually think those guidelines are pretty good. But we do find that many, many patients who may not have genuine heart failure may have BNP somewhere in the region of four hundred to eight hundred just if they're in their eighties or 90s, just because they're elderly. Sometimes it needs an echo just to reassure everyone. So yeah, I don't think just swollen ankles is enough. And when someone's got swollen ankles. We should be thinking about other explanations. Calcium channel blockers, particularly at high dose drugs like Doxazosin, for instance, used to treat hypertension, are very, very commonly can cause peripheral oedema. Almost any vasodilator can worsen peripheral oedema. So, a little bit of clinical assessment for sure. But the BMP is helpful but perhaps not jumping immediately to conclusions. It's definitely heart failure if the Bnps were four hundred in an elderly age group. So, I think the BNP is really helpful and I think the nice guidance is pretty good. But sometimes you do need the echo as well as the BNP to really be more certain about the diagnosis.

MG: Yeah, a very helpful clinic appointment for those patients. If they're told your heart is fine, you've had a full checkup and now you can move on. And I know you alluded to this before, but if you don't mind, I think it's important for us to briefly cover heart failure with preserved ejection fraction because I knew when I was more junior, I thought it was just any form of clinical heart failure where the ejection fraction was normal. But I think the more that I'm reading that actually there are other echo findings that are associated with this. And actually, it's not such an I don't want to say easy diagnosis, but it's certainly one that we do need to take pretty seriously. So, do you mind just giving us a brief overview of how we should be diagnosing heart failure with preserved ejection fraction?

SM: Absolutely. Well, first of all, it's a really monstrous problem. It actually accounts probably for about half of admitted patients with clinical heart failure. And I think really what has happened is that we've not had appropriate language to explain the diagnosis for many years. I think the language is better now. I think I can go along with the expression heart failure with preserved ejection fraction better than maybe with some of the older terms, such as diastolic dysfunction, Etc. and it was actually quite helpful there. What you said with patients with preserved ejection fraction, because in the past, I think very often that was all that we looked at was left ventricular function, and we weren't really looking at the echocardiogram properly. So, there are other features to look for. Things like atrial size, presence of left ventricular hypertrophy, the filling index through the mitral valve, for instance, left ventricular mass. All of these features can give you a clue that the patient may have heart failure with preserved ejection fraction. It's a really, really common phenomenon, and one of the difficulties about it is that there is no single test that makes the diagnosis. I've sometimes suggested that heart failure with preserved ejection fraction is a little bit like our me syndrome, or chronic fatigue syndrome, and cardiology, insofar as we haven't really had one good specific test for it. We kind of know there's something there, but we almost won't ignore it because we don't really fully understand it. I think we are understanding it better. Most of these patients will have some elevation in N-terminal probnp and therefore would fit with the universal definition of heart failure. So that's one thing. Secondly, I think they will have echo appearances, but you actually need to read the full echo. You can't just skim and go straight for left ventricular function and expect to get the diagnosis. With that, you need to look at the atrial size. You need to look at the mitral inflow how that's reported. As time has gone by, the physiologists who do the echoes have tightened up their criteria for reporting. The British Society of Echo have improved the reporting criteria. And I think we're now in a position where we do get a lot more information from the Echo than we used to before. The other big frustrating thing, as I say, is that there's no specific tests. We tend to use scoring systems. There are a couple of competing scoring systems. There's a European system which is almost a strategy of investigation for heart failure with preserved ejection fraction. And then what I find practically to be a little bit more useful is the so-called HFpEF score, which is an American classification, and that gives weight to a number of pretty simple clinical factors, such as weight treatment with hypertensives, presence of atrial fibrillation, presence of pulmonary hypertension, age over sixty, and then finally the filling pressures through the mitral valve. And you get points here and there for these various criteria and add them up. And more than six points gives you a diagnosis that's highly suggestive of HFpEF. So, it is a complex condition, but the shortcuts, if any, are maybe if the atria are dilated, maybe if the patients get AF and if the ventricle looks normal, but yet they've got high BNP. They're manifesting clinical heart failure. It's probably half pemf in many cases.

MG: And just following on from that, because you mentioned that, for example, in that scoring category, BNP isn't a part of it. So, should we still be looking for BNP and is there BNP still important for us to diagnose?

SM: I think it's really important firstly to diagnose. So, there are not many people who've got true clinical heart failure with a low BNP. The one group perhaps that may be an exception. Obesity actually ironically can sometimes cause an erroneously low BNP. But for most other patients, if they've got clinical heart failure, they'll usually have elevated N-terminal pro-bnp. And more than just sort of being a binary classification. If it's above the threshold of four hundred, the level of BNP is a very good guide to the severity of heart failure. So really high levels of BNP mean a really sick patient and a patient that you would be more keen to admit and treat aggressively. So, I think BNP is very important. So, the universal definition of heart failure, which came out a few years ago and very much an international consensus, was that heart failure needs to be diagnosed really with partly naturetic peptides. For the first time, peptides were given a very, very prominent role in making the diagnosis of heart failure. And I do think that is valid. Most patients with a low BNP, certainly below four hundred, we would not be too concerned that they've got true heart failure. Okay. And in terms of treating these patients, obviously you mentioned the four pillars of heart failure for heart failure with reduced ejection fraction, how these can be disease modifying agents. But given that the pathophysiology is so different, and I guess still relatively poorly understood, how should we be treating these patients and what options are there? So, I think again, this is one of the reasons why we've almost ignored the condition in cardiology or we've almost not wanted the condition to exist. I know even now some colleagues are a little bit. How would I say blasé about the treatment of heart failure with preserved ejection fraction without having had what are definitely effective treatments? For a long time, it was a difficult condition to feel good about treating. It seemed so much easier if you've got reduced left ventricular ejection fraction to treat it using Ace inhibitor, use a beta blocker. You know, there's great evidence. So, the first class of drugs that have really definitively been shown to produce an important benefit for these patients over and above, just treating the fluid overload with diuretics have been the sglt two inhibitors. And we've seen that now it's almost a class effect with Sglt2 inhibitors. And that certainly seem to reduce combined endpoints of mortality and hospital admission with clinical heart failure. And this effect is so powerful that in the American guidance now, which had the benefit of being just a little bit more recent than the last European guidance, they actually recommend an Sglt2 inhibitor as the first treatment for a patient with Hefh path. We would obviously often use a loop diuretic as well, and there is accumulating evidence for the benefit of MRAs as well. Unfortunately, the last really large study looking at the use of MRAs may not have been conducted entirely smoothly, but more recently, one of the newer MRAs, Finerenone, has shown good clinical benefit when being used in heart failure with preserved ejection fraction as well. So, I think loop diuretics for lots of congestion, if we would definitely consider sglt two inhibitors for these patients and would often consider MRAs as well, especially in the patients that are resisting treatment with a loop diuretic who are resistant to treatment with a loop diuretic. So those would be the key classes of drugs, not as many pillars as reduced ejection fraction. But I think we have made inroads into this now, and I think we're able to keep more of these patients out of hospital more often nowadays.

MG: And again, when we're considering Sglt2 treatment in these patients, we've already mentioned that a lot of these patients may actually have high BMIs. And kind of if we take a leap from that, they may actually be diabetic in the context of HFpEF. So, can we safely prescribe Sglt two in these patients that have concomitant HFpEF with diabetes?

SM: Yeah. Well, generally speaking, we would avoid them in type one diabetics avoid the use of these drugs just due to the risk of acidosis, etc. We also in my service locally, after a lot of work along with our endocrinology team, we also would use them with great caution in people with really poorly controlled type two diabetes as well. We'd be very concerned about that. But endocrinologists are out there, or the diabetic services out there, and you can often get a bit of advice if you're anxious about using them. In particular patients we would consider in a really poorly controlled diabetic involving the diabetic team anyway. But we would obviously be pointing out to them that one of the things that we want to do is try and get the patient on to an Sglt2 inhibitor, if at all possible. They're not without side effects. Thrush in particular, is fairly common, probably about one in twenty patients. And really nasty conditions like Fournier’s gangrene as well that it's said to occur in about one in three thousand patients. And we have seen a couple of cases locally of that, but very effective drugs when they're tolerated. But you do need to use them with caution. Obviously, the whole use of these drugs was kind of a fortuitous discovery after long term surveillance. After the introduction of Sglt2 inhibitors due to concerns about new diabetic drugs. So, they were being used widely in diabetics. And it was only with that experience that we started noticing that patients were having less problems with heart failure. And obviously, now we know that the drugs are effective even if you're not diabetic as well.

MG: Great. No, I think it's just really important for us to highlight that because now everyone is prescribing Sglt2, I think without always thinking about the possible side effects of them. And yes, they're really effective. But I think we just need to remember the holistic patient approach to that. I guess my last question is using your experience of which you have vast experience, what do you think are the most common mistakes that resident doctors make in the treatment of patients with heart failure, and how should we go about preventing them?

SM: Good question. Well, the number one mistake, and it's not just resident doctors. It's a lot wider than that. But the number one mistake, I would argue, is that we Probably don't treat aggressively enough with loop diuretics after admission. Again, we've become quite seduced by the modern treatments available by the four pillars of heart failure treatment, for instance, and we sometimes can really forget the basics if a patient is unwell enough to be admitted to hospital. That means probably that primary care hasn't been able to treat their problem. So, I don't really understand why you would keep going with an oral diuretic for that patient. You're going to accelerate their recovery in hospital if you use intravenous diuretics right up front. So, I really encourage the use of intravenous diuretics early not being too worried about renal function. You need to monitor it. Absolutely. But if the patient truly has heart failure, we often find that the renal function actually improves over the hospital stay as the patient becomes decongested so that the use of intravenous diuretics, not obviously at massive doses, unless the patient proves to be resistant after the first couple of days. But I would say as a single error that I see is probably not giving enough diuretics. And I say that I speak sometimes to my advanced heart failure service locally, and they give just extraordinarily high doses of diuretics that make me cringe, actually. So, I think we probably generally just tend to use a bit less than we should. So, I'd encourage loop diuretics and usually meaning frusemide and giving it in a pretty decent dose to start with, often maybe one hundred milligrams intravenously early on in the admission. And watch for the response.

MG: And any other last parting pieces of advice to anyone treating these patients. It doesn't necessarily have to be a mistake that is made, but what you would say to any resident doctor who is on your ward that you know, this is what I want you to look out for, or this is how we should be effectively treating these patients.

SM: Well, I think you need to look for the patient getting better and getting stable. Of course, it's not any one thing, but it's patient's weight, their degree of congestion or the ankles visible again. Is the patient less breathless again? Whenever you feel that the patient is approaching that point and my personal practice, I actually keep the intravenous diuretics going right up until just about the point of discharge, because there's a common tendency to. Well, let's switch to oral diuretics and see how it goes for a couple of days. The changes that you're likely to see often will take longer than that. You're almost falsely reassuring yourself that either you're not going to see a change in kidney function over forty eight hours before the patient goes home, and equally, as soon as the patient does go home, they can easily fall in a heap because you may not have got the dose right. So again, I'm very glad that we have a service. We can pick up the patients early after discharge because if we haven't got the discharge dose of oral diuretics right. We can make that adjustment very early within a couple of weeks. And it's really important to know the infrastructure that you work within to know the service that you work within, to know what services are available. If that sort of service isn't available to you. The flexibility may not be there, but it's usually a good idea to have someone look at those patients with a check of renal function with a check of fluid status within a couple of weeks of discharge. That's part of nice guidance, and I think it's a very, very valid piece of guidance. And it hasn't changed over many years from the advice from NICE.

MG: And I guess it just goes to highlight that we're all one big team trying to aim for good patient outcomes. So always feel free to ask, I don't know a single, especially heart failure cardiologist that doesn't want to know about their patients. So, for anyone who doesn't necessarily work in cardiology, that doesn't mean that we don't want to know about these patients.

SM: That's right. And there's a lot of specialism in the paramedical side. You know, the heart failure nurse specialist. We have a number of heart failure nurses, pharmacists and our service as well. And it really, really is a team approach. So really important to rely on them. Some of the heart failure nurse specialists are fantastic. You know, they'll see the patient as in-patients and follow them through, perhaps seeing them even on home visits after discharge. So, there's a lot of expertise to help you along and caring for these patients.

MG: Great. So, to summarize for our listeners, offload your patients, offload them properly, check their weights, check their renal function. And I think be very strict with their weights because I think a lot of the time, you know, the weight isn't done and we say, oh, it's fine, we'll weigh them tomorrow, be strict with their weight. It's part of their treatment. Be strict monitoring their renal function. And don't forget you work as part of a team. Make sure to escalate as you need to. Does that sound about right as a take home messages?

SM: Sounds about right. Lots of other team members. Geriatricians. Very important. Nephrologists and palliative care consultants as well. Very important to remember the other people that can be really helpful in the care.

MG: Yes. Great. Well, Doctor McClure, thank you so much for joining me today and for going through an overview of heart failure. It's such a big topic that I know that we can't go into all the details for all our listeners. Thank you for tuning in. I'll make sure that you have lots of resources to read in your own time. Please feel free to keep listening to other episodes in clinical conversations for all things clinical and what you may encounter on the wards. And we've also got career conversations for any aspiring cardiologists, nephrologists, and all other specialties. Thank you so much for joining me yet again.

SM: Thanks very much, Marilena.