Hey, hello everybody. Well, thank you for joining us, and we are going to spend the next 50 minutes or so talking about heart patients that have something else, comorbidities, or patients that have something else that By virtue of having the disease or its treatment can affect the heart and how best to manage these patients. So happy to be here.
Well, let's just jump right in. OK, useful resource cardiac education group, go to it. Some of the leading cardiologists in our profession contribute.
It's kind of updated frequently, and one of the things I like most about this is that we have both a dog and cat formulary, all the drugs, all the dosages, one stop shop, really like it. So some of the things that we're gonna be talking about today, you can see on this list here. And some of these things we can do something about.
We can maybe prevent stress, we can monitor electrolytes, you know, adequately and prevent, you know, abnormalities from developing or identify and correct them as quickly as possible, be on the lookout for things like primary hyperaldosterism in cats which we'll talk about maybe an underdiagnosed and the most common adrenal gland disease cats get. So if we know what to look for, we may be able to prevent or at least, you know, have a full assessment of our patients. So by treating their comorbidity, we can minimise any adverse heart effects.
All these things affect the heart by affecting the key parameters of this crazy formula, oxygen delivery, the formula of life, I would say. And in order to live, you need to get oxygen to the tissues and that means having adequate cardiac output to push the oxygenated blood around and then you have to have enough oxygen in the arterial blood to be delivered to the tissue beds. Yeah.
So for something to affect cardiac output, it has to do something to these, right? So we have in our minds already probably, oh, I bet I know how to say . Excessive fluid administration can affect the heart by causing excess preload and we can have congestive heart failure or Hypertension can cause increased after loading and decreased cardiac output.
So things that affect our cardiac output are do so by changing these things, including the heart rate, yeah, or rhythm. So arrhythmias, brayardia, tachycardia, etc. Can also decrease cardiac output and then conditions that affect the amount of oxygen in the blood, arterial blood.
Mostly do so by affecting the haemoglobin because the vast majority of oxygen carried around in the arterial blood is bound to haemoglobin, and if we have a lack of haemoglobin, then we have a decreasing, you know, cardio, arterial oxygen content, which can affect. Our patients' outcomes. So we're gonna be looking for these things and thinking, do I have a disease in this patient or am I gonna do something to this patient that could affect these parameters.
I think one thing to keep in mind obviously is that this in people it's kind of referred to as cardio renal syndrome, where problems with the heart can affect the kidneys and vice versa, and because we're, you know, on the ball. In veterinary medicine, we consider that to be cardiovascular renal disorders, recognising the importance of the vasculature in overall health of both organs. Think hypertension, think thromboembolism, think heartworm disease.
OK, so we need to consider the heart, the vessels, and the kidney when we're trying to decide, do we have a comorbidity that can be deleterious to any of these structures, or do we have a disease in these structures that could impact heart or kidneys. And the links between these structures are anatomical, physiological, and I think makes a lot of sense, yeah. You know, in order to have an adequately functioning kidney you have to have it adequately profused and that relies on, among other things, you know.
adequate oxygen delivery, so we've got to have enough preload after load contractactility to get that cardiac output normal, normal heart rate, to perfuse those kidneys because they receive like 20% of cardiac output. We also know that hyperthyroidism, you know, is something that can increase renal perfusion, renal blood flow. And sort of mask kidney disease.
We have this false sense of security about how kidneys are doing and as we treat the hyperthyroidism, we can unmask kidney disease, so they're definitely You know, those physiologic parameters affecting volume that can affect renal blood flow and profusion, and then the kidneys have this effect on controlling things like blood volume, electrolyte acid base status that can have cardiac effects. So bottom line is disease in one can cause disease in the other, and it's happening more. We're recognising more animals that have comorbidities because we're doing better at keeping them alive longer.
Yeah. And also we're doing better at monitoring things like blood pressure, so we can identify that and address it. OK.
One thing we have to worry about when we're talking about how the heart can affect the kidneys is, or anything that can affect the kidneys. The tubule of the nephron is the most vulnerable part of it because the tubules have the highest. Metabolic rate, they do most of the work, so they need adequate blood flow and oxygen, right?
So anything that compromises that to the kidneys is going to affect the tubules first, OK? And this can be a primary toxic insult like from non-steroidals, grapes, raisins, lilies, or it can be a problem that's indirect like. Sepsis, severe pancreatitis, inflammatory cytokines and circulation, they bombard the kidneys and the tubules do not like it, and hypertension as well can have that effect.
So, tubular injury markers often appear earliest as an indicator of a kidney problem, and they are found in the urine, not the blood. So in order to identify early acute kidney injury, we need to be looking at the urine, and they can be present, these injury markers in urine for up to 2 days before we see an increase in our GFR functional markers in the blood. So we have our traditional injury to injury markers like granular casts specific for tubular injury, eugglycemic glucoseuric, specific for proximal tubular injury, but we don't always see these in animals with acute kidney injury.
We have a newer parameter available now asystatin B, which think of it as a leakage enzyme of the kidney like ALT in the liver, where if you have Active tubular cell damage, this leaks out of the tubular cells and you can identify it in the urine. So we want to consider this parameter as a marker for acute and active. Right now it's happening, tubular damage whenever we have obviously anything that would cause a primary or secondary acute insult to the kidneys.
So things like toxin exposure, shock, nonsteroidal antiinflammatory drugs, both toxicity and monitoring, OK, and also some unfortunate animals have chronic kidney disease and an active injury component. And if they do have this act active injury component, they tend to progress more rapidly through the iris stages of CKT. One way to identify this active injury component that's concurrent to the, you know, sort of stably slow stable, slowly progressive CKD is to get a cystatin B and if it's increased, it's predictive of more rapid progression.
Should we, should we be getting these tubular injury markers, maybe including cystatin B in patients that have heart disease as a clue that there is a perfusion problem that we need to address, heart disease more aggressively, perhaps. One study looked at dogs that had mitral valve disease, and in all. Stages, there were increased tubular injury markers.
Now stage B1 and B2, these are asymptomatic dogs that have evidence of structural heart disease, right? No clinical signs. C stands for congestive heart failure.
So even asymptomatic, earlyish stage B1, stage B2 dogs with mitral valve disease had in one study increased in two bitter injury markers, and if that's present, then we would pay more attention to what's going on with that heart status and maybe. If you haven't done a full workup, consider doing that and and adjusting or starting therapy to minimise, to optimise cardiac output so that we can minimise renal tubular injury. Not many studies in cats aren't using ystatin B so far, but some, we need more, and it looks like it can be predictive of survival.
It's higher in cats when it's increased compared to . Survival is lower in cats with an increase of statin B versus cats that have a normalcystatin B and the same rules apply. Any sick cat, you know, severely systemically ill cat or cat that's exposed to lilies or eth glycol, you know, heart disease, think about assessing the kidney impact from the cardiac disease by looking for injury markers and this is a really good one.
OK. So obviously another factor that can affect the vasculature, so the cardiovascular renal disorder is hypertension, and I'm sure you guys are aware of the ACVIM consensus statements. These are open source available to anyone, and they publish these when something new has been uncovered that's important enough to spread to the veterinary profession, and there was a hypertensive hypertension consensus consensus statement a few years ago.
Which kind of changed the game with a new normal being less than 140 versus the previous normal blood pressure was considered to be less than 160, and there's this pre-hypertensive group now between 140 and 159, and it's important to identify these animals because they're more likely to become hypertensive in the ensuing months. So we would monitor them more frequently so that we could prevent hypertension and the deleterious effects on heart. Kidneys, eyes, and brain.
OK. When you identify hypertension, it's most of the time the vast majority of cases secondary to some kidney, any kidney or endocrine disease and you can see the lists here. So you identify hypertension, you assess for these things, you identify these things and you be sure if you already have it, to measure blood pressure and it's systolic.
All decisions about treatment. What stage are you in? Are you pre-hypertensive, normal intensive, it's all systolic blood pressure, we can do that.
Ideally, it would be mean blood pressure because that's truly what affects and determines vascular bed perfusion, but that's a tough one to measure, in most instances. So we rely on systolic, so get good at that. Start early in your patients and monitor so you can identify early problems.
Let's see, what's the news about treating it? So in cats, good old amlodipine. Great drug.
And telmisartan, a newer drug, hypertension, that's also good for protonuria. So if I have a hypertensive proteinuric cat, I'm kind of reaching for telmisartan cause with one drug, we can, you know, address both conditions. And then I think just keep in mind that now we base the initial dose of amlodipine on blood pressure, not body weight, with 200 being the caught up below 200, the 0.625 MB per cap per day dose, 200 or greater, double that.
OK, if you have a hypertensive cat who happens to be hypokalemic, likely that's gonna be kidney disease, chronic kidney disease, or hyperthyroidism, but if it isn't, it could be this. So primary hyper aldosterism is the most common adrenal gland disease in cats, and they come in for signs of low potassium, so they're lethargic, they're weak, they have maybe ventral neck flexion or visual changes because hypertension is caused retinal haemorrhage or detachment, right? So suspect that and then.
You're going to like work the cat up and it's hypertensive, it's hypokalemic and you'll think, well, I'm gonna assess it for chronic kidney disease and hyperthyroidism. I mean, it's usually one of those two things, but if it isn't, remember this is out there and you'll find it because while while working up the other problems, the T4 will be normal and instead of finding two small irregular kidneys on abdominal imaging, if you have an ultrasound, you'll see an adrenal mass in one kidney. And then You'll do an aldosterone level and it's usually high, so the well it's almost always high.
So the combination is Low potassium, high blood pressure, no high T4, adrenal mass, not too small kidneys. And high aldosterone, it's this drug. Other clues that you're dealing with this are, if you have an indication of acid-based status on your panel, like total CO2 or bicarb, then it will be high in this disease and obviously with CKD, if you're going to have a change, it's going to be low, right?
They're aidedemic versus alkalotic, and with CKD phosphorus is usually high, at least in advanced stages, and with this disease, phosphorus is normal or low. That would be a clue. The other clue I hear, cause I always ask people when I speak, has anybody seen this and it's surprising.
Almost one person in every talk I give has had a case. It's out there, it's underdiagnosed, and I'm like, how did you figure it out? And they said, Well, I was, I saw this low potassium in a cat, and it just didn't budge when I started potassium gluconate.
And that's super common because the potassium is often so low, driven by this high, high, continually secreted aldosterone that it's really hard to budget with potassium glucoate. If you identify this disease, prognosis is good. With surgery.
All right. One vet who had a case, I'm like, well, how did that go? She goes, Well, we identified it when the cat was 6 years old, and I go, how did it do?
And she goes, it's 14 now. OK, curable disease. As long as we are aware that it's out there and if we aren't finding CKD or hyperthyroidism in these cats, we have, we should be thinking about this disease.
It's really hard to control medically. You can Improve the values, but it's really hard to normalise blood pressure and potassium with medication in this disease. So it's out there.
Hypo hypokalemia, hypertension, it's not CKD, it's not hyperthyroidism. Think this, get an aldosterone level, especially if you see an adrenal mass, and then get it out. OK, hyperthyroidism, we all know, can have deleterious effects on the heart and kidneys, so over time.
So, this I think is probably, I haven't found a more recent better document about all things hyperthyroid than this again, open source, really useful and the point here is When we have a cat that comes in, we should be screening all cats 6 to 7 years of age or older for hyperthyroidism. Just no signs, whatever. Just put T4 on the panel in cats of that age so that we can identify what they've considered this group 6 cat, who is a cat that has no signs, no blip, no nodule, but has persistent, a few months apart, elevated free T4s.
That's pre-clinical or cult hyperthyroidism, and we want to treat it. So that we don't end up with deleterious effects on the heart and other structures, all right? So let's say that you're working up a cat and it's the right age, 6 or 7 or older, and you find a borderline total T4, so a little bit higher than normal or sort of high end of normal, and an older cat like 8 or 10 years of age where it shouldn't be that high, so think about that cats in that age group, 8 to 10 or older, their T4s have no business being in the high end because if we had a specific age.
Range for T4, it would be lower cause T4 goes down with age. So you're thinking, well, is it, it's too high for this cat given the age, or is this slight increase real or not? Well, how do you confirm there's a couple of ways you can just repeat the total T4, no harm, no foul, as long as the animal's stable, nothing urgent about if you knew you would treat.
You can do a free T4 and that can be ED or not, you know. For this use, and don't forget using TSH in cats. It's like in dogs, right?
So with dogs, low T4, high TSH, hypothyroidism versus your thyroid sick or anything else. In cats that are hyperthyroid, the TSH is really low. So if you have a borderline total T4 and a very low TSH, the cat is hyperthyroid and should be treated even in the absence of clinical signs, and hyperthyroidism can affect the heart by both indirect and direct.
Mechanisms, I think you can read them here, it's no surprise. Hyperthyroidism can also cause hypertension, but you're not off the hook. If at diagnosis of hyperthyroidism, blood pressure is normal, it doesn't mean it will stay that way because it seems like 20% of cats that are normal tends so that diagnosis, develop hypertension within 5 or so months.
After treatment has begun. So the point is, if it's good, great, start at the start of therapy, blood pressure is normal, no reason to treat it to treat the hyperthyroidism, but continue to monitor blood pressure for at least 6 months to make sure it doesn't develop as these cats are treated. Usually this is an older cat disease, of course, and that's when we start to see the deleterious effects from hyperthyroidism on the heart.
One thing to keep in mind is that at diagnosis of hyperthyroidism, if you find changes on radiographs or ultrasound that suggests also like cardiomyopathy, no way to tell if it's due to the hyperthyroidism or a separate primary heart problem. No way to tell. Eventually you'll be able to determine that by using antipro B&P.
At diagnosis, if you have evidence of heart disease, then get a pro B&P level. That should normalise after 3 months of being your thyroid if the heart disease at diagnosis is due just to the hyperthyroidism. So monitor.
If 3 months after your thyroidism has been attained, your Pro BMP is normal or way lower, it's likely one disease, hyperthyroidism treat that. If the ProbMP does not go down. Then you've got two diseases, continue to treat the hyperthyroidism and then determine if the cat needs therapy for heart disease as well.
Tachy arrhythmias or arrhythmias with hyperthyroidism are usually tacky arrhythmias, and that can be atrial or ventricular in origin. They can be atrial or ventricular in origin, and a good drug for either of them is atenolol, which is fine in most cases. If you have asthma, then we don't want to block the bronchodilating beta 2 ad adrenergic receptors.
So we might want to avoid a beta blocker and use diltiazem instead. OK, what about hypothyroidism in dogs? This doesn't really do much unless they have significant heart disease when they eventually get hypothyroidism.
OK. So this is pretty much spares the heart in most instances, but what it does make you do is be more cautious, excuse me, about treating the heart the hypothyroidism if heart disease is present. We don't want to increase the metabolic demand and rate too fast to tax the heart.
So we will start at 25% of the standard dose of thyroxine and gradually ramp up just to allow the heart to adjust to the increased demands over time. OK. What about Cushing's syndrome as another endocrine disease that can have cardiac effects?
Obviously, both dogs and cats get this disease. It's more common in dogs than cats for sure, and it rarely causes but can exacerbate heart disease by changing those parameters we talked about earlier under cardiac output. So the cortisol can do two things.
It can increase preload excessively, volume overload, and it can also increase after load, OK, by causing a peripheral. Vins to constrict arterials to constrict. So we've got increase in systemic vascular resistance, increase in volume, and that can be a trigger or exacerbator of heart disease, and it can also cause hypertension, of course, right?
And then devastatingly if we have an unfortunate dog with Cushing's, we can see a vascular component of the cardiovascular renal access disorder, that would be thrombobolic disease, usually the lungs. Also, pushing our dogs can be proteinuric, right, which can lead to hypertension, and if it's severe enough and the albumin drops significantly, that can also contribute to the risk for thrombobolic complications. So monitor urine in these dogs, and if we've got persistent renal protonuria and our UPC is elevated, we want to treat that concurrently, to their treatment for Cushing's disease.
OK. Because protonuria is a risk factor for both hypertension and for thrombolic disease, we want to know how to deal with that as a comorbidity to prevent or further prevent further exacerbation of cardiac problems, and this is the updated guideline recommendations from, these are the updated guideline recommendations from Iris and what we like to point out is that we use renal diet and telmisartan to decrease intraglomerular hypertension. Which if we have a persistent increase for long enough, will develop fibrosis and sclerosis.
So these drugs both are aimed at lowering intraglomerular hypertension. They don't do, they they're not gonna control systemic hypertension. If that's present, that's treated separately, right?
If we have a significantly decreased albummen, then we want to get animals on clopidogrel to minimise the risk for thrombobolic disease. And what we now go our goal for treatment not treatment now for Iris International Renal Interest Society has changed. It's great if you can get to a normal UPC.
It's hard though, especially if the initial value is high. So a decrease of 50% is what we're looking for and how that impacts therapy is, we kind of start with telmisartan and if you haven't gotten that 50% drop from baseline, we gradually increase the dose as you can see there. We control blood pressure with amylodipine if that hasn't changed cause that may prevent further, that may give you some further benefit in lowering the UPC.
We do the omega 3 fatty acids and then we kind of stop because if we then add on other renovvaoactive drugs like ACE inhibitors, benazapril, enalapril, when we've maxed out the elmisartan dose, then we're at an increased risk of severe drop in GFR. And that's, it's safer to be fine, happy with a 50% drop in the UPC then potentially piling on additional drugs that could have adverse effects to drive the UPC lower, OK? And then you can see the monitoring here, all right.
OK, now in cats, we were talking earlier about preventable, potentially reversible causes of heart disease in cats. If the cat has any of these, it's better because we can do something about the heart disease, right? Versus just having primary cardiomyopathies.
And one way to Determine if you've got an issue to begin with, or if it's safe to administer high rates of fluids or anaesthesia or corticosteroids. Is to get a baseline pro BMP, and if it's increased, be careful, OK? So we want to control stress cause there is a tachycardia induced congestive heart failure with tachycardia.
You don't have enough time for diastolic filling, right? And so you end up with decreased cardiac output decreased preload, not good, right? And then With IV fluid therapy, especially if it's a cat that's gonna require increased amounts, and we'll talk about high amounts.
We'll talk about what to do with fluid therapy when you have heart disease and an animal that needs fluids, things in cats that require maybe the highest fluid rates would be say DKA or post obstructive diuresis after you've unblocked a cat. So. Cerrorob and pes can help you determine if it's safe to continue.
If your initial one is normal, right? If your initial one is increased, you need to give these guys fluids, but monitored carefully using an accurate gramme scale, maybe 4 times a day, in that acute phase where you're getting pretty aggressive with your fluid therapy. General anaesthesia, same thing, you might want to adjust protocols, control your fluid volume administration rate, minimise stress and pain in the whole per-anesthetic period.
And then let's spend a little bit of time talking about corticosteroid induced congestive heart failure. This happens from two in two ways. One, if your corticosteroid has a mineral corticoid component, methylpred, prednisone, prednisolone, then the sodium retention can cause fluid retention and you can have increased preload volume overload.
But All glucocorticoids can increase blood glucose, and that can cause an osmotic shift from the intracellular or the extravascular space into the intravascular space and raise volume that way. OK. And they can also cause increased systemic vascular resistance increasing after load, yeah.
So what do we do? Well, we get steroids when we need to for sure, and most of the time it's fine. Yeah, but cats are so good at hiding their heart disease that one way to see if they've got some heart disease to use your Pro B&P again.
And if it's increased at the start of glucocorticoid therapy, then you're definitely gonna want to monitor it during treatment. And if you see an increase from baseline, and it one study that looked at this showed that baseline increase. By 60% in 60% of cats on prednisone at this dose after one week, right?
Right? Or and some cats went from normal pro BMP to elevated, yeah, higher than normal at 40% of cats. So bottom line is.
If you're gonna need to be on corticosteroids, let's say you hear a gallup any or it's an at-risk breed in particular, consider Pro BMP to begin with, monitored during therapy. If it starts to go up, then switched up. Glucocorticoid may be considered redeinide or some other immunosuppressant.
One thing to remember, you could absolutely use a Snap pro BMP in the clinic to rule out moderate to severe heart disease. So you would consider it in a cat with respiratory signs to determine if it's asthma, or congestive heart failure, if you have a murmur or gallop and want to determine if that's significant, gallops are usually always significant, murmurs may not be, and any of these other conditions here. If it's normal, you can say, well, I can go to anaesthesia today, right, cause if I have heart disease, it's very mild.
It has increased, you need to think twice about it and adjust protocols, fluid rates, etc. OK? The reason that you can't use it to say this cat has no heart disease, if it's negative is that.
In like the cutoff for abnormal pro BMP in a cat is above 100 pea moles per litre. The snap turns positive at about 115 to 120. So a negative snap doesn't mean you don't have any heart disease cause you could have between 100 and 115 or 120, but You don't have significant heart disease.
Probably clinically you can proceed with whatever you had planned for the day, but you can't use this test to screen say at-risk breeds for heart disease to determine if they should be in the breeding pool or not. That requires ultrasound. OK.
Obviously, diseases that change electrolytes can affect the heart by causing arrhythms and in particular or decrease contraactility and potassium is the big one that we're concerned about, but it's not just when it's high. Obviously, a high potassium, we can see these devastating effects on heart rhythm rate and rhythm, right? But mortality increases when you have both increased and decreased potassium, right?
If you do have high potassium, first thing is to make sure it's real and not pseudo. OK, so make sure we don't have thrombocytosis or we don't have EDTA contamination of the sample, those sorts of things. We don't have any molysis in a Japanese breed of dog, I think that's on the next slide.
But with hyperkalemia, you can have, I'm sure you've seen this, you can have some cats that have potassiums that are kind of scary high and they don't care. They're not bradycardic, they're not hypertensive, they're not hypothermic. You've got time, OK.
Some cats with potassium is lower than that show signs. So it's not the absolute value per se, but it may be the rate and magnitude of change increase because other minerals, electrolytes, and acid-based conditions can affect what potassium does to the heart. But if you have a cat, especially, specifically that's bradycardic and hypothermic, then you know your potassium's above 8.
Deal with it. If the cat has a potassium above 8 but is not bradycardia or hypothermia, you have more time. OK.
Again, these are the conditions, these are the causes of pseudo hyperkalemia. Make sure you don't have these, before we do some extensive or expensive treatment and thrombocytosis increases potassium in the tube, not the dog, because there's a lot of potassium in platelets. So when they contract in the tube, then the potassium enters the serum and then is picked up on your analyzer, but that doesn't happen in the dog.
OK. OK, so I think we all have our protocols for treating life threatening hyperkalemia. Your first bet is to get them on some isotonic crystalloid, and it's fine if it contains potassium because the amount of potassium say in lactated ringers or plasma light, trivial.
It's not going to increase the serum potassium further. Potassium, calcium gluconate is your cardiac protective agent that buys you some time to get everything else lined up if you need it. And then we use our, in my experience, the combination of insulin and 50% dextrose is what drives potassium into the cells the fastest.
Bicarb rarely necessary only if you have extreme asidedemia, pH less than 7.1, bicarb less than 12. If you have that, you need to give it, right?
But we don't rush to it unless we have these values and we start by calculating the dose and giving one quarter to 12, and then doing that repeatedly if necessary until we get our values above these cutoffs, OK? Hypokalemia, on the other hand, is a contributing cause, an aggravating factor to arrhythmias as well, right? So.
I listened to a lecture that a cardiologist get. I'm not a cardiologist a few years ago in England, and it's not uncommon for cats and dogs, at least at her practise, to come in hypokalemia or obviously to develop hypokalemia on diuretics. So her protocol is the following.
If at diagnosis, they need their potassium is less than 4, when you start their treatment for congestive heart failure, Lasix, and others start supplementing their potassium. If the potassium is normal at diagnosis before you start diuretics, go ahead and rock and roll, just recheck the electrolytes a week later, and then you can decide if they need supplementation or not. And then continue to monitor, OK.
Point is, don't let their potassiums hang below 4. 4.5 you know, below 4 3.7, fix it, OK.
OK, now, we've got heart patients that need fluids because they get other things. They might be dehydrated, they might be hypovolemic, etc. So we need to give these guys fluids.
Let's just put it this way. If it's possible to give them fluids by the oral route, by placing in any tube, it's really hard to cause volume overload doing that. That's a very physiologic, safe way to correct mild dehydration in dogs and cats with heart disease.
But in general, we just want to avoid overdose. In all patients that we administer fluids to, especially patients with compromised cardiac status, right? I always say.
You need to replace the fluid at the rate the animals lost the fluid. So with hypovolemia, that's an acute loss, you need to replace the fluids quickly, and if they're dehydrated, that's a gradual loss, you replace the losses gradually. And if you remember that, it's one way to keep from overloading our patients with fluids.
So you can see the fluids that we resuscitate with, it's not saline anymore regardless, right, especially in heart patients because of the higher sodium content. Good old lactated ringers is fine, doesn't matter which one you pick, right? If you do have a heart patient that has traumatic brain injury, right, and their critical condition, you, you can give them hypertonic saline if they're hypovolemic, right?
But once you get their deficits. Corrected if they continue to need fluids. We got to, we have to get them off, and this is in general, not just heart patients, get them off the higher containing initial fluid we chose, higher sodium containing the initial fluid we chose to a fluid that has half the sodium content.
And you can buy it, so you can buy a half strength saline into net% dextrose, or you can make it dilute whatever crystalloid you use 1 to 1 with D5W and mostly you have to have in most instances adding say 20 mL equivalents per litre of potassium is is a good idea. OK. And in general, certainly in heart patients if you don't need it.
Avoid sodium chloride because it's acidifying, no buffer, and chloride is a metabolic acid, and then chloride can also cause renal vaso constriction, so that's not great, yeah. OK, let's see. When we're monitoring how our patients responding to fluids, we want to monitor perfusion as well as blood pressure, OK?
This is. You can see this or not let me get rid of that. OK.
I'm a big fan of using the dorsal pedal or metatarsal artery pulse to start with, because if you have a pulse there, your blood pressure is normal, near normal or normal. Having a femoral pulse just tells you that your blood pressure is above 50 or 60. Better than having a blood pressure lower than that, but you wanna use your Physical exam and get good at doing dorsal pedal or metatarsal artery pulses because a pulse there means blood pressure is adequate.
Also pay attention to what happens to the pulse when you have simultaneously aus when you're simultaneously auscultating the heart, so to detect arrhythm is pulse deficits and then pay attention to the strength of the pulse. If it waxes and wanes with Respiratory phase. So if it decreases the strength of the pulse goes down with inhalation and increases with exhalation.
That's called pulses paradoxis. And when it comes to cardiac patients that usually is due to pericardial effusion. So if you Feel that on a physical exam in a dog or a cat, the very next thing you do is put a probe on the heart to see if there's pericardial effusion.
OK. How do we administer fluids safely to cardiac patients? Well, if a stable heart patient needs fluids, let's say for general anaesthesia, then we kind of start with fluids.
Go get fluids under anaesthesia, but at a lower rate than we might in other perioperative patients. If the heart disease is more severe, if you're concerned, then you can get off the lactator ringers. By the way, lactator ringers has the lowest sodium content of the crystalloids we usually reach for.
So that's an OK choice with heart patients, but if you're concerned or the patients had a history of heart failure or problems with fluids, then you want to go to that half strength saline fluid. And if your congestive heart failure patient is hypovolemic from vomiting or any other cause, you have to give fluids quickly to restore volume perfusion, that's oxygen delivery again. And lactated ringers is fine with careful eloquats of fluids or sort of maybe 5 to 10 mL per keg in a dog, 5 mL per keg in a cat, with heart disease, you'd go higher than that if they didn't, and then repeat as necessary following your response by perfusion parameters like lactate or pulse quality, that sort of thing.
And then if they need ongoing fluids, then once they're resuscitated, you get them on their lower sodium containing fluids. If a congestive heart failure patient is dehydrated and it's mild, you can correct that with a nasal esophageal tube or gastric tube or sub-Q fluids. If they are, if the dehydration is severe, then lactating mingers or low sodium fluid gradually will be safe.
And then with pericardial effusion, the issue here is they've got pressure on the right side of the heart right a right ventricle, and that makes it hard for Venus return, right? So you have to give these guys fluids to overcome that increased feeling pressure. These guys need fluids and then they just need to have pericardiocentesis.
OK. Obviously one of the severe vascular, you know, complications of our cardiovascular renal syndrome is arterial thromboembolism in cats, and you can read this slide here, the important thing I like to point out is that They're often not in congestive heart failure when they present. They're always super painful, and they come in panting open mouth breathing and you train your technicians if you see a cat with open mouth open mouth breathing, bring them to the back and get them an oxygen.
Something's going on with the lungs. OK, that's certainly keep doing that, but in this scenario, it could just be the pain. And what we don't want to do is give Lasix to a cat that has thrown a clot that doesn't need it because if they throw a clot, we're relying on.
The, collateral circulation to profuse distal tissues, and we don't want to give a diuretic that might compromise that, right? So just pain medication, see if that improves respiration. Obviously, if you hear crackles and Increased lung sounds or you see frog coming out of the nose that you know you're in congestive heart failure, but hold off on LASIK administration that's just a matter of course on these guys because the majority of them are not in CHF when they present and if they're not, or if it's one limb.
They can have a really good prognosis. I mean, it's not so great if there's, you know, bilateral limb involvement and congestive heart failure at presentation, but still I'm sure we've all seen cats that really shouldn't have done well, kind of do well, OK. All right, so We all can recognise this syndrome, but think about the five pieces of arterial thromboembolism when you're trying to make the diagnosis, and when it comes to, you know, pulselessness, it's usually pretty straightforward, but you can use a Doppler probe on the distal limb to see if you're picking up any flow, but I think we know what to look for.
And then treatment wise, it's pain, pain, pain management, all right? And then we can use either clopidogrel or rivaroximan. In one study that was reported last year, they were equal in preventing recurrence, right?
And actually I think it may be not too long before more people recommend using both as some cardiologists are doing now to have the antiplatelet effects of clopidogrel, anti-clotting effects of the rivaroximab, the factor 10A inhibitor, OK? If you are lucky enough to catch them early and have TPA accessible or referral centre that can administer TPA, that's fine, and then we only treat congestive heart fail, Lasix if we determine it's present. And then the key here is if we're lucky and the cat makes it.
And starts to reperfuse the limb, potassium can shoot up in the blood because when muscle cells break down, they release potassium into the tissues of the whatever limb or limbs are involved. And when you start getting blood flow, that potassium gets reabsorbed into the circulation and then it can have its deleterious effects on the heart. So we don't want to get a cat through the crisis of the clot, only to have them succumb to undiagnosed hyperkalemia.
OK, so electrolyte monitoring is critical in these guys. And then you can see here, these are your drugs for preventing recurrence. It could be clopidogrel or rivaroxaban or both.
If you have a real cooperative cat that likes getting medicated and is not gonna be stressed by doing so, both is fine. If you have an owner that doesn't mind giving injections and injections and oxaparin works as well. OK, I think we want to end on like a pretty positive note, which is we finally have a drug that has been shown to delay the onset or the progression of Cariomyopathy in asymptomatic cats.
We have good old immaendan in dogs, right? Stage B2 dogs where they have valvular disease or dilated cardiouropathy, if we start them on Pimabendin. Stage B2, not clinical, but have structural changes that are severe enough to warrant possibly intervention, immaendan, go for it.
Nothing like that has been available in cats until now, so we have this. Conditionally approved, CA stands for a conditionally approved drug based on initial studies of efficacy and safety. It's a one time per week drug that has been shown to prevent or delay progression of left ventricular pertrophy in cats that have clinical HM, which they are so good at hiding that.
You might, you know, this is crazy because first you have to have had Some suspicion that it was there to even diagnose it. So if you have a gallop, never ignore a gallop, that's not normal. A murmur, pay attention, maybe work that up as well.
So the next step would you have any concern at-risk breed, gallop, murmur, if possible, get an ultrasound. If you show that that study shows evidence of cardiomyopathy, now we have this drug that can be used to delay the progression of it, which is great news. Also, pretty, pretty safe, minimal side effects, some GI, but one thing is, there are two MTOR receptors.
This drug can affect both, and one of them, I think it's MOR C2, . That can cause hyperglycemia. So we would be careful about that and pre-diabetic or diabetic cats.
And I think that's it. So I'm super happy that we had a chance to have this conversation. I wish it was a conversation that we were together, and someday, hopefully, we'll be meeting in person and if you have, attend one of my lectures online, come up and introduce yourself.
OK, have a great rest of your day. Thank you.