Hi, welcome. So today we're gonna talk about cardio renal patients. So, most of you will be familiar with dealing with the cardiac patient or renal patient.
This is kind of just both of them together, really, if we simplify it. So in human medicine, they've kind of brought out guidelines, and they've been doing this for quite a while. In 2015, 16 boarded veterinary surgeons, in medicine kind of reviewed this syndrome within the veterinary context.
So they defined this cardioreal disorder, as a disease, toxin or drug-induced structural or and or functional, damage to the kidney and or cardiovascular system. And then that leads to disruption, of the normal interactions between those. So, we know, we'll go through this today in the, in this webinar of how those systems work and therefore, how they affect the other system.
And there's normal interaction between those systems and that, that. Abnormal interaction then causes an ongoing detriment to the, either the heart or the kidneys. And we'll discuss again, kind of the grading between those, because it might be that you have a cardiac syndrome as your primary disease, or renal, disease as a as a primary disease, and that then leads to that imbalance between the kidneys and the heart.
So they came up with primary cardiovascular, primary renal, and then concurrent disease, so both of those just exist together. Mm So we're gonna do a brief overview. I'm not gonna spend tonnes of time going over how the heart works and how the kidneys work, but we're gonna kind of pick up on those main things that are going to cause disruption to the other system.
So we know that the heart pumps out blood, it receives the blood from the body, I'm into. Though I'm into that, I'm right atrium, through the right ventricle, out towards the lungs, where then it's oxygenated in the lungs, brought back, into that left atrium and then ejected out through the left ventricle to the body, where all of that blood supply is taken to the body for, for oxygen supply, for that energy, for, you know, for that metabolism for that patient. And all the cells within the body require oxygen for metabolic function, for homeostasis, and if they have short supply of that, that's when we start to see things like cell cell death, apoptosis, ischemic injury, we start to see that those cells start to die.
The other thing that starts to happen as well is when we have heart failure or heart symp heart disease, is that now the heart that's receiving that blood is no longer able to pump it as effectively and whether that's because it is not strong, the muscle is not strong enough, so we don't have that inotropy, . Or it's not going fast enough, so coronotropy, or it, there's some sort of, back flow. So we think about this when we have mitral valve disease, is that those mitral valves, are not snapping shut properly, and what they're doing is letting blood flow back into, back into the left atrium.
And then, therefore, there's not enough blood that's being ejected out through that, left ventricle. When we see poor blood supply, what we start to see is that now that affects the kidneys, and in a minute we'll talk about how that affects the kidneys, but what happens is the kidneys recognise low blood flow, within those vessels, and they say, OK, well, we need to do something about this. We need to be able to get the heart to pump faster, we need to be able to increase our blood volume in order to do that.
And so there's a couple of ways that they do that through that running angiotensin aldosterone system. In the meantime, the heart is trying its best, it's pumping as fast as it can. We then pick up heart murmurs, we pick up a potential syncope, arrhythmias that the heart's having and potentially we recognise that primary cardiovascular disease.
So, in our heart disease, we have, 22 things. So, they used to be called left and right. Now we have forward and backwards failure.
So, forward failure or low output failure, often as a result of things like cardiogenic shock, and it's basically that the heart isn't pumping enough blood to meet the body's needs. So we result in the under perfusion of tissues. So in forward failure, we end up, With I'm.
Again, congestive heart failure, but we have this low output, so we start to see that that renin angiotensinal deerone system is, is triggered. So we get cardiogenic shock because we get this back up into the atrium, they're not pumping that effectively, we get our increased preload. So now with backwards failure, what we see are congestive heart failure, occurs when the heart again can't effectively pump blood out.
And it leads to fluid buildup, so we end up with pulmonary effusion, pleural effusion, plural, Pulmonary edoema, leaky capillaries, free abdominal fluid. All of these things suggest that there's, again, that there's an increase, in pre-load and afterload. What happens now is all that blood is sitting in those vessels rather than being ejected by the heart.
It's now just sitting, getting backed up and leaks out of those vessels, causing that congestive heart failure that we see classically with those symptoms of pleural effusion, pulmonary edoema, free abdominal fluid. In cardiovascular shock, like I say, what we see now is that there is enough blood in the system. We've not lost blood like in other shocks such as hypovolemic shock, but with cardiogenic shock, there is enough blood within those pipes.
But now what's happening is that the, the, the main engine, the heart, is now not pumping out that blood effectively. And so when, by the time that that blood reaches places like our kidneys, is that now that the, that the blood pressure is very low. And so those kidneys recognise that that patient is in shock.
And so the kidneys require a blood pressure, I mean arterial blood pressure of a minimum of 60 millimetres of mercury to auto regulate themselves in order to control the glomerular filtration rate. So this glomerul filtration rate is how much pressure is in that glomerulus, which we know that then goes through the loop of Henley. We don't want too much pressure cause we're gonna burst those vessels, we're gonna cause damage.
If we have no pressure and we're not able to regulate and get that to the normal pressure that it needs, there's not enough flow coming through for us to filtrate out the toxins, so we know that the kidneys are responsible for those toxins. So as a result of that low flow and that low blood pressure that's coming from the heart because it's not affecting, it's not pumping effectively and therefore, the cardiovascular system now suffers. It's a now it's a domino effect and those kidneys are now suffering.
So those kidneys can no longer auto regulate. They're no longer able to filtrate all those toxins. So now we start to get a buildup of things like a urea, and we might get electrolyte imbalances as well, because we know that those are responsible, that the loop of Henley within that glomerulus is responsible for filtrating and, and, using the osmotic radiant to create an, an equilibrium.
So we might get an increase in salt, so sodium, we might have increases or decreases in potassium because there's no longer that philtre system working. And so, again, all of these things are gonna affect things like our pH which we know is very important to our patients to maintain between 7.35 to 7.45.
If we go out of those ranges, we start to see, deliterous effects on our patients. So we start to see that the patient might start vomiting, they might be anorexic, they might have arrhythmias. Again, this is going to affect our heart and further compound our issues.
So it's kind of like this ball rolling down the hill. And once we start to get bad, everything else gets worse, and it continues in that vicious cycle. So running ang angiotensin aldosterone system is really important for our patients, for, for any patient that we treat, but in particularly both the cardiac and the renal patients.
So I've just mentioned about that I'm. That the kidneys need and the brain as well needs a minimum of 60 millimetres of mercury, so that's why we have that figure there to auto regulate. If they don't have that, they send this messaging system to basically say, OK, let, we're gonna get, we gotta get our butts in gear.
We've got to make sure that we are now, you know, creating blood volume to be brought to the kidneys and a sufficient blood pressure to be brought to the kidneys so that we can filtrate out those toxins so that we can have equilibrium on our, on our blood, sodium contents and making sure that we have a You know, balanced plasma. So what happens is Within the kidneys, we have these stretch receptors, and those stretch receptors are responsive to the blood flow. So, we get that blood volume coming round through the, cir circulatory system that again, is coming from the heart.
The heart isn't pumping enough. That circulatory system is weak. The kidneys now recognise that they're not getting enough stretch.
Those stretch receptors go, hey, we're not actually stretching at all. So they release renin from those juxtaglomerular cells. And that wreniness released into the cardiovascular system is circulating within the blood.
I'm and Now, when this renin reaches the blood system in the cardiovascular system, is that angiotensinogen that has been produced by the liver, which is always produced by the liver, that again is just within that circulatory system, is now cleaved into angiotensin one. So angiotensin one is now circulating within the system. This angiotensin one again, because of the circulatory system makes its way to the lungs, and within that we have our angiotensin converting enzyme to our ACE.
So think about the medications that we give for our patients that are in heart failure, we often give ACE inhibitors. So this is where it's working. And it's stopping that action of is angiotensin converting enzyme from being released in order to create this next step.
So the next step is that angiotensin 2 is made once this angiotensin converting enzyme, this Ace is released from the lungs. Angiotensin 2 is the thing that causes those changes to happen. So angiotensin 2 acts, on the adrenal gland and causes release of aldesterone.
This aldesterone, again, is circulating within the system and creates the need to stimulate reabsorption of sodium and water. So rather than excreting, water. Or sodium, what now happens is we get that retention of sodium.
And the reason why it does that is because when we when we increase our intake of sodium or we don't let go of our sodium. Now the blood that's circulating within our system is very salty and and sodium is our main o Osmotic gradient influence. So the more salt that we have, the more that water is drawn from, our extra extracellular spaces, or intersectional spaces in order to draw water to balance out that sodium so that we don't have a, a large volume of sodium versus our blood.
So now what happens is that water comes from our cells within our body, so again these patients get dehydrated because they're sucking cells from the extracellular space, or all those cells that aren't within that intravascular space from the interstitium. To balance out that sodium. Again, the water, so again these patients, start to become oleguric and uric because now what they're doing is retaining that water in order to balance out that sodium.
Oh man they're not urinating out of that water, they're not getting rid of any water. So what we start to see is potential cell swelling as well. Andretensin to itself, as well as obviously releasing this aldosterone, is a potent, constrictor, so vasoconstrictor.
So it causes peripheral vaso vasoconstriction of all of those vessels within the body. And now what we see is That we've increased our blood volume from this aldesterone, so we've increased the blood volume because we've increased the salt, and now we've increased the water to match it. So our blood volume has increased.
And now we've got this vasoconstrictor that's causing this, all of this extra blood volume to be squeezed around the body at an appropriate, circulatory, kind of blood pressure. So we've increased that blood pressure by by releasing the angiotensin too. So all that smooth muscle.
And again, the heart is a smooth muscle that again causes that, a, a little bit of positive ionotropy in those patients as well. So you say, like, this is great. We've increased our blood volume, we've increased our vasoconstriction and therefore our blood pressure.
Why, why is the system bad for our patients? Why would we want to stop this patient, this in our patients? And this is where It comes into play with our cardiac patients is that they didn't have low volumes to start with.
They have appropriate volumes, and now what this Renintenin, this RAS system is doing is increasing our blood volume. Well, the heart already can't cope with the blood volume that it had and. We've increased the blood volume, so the heart's gonna cope even less with that.
And we're just gonna get into this vicious cycle because the heart's not coping, it's not pumping the blood. The RAS system is triggered. We've increased our blood volume, we've increased our vasoconstriction.
Meanwhile, our patients getting super dehydrated, they're not urinating as much. It, it is a, it's, again, this is another one that it's a very vicious cycle. Initially, this RAS system is really good for those hypovolemic patients that have had a bleed and have that low blood pressure or potentially like saying decompensated shock or when they're compensating in shark, before they decompensate, I should say, is that it causes that initial bump in blood pressure in order for us to, to keep that patient as alive as much as possible.
This is our, our fight or flight, you know, our, our. Sympathetic kind of system kicking into place. Long term, this does not work for our cardiac patients, so we need to stop this really.
But when we stop this, what we now do is that we are again, we're going, we need to address the fact that there's low blood pressure to those kidneys, and how are we gonna do that without triggering this RAS system or relying on the RAS system. So both of those really important kind of systems. So when we look at this next, schematic view, this was taken from the, American Journal, the American Heart Association journal, so human medicine, hence the human skeleton, but it's just a really good schematic of kind of what happens when we, and, and how much those systems really kind of, Balance each other out on the scale.
So we have a acute cardiac insults, let's say a patient has a primary, you know, has a, has been identified as having a, a primary cardiac disease that's just been identified and maybe have cardiomyopathy, arrhythmias. Now what happens, we have that reduced cardiac output. Reduced perfusion, therefore, but now what's happening as well, because we get this backup.
So remember that backwards failure, we get this backup in our system as well, is that now the venous pressure is much higher because it's really trying to have to, it's got a lot of systemic vascular resistance because we're really trying to push against these small vessels with all this backed up volume. And again, this can cause congestion in the kidneys. Again, we get this peripheral vasoconstriction which might cause vasoconstriction within the kidneys.
So again, the kidneys aren't getting the blood supply that they need, . And again, that RAS system is triggered as well. I'm.
So again this works in both ways, and that this rash system then causes peripheral vaso constriction. Now there's not blood, you know, now there's too much blood going to the heart, we we're also causing vasoconstriction, . You know, everywhere I, we are, I'm potentially gonna cause our patients to end up with, I'm acute kidney injury versus our acute cardiac insult.
So how are we gonna go about identifying with our patients have cardio renal syndrome? And so we know about, obviously, how we would go about doing our heart patients and our kidney patients. And, and in, you know, simplified, we do need to just basically do the test that we would do, when we are thinking about our patients that have, cardiac disease or renal disease.
But now what we're doing is we have a little bit more consideration that, OK, these two systems are intrinsically linked. And so what we need to look at is biomarkers kind of cardiac or kidney injury. That provide us information in the context of cardio renal syndrome.
And kind of identify early cardiac or renal injury so that we can kind of look at how we're treating those patients more effectively rather than just going all in with cardiac, medications and not thinking about those kidneys and, you know, a lot of those kidney medications, so like a lot of the heart medications like those diuretics, those ACE inhibitors, things like that, they are going to have that direct effect on our kidneys. And so for our diagnostics for heart disease, what we're gonna do is obviously thinking about the auscultation, thinking about whether those patients have murmurs, arrhythmias, pulse deficits. I'm potentially thinking about screening patients, for heart disease.
I'm particularly. If they're older patients, or they're a breed that is specifically, pre predisposed to things like mitral valve disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy. All of those patients, that we know that there are certain breeds that are predisposed to those.
And then basically we're just going and using the AI classification. So this is from AIM, for the Class A, Class B, Class B2, class C1, Class 2, C2, class D1 and class D2. And we're gonna use things like our, our natic peptides, pro BMP or sorry N terminal pro BMP or our, BNP, so our B type naetic, peptide.
So most commonly in practise, we're gonna be doing that pro BNP. And you can do them and within the practise or again just send those off. And they're reaching the uses and they're also, there are kind of a Links with acute kidney injury and pro BMP as well, so, so again when we're thinking about looking at our renal disease, we might also think about running those pro BMPs as standard alongside those.
Other ones that might have, are, are cardiac troponin, one. And so these are already established kind of indicators for cardiac injury, or disease, and we use these regularly. And again, we use them in-house, we might send them off.
So it's kind of thinking about those biomarkers that we commonly use with those and thinking about the, potentially looking at those patients that, they are at risk of cardiac disease if they, if you've identified a primary renal disease. I'm So cats in particular are kind of a bit trickier with this one. They often can have kind of substantial pre-clinical heart disease, without any abnormalities or potentially with abnormalities, during physical, examination.
You know, sometimes we have patient, cats that have heart murmurs and they have nothing wrong with the heart when they're sent for a cardiac scan, versus patients that have had no heart murmur and it turns out they're in, they're in congestive heart failure now. So, again, thoracic radiographs of cats might be unremarkable. And so, the recommendation is that actually cats would be better to be screened via cardiac ultrasound, whereas dogs, we might just do a thoracic, radiograph.
So again, any, any cat that has a murmur, a gallop rhythm, or definitely a, you know, a radiographic cardium megaly in a cat as well, that should prompt, . Further evaluation for heart disease. Again, pro BMP, I'm in these patients, I'm sort of elevated values.
I'm suggest a high likelihood of, underlying heart disease. And so again, it's not realistic to to heart scan all patients that you're coming in that you think have renal disease, but particularly if the patients with renal disease, so acute kidney injury patients that you've got, and you suspect, you know, you listen to, you've done an assessment and potentially you're suspicious of heart disease or, . You're worried about this cardio renal syndrome, then they are a candidate for thoracic radiographs and ultrasound as well.
So, same with kidneys, and following those, international renal interests aside to the Iris guidelines. So they have the iris guidelines for AKRI for acute kidney injury, and they also have them for the chronic, kidney disease as well. And they're just the most widely accepted, and they have this nice handy kind of grading criteria for you to grade that patient, 1 through 5.
And other things that we might do is, look at, biomarkers of early kidney injury. So, I'm, clustering, but particularly NGAL, so neutrophil gelatinase associated with lipocalin, is a protein that's found in neutrophil granules and that are secreted by the renal tubular, epithelium, by the myocardial cells as well. So again, there is that connection between that cardio renal syndrome.
And other specific organ sites as well, so. It has been extensively kind of studied within, cardio renal, syndrome, and has that diagnostic and prognostic value, in acute heart failure as well as, chronic heart failure. And within the context of acute kidney injury, is actually the most up regulated protein.
So actually it's a really good biomarker for our kidneys and particularly in our cardio renal syndrome. And so you'd need to send that off to the lab, but, is available. And then system C.
And as well as that looking at our urine samples, so if we've got protein in your ears, that I be in your ear, those are biomarkers of glomerullar filtration, and that integrity, within the context of cardio renal syndrome. So again, it's a cysteine, protease, and it's in all nucleated cells, and produced at a constant rate, so it's freely filtered, completely reabsorbed, and not secreted in renal tubules, so it is that I'm very specific about the glomerul filtration. And therefore we can keep an eye on those patients that have heart disease.
We might start thinking about running, cystatin C alongside to see what our glome infiltration rate is and therefore do we need to do something about this? Are we at risk of acute kidney injury because we have a low glomerufiltration rate. I'm So these are the ones that we're gonna send off to the lab, but then a useful kind of biomarker in early chronic kidney disease in dogs is our serum, symmetric dimethyl argen, the SDMA.
And that again, correlates really well with measurements for glomerullo filtration rate, and usually increases before serum, creatinine increases that we see with the iris guidelines. And so that suggests renal compromise. So again, more widely available, can do it in-house on your biochemistry machine, that SDMA.
And again, thinking about, whether our patients have, concentrated urine, with substantial, protein in your ear. Again, that's a kind of a, a, a trigger for us to think that that patient might have significant renal disease, and thinking about things like her urine, protein creatinine ratio. Again, because cats are cats.
Cats naturally have, like, kind of well-concentri urine. So early chronic kidney disease is kind of overlooked, and it's where it's really important within the context of cardio renal syndrome, is that we're trying to avoid, the early chronic kidney disease because once one system fails, the other one is gonna fail as well, and then they're gonna kind of compound each other. So, specific gravity, I'm underneath, 1.035.
I would suggest chronic kidney disease in these, cats, and therefore, further staging. So imaging, doing your urine protein creatinine ratio, urine culture, potentially, I'm thinking about things like, if a patient has muscle wastage, I'm therefore thinking about things like serum, SDMA concentrations, because of that, I'm. They're gonna be more accurate than actually our creatinine values, .
As a, as an indicator for our renal function. So now we kind of come to our different categories. There's lots of categories to remember, and they are out there, in tables that are much easier to kind of digest.
I'm gonna break them up into the different cardiorenals. So we have type one. So this is an acute, impairment of the cardiac function leading to acute kidney injury.
So we have a primary cardiac disease, so we have this acute cardiorenal syndrome. It's acute onset, and we have that rapid impairment of cardiac function, and therefore, that leads to acute kidney injury. There's kind of multiple and complex mechanisms of, by which acute heart failure or of onset of an acute onset of chronic heart failure leads to that acute kidney injury.
So thinking about arrhythmias, in particular, would be a good example for this one. Myocardial injury would be a good one. I'm.
As a as a good example for these. Acute heart failure, cardiogenic shocks, that's forward failure. And again, this is another classification rather than type one is CVRDH unstable.
So these patients are often unstable, because of that acute onset, there's no coping mechanisms that a patient has now, put in place. Type 2, is our chronic cardiovascular disease causing progressive chronic kidney disease. So, again, this is a chronic type.
So we have a chronic cardiorenal syndrome, chronic cardiovascular disease, progressively worsening chronic kidney disease, so. Chronic heart failure, is likely to cause persistently reduced renal perfusion, as I talked about, that chronic renal congestion, so congestive kidney failure because of that, I increased pre-load, increased after load, systemic hypertension that we see with these patients. I'm I'm what we often see is these neurohormonal changes, because of chronic sympathetic stimulation, because of that cardio, that that chronic cardiac disease.
So things like production of epinephrine, adrenaline, angiotensin from the kidneys. Endothelin and as well as that things like release of nitroretic peptides that BNP and nitric oxide as well, which we know causes cell damage. So chronic heart failure is our main one that we see with this one.
We see this congestive heart, kidney failure as a result. And this is considered a stable one because the patient has been dealing with this over a longer period of time, but has, developed, developed coping mechanisms. They're not, they're not serving that patient very well, but there are things like this epinephrine, this angiotensin, nitrotic peptides, and nitric oxide that are, trying to trying to create a balance between the two systems.
And so type 3s are acute primary worsening of kidney function that leads to cardiac dysfunction. So now we're switching from our cardiac disease to our renal disease as the primary cause. So we have this acute, kidney injury that can affect the cardiac function through multiple mechanisms.
So, for example, with acute kidney injury, we get fluid overload because the kidneys can no longer filtrate, that fluid out, so we get increased volume. That's gonna cause cardiac dysfunction because now there's too much, there's too much preload time. There's too much going into that heart.
It, it's not gonna be effective for that, it's gonna be overloaded. Electrolyte disturbances, so again we know that the kidneys are responsible for filtrating. They might have an increase in sodium and therefore we can we get that increase in water retention.
And there's to get that vicious cycle of that fluid overload in those patients. Neurohormonal neurohormonal activation. So again, the RAS system is triggered because that kidney is injured.
It's not receiving the blood supply. It still recognises that it doesn't receive the blood supply and and it's releasing those. It's also releasing things like free radicals as well.
And myocardial depressant fact as well. They, so they can all cause things like our development of arrhythmias, pericarditis, and acute heart failure. So, we get this acute kidney injury, and we might have things like hyperkalemia, we might have urea, which we know, and toxins to that patient.
And so now this means that this patient is unstable because of that high potassium that's going to cause arrhythmias to the heart, potentially even death. Uremia again, if they have a buildup of that it's gonna cause neurotoxins, and it, you know, gonna cause death to that patient pretty rapidly, as well as the pH imbalance as well that uremic acid influences the pH so. This is considered an unstable cardio renal syndrome.
So CVRDK unstable is the name for it. We have type 4, which is our primary chronic kidney disease that contributes to cardiac dysfunction, so. Things like chronic glomerular disease.
So what we start to see is because of, detriment to those glomerulus, and we start to see that we're not filtering out all those, electrolytes. We're not, we're, we're having neurohormonal activation. We're having release of free radicals, nitric oxide, .
And as a result of that, that causes a decreased systolic function to the heart, left ventricular, left ventricular hypertrophy, a high output state, and that's secondary to anaemia because we know again that the kidneys are responsible for, production, of red blood cells. So when the kidneys start to die, and when we start to see that chronic kidney disease, where they're not, we start to see a chronic anaemia as well. So because of that, the heart creates a need to pump more blood quicker, so that we pump the blood to the lungs as as quickly as possible within a minute, so that we get more oxygenated blood circulating in the body.
And there's a kind of, potential long term, cardiac, sequela of, chronic kidney disease. So, as I said, we get this anaemia, we get the systemic hypertension, and that's because, that we're constantly trying to push blood out as quickly as possible to get it oxygenated, to get it back out to the body. So it's considered stable, because that's not gonna kill the patient immediately, it will potentially kill the patient eventually but that's kind of how we remember it.
And then finally, within our category. Is we have Type 5 cardio renal syndrome. So this is secondary cardioenal syndrome, and that's characterised by cardiac and renal dysfunction, secondary to an acute or chronic system, condition.
So, sepsis is the most acute condition that affects both the heart and the kidney. Diabetes, meitis and hyperadrenic vorticism are also kind of typical chronic diseases in dogs that have, a similar effect on the urinary and cardiovascular systems. So within diabetes, we know that we get this increased thirst response, therefore we get increased fluid, .
Fluid retention, fluid intake, I'm. Potentially if our patients have diabetic ketoacidosis, we then start to see the kind of deleterious effects of that as well and that I'm we can see acute kidney injury with that. And so kind of this works both sides, so we see this acute kidney injury, but we've also got this fluid retention.
That's causing the increased demands of that heart to pump out, so we get this concurrent kidney and, cardiac disease. Again, hyperadrenal corticism we see changes to the fluid shift, fluid balance. We see increased salt, within our hypoadrenal courseism or Addison patients.
So we now see that our patients become dehydrated because they're sucking all of that fluid into the intravascular space. We're now potentially fluid overload in that heart. We're also potentially fluid overloaded, fluid, with, with these patients as well, they have peripheral vasodilation.
So we're now seeing that we have a low blood pressure within the kidneys, the rash system's triggered, it becomes this vicious cycle. I am sepsis again, so with sepsis we have this distributive shock, so we have those leaky vessels. So now we have a blood loss, a blood volume loss within the circulatory system that is going to affect both the heart and the kidneys.
And this is called CVRD 0. So what are our treatment options for these patients? It kind of makes it kind of a bit difficult.
I mean if we're trying to deal with both of them, I'm and it is challenging. And sometimes we may need to prioritise one system over the other, and that's a difficult decision to make, because both do, you know, the heart is doing a great job pumping blood and getting oxygen to where it's needed, and the blood pressure to keep those vital organs, from getting the ischemic injury. And from getting multiple organ dysfunction.
But if you don't have kidneys that work, then you no longer have, you know, good fluid balance because you have electrolyte imbalances. You have arrhythmias because you have electrolyte imbalances. You have, toxin buildup.
So, you know, you have eremia, and therefore you get changes to your, you get metabolic acidosis as a result, and therefore, that's gonna kill your patient anyway. So, it is kind of like being stuck between a rock and a hard place. And so, but the overall goals in these patients that have cardio renal syndrome are to maintain appetite and body condition, decrease clinical signs of, of what we're seeing.
And ultimately provide good quality of life for these patients, it's not, it's more kind of like, we're not gonna reverse the causes of these, it's more of a palliative kind of prolong life prolonging treatment options. So again, when we're thinking about balancing these, we're thinking about the drugs that we're given, so as I mentioned earlier that I'm there's loop diuretics at rozamide that we use. When we see patients that have pulmonary edoema as a result of congestive heart failure.
Great for that congestive heart failure, we're getting rid of all, well, great for that patient because we're getting rid of all of that fluid that's on the lungs. We are reducing, we're getting rid of that, you know, we're getting rid of all that water, and therefore, creating less volume for that heart to have to pump. But now, what we're doing is we're also getting rid of our potassium.
We're also getting rid of our fluid. We're reducing our blood volume. Therefore, we're gonna have low blood volume that's gonna affect our kidneys.
And so, again, this is where we're kind of stuck between a rock and a hard place. So our primary heart disease, when we're thinking about those classifications, if it has the primary disease, often what we're gonna be doing is treating the primary disease as the first, I mean, as the first one to reduce those clinical signs, because those are where the clinical signs are coming from. And so immaendin is a positive inotrope, and that improves that systolic function, which may also increase, our glomerular filtration rate.
It doesn't suppress that, furosemide induced a rash activation, so just kind of bear that in mind. So, again, it's gonna depend on our patients and what heart disease they have and thinking about the complications that they have. So, for example, a dog with dilated cardiomyopathy and reduced ventricular systolic function, might have reduced cardiac output, a systemic hypotension, which may reduce glomerul filtration rate and trigger that randomly.
So, for those patients, we're thinking about positive viotropes to, create more, to get, to get that blood pressure, . Because we're increasing that systolic function. So we're maintaining adequate output, blood pressure, and renal perfusion.
But dogs with congestive heart failure that we're seeing, we are looking to things like our diuretics, because we want to resolve those clinical signs, we want to resolve that respiratory distress. And so with those, we need to then think about, kind of using them at the lowest doses possible. And that's, again, to prevent that damage to the kidneys and that, you know, low glomar filtration rate and that RAS activation that we see with furosemide.
I'm, so again, we might do, I'm. We potentially are gonna use furosemide, imabendan and an ACE inhibitor, so . So, again, thinking about the RAS system, how that's gonna affect the kidneys if you're now stopping that RAS system that's actually just trying to do its job to get a good liar filtration rate.
How's that gonna affect it if you're gonna use an ACE inhibitor? And so thinking about your electrolytes as well, your blood pressures, because those are all influenced with this as well. For some patients you might have to reduce or completely stop your ACE inhibitors, if they're poorly tolerated, or if you now get a substantially increased creatinine level.
So when we start cardiac medications, we should be looking at our kidney function, our electrolytes. So creatinine and electrolytes should be kind of reassessed within 10 to 14 days of start in our treatment as well. And again, thinking about arrhythmias as a, as a result of any electrolyte changes.
I'm So digoxin, and other kind of drugs that I have a predominant kind of renal excretion again might require kind of closer monitoring, and a potential reduction of the dose if we start to see renal diseases, you know, this cardio renal disease in our patients. But the kind of a good recommendation above and beyond the medications that we give is this omega 3 fatty acids. I mean that's recommended as an oral supplement, and has been used as kind of an antioxidant and an appetite stimulant in patients with heart and kidney disease.
So again, in these patients as well, we want to reduce their salt intake, so thinking about their, their diet that they're on and reducing the salt that's in their diet. So I mentioned the ACE inhibitors and kind of, but with our renal disease, what we're starting to think about, is that, we know that those ACE inhibitors block the angiotensinin and that aldosterone, but they do have an inconsistent effect, especially in cats, and so. Again, with those patients with congestive heart failure, particularly cats, we might initially start with rosamide and ACE inhibitors.
We might then drop the ACE inhibitors, and think about our systemic hypertension dehydration in these patients as well, because we equally don't wanna, we wanna try and avoid giving fluids to these patients, especially if they've got, heart disease, because we don't want to overload the heart. So, in our patients with kind of primary renal disease, I'm, again, thinking about whether we're using ACE inhibitors or those angiotensin, receptor blockers, and those mineral corticoid, receptor agonists as well, so our detroone blockers. So, Those are all things that we kind of, I'm thinking about.
I'm so that those aldosterone blockers have potential for renal and cardiac protection. So things like spirolaxolone, is actually much better in these patients and loop diuretics, because we're, we're given a diuretic, but we're also, causing a, we're not causing the activation of that raft system. And so loop diuretics, again, have conflicting effects on that, renal function.
So they reduce renal congestion in those some patients, and might improve that glomerul filtration rate, and delay the chronic kidney disease. But on the other hand, excessive doses of those diuretics are gonna cause reduced renal perfusion, therefore, reduced glomer infiltration rate as well. And so, I'm kind of the combination of loop diuretics and thiazide, diuretics, they might have a synergistic effect, but also might cause excessive volume depletion, and electrolyte disturbances as well.
So, we shouldn't be using those concurrently in the cardio renal system, syndrome patients. Thinking about patients with renal disease, often we put these patients on fluids, and so with patients like cats, what we often see is we give them fluid therapy with chronic disease, and we quickly unmask, occult heart disease. So, you know, we all know the patient that we've had on fluids and all of a sudden it's now got a gallop or it's got a murmur.
And that might be regardless of whether it's given subcut or IV. And so, in severely aotemic cats, long term subcut fluid might maintain well-being, but again, with modest, chronic kidney disease, it actually might be best, . To avoid, I'm because this this sodium load and I'm And that can cause an increased systemic blood pressure, .
So with dogs with acute kidney injury, and degenerative mitral valve disease, we can give these patients, you know, fluid therapy, should actually be given to address a renal injury and optimise the chances of recovery from that acute kidney injury rather than turning it into a chronic kidney disease, but we just need to closely monitor for fluid overload. Again, dogs with primary renal disease that show signs of overload, in these, when they're being administered fluids. They should be discontinued and thinking about our fluid volume, so these might be the patients that then we're referring on potentially for dialysis, .
If that's a possibility. So diuretics can be administered if necessary, but I'm, again, thinking about those fluid overload signs, so increased respiratory rate, potentially kind of regurgitation, lots of excessive swallowing. You might see it on ultrasound scan, that kind of nasal drip, the swelling of the sclera.
But most importantly is that respiratory rate. And so that's the thing that should be primarily checked, that rate and the effort. Every hour, if you have a patient that has, underlying heart disease and they have an acute kidney injury or a chronic kidney injury that they're having fluids for.
Heart rate may also change as well, if fluids are kind of, so they might increase if fluids aren't tolerated. And thinking about things like monitoring our body weight. So if we have an increase of more than 10%, Within 24 hours, then we've overloaded our patients.
So, inevitably, some of these patients will need fluids. We've just talked about that. We've just talked about, especially in those renal disease patients, it's, it's really important, to maintain fluid therapy, to maintain our blood volume.
And there's various reasons why it's not maintained, and that might be because of, inappropriate excretion from the kidneys. They're not able to concentrate and they're just getting rid of all the water. They might have more sodium and therefore they're now dehydrated, so we need to correct that problem.
They might have that concurrent disease, they might have sepsis, we now need to think about, or they might have hypovolemic shock. So we now need to think about that we need to give fluid therapy to these patients to correct electrolytes, to correct any circulatory deficits. And so fluid choice is really important in these patients.
I've just talked kind of about monitoring for fluid overload, but thinking about our fluid choices as well. And so think about those sodium levels, particularly with those heart patients, and in sodium content in the maintenance fluids that we're giving these patients. So things like Normasol and, .
With 5% dextrose, or 0.4 0.45% saline might be a better choice because of that lower sodium content in those patients with increased sodium levels, so we're gonna be guided by our electrolyte levels that we're looking at.
Again thinking about the fluid that's lost, that's equally important. So, again, in a hyperadrenal corticism dog, you might have horrific hemorrhagic gastroenteritis and therefore there is a loss of, plasma, and therefore is plasma more appropriate, . Is that plasma gonna cause better volume expansion with smaller, smaller volumes of fluid therapy, rather than giving lots of crystalloids that are only maintained within the body for 40 minutes.
But now we're gonna cause that, kind of untold damage to the heart or to the kidneys. The patient doesn't need shock replacement. I'm potentially thinking about those oral fluids, so reducing the need for those intravascular fluids that are gonna cause overload signs, particularly gonna cause increased demands on the heart.
So we have, primary renal disease, but we're just trying to treat it, a chronic kidney disease in the patients think about oral fluids, and that might be, what you, you know, giving you offering water to your patient, but also might be putting in things like a nasogastric tube, nasoesophageal tube and putting fluids down that so counting those as liquids, and using water for that in those patients. Thanks very much for listening. If you've got any questions, I'm free to feel free to email me.
My name is Chloe Fay RVN at gmail.com. I thank you very much for listening.