hi everyone oh I'm gonna do a quick intro yeah that's fine thanks H hi everybody I'm liisa Watsky from the Calgary Academy of veterinary medicine thank you for joining our CE session this evening with Dr etan cot on updates in cardiology and thanks so much to Pina for sponsoring this session Dr Laura hartney is here from Purina and we'll be doing our speaker introduction in just a minute and a short presentation at the end today so if you could please stick around for that it would be greatly appreciated uh for all participants today please keep your microphones muted and your cameras off if you're having technical difficulties please leave and rejoin the meeting uh as this will fix most issues Zoom will track your minutes of participation and I will send you a c certificate within the next few days we are going to uh hold questions until the end of the lecture at which point you can type them into the chat box and this lecture is being recorded So if you have a bad connection or need to leave for any reason you can request a copy of the recording and the quiz to get your CE credits if you have any questions for me you can send me a private message in the chat box or you can email me at info@ cm. a.ca and please note the views of the speaker do not necessarily reflect the views of cavm our members the participants or the sponsors cavm does not censor our speakers so now I'd like to turn it over to Dr Laura hartney from Purina who who's introducing our speaker this evening thanks Liz um yeah Perina is very excited to be um able to uh sponsor this lecture by Dr kot so I'm just going to introduce and read you a little bit of his bio um Dr Ain cot is a professor of companion animal medicine at the Atlantic Veterinary College faculty of veterinary medicine at the University of Prince Edward Island atan is a very a Veterinary cardiologist and his professional interest are cardiovascular disease of different species interpersonal communication between veterinarians and animal owners and the intersection between human and animal heart disease he teaches this in the classroom laboratory and especially in the veterinary teaching Hospital on final year clinical rotations um giving experiential learning um atin has um many many accomplishments uh and he is perhaps best known as the editor of the clinical Veterinary advisor textbook and now co-editor of ur's textbook of Veterinary internal Internal Medicine he is a 2015 3M National teaching fellow and his favorite quotation is everybody is a genius but if you judge a fish by its ability to climb a tree it will live its whole life believing it is stupid from Albert Einstein and I recently heard that quotation for the first time and I thought it was great so I did want to share that with everyone so um welcome Dr cot take it away thank you so much uh it's really flattering I uh I can't tell you how much it means to see uh this many folks being here uh because I know what a veteran time represents you know we all have too little of it and so many demands and opportunities uh so I'm really uh I'm flattered and touched that uh this many of you are here this evening I um have the privilege to speak about two topics that uh that I hold dear uh one is updates in feline cardiovascular Therapeutics so the mystery of cat hearts and what uh you know what latest tools we have to to deal with heart disease and the other is general anesthesia and dogs and cats with heart disease so both quite practical topics and I guess I'm I'm taking my task to mean uh making the most of this precious time uh to try and make it both insightful and also practical um I wanted to thank Liz thank you both uh very much for the the warm welcome and uh I was hoping to clarify Liz for taking the questions at the end of the lecture I'm hoping that's at the end of each lecture so that uh we can go for maybe 45 minutes or so on this first topic and then have 1015 minutes of question and answer uh as well as a breather right and then uh move on to the second for sure yep that works great okay wonderful well thank you well um I will um as a as a matter of uh kind of habit and and and just for both Visual and auditory um um information um rely on PowerPoint and so here we go so if you do have questions um please it's so much more interesting when it's a dialogue rather than a monologue so I I really do have in mind to cap this out at about 45 minutes so that there's room for for building off beyond that so uh this is my first topic I really do want to thank uh the folks who've made this possible um and so here are the the the members of the academy in particular and uh the sponsor and my home team so that I could put together this lecture and be here now and I'd like to dedicate this lecture to uh two folks who invited me into the most unbelievable collaboration um which is the creation of the current edition of tingers which just came out uh this past year uh the the wisdom and experience of these two people Steve tinger and Ed Feldman is just immeasurable um and so uh this one's for them these are my research and sponsor disclosures and this is in uh U you know consideration of transparency so that you can decide as I work through what I'm talking about tonight um whether and how much uh that has influenced what I tell you um I hope not but uh but this is uh for you to decide so when we talk about uh cardiovascular medicine and cats there's a lot that we rely on that's been around for a very long time I mean fosite is still the diuretic of choice um but you know we also have pimo bendan and so should we be giving that to cats or not we have rapamycin we have River oxyen these are new drugs that are kind of talked about um but I can't say that they're in widespread accepted use yet and so my thought was if you're interested in in uh you know sacrificing uh time in an evening to learn something then it should be maybe about what's on the horizon and and to be familiar in a kind of non biased way I hope um with these things I have no like Financial connections or or or whatnot with any of these products so I'll take them one at a time they each have a different sort of method of action or reason for being uh for cats with heart disease and uh I'll try and and and make that clear one by one um so here we go so rap ay um fascinating substance actually um this is something that's been around for a long time it's a uh it's a derivative of a fungus that was discovered in the soil of Easter Island like with the the you know the gigantic sculptures so that's why it's called rapy rapanui is the the indigenous name for Easter Island and uh somehow somebody discovered that this fungus that grows on Easter Island has anti-proliferative properties and we've known about that for a long time because in human coronary artery stent like if one of us gets a stent placed one of the problems is a so-called candy wrapper lesion where the the stent keeps the the area of tube where it is patent but then at the ends like a candy wrapper there's stenosis on either end just where the stenosis or where the stent has ended and so that tips of coronary stent have been embedded with rapamycin slow release rapamycin for a long time to try and and prevent that uh uh stenosis um but what hasn't really been explored very much until recently is systemic Romy therapy like it's fine to have it on an area coronaries but what about having it you know uh in you uh systemically so um why would you want that well because this idea of an anti-proliferative antifibrotic effect could have wide- ranging implications maybe there are individuals who have diseases that have a particularly strong profibrotic effect and so could this in some way mitigate that uh there's a number of different ways that rapy has been found to work mechanistically like individual um um receptors and and and individual Pathways and so all together they they um uh produce this impressive list of of mechanisms this is just the cardiac side of things so I just skipped over this slide um here's an experiment that dates back 20 years now um and yet was in mice and has since been uh investigated in cats as I'll show in a minute looking at basically giving rapid M to cats that had a predisposition for cardiac hypertrophy and comparing the treated cats with Placebo cats or mice I should say sorry and U what this this graph is meant to show is the change in heart weight or in this case heart weight to body weight ratio uh shows that uh a truly Placebo treated Mouse experienced uh no change in its heart rate um whereas an individual that received uh that that was uh predisposed to becoming hypertrophied had less hypertrophy if it was treated with Romy this gry bar uh than if it was treated with vehicle meaning inactive substance U not surprisingly vehicle is Placebo and same as no treatment so what this shows is that giving Ramy experimental mice reduced the process of ongoing cardiac hypertrophy it seemed to put the brakes on it that is for for a cardiologist like me that is just a Thunderclap of of information because one in 500 humans has hypertrophic cardiomyopathy so we're talking about Millions upon millions of people around the world and yet there's nothing that can take the hypertrophy away or so we thought so what about rapy and so the the idea of exploring rapy treatment for cats that have hypertrophic cardiopathy is intriguing for cats and potentially intriguing for people in terms of broader Veterinary applications before I get to the the cardiac stuff this idea of being antifibrotic is is almost it borders on the idea of the Fountain of Youth because you know aging is fibrosis so it has been and is continuing to be investigated in a number of Veterinary applications not just feline hypertrophic cardiomyopathy but just the simple project uh process of Aging in dogs uh the DAP the dog aging project has undertaken uh a prospective clinical trial of rapy to see if it produces differences in lifespan and in biomarkers I should say of of Aging along the way uh other processing dogs we know that satic stenosis SAS that uh in in my field of work so many golden retrievers and and and Rottweilers and many other breeds have uh that's predominant a fibrous lesion that obstructs outflow from the left ventricle out to the yorta A congenital lesion that progresses during a puppy's growth to adulthood and so maybe if those pups were treated with rapamycin maybe that would delay that process so all of this sounds really exciting and promising but of course it's one thing to speculate and then another to take inventory story of what are the the potential drawbacks or or does it really work and and does it work equally well in everybody uh and so that then led to this this remarkable clinical trial of rapy in cats with HCM so uh I love this this you know acknowledgement of the realities of pilling a cat uh delayed release rapy was the product that was investigated it's a pill given once a week I mean you can't beat that so uh this was the the the test dosage .3 milligrams per kilogram given orally once a week uh for 24 weeks six months and the idea was to uh take cats that had subclinical feline hypertrophic cardiomyopathy meaning cats that were asymptomatic this is the bread and butter of feline Cardiology as far as I'm concerned the cat with a heart murmur that comes in for no cardiac reason just some other health concern or a wellness visit has a murmur and investigating it reveals that the murmur is caused by HCM uh a bunch of those cats were enrolled and treated with Romy and an equivalent number of cats were enrolled and treated with Placebo so to be able to compare the two groups and and minimize bias and uh here's the result and so I I'll walk through this graph a little bit very exciting stuff um the y- axis here is uh maximal wall thickness so this is echocardio graphic data measuring the left ventricle of cats and when the left ventricle is in maximum diast so fullest is when the wall should be at its thinnest and if you measure the thickest segment of that it should be under 6 millimet uh that's basically all healthy cats so anything above this anything that shows up on this graph would be the kind of finding we'd expect with hypertrophic cardiomyopathy so okay so at Baseline uh the placebo group of cats the cat's given a low dose of Romy and the cat's given a high dose of rapamycin all had surprise surprise uh maximum wall thicknesses that were you know somewhere between seven and eight uh mean uh in that group so of course what's interesting is what happens to them over time so by by the time the the the two-month Point has been reached there really are no significant differences between groups but by the time we get to 6 months the wall thickness of cats that received either low dose or high dose Ramy hasn't budged as if the process of hypertrophying had been arrested whereas the placebo treated group had a significantly as indicated by these asteris a statistically significantly greater um Dimension or or wall thickness so meaning that unchecked uh hypertrophy continues which you know can happen uh and that didn't happen in cats treated with rapamycin so this was really first of all it's rigorously studied you know the idea of having this be Placebo controlled so there was no maybe Observer Observer Bias or observational like confounders uh that it was as objective as possible a randomized blinded study meaning that the investigators uh you know were were blinded or or had coded the treatment but they didn't know what the code was so they couldn't speculate all of this to say that when uh the the study was over and and the codes were revealed and so on it showed this so this is phenomenal um really groundbreaking and you know at the same time we have to consider the limitations of a study like this where this is a limited number of cats and it says what happened over six months but who knows what that would mean over the scale of an entire lifetime so uh the the the results can be summarized as there was no change in left atrial size an important marker of the consequences of hypertrophic cardio opathy uh in treated cats and however there were adverse effects in one6 of the cats so 24 uh 12 cats received low dose rap 12 cats received higher dose and then uh 12 other cats were Placebo treated and so four of the 24 treated cats had adverse effects but I mean two of them had congestive heart failure and one had sudden death who's to say that that was drug related as opposed to just being being part of what might happen with any cat who has hypertrophic cardiomyopathy so early days yet and so I I think what I take away from the rapid trial from the rapid cat trial is that this is exceptionally promising but before my inner Optimist gets too carried away I'd like to know a little bit more about targeting like which cat should have this because uh the risk of adverse effects is seemingly limited but at the same time when a cat has early stage hypertrophic cardiomyopathy like lecular thickening with no left atrial enlargement yet completely asymptomatic cat uh we know from Phil Fox's reveal study just looking at at uh 1,700 cats uh just following them over time we know that uh 77% of cats that have mild asymptomatic HCM 70% of 77% of them are still alive 10 years later after the diagnosis so HCM it's such a kaleidoscope of severity you know it it in a majority of cats it probably behaves fine uh that's why so many cats with HCM can undergo general anesthesia and do okay as I'll talk about in the the second session um but the there's a a substantial minority of cats that can worsen and so perhaps those are the ones that we should try and figure out and Target with rapamycin um one of the cats had diabetic keto acidosis in this this study one of the rapat treated cats and that's really important because that's a recognized possible complication of Romy so that would be much more sus suspicious or suggestive of a drug rated adverse effect um perhaps cats that are already diabetic and have HCM shouldn't be getting this treatment um and so overall with Romy I think what this tells me is that it's really promising uh it's the only treatment that has undergone clinical trials like this that point to slowing down or even potentially reversing spontaneous LV Elric hypertrophy and so before like if my own cat had hypertrophic cardiomyopathy and I had a box of rapidy for free I actually don't think I would give it to my cat because the enthusiasm for starting a new drug on the basis of a six-month study and then proceeding to give the the drug to the cat indefinitely which is going to be years that's a that's a leap that that we don't have the the knowledge to make yet and so what I'm trying to do by presenting here uh this here tonight is is maybe two things um to raise awareness that this drug exists and is worth following because it's really promising and then paradoxically at the same time to maybe calm the the the art or and the enthusiasm for it for starting it you know right away on on a cat that is expected to take it for life because we don't know that that is any better than the you know 10-year survival of 77% of cats that have idiopathic hypertrophic cardiomyopathy already and we we don't really know the safety profile not at least in a way that justifies you know years of use so rap ay a very promising intriguing frankly fascinating thing certainly you'd have to think with uh human implications yet uh I don't know of any yet that have been um any human trials that have been published um and so maybe the cat will serve as a as a sentinel and as a a Trailblazer for human HCM patients later instead of the other way around as we've done it for so many years no I need it I need it did you just sorry there sorry that I muted that person I'm so sorry uh but do please keep track of your questions because I I want to get to them it it's there's great I know that there's great stuff out there uh in terms of of discussion points so wrap a mice and the first um uh feline uh treatment that's that's uh on the table for today the second one I'd like to talk about is something to prevent saddle thrombi and any of us who's had even I'd venture to say even just one cat with this horrendous disease would wish for something more effective and so let's go over the options and then I'll talk about River Ox aent so if I look at a casebase uh sort of example um here's a cat that we had in probably a few months ago now uh this is a 2-year-old male castrated Sphinx cat we see a lot of sphinxes and as meaning on on you know Cardiology Service uh here at the Atlantic P college and so I recognize that I have you know a bias just by virtue of the clientele case load um but even young cats like young sphinxes uh can get uh fairly rapidly Progressive uh hypertrophic cardiomyopathy again recognizing that I probably see the worst uh as selection bias but here's a cat we see uh that we originally saw at age two years uh some years ago and so at that time uh this was the cat's echocardiogram and I'm recognizing that echos play more or less well when they're streaming um so let me just point out the features of what I see here uh this is a short AIS right-sided view on the cat's first visit which is now a few years back this uh round structure here with lines bobbing in and out of the middle of it is the aorta uh and then occupying kind of the the 8 o' to 4 o00 uh position here uh as the the comma or or teardrop shape or uh Dr sfer said the cartoon whale kind of image with this is the body of the whale here and then the tail of the whale back here this is the left atrium and uh wrapping around these structures is the right heart so aorta and left atrium and um anyone who's done much Echo um including point of care uht fast will know the value of this view because when we can compare the aorta to the left atrium um setting aside the right atrium here for a second we expect that the diameter of the aorta and the diameter left atum will be more or less the same uh upper limit of left atrial to aortic ratio 1.5 to one left atrium can be one and a half times uh as big as the aorta and still be normal that was this cat on the first visit looks fine so there's certainly no consideration for anything to try and prevent saddle thrombi on this cat who had hypertrophic cardiomyopathy I'm not showing you the left ventricle but it was thick but there's no repercussions to allow blood stagnation like left atrial enlargement so no treatment on this first visit two years later we have this appearance where the cat now has this same left same iort here left atrium I don't know I could probably talk myself into it looks a little more generous but it still measures well within that normal ratio four years later uh so this was a year ago when we saw the cat in uh the cat now has the same aorta but proportionately we see very substantial left atal enlargement including left oric enlargement and that's what nobody wants to see because our left Oracle Yours Mine and this cat's is sort of the attic um where you know blood goes to to kind of of of stagnate um and so uh this is probably where spontaneous clots can form and they just get kicked into the the body left atrium and swoop Downstream and so uh that was a year ago this year we are now 5 years post diagnosis we have again for a reference aort here and this grotesquely enlarged massive left atrium with a colossal left Oracle and basically just a you know a clot waiting to happen when we think of how sluggishly BL blood must move as it goes through here if what it meant to do was to move through a left atrium that's the same diameter as the aorta so so cat is still fully asymptomatic so on one hand you know premum non no like first Do no harm I don't want to start a a drug that you know the owner is going to have to give every day so maybe the cat doesn't like it inevitably there's always the risk of some adverse effects with any drug but on the other hand how can I look at this huge left atrium even though the cat's asymptomatic and leave it alone so what do we what's the evidence that we have to guide our decisions I mean I can just shoot from the hip and do the same thing I want every time uh but that's that's not really very objective or or uh supported so so I like to think of like what are my options uh given that this is the evolution of this cat and yet the cat remains fully compensated asymptomatic well I guess I I I struggle most with something that I finally found a name to which is optimism bias um so this is a a a topic that's recently been popularized uh uh and and really what it amounts to is that um optimism bias is a form of bias that is uh an illusion is illusory and what it consists of is basically to believe that the future is going to be better than the past or the present um so the these researchers uh Dr shat and and and her team uh looked at things like telling folks that um you know cancer is the leaving CA is the cause of death for say 30% of humans in industrialized countries uh in in our Modern Age and how do we feel about our own mortality for cancer people reportedly not being concerned about it at all uh the sense that you know maybe it can happen to somebody else but not to me and I think that's a uh it it's familiar even if we're not familiar with this this name um Dr sh's team has investigated this across uh in in numerous cultures uh socioeconomic statuses um geographic regions and and consistently found that it affects about 80% of humans which I think is hilarious because it takes a certain stretch you know in this day and age to think of ourselves as uh like excessively optimistic um but sure enough in in in the context of bias of optimism bias we we uh we evidently we are and I think for me uh the the the greatest example I see of that is when I send out a group email so I I you know send an email to announce something interesting that's going to happen or ask for volunteers or whatever somehow in my like foolish optimism I think that a people are going to read it and B people are actually going to act on it I mean that never happens you know there might be a a couple of inquiries or replies um and so I think group emailing is inherently uh imbued with optimism bias um and even within just the context of veterinary medicine I mean we see this every day clients who who ask sort of expectantly it's not not as bad as you think or is it that bad and and and it turns out it's not I get that a lot with heart murmurs uh I never mention the grade of a heart murmur anymore there I might be the only cardiologist who shies away from that and I don't understand why because time and again I I have clients who come in on referral and say Doc you know is it as bad as as we think like well how bad do you think it is your your dog or your cat is asymptomatic well we heard that the murmur is a grade four out of six as if that carried an implication you know of of being I don't know 23s gone or something so I I never go there anymore um because I I I I recognize the bias that come comes along with maybe those implied uh numbers but I digress uh we want to talk about about how do we help a cat that is asymptomatic but through marked atrial enlargement has uh the risk of aortic thromboembolism and I'm going to battle my inner optimism bias that any treatment that I come up with might be helpful for a cat that's in that situation because the truth is and I'll say it right now there is no drug that has been proven to delay the onset of the first blood clot satle thrombus in a cat not a single one so I'll go through the drugs that we do have and talk about what they have been shown or not shown um to to do so that we steer clear of optimism bias and other biases and know the real truth uh aspirin so I over the years like been at this for a while so especially in the earlier days I prescribed a lot of aspirin and its main attribute was safety uh I can't remember a single cat receiving this kind of you know low dose 81 milligram or even the the micro dose of 5 milligram per kilogram was like you know 2.5 milligrams of aspirin I mean all that stuff is very safe and probably uh because in lock step it is minimally uh effective if at all the only evidence ever shown uh for uh the efficacy of of aspirin on cat uh clots was in vitro uh work showing that cat platelets were less uh aggregable when they were bathed in an aspirin solution and so somebody said well how long does a cat platelet live in a cat circulation somebody else said 6 days and so somebody else said well let's do it every three days so that we catch them you know when like half the turnover half the platelet population is turned over that's the only reasoning behind this this therapeutic recommendation so it really has never uh been successfully shown to prevent clots and I just don't use aspirin anymore morphine however is extremely potent and highly effective um I've used quite a lot of that back in the day the problem with warrin is it can be too effective uh so pulmonary uh bleeding uh I remember several memorable cases of that uh bleeding into your lungs looks like pulmonary edema so you have a disant cat with interstitial infiltrates or beines on on tfast and then then what we think it's edema but it's not and and and then there's the GI blood loss and so on and then it has to be tight Tred to weekly uh proen time measurements which is a real pain so I don't use that anymore either even though frankly I think some of the successes that are reported um you know in the earlier studies of of cat clots were from warin treatment and then finally there was a time kind of the late 90s and early 2000s a great flurry of excitement around low MCU Hein which in people uh are just pharmacologically or pharmacodynamically more predictable than regular Hein and uh can be dosed supposedly just once a day and so on and most of that has has kind of been disproven uh and it's more expensive than unfractionated Hein so I don't use it as prophylaxis for preventing clots I use regular unfractionated Heparin in the treatment of active clots when a cat presents on emergency so uh prevention the one thing that has been proven to prevent satle thrombi is Plavix cigil but it has never been proven to PR vent it the first time it was only ever studied for prevention of re-embolization in cats that had already had a clot and I don't think that's because it's ineffective um you know for preventing the first clot it's just that it's a lot harder to predict will a cat develop a clot when they haven't had one before uh some cats look like the echo that I just showed you and live impossibly long I me I'm sure you know this I I'm I'm not the only one who's seen this and others you know at the slightest whiff of left atrial enlargement the next thing we know the cat comes in um with a horrendous sat thrombus so predicting which cat will develop a a clot and and acting on that is extremely challenging the best that we have currently is left atrial size assessment with various other intriguing uh measurements tried but none n really convincing so okay so would I start a a cat like I showed you uh onle pitl even though the cat's never had a clot uh maybe and I'll talk about it when I wrap up this case when we go through the the different drugs so uh is that the best we can do it's a rhetorical question the answer is is uh perhaps not because there's a new class of drugs that River oxan belongs to that is uh really the first line of treatment in people and so let's talk about Rivero oxan um this is a drug that instead of acting on platelets like citril does it acts on the coagulation Cascade so if you recall uh plat gets activated when the blood vessel is damaged or thrombus forms and so the platelets congregate and uh coagulation Cascade uh independently uh uh operates in parallel to that and so that's important because it means that we can uh consider both treatments without having uh um duplicative effects so it would be possible to consider giving both River Ox event and cogil if we thought that that was necessary in a patient um here's a lovely study that looked at doing exactly that so uh dual therapy with cogil and river oxan and cats who have already had a clot so this was 32 cats and they were evaluated retrospectively uh so that's important uh five of 32 cats had adverse effects of bleeding not surprisingly given that individually these drugs are meant to to make the blood thinner so together they might well be expected to do that but perhaps in these cats that have already had thrombolic disease that would be acceptable if we consider perhaps if they were minor events uh that that's a price worth paying if it's worth it therapeutically well the median survival time in these cats was two years if they had a satle thrombus that Ed two or more limbs which is this isn't you know a partial one or a one leg one uh these are are serious cases and to to have a median survival time of two years is really remarkable um but I will say you know if we if we look at this study in some detail there are some additional things that can they give me a little bit of pause so let's look at at what was done um first of all the cats that were studied had uh previously had aortic thrombo embolism at in 18 cases or had a blood clot in the heart which is to me even more devastating than having had a clot because that's um ready to to dislodge and embolize anywhere um or and or had spontaneous Echo contrast meaning micr clots floating around in a dilated uh left atrium five of those cats as I pointed out in the previous slide experienced adverse effects and those consisted of uh epistaxis vomiting blood uh defecating FR Frank blood and blood in the urine but no cat required hospitalization as a result of these events uh the median survival time from the onset of therapy was 257 days for all cats 502 days for cats with all saddle thrombi and um 725 days for cats with an atic thrombus to two or more limbs um interesting that the the longest uh survival was cats that had two or more limbs affected uh even though that's more severe I suspect that's because they just had more cats that fit that description and and uh the uh these shorter survival numbers uh were influenced by smaller uh numbers of cats recurrent rate of aoic thromboembolism while receiving both River oxan and Citra was 1 in six 16.7% and no cat developed uh a new um aortic thrombo embolism uh while on Dual therapy and so um that's a that's a very promising set of information um it's really tempting for me to look at those findings and start to think maybe I should be reaching for both uh instead of just clig but clearly if we go back to this cat case that we started with there was no basis for any of that based on normal left atrial size five years ago or four years ago two years ago with a little bit of left atal enlargement I mean I just feel like I see so many cats like this that never have a clot so would it be worth it to treat it all and if not then maybe now as opposed to a year ago we should or if we started then do we keep it the same or do something different here I want to point out what we did which is this on the basis of this is not a formula for every cat this is the result of discussing with owners both the meaning of these treatments and then the limitations inherent within them because if this cat now that I've started dual therapy on a cat that never even once had a clot I mean that's extremely Cavalier but if this cat so if this cat bleeds then then that's my fault I mean I may have made this cat worse than not treating the cat at all cat's never had a clot before but with this degree of of agal enlargement there's a basis for starting one or both drugs and what I'm trying to say is that that decision in my hands anyway is really made in consultation with the owner and it becomes a caseby casee decision uh this cat has done fine so far uh so the last followup that I knew of was uh still no clot but is that treatment necessary would this cat continued to have had no clots is the cat uh unhappy being pilled every day uh you know with medication that maybe doesn't taste very good or my point is that this cat tolerates it fine and the owner is delighted to do it so it works but to apply a blanket solution to say every cat should have roxan or not I think would be a mistake at least in this preclinical state and to some degree even in cats that have had aortic thrombi so I do struggle with my optimism bias I'd like to help and I think we all do kind of why we became veterinarians and yet in the spirit of making a difference for the better we have to acknowledge the limitations that we have in our toolbox and I think River oxan a little bit like Rapa is um yeah promising um but it would be incomplete borderline misleading uh to have this come across as the new standard of care because it's it's not so wow that's a lot of ground to cover um I've talked about rapamycin as a drug that affects the my cardium itself in hypertrophic cardiomyopathy I've talked now about River roxan as a new category of uh thromboprophylactic drugs to try and reduce the risk of blood clots and cats and now I'm going to talk about a a third uh drug that we're all I think very familiar with for use in in dogs and how it applies in cats so pimobendan what is its current role in cats with heart disease and here I I actually want to take a track that is kind of historical and timeline based so I'm going to present our knowledge of pimo Benda and use in cats from 10 years ago till the present day and I want to do that because there have been different findings along the way so unlike River roxan and rapy which are both wholly new I mean just entirely new uh discoveries and and and very few papers uh the Pim ban story in cats is 10 years long and and I want to go through those 10 years so that there's some understanding of why there would like the fact that there's been conflicting results and and where we stand today so um so a a bombshell exploded uh 11 years ago when this paper from North Carolina State University was published in the avma journal titled a case control study of the effects of pimobendan on Survival time in cats with HCM and congestive heart failure and this was just the craziest paper because pimo bendan is a positive inotrope it makes your myocardium squeeze harder great idea if you're a Doberman with dilated cardiomyopathy but when you have hypertrophic cardiomyopathy your problem is the opposite you want to fill more you need to relax so a drug that makes you squeeze harder seems to be the exact opposite direction to be headed in and pimobendan is a vasod dilator so inotropy is contractility uh vasod dilator is is you know arterial dilation to ease the workload on the heart Downstream so an IO dilator but if you have hypertrophic cardiomyopathy you have abundant contractile strength so you don't need a vasodilator if anything lowering your blood pressure might elicit reflex tachicardia to bring it back and tardia is the last thing that you need when you have hypertrophic cardiomyopathy because it consumes more my cardial oxygen and it decreases how much time you have to fill between beads so it just seemed like who would ever think of giving pimo Bend to one cat with HCM and then Along Came this paper 27 cats with recent onset congestive heart failure due to hypertrophic cardiomyopathy treated with furosemide an Ace inhibitor and pimo compared to 27 other cats that were treated that also had HCM and congestive heart failure treated with fos inhibitor no pimo how did the groups compare so it was just mindboggling uh these are meant to be this is the same radi graph twice just to show that there were two identical groups except some were treated with pimo and some were not look at these numbers the cats that were in the pimo group had a median survival of 626 days after the onset of heart failure imagine a median survival of two years I mean for us a median survival of a year and a bit is really kind of what we hope for for cats who have gone on to develop convincing congestive heart failure from their hypertrophic cardiomyo thankfully it's a minority but once they're there that's a big step towards worsening the onset of heart failure is so to live another two years on average was really amazing compared to cats without pimo lived an average of three months you know one sixth as long just startling and so then the question was why you know I've just explained it should be absolutely cont contraindicated because it makes your ventricles squeeze squeeze harder and that's the last thing you want when you have HCM and it dilates your vessels but you don't need vascular you don't need arterial dilation when you have HCM and so how could this be uh a question was raised well maybe there are other effects of pimo like maybe it's an antiplatelet it has antiplatelet effects you know innocent bystander benefit but uh a wonderful study from a group at Georgia showed that actually when you give pimo cats their plate function doesn't change what about maybe these positive inotropic effects of squeezing that we keep focusing on affecting the ventricles maybe it also causes the Atria to squeeze harder now that's an interesting idea because of course when the ventricles are filling is when the Atria then squeeze so maybe pimo is helping a dilated Atrium to better top up a left ventricle and and and you know improve the fact that the the space in The ventricle is crowded out by hypertrophy and that exact thing was in fact demonstrated that giving a single dose of pimo bandic cats increased their left eal fractional shortening the the change from maximal diameter to minimal was was furthered by 16% uh just by giving one dose of pimo so well that would make sense like why you would give people bend that and expect it to help and it C with HTM so okay so we have these conflicting sort of things back in 2014 we have a benefit uh we don't know why because it like the fact that it makes ventricles squeeze harder and Diles blood vessels is no help to us and it doesn't help with platelets but it does seem to make Atri like okay so what do I do with that do we do we use this drug in cats or not and it took another seven years to conduct a prospective trial and I just want to point out why that's happened uh why why that happened and why it's important uh the title of this paper is effects of P bandan cats with HDM heart failure results of a prospective double-blinded randomized exploratory non-pivotal field study in other words uh as little optimism bias or any other form of bias as could be um you know expected in a trial and so why would we want to do that well one reason is when we look back at at this this remarkable trial here back in 2014 uh the cats that were treated with pimobendan had been treated in the last year to they were the most recently treated cats at all uh at at NCSU but since they had started using p ban in order to have controls without pum bendan it was necessary to go looking in historical records and we know that with the passage of time the general Improvement in care and so on increases we know that using retrospective analysis means that we're reliant on what's written in the record which may not capture it might capture only the exceptional cases and so there's a real risk of bias influencing our conclusions when we rely on retrospective uh evaluations and the investigators acknowledge that they didn't claim this to be any more than it was but it's up to us to recognize the limitations of retrospective analysis for treatment conclusions so here's this great prospective study that looks at uh pimo and cats perspectively and uh it's not a particularly complicated study design but let me work through it step by step because it it's it's detailed so there were 83 cats enrolled in this study and they all had to have experienced congestive heart failure and survived um and to start pimobendan or Placebo they had to have all had that within the past 60 days so that it was still active disease and recent enough and the idea was that if you were a cat who had hypertrophic card ay when a congestal heart failure got bailed out of it and you were in pretty steady state kind of situation then you could be enrolled and you would either get pimobendan added to your furosemide or you would continue on just furosemide and I think yes of course have Placebo added instead of the pendon added to your fide therapy so you're getting two pills or at least two treatments one way or the other one is Pon fide the other is fide alone roughly equal groups how are we going to decide um what constitutes an end point because following all the way till the patients died well some these cats chuggle along for a long time and there's other things that start to come into play um other health issues for example that that can muddy the waters a little bit so why not Define it like this we'll follow these cats and if they have recurrence of pollary Edema or plural diffusion if they have recurrent congestive heart failure that requires bumping up the furosemide then we'll consider that that was a point where the uh uh where treatment failure was experienced and so we'll call that an endo um so treatment success whether you're treated with pimo and furosemide or with furosemide and Placebo you'll be considered a success in this clinical trial if you live 180 days or more without having had to increase your fosite and of course the point is let's have a look do we have more treatment success cases with pimo or are they essentially the same and the answer is they're essentially the same because out of the uh 39 pimo treated cats that finished the study for drop down uh 12 of The 39 were successful didn't need a bump up in in their fosite and then of the 39 cats that received just furosemide no pimo two dropped out and 13 of the 30 seven required uh no increase in their furosine so a difference of 31 uh% of the pimot treated cats lasted the six months with no train change in treatment versus 35 basically a P value that's not significant so the story here is again to emphasize that when something sounds really promising a big part of maybe our desire to do good um and to help our patients kind of Taps a little bit into the optimism bias and along comes uh a little while later a trial that prospectively and objectively evaluates the the usefulness of a drug and then that can be a little bit more sobering it almost always is um and that doesn't mean that the drug is wrong it might mean that it's maybe more useful for certain specific subgroups uh I still give pimo bandan to very few cats but if a cat has hypertrophic cardiomyopathy and I can see on Echo that the left ventricle is is is uh has systolic dysfunction it's not pumping very well there's massive left agal enlargement then I'll talk to an owner about trying it and if a cat perks up visibly in a couple of days which I've seen then I say well why don't you keep giving it and if if the cat shows no change then I don't have evidence to support continuing to give it there's never been a single trial by the way in dogs or cats of Pim bandan that looked at the effect of of withdrawing it um you know I think many of us think that P benden produces really striking results in a small subgroup of dogs or cats and then ham results and then when we do these large studies those get Blended together so we we don't uh subgroup them very well so anyway my point is that I I do do that in cats for lack of any other uh information if I think that there's systolic dysfunction or in the rare cat who instead of hypertrophy cardiomyopathy has you know dilated cardiomyopathy so my current answer for using pimo and cats yes or no is sadly is no and uh and I do that partly because we haven't even talked about how the drug is is handled in a cat the halflife of pimo bandan is two and a half times longer in cats than in dogs so one dose will last two and a half times longer by which time we've given the next dose and then the next one and so there's a tremendous mismatch between how often it's given or should be given in a dog versus a cat but we just treat cats like they're small dogs the peak plasma concentration of p bendan is 10 times higher after the a dose in a cat than in a dog what are the effects of that we don't know so currently I don't give pimo bandan cats period with the rare exception of a cat that has ventricular cystolic dysfunction um I'd like to summarize to leave what I thought would be more time than this but will'll be at least five minutes for talking uh and let's maybe eat a minute or two into the next talk uh to to talk about these fascinating feline Therapeutics the summary is that rapy is promising um and still has to have pros and cons elucidated a little bit of the same story with River oxan also promising certainly indicated for a cat who cannot tolerate cigra for example a cat that drools everywhere and hates the taste of CIT River roxman doesn't seem to be like that and if a cat has already had a SLE thrombus and survived it then I would happily use River oxyen um in terms of teaming it up with cigil still to be elucidated and for people currently yes with systolic dysfunction but that happens in such a small number of cats with hypertrophic cardiomyopathy so more likely no um so with that I'm very very happy to answer any questions that have uh come up and uh please if you would uh I think uh are Liz are we asking for drop in the chat or unmute I usually ask people to type them into the chat um and do you want me to read them for you I mean I have uh a nice question here from Anna villal which I can read and then I don't know if you're seeing more I just have that one yeah I've got one too after yours okay perfect so um uh Anna thank you for the question it says if a client is declining referral as well as other Diagnostics like radiographs is there a certain Criterion I use for starting dogs and cats on P bendan is there a certain murmur grade that's loud enough or or any other physical sign to start medication I love that question because that is uh a real world question I see that uh be acted on all the time so um I think I can comfortably say um I I don't I don't often have all Yes or all no and answers um but this one is is real straightforward and the answer is no and I don't want that to be the answer I'd like to say that yes if there's you know this physical finding or this feature or whatever that in order to help the patient we should do this but the reason I say no is because depending on the study somewhere between a third and a half of cats that have heart murmurs have structurally Normal Hearts so they have physiologic murmurs no heart disease so before starting to pel those cats when they're getting a medication that not only may not help them but they actually don't require I don't want to set up a situation of doing something to one of my patients that that patient doesn't need and that is a very very real possibility for cats with murmurs of any grade of intensity uh you know in in an incidentally detected murmur same story with dogs um you know to have into the dog thing time and again we have dogs that have grade three or grade four out of six systolic murmur due to their mitro valve disease they get referred to us they're already on P bandan or or planning on starting it and we see we have great Echo machine we can see with Echo that the mitro regurgitation from the left ventricle back into the left atrium is obliquely directed headed right for the left atrial freeall well where do I put my stethoscope when I escal the heart right there so no wonder hear really loud but it's not a lot of mitor regurgitation it's a little bit that's aiming right for where my ear is through the stethoscope so no wonder the murmur sounds loud no basis whatsoever for treatment on a patient like that when the left adum is normal size so I really want to emphasize that in our good graces in in the the the responsibility that we take on as veterinarians our duty that that that doesn't mean starting medication might be unnecessary and and there's a lot of that based on the physical exam alone of a patient with heart murmur great thank you uh someone has asked if you happen to have a video to show how best to get the view of the left atrium I I do it's it's just it's It's tricky because what you see is a hand on a probe on a chest um I I would gosh I mean the answer is yes and the ultrasound beam which you'll notice on your ultrasound probe uh is indicated by the marker on the probe there will be a a logo uh from the the manufactur the machine or a DOT or something that should be pointing in in a a cranial ventrol to cardo dorsal axis on the right side of the dog or the cat and I think beyond that I think it's a matter of practicing I encourage you to to try that uh with patients that are anesthetized for other purposes okay um and I'm I'm getting several questions I don't know if you're seeing them because they're I'm seeing message yeah I think they're sending them directly to you so I don't have any other questions but you can go ahead and answer those okay great um I have four so I'm going to do hardest thing for me which is to keep it short so uh Jesse Pac asks what do you think about the use of Inhibitors or a Inhibitors plus spironolactone for Rass suppression in cats with congestive heart failure really interesting idea because it makes sense mechanistically a diuretic which we give for congestive heart failure inherently increases renang aldosterone system function the problem is same story when we actually try it to see does it make a difference in the Natural Evolution of disease wonderful study of 151 cats that receive bonaza Pro uh an Ace inhibitor there was no survival benefit to doing that even though it was an extended very thorough study so I don't use ACE inhibitors for cardiac uh treatments in cats anymore so let me say that again because I know this is this is like different from what we did for at least a decade if not two the principle of giving an Ace inhibitor makes sense to a cat in congestive heart failure along with furosemide and that has not proven to be beneficial to cats that's in Stark difference to dogs where several ACE inhibitors so bazail and an alil for starters but I'm pretty sure a mid April maybe ril uh have been shown to extend uh survival uh in cat in dogs being treated for heart failure so um I I don't use ACE inhibitors U for Ras suppression in cats uh is Parental use of Romy from ano is Parental use of Romy being done in human medicine or is it still being used uh in medical implants so great point so yes for the implants uh parental use I I don't think so I just can't imagine that it wouldn't be um but I I'm not aware of of a clinical trial like the rapic cat trial in cats that looked at ripy in in humans with HCM great question uh Susan L Point asks what's the success rate of treating aortic thrombo embolism and does this play a role in deciding when to start cigil and or a river oxan a wonderful question so uh a cat that has a saddle thrombus uh if we look at surveys you know of general practice treatment um the the survival rate for cats that are actively treated is about 30% however surveying like on on a a session like tonight's surveying practitioners and asking how many of you recommend euthanasia on initial presentation with tic thrombo emsm the the response rate is uh yes to about 70% so it's hard to know the real survival of cats with saddle thrombi because the fatality is is a little bit of a self-fulfilling prophecy um you know we we recommend euthanasia that's not a wrong recommendation let me be clear I mean a cat that has a satle thrombus almost certainly has underlying heart disease that a is going to be irreversible and B is going to cause another sdle thrombus at some point so it's not for everybody uh maybe not even for a majority of clients I don't know but the point is that there are clients who are interested in pursuing treatment and when they do about a third of those cats survive so does this play a role in deciding when to start either an antiplatelet drug like Plavix or uh anti coagulant like River oxan I would say yes uh preventing these kinds of problems you know is a whole lot a whole lot more Humane than trying to catch up with treat treating them because of the excruciating pain that they cause but then I'm thinking well there's daily pilling of medications that a cat may or may not need if it's never had a clo before so really for me the decision is very strongly owner Centric it's based on compliance owner wishes uh so many owners say I don't want to give chemicals to my cat and so many other owners say I absolutely want to do everything I can and you know this as well as I do I mean in that mix is where I find my answer because there's no single right answer um the very last question um on this topic and thank you all for uh for these terrific expressions of Interest please keep track of them for for the second Q&A session here uh in in you know 45 50 minutes um um Ian UHA asks a 19-year-old cat presented with vocalization visual impairment suspected re Detachment blood pressure was 220 mm of mercury I'll presume systolic and the cat had a grade four out of six heart murmur no further Diagnostics were approved what would you choose to treat holy moly what a great question uh treat for feeling hypertension start citril or benign neglect given the age and the problem is there any benefit to lowering blood pressure if I'm concerned about at in a cat wonderful question so to me the the most striking thing that that you've described in this case is the retinol Detachment because there are very few things that'll do that apart from blunt trauma and I'll assume the cat wasn't hit by something or wasn't known to have been traumatized spontaneous retinal detachment makes me think of systemic hypertension until proven otherwise and here you have a documented blood pressure of 220 so I would treat that cat for the hypertension as well as whatever inciting cause it might have chronic kidney disease would be the classic hyperthyroidism sometimes Etc looking for the inciting qua um I would not start cigil because the heart murmur I think would be the thing that makes me suspect um you know heart disease but let's be clear as I just said earlier somewhere between a third and a half of cats with heart murmurs have a benign cause if I don't have an uh some form of Imaging and most certainly preferentially Echo um then I'm very reluctant to treat because I know I might not be doing anything or I might make things worse here I'd be concerned that giving cigil uh is going to make the blood thinner and make retinol detachments and retinol bleeds potentially Hema uh you know much worse so I would stay away from anything that decreases coagulation or plat function um you know with with a with a 10-ft pole but I would treat the cat's hypertension yeah excellent um I will uh pass on on the last couple of questions in the interest of time um because time does move quick and so let me um stop sharing for a moment so that I can switch screens and thank you again uh for your uh patience I you won't believe this but it's true just had a popup window uh say update available do you want to restart now or try tonight so I'm not going to restart now but I'm going to put try tonight keeping in mind that I am several hours ahead of you and I hope my computer doesn't think that means now um if you happen to get kicked out I'll be here you can rejoin you're so kind thank you I'm counting on it no problem so far so good I think um well thank you so much for your your ongoing interest I I'll I'll do my best to make this last uh or the second half uh worth your while what I'd like to talk about is another Super practical and very common topic that I get asked about uh in the veterinary teaching Hospital which is telephone consults on how do I anesthetize this dog or cat that has a heart problem and it might be a suspected heart problem like we've talked a couple of times now about heart murmurs with no further information or it might be a mostly confirmed one like cardiomegaly on radiographs or truly confirmed one like echocardiographic diagnosis so let me thank uh my colleagues drors Lee Lamont and Stephanie Hamilton of the uh anesthesia Department here at the Atlantic vet college for some slides they've contributed to this talk and uh summarize what we'll talk about here with the following Four Points um I'll move through this with a kind of interweaving of you know rationale like what's the reasons and mechanisms uh and just mostly just plain practical applications here's what we do and why uh and then welcome questions on on clarifying that or or further detail so I want to talk about uh general anesthetic approaches and and specifically risks in cardiac patients and then what pre-anesthetic and anesthetic drugs do we use and why and then monitoring and troubleshooting so you know no great surprise to anyone general anesthesia on principle alter's cardiac function uh and workload and so on and these things are well tolerated by individuals that have healthy Hearts but even so we know that uh there's you know all of our potential nightmare uh a collective nightmare is the the patient that uh rests and and seemingly had a normal physical exam and no suspicion of heart problems so even a normal individual can have an anesthetic risk with the heart and and that's increased with heart disease so with that in mind it's worth uh considering that uh when I approach a patient who has heart disease and I want to decide how to how to anesthetize them my first question is going to be to ask myself is this patient asymptomatic or symptomatic so to use the you know more Veterinary lingo is the patient compensated there's a dog named Peanut and uh this dog shows you know really the the embodiment of well-compensated um mitr valve disease this is a dog with with uh mitral disease that shows you know curiosity and interest in its surroundings awareness and alertness normal respiratory effort and rate um I especially want to emphasize the dog's curiosity and responsiveness to its surroundings that to me is one of the most satisfying signs of the absence of congested heart failure a patient who has this kind of physical exam to me is most likely in a compensated state of its heart problem so if this dog has mitro valve disease I don't know it and a patient with compensated heart disease of course has a much lower anesthetic risk that's uh in in comparison or contrast to uh this is Peanut the same dog who has uh congestal heart failure so this is taken at a very different time but in the same kennel as it turns out and uh here we see uh the the kind of labored and rapid and and persistently rapid uh respirations typical of a patient with pulmonary edema and I I just you know you couldn't uh invent a more clear manifestation of the feeling of congestive heart failure uh and almost sort of vacant or not all their expression total lack of Interest or responsiveness to surroundings a kind of a a dazed you know looking off into the distance perspective why because peanut is only thinking about breathing and so when I have a patient who's like that my first goal is to get them not looking like this anymore and looking like the previous clip before anesthesia it would be very very rare for us to anesthetize a patient who looks like this with their heart disease instead first treating the congestive heart failure and stabilizing them every now and then I mean I students are are often worry about well what if I have a dog who's just been hit by a car and has a fractor that we have to repair and they're also in congestive heart failure and I would still say that the the congestive heart failure has to be managed first uh because the anesthetic risk is prohibitive if the patient is has pulmonary edema before even being induced so first deciding is the patient compensated or decompensated in their heart problem we want to make sure that for anesthesia they're compensated second what is the nature of the heart problem so of course there's dozens and dozens of different types of heart diseases in order to know what it is ideally just Echo everybody but that's not realistic um and I would argue perhaps not even necessary so I use the signalment of the patient the history physical exam for a lot of just basically presenting in my mind a list of differential diagnoses if it's a 12-year-old Chihuahua or malti or Cavalier or whatever with a systolic left apical murmur then I'm thinking that my top you know several diagnoses are just mitral disease but I'm also careful to be thorough in my oscilation because maybe it turns out that dog actually has a point of maximal intensity louder over the right heart base in which case I have no idea what it is and I really do need no matter what more diagnostic information I I don't have a suspicion anymore um so thoracic radiographs are very helpful both for assessing the lungs for the presence of pollary Edema the plura for plural diffusion and getting some idea from the appearance of the heart in terms of secondary changes to the cardiac silhouette and basic blood work so these things are all really I mean they would be reasonably considered at least the blood work in history physical in pretty much any uh patient being anesthetized short of a shelter or high volume spu type setting and thoracic radiographs make sense for a patient who has a cardiac concern I put here Pocus uh tast with question marks because I think there's a very good case to be made for uh assessing every dog and cat that has say a heart murmur or suspicion of cardiomegaly on radiographs or any other reason to suspect a heart problem with a point of care ultrasound fcus before uh anesthesia if nothing else then just to gain reassurance from seeing normal left and right atrial sizes but it requires skill familiarity with the technique and ability to interpret the images and folks who can do that I think are wise to include it in preanesthetic evaluation and so first I've tried to stratify whether the patient heart problem is decompensated or compensated okay let's say it's compensated the you know 11-year-old mixed breed dog with dental tartar that has a left apical systolic murmur and needs uh work done on its teeth so when I next have decided after deciding it's it's compensated based on the physical exam if the patient uh if the client rather doesn't consent to say an echocardiogram I'm going to want to use the information I have to formulate a working differential diagnosis and to pick my top differential as one of two disease processes there are dozens of heart diseases but they really all can be C categorized broadly as one of two types of problems either it's a diastolic dysfunction problem like we see on the left like hypertrophic cardiomyopathy or it's a systolic dysfunction problem like we see on the right with dilated cardiomyopathy so let me start with d CM we all know that you know if the heart's not working well it doesn't pump well and so we think okay that means that the squeezing power is lost and so like dilated cardiomyopathy it doesn't squeeze well anymore that's a fairly logical and easy to considerer thing it might be for example that drugs that temporarily increase the squeezing power would be helpful sure enough maybe vasod dilation Downstream is helpful because then there's less resistance to forward flow of the weakened ventricles makes sense too and excuse me largely these things are the opposite of what can be helpful for a patient with diastolic dysfunction so a cat with hypertrophic cardiomyopathy does not need dobutamine to have the ventricle squeeze harder when it's already equipped with more myocardial mass than it wants a patient like that does not need a vasod dilator when it it really has no difficulty moving blood forward if only it can have enough blood accepted into it in the first place so I want to comment on how all heart diseases more or less can be slotted in one category or the other uh paracardial diffusion squeezing the a heart the heart might be normal but by virtue of it being squeezed by paracardial Fusion this is now a problem of diastolic dysfunction so we don't want to give dobutamine to try and make it pump harder because its problem is not pumping its problem is filling etc etc uh mitro valve disease that's not necessarily immediately a problem of systolic dysfunction but a patient with mitro regurgitation this is the mitro valve is having trouble moving blood in the forward Direction and over time the left ventricle does come to dilate and eventually can lose some of its systolic ability and so mitro valve disease even if it doesn't yet show systolic dysfunction is treated anesthetically like a patient with systolic dysfunction like d cardiomyopathy so again step one I want to observe the patient and decide is this heart problem compensated like asymptomatic or decompensated like in heart failure if it's decompensated we're not doing anesthesia for an elective procedure assuming it's compensated I'm going to try and decide do I think from the sement and my physical exam that this patient most likely has a diastolic dysfunction problem like just about every cat versus with heart disease that is because cardiomyopathy is by far the most prevalent problem in cat Cardiology and uh hyperopic cardiomyopathy is is the most prevalent so I want to know that because if I have diastolic dysfunction then I don't want a vasod dilate it will it will lower blood pressure that elicits a reflex tardia that now is the opposite of allowing enough time to fill and empty and fill empty so I wonder if any to increase or maintain a normal to upper limit of normal blood pressure because the left ventricle is equipped to meet that challenge and that will probably reflexively slow my heart rate while maintaining the blood pressure so I have more diastolic filling time that's a good idea I don't want to fog I do not want to fog this myocardium to beat stronger with drugs that increase myocardial contractility because usually doesn't need that the rare exception that I alluded to the last hour is the cat with end stage hyper trophic cardiomyopathy where where the left ventricle is is not Contracting very well and so notice how that category of disease hypertrophic cardiomyopathy restrictive cardiomyopathy cardiac tampeno from paric cardial Fusion these diastolic dysfunctions are managed by you and me anesthetically in the exact opposite way of the rest of the heart diseases because in systolic dysfunction we want to avoid uh we want to use or we want to consider drugs that increase uh my cardia contractility because they could be helpful I wouldn't do it for a very long time um I'm asking the my cardium to work harder but maybe just to get us through the anesthetic episode for for a short time and I want to avoid drugs that increase systemic arterial resistance so if this patient's blood pressure is dropping I going to give something that makes the left ventricle squeeze a little bit harder rather than trying to Vaso constrict to raise the blood pressure and so what I'm trying to paint is this idea that there are two different broad kind of mechanistic categories of how the heart misbehaves diastolic dysfunction and systolic dysfunction and I think intuitively we always think of systolic oh the heart's not working so it must not be squeezing I better give a vasodilator but in the anesthetic situation where we have you know the ability to control uh blood pressure through different means uh vascular drugs or heart drugs so on we need to consider what the heart disease process might be in order to give uh the the best drugs for anesthesia I don't think I need to to sell too hard about the value of a preanesthetic evaluation uh because we all know it and if we could wave a magic wand and have Echo results for free on every patient we would we would want that so it's more a question of remembering um you know why we do it and and perhaps you know providing this to the owner as justification for why in a particular case especially we might want additional information I want to talk a little bit about anesthetic risk in cats and dogs not specific to heart disease but just what is it that helps us maybe in addition to the heart problem start to be thinking of like geez maybe there's really quite a bit of anesthetic risk here maybe a little bit more sort of forward in in in recommending or wanting additional diagnostic information like an echocardiogram versus the overall anesthetic risk outside the heart is is pretty low so maybe I'm a little bit less worried or concerned uh amazing study uh looking at several tens of thousands of cats that underwent anesthesia and the small number of them that died under anesthesia I think it was oh something like 200 cats out of over 100,000 I think uh anesthetic EP that were surveyed um yeah so something like a 0 2% uh risk of fatality under anesthesia and what was found interestingly is that these four variables that were examined had very clear risk associated with them cats that are 10 or more years old uh had a two and a half or 2.1 times increased risk of death because associated with their age uh the American Society of anesthesiologist classification is essentially a grading scheme for the stability of the patient heading into Anesthesia where ASA grade 1 is a perfectly stable patient and ASA grade 5 is a crashing patient and not surprisingly the risk increased uh the higher the the instability of the patient whether it was a minor or major procedure in increased uh the risk of of anesthetic death in cats probably at least partly because of the duration of anesthesia and the biggest uh one of all 15.7 time increase in risk of death death in cats if their body weight was uh less than or equal to 2 kilg which I take to mean uh if they were kittens uh and so many things can factor into that the ability to deliver therapy fluid therapy or anything else to a kitten effectively uh the uh late stage of illness at which a kitten can be presented and so on their their minimal reserves for for responding but the point being that each of these factors that was examed had a significant uh contribution to anesthetic risk of death so I think of that because if I have a if I have a a cat with um a murmurer and the owner declines all uh further diagnostic testing radioraps Point all of that is uh biomarkers everything is out of the question then I think to myself well if this is an 8-year-old cat with an elective procedure and no other illness that's stable who needs a minor intervention and is a 4 and a half kilogram cat then all things considered that is a relatively lower risk than it otherwise might be uh with these factors and so what do I do maybe do I just assume that the cat might have hypertrophic cardiomyopathy and proceed with anesthesia accordingly that would I think be a very good idea what about anesthetic risk for dogs um you know the the exact same group looked at an also an incredibly impressive number of anesthesia events uh that dogs underwent and looked at case fatalities and essentially looked at the same variables with very similar results uh although it was a Sevenfold increase in risk of death uh if dogs were greater than or equal to 12 years old versus uh young or middle-aged adult uh more and stable dogs uh had a a worse prognosis uh scheduled versus urgent versus emergency also increased the risk of death and uh so did weight again with less than 5 kilos presumably indicating a fair number of puppies so um this deviates from a purely cardiac standpoint um but intentionally to point out that as we think of anesthetic risk in uh dogs and cats from the heart standpoint purely that also fits in with the the larger picture the amount of objective information we have actually anesthetizing animals that have spontaneous heart disease is appallingly small uh one paper and here it is and it's in dogs so we got nothing on cats so let me tell you what this paper uh says and I'll say off the bat this very much mirrors my own experience and I'll also go one step farther and say it likewise mirrors my experience in cats uh with heart disease so let's say cardiomyopathy and this study in dogs uh 100 dogs that had heart disease the majority of which was degenerative mitral disease uh were anesthetized for an elective procedure and uh the result was you know it was examined was pretty straightforward uh did they live and did they have complications and the answer was basically yes and no U there were 100 controls that had no heart disease that were essentially the same types of dogs uh seen at the same institution and so on and so there was no significant in difference in complic between dogs that had heart disease and those that didn't and no deaths uh in in all the 200 dogs so that speaks to maybe having a heart problem is a concern for an increase in anesthetic risk and even anesthetic death yes but the flip side of not administering anesthesia and not performing whatever procedure carries its own set of risks um I think uh you know it's the age-old thing that I already mentioned prom no no is um you know first Do no harm and it's like maybe there's another side to that coin you know but also let's not harm by withholding treatment that is necessary or going to be indispensable in the future so I do find myself with the dog that has you know very impressive periodontal disease or cat that has advanced asymptomatic disease so stage B2 hypertrophic cardiomyopathy or Degen mitral disease I mean many many lay people have heard horror stories about anesthesia and don't want that for their companion and at the same time so I acknowledge that in discussing the findings of say an echocardiogram with a client and while I acknowledge that I say you know let's keep in mind that most heart disease that we turn up are going to be irreversible so let's say mitral disease in a dog or cardiy again I say you know let's also keep in mind that this isn't going to get any better anytime soon it might stay stable for some time but if we put this off there's a possibility that if we'd ever decide to go forward with anesthesia in the future that har will be worse off and it's certainly possible that the reason for the anesthesia dental disease or whatever else it might be is also going to worsen so while it's not great to have an increased anesthetic risk now perhaps it's worse to put it off to try and avoid the risk altogether and then six months or a year later have worse heart disease and now we have an emergency dental procedure and a two three obsessor or what have you so I think oftentimes owners come to a Cardiologist wishing that it's not as bad as they fear and and I will say that I I do feel not in any sort of negative way just really a a purely optimistic way quite a strong pressure for many clients to to have it you know Doc is it is not as bad as it might be um so when I deliver this news about uh a diagnosis of a particular heart problem and it's with the intent of it's a part of a pre-anesthetic evaluation I tend to be relatively um like encouraging for proceeding not because I think it's without risk I'll often say something like you know say a dog has B1 mitro valve disease so mitro regurgitation but no secondary Distortion no enlargement of left agum left ventrical mild disease I'll often say to a client in explaining this at discharge that this increases the anesthetic risk and I'm just going to say like from experience somewhere between two and threefold so 200 to 300% increase in anesthetic risk compared to an equivalent dog with no heart disease and that's meant to be a shocking thing so that's a lot but if there's 2% chance of that risk for dog that has a normal healthy heart then we're now talking about with this dog it's more like4 to 6% and that's still 99 plus percent likelihood of coming through okay and so I paint it that way so that owners are aware when they read on the internet about how terrible anesthesia is when you have a heart problem that that's true in absolute terms but when we look at the relative bigger picture that it's still probably favors going ahead with the procedure and so this paper is supportive of that so what did they do these North Carolina people that that had such an amazing result of no deaths and no complications and this hund dogs did they you know what kind of of phenomenal you know uh Platinum standard treatment that they offer well frankly I mean it's wonderful and how underwhelming it is uh they administered Hydromorphone and premedications fairly routinely done and they gave mzm as a benzo dipene uh to back up the hydrophone just prior to an anesthetic induction and they have either etomidate or propofol we use propile all the time alax alone as well we don't have a tomate but but it's not available in Canada I used to be disappointed about that so I had a chance to give a series of talks just over a year ago in Upstate New York about 200 veterinarians in attendance and and so I I did a a polling question I said here we are in the state of New York where atom is you know widely as WI available as as propop ax alone I said who routinely who has atom8 in their Hospital uh right now and uh the response was one out of 200 plus participants so I don't I don't miss it uh atom can produce the same kind of recovery as ketamine does for those of us who remember so a fair bit of dysphoria and and not the smoothest anesthetic recovery um it just has the the the wonderful virtue of of having a essentially no cardiovascular depression but then propofol and alfaxalone when they're used in small amounts titrated to effect really have minimal uh cardiod depressant effects too so anyway the the the study looking at dogs with heart disease Premed them with Hydromorphone gave a touch of medz and then induced them with propol maintain the mod isof Florine and performed comprehensive monitoring which consisted of puls oxymetry uh I believe they did ntial Co two which has its value but it's probably certainly not indispensable and then you know like anesthetic plane monitoring and pulse and temperature like things that are accessible to all of us so really what I like about this paper is that it showed that minimal to know increase in Risk was possible using means that are accessible basically to all of us okay so what do we what do we do it's nice to look at this evidence and this is you know kind of how it's how it's been done or or or like what what people have shown on studies what about you know get down to Brass tax so let me talk about the drugs that that we use with no pretense that these are the only drugs just to describe an approach that seems to work so um I like atropine or glycopyrolate a lot uh it's been a fair bit of hay that's been made about you know maybe glycopyrolate is less protac cartic which actually was shown in a study of healthy dogs that atropine intended to produce more rapid heart rate uh than glycome okay um I think the bigger point is that when a patient has heart disease what we don't want is to make that heart work harder than it needs to and so for that reason I never recommend pre-treatment with glyco or atropine uh glyco atropine would not cannot be part of the pre meds of a patient who has heart disease because if the patient is doing fine with the heart rate of I don't know a dog of 120 or a cat of 170 then why give these drugs that immediately crank them up by an extra 50% with the mitro valve being beaten upon and turning away or or or the hypertrophied myocardium of HCM you know having to beat so fast for nothing and so uh I don't do that I instead make sure that the patient has a catheter in and even if it's the most kind of benign In-N-Out piece of cake elective thing that's going to be really fast if the patient has heart disease and they're going under anesthesia they need to have an IV Cath and so I would give um you know literally like quarter quarter dose maybe half dose but even quarter dose of glyco uh as needed for a patient who is bradaric and bra cartic and you know low normal tensive or hypotensive if a patient is braic cardic but hypertensive because they got Dex metodine you know Vaso constrictor the Vaso constriction is offset by lowering the heart rate to maintain normal blood pressure and we don't want to like we don't want to chemically speed up the heart then so to to to keep in mind that X metodine routinely produces lower heart rates in a way that does not require intervention with glycopyrolate or atropine um but let's say Dex metaton is not part of the picture then I use atrop and G glycopyrolate as needed to maintain what's an appropriate heart rate well I think to myself of if the patient wasn't anesthetized so a dog with a heart rate between 70 and 120 to me is as you know stable in status quo as can be cat 120 to 180 seems fine um and and uh with blood pressure measured concominant acepromazine so very few of us I think are still of a vintage um who still use this prosine but I I like it for uh young healthy cats and this should say dogs as well uh so a patient who uh needs an elective procedure and and has mild subotic stenosis or cat with a mild or a moderate ventricular sepal defect or or whatnot um patients that are compensated and have minimal secondary changes to their heart I'm very comfortable giving these promazine and I do like intramuscular or I suppose you could do subq but intramuscular to to um have it work uh fairly quickly it's a very small volume so concentrated so it's not a painful injection and I like it because it's a a gradual onset and an extended slow offset of sedation um so for extended effect we wouldn't want that in an elderly patient for example or a patient who is hemodynamically unstable and Alpha 2 Agonist like Dex metodine um that's a good idea with hypertrophic cardiomyopathy in terms of arterial constriction um but it can be controversial to some with hypertrophic cardiomyopathy because it's yet to be clarified whether that vas of constriction can in some cats and dogs also apply to the coronary arteries which we would not want so um I personally like using Dex metodine quite a lot in cats and I use it at you know doses that are microscopic compared to the the package label dose um so 1 to two microgram per kilogram would be a a typical go-to for me Bodines like mazam uh these are also pre-anesthetic drugs like I showed in that protocol that North Carolina State used for those 100 dogs uh maalam or or diazapam of course their effect is very limited it's brief and and of low magnitude but together with anopia is is a classic combination I find this gets talked about so little maybe I don't know maybe maybe it's just a thing around here or but the the stimulation and especially the noise sensitivity of opiates um you know it's really important um somebody you know just drops a syringe on the other side of the room and a dog uh lurches uh in response to it uh that's important and so we want to consider that in the patient's well-being and and and use of opiates ketamine was was recommended for a long time I don't think it's used fairly little again except in maybe shelter or or kind of bulk surgery uh contexts C is used as part of infusions like MLK for morphine like ketamine and and many other combinations um it it got a bad wrap for the heart because of the tachicardia that it produces but that's much more of a concern with high doses like these astronomical you know 22 Ms per kig uh that used to be given im to like spay a cat which is appalling when we think about it because ketamine confers no visceral anes anesthesia so this is essentially a solid never but uh if it's given in a low dosage especially if it's together with something else then ketamine and the heart are okay uh the the amount of increased myio cardial oxygen consumption is is very minimal uh at these lower dosages and and this rough recovery thing is is really much less of a concern propile I mentioned is is one of my two favorites along with alfax alone yes it can cause apnea um but that's to me really only if it's given like a a giant Bolis uh you know I mean there may be a brief apnea anytime so titrated to effect um it's as far as I know you know every cardologist feels comfortable uh using it or most anyway and uh likewise Al axone um it has the advantage that it can be given im or propol can't but that's kind of body size dependent because we quickly run into several milliliters to inject IM in a mediumsized dog and that's just prohibitive uh I do find it has a wonderful both induction and Recovery profile uh just like propal so Okay so we've covered a lot of ground I talked first about looking at Peanut the dog that was breathing well and then breathing hard for choosing compensated and not decompensated patient has to have compensated heart disease before we consider anesthetizing them and then we want to know what kind of heart disease do they have and that'll require discovering or or even just thinking in our own differential diagnosis with the information we have from sigment and physical exam is it more likely to be a diastolic dysfunction problem or systolic and then having established that we get the information that we can ideally with an EOC cardiogram or at least a tast and then in our selection of pre-anesthetic and induction drugs we follow some of the pointers that I mentioned for choosing which drug is best I want to mention that there are a couple of things we can do for pre-anesthetic support and for monitoring one is continuing the same cardiac medications even the day of like the morning of anesthesia so since the patient's fasted we'll want to give it on you know the tiny meatball and then uh maybe a a syringe with tap water for a few milliliters of a water Chaser to make sure that it's swallowed and reaches the stomach that's a good idea for all drugs except ACE inhibitors like the pills and the reason for that is it's been shown that ACE Inhibitors cause significant hypotension during anesthesia if they are administered on the morning of general anesthesia so we would skip a dose of those but give all the others preoxygenation is is to me was a classic so I I come from private practice background so when I came to the Atlantic vet College I thought I was just doing the teaching thing for a year and move on um but it's been 20 plus and so my my 10-year career in uh private practice uh pivoted to Academia instead of the opposite path that seems to be more common uh and so I remember when I first heard this this this idea of let's preoxygenate this patient for their benefit I thought holy smokes like the number of patients with heart disease that I've seen and estheti successfully without doing this like is it even worth it and I think at the root of my skepticism was this idea that you know they'll breathe the oxygen like whether you do Flow by or a mask let breathe in and out we do it for like three minutes let's say okay then turn off the oxygen put the thing aside and now induce the patient and intubate them I mean the oxygen was gone in three breaths but it was pointed out to me um in the most generous and diplomatic Way by Dr Sheila Robertson at University of Florida that a kind of a Depo effect exists with preoxygenation so I do recommend this for patients especially that have more advanced heart disease so a patient with substantial secondary changes or a patient who was in congestive heart failure who's now been uh treated and is is more stable but still has advanced heart disease uh when a patient like that has an oxygen mask in front of its mouth for 3 minutes or so and breathes 100% pure oxygen for those 3 minutes that oxygen isn't just tracheal and bronchial over that kind of time frame of three minutes It'll reach the bronchioles and even the Alvi and so it's been shown that the concentration of oxygen in your Alvi remains elevated for several minutes after just a two or three minute preoxygenation so that Depo effect I think makes a lot of sense and so it's not practical to do that with every animal that has a murmur but it is an extra tool that we can reserve for increasing the risk of a stable anesthetic in a patient with more significant heart disease uh and then the big you know one of the big questions is what about fluids so of course giving fluid therapy uh to any patient assumes that the heart can uh uh receive a larger blood volume and move it on through and and that's true in healthy Hearts um but it's less true in a patient with heart disease so we want to find a fine balance between giving enough fluids to keep the patient hydrated keep the kidneys working properly and yet not overdo it and I find that a good way to do that is just to use this kind of reduced surgical maintenance rate and if possible to use a an isotonic fluid that is weaker in sodium content because there's not a need for a high sodium content in a patient that is hydrated uh the 0.9% sodium chlorides and lactated ringer Solutions are replacement fluids that are given an individual that has for example lost sodium and chloride and potassium through vomiting or diarrhea but in a stable uh uvalic patient then a lower sodium content to the isotonic fluid is is actually um more heart friendly uh I think this this slide speaks for itself in terms of methods of hemodynamic monitoring and the repercussions of even this simplest monitoring on a patient's survival are remarkable U here's a that same study that I I I cited earlier in cats and anesthetic death if you can believe it uh these authors documented a fivefold lower risk so 500% decreased risk of anesthetic death if the pulse and pulse were assessed versus neither one I mean this is really entry-level stuff and so I'm going to guess that you know the majority of folks who have sacrificed two hours on a you know a fine Wednesday evening to listen to this kind of stuff or probably already doing this and then some and if you are then good please keep doing it because as you can see that makes a difference and if you're not you should consider because this is simple stuff and it can help all patients that go under anesthesia so um that's really the long and short of what I wanted to talk about except for troubleshooting so I'll talk about a couple of complications I think some are straightforward others like a couple of EKG slides or more uh maybe cardio informative specifically and then we'll have about 10 minutes or so for questions and then uh a short presentation um from our sponsor from nesle Pina so managing complications um hypotension is really important to monitor because it elicits or reflex tardia and it decreases profusion of vital organs so when it happens in a patient who has heart disease there's no reason to do it any different than a patient with a healthy heart would just decrease the inhaled isophlorin concentration lighten them up uh that's to to help with the low blood pressure the patient's blood pressure is still low and they're light enough that we can't lighten them anymore like maybe there's starting to be some movement or whatnot then we could address that with a vasoconstrictor substance like phenoline or a fedrin and a Bolis of IV fluids is also possible but remembering that patients with heart disease are at greater risk of having that fluid spill into surroundings and and Trigger pulmonary edema just a heart failure so we we would perhaps want to make sure that you know is this a patient that did have fluid deficits that we were still catching up on then maybe a fluid bis is okay hypoventilation you know if the patient stops breathing then no surprise we decrease the vapor vaporizer setting and bag them intermittent positive pressure ventilation is a good idea in patients that have significant cardiovascular disease we want to try and avoid really high peak airway pressures because those can inter interfere with Venus return um but that's that's more of a technique issue and if it's done um properly in patients with normal heart Heart s than it can be done properly in patients with heart disease my last couple of slides are on ECGs because that's an important component of anesthetic monitoring and even more so in patients with heart problems so let me show three examples of ECG abnormalities that come up and just quickly mention how to address them the first thing I'll say before going there though is recognizing ECG artifacts is really important because anesthesia is is just ripe for those the alcohol has dried out so the skin contact isn't very good and now we have what looks like atrial fibrillation with a squiggly Baseline maybe it's just that the alcohol dried out um a patient that has uh movement can have that look like premature ventricular complexes vpcs and we don't want to misinterpret those so uh looking for artifacts is really important if you're not sure you can always take a picture and uh give us a call at the Atlantic back College um that's play it well we're three hours ahead of you uh so probably be good for morning concerns and less so this time of day but it's uh it's always worthwhile for us to share with students what questions or concerns you have about ECGs and specifically with artifacts too because then they get to to to learn what the imposters are um so um when an arhythmia is present It's always important to address the cause because in a sense giving an anti- rythmic drug uh uh is is a little bit like a Band-Aid solution and arhythmia almost always happens for a reason and if we can fix that reason like uh if the patient has a low uh spo2 that can be rhythmogenic so fixing that can make the arhythmia go away like PVCs if the patient has acidosis has hypokalemia a number of other disorders can be themselves AR rhythmogenic and so we want to fix the problem at the cause not just immediately given anti- arhythmic so the ECGs I wanted to show you one is sinus Brady cardio here's a cat with a heart rate of 100 and sometimes that can be in response to Dex metodine phasal constriction elicits an appropriate slowing of the heart rate so as to not blow something out and so uh sinus braic cardio by itself doesn't warrant treatment but if the patient has sinus braic cardia and a normal or low normal blood pressure or if the patient has sinus braic cardia and never had an alp like Dex Med then we would want to drop the inhal and concentration bag the patient if the patient is not breathing and then consider uh repeated doses of glyco as needed for a cat to Target 100 to 140 beats per minute and a dog maybe 70 to 100 um here's perhaps my favorite finding on an ECG and and please go ahead and take a screenshot of this uh I recognize that there's also the recording if you want to go go through it let me let let me uh analyze this with you so here is a p-wave so that indicates the Atria depolarizing then the pr segment is here that's impulse going through the AV node and then the QRS complex is here and the Qs complex ends here this is the t-wave but the t-wave sorry this is the uh the the um swave so QRS here this is the ST segment and this is the t-wave here all of this wound up in the basement here when we're used to seeing it happen here like s segment and then d-wave and then back to the next one so how do it wind up here and the answer is it's called SD segment depression and so it's a repolarization abnormality and the thing that causes this is myocardial hypoxia every year I see a case of a patient who showed this where you know 20 minutes earlier this wasn't on the ECG so this came on and it's due to an anesthetic circuit problem somebody forgot to reopen the Popoff valve ran out of o2 or forgot to start it back up again after reconnecting the patient uh turned the patient from one recumbency over to the other so the tube got uh twisted or or kinked anything that deprives the patient of oxygen May first deprive The myocardium of oxygen and that shows up as the onset of s segment depression so you should know this finding because if you see this happening where it wasn't there just a moment earlier then checking the anesthetic circuit for appropriate oxygen flow is really important and then finally what about PVCs well uh we know they're also called vpcs uh same thing basically a spontaneous heartbeat originating in the ventricles that doesn't belong there those this is a a string of a whole bunch of them happening at about 150 beats per minute when a patient has these under anesthesia it's really important to follow a stepwise approach approach and by that I mean I use an algorithm uh this is out of textbook called the clinical Veterinary advisor the the the great privilege of having edit edited and uh this is half an algorithm I'll show you the other half on the next Slide the whole thing is a PDF that should have gone out to you along with uh these slides um but it's also thead visor if you want to look it up you can follow a step-wise manner that that or process that asks first of all is the rate high because the rate is not High then it's not ventricular tachicardia it could be these other things none of which is treatable with anti- rythmics if it is then is there a pewa for every QRS at a constant PR interval so on to work your way through eventually you get to is there an underlying problem that may be triggering ventricular tachicardia and must be dealt with and here are those reversible causes that I was talking about I mean just about any dog who has um you know a splenic mass is going to have PVCs and the treatment for that is take the spleen out so it's not surprising that the arhythmia is there under those circumstances and we treat the underlying problem uh rather than the arhythmia itself so this is the whole algorithm what I've tried to do with this talk is to both bring out existing evidence and and also weave in basically preferences and and personal kind of um day-to-day use and I tried to do that in these categories so with that I I do see we're at seven questions which is a you know a lofty ideal and uh and let me try and and answer those um Liz I I see them here as uh let's see I think direct messages so I I don't know if you're seeing them too yeah I've got uh you'll see the ones that come to everyone um but you go ahead and answer whichever ones you want and whatever doesn't get answered um people can email me or I'll give them your email address and we can figure it out later that's uh I think that's yes let me let me do my best here and if I think of what my inbox has been looking like lately let me concentrate more on trying to answer them here for sure um so um uh Melissa we asks uh these are thank you for these questions uh with major surgery and a long anesthetic how can we minimize the risk for for say dental work this is the main surgery I think we all perform I see a clear benefit to the patient but is there any information about about the duration for example greater than next hours increases the risk by why um an awesome question I you know since the since we were Veterinary students we've known this and yet in terms of an exact number I do not have one for you I I don't know that one exists so I think um it's again a matter of we're just weighing pros and cons if I can get this procedure done properly maybe the dog doesn't need it again next year versus do I accept that it's imperfect and just get in and get out and I I honestly I think I would use the degree of severity of heart disease and the means that I have available to me to to address that but I'm sorry I don't have a solid answer I don't know anyone who does either uh Kathy Wright asks if a dog does not have a heart murmur preop but develops one after induction I love this uh with Dex omine is this a concern for cardiac pathology so wonderful question and the answer is it can be but it doesn't have to be so I've experienced that in dogs that had a normal echocardiogram and I've also experienced that in dogs that had an underlying problem unmasked essentially uh by premedication or even just Jal anesthesia altering hemodynamics um I will say that in general and this is sticking my neck out but it just reflects my own experience that uh when that has happened it tended to be a minor heart problem um so I don't remember a situation where that was catastrophic although perhaps it's happened to others so yes it's a concern for cardiac lesion but not automatically one you might still have a normal heart and if you have a cardiac leion it doesn't automatically have to be a bad one awesome question uh Britney is asks when comparing alphaxalone to propofol for induction in cardiac compromised patients is one considered safer or preferred over the other is so such a great question um I've I've heard and and kind of felt a little bit of of uh a preference towards alfaxalone in that regard and then I think of my optimism bias like I've used propol in so many dogs with such like catastroph I mean what we're talking about here is is not cardiac procedures right what what I'm I'm what I'm proposing is managing situations that are um not specifically intracardiac interventions but intracardiac interventions is what I do um pacemaker today uh PDA tomorrow as it turns out and so those are patients where there's a greater anesthetic or arhythmic risk because we're dinking around within the heart and patients that have cardiac compromise to begin with even in those patients I find I'm happy to use alphaxalone or propofol interchangeably nice question thank you um Angela anet asks uh would dexmon be okay in a patient with diastolic dysfunction but not in systolic yes that's exactly what I was trying to get across the one Shadow like the one question mark is to what degree does me Dex metodine cause coronary vasal constriction as well as Peripheral arterial constriction um if it's used at little mini doses like one or two micrograms per kilogram um and we I I don't know what the answer is to that but yes it is par excelance a drug Dex metaton for diastolic dysfunction cases excellent Tracy ho would lrs be more appropriate for fluid therapy for dogs with compensated heart disease versus 0.9% sodium chloride wonderful question so the answer is actually no because they're both sodium Rich if I look on a bag of lrs like the print on that clear bag if you if you squint your way through the all the writing you find a sodium content of lrs is somewhere around 140 mil equivalents per uh per liter and for um uh for 0.9% sodium chloride I want to say maybe one is it 150 or the point is that they're both essentially identical to the value you get on blood work so you're you're replacing you're putting back into the patient what is missing from their circulation so if you've lost a lot of blood like Hemorrhage or if you vomited and losing you know a lot of sodium chloride but a patient who's UIC dayto day through breath urine you know sweat tears whatever uh those are are quite sodium conserved losses so the the cumulative sodium loss in in concentration of sodium in like urine and breath and so on is like 30 mil equivalents per liter it it we do a lot to conserve sodium so lrs and sodium point9 sodium chloride percent quer equally uh kind of more sodium Rich than you need when you're already well hydrated um Anna smid thanks for the question Anna smid asks what was the dog heart rate under GA that you mentioned so a Target would be uh a reasonable Target would be 70 to 110 for a dog and uh probably 120 to 160 for a cat uh Brian McBride what are your thoughts on using cardalis for CHF and dogs with micral disase so uh really interesting question a little bit of deviating to a a different topic from tonight but yes I mean cardalis has uh components that are individually effective and so has been investigated and shown to be um you know to carry the advantages that would be expected with its components um K brunfield thank you so much thank you that's uh that's really kind of you uh and Kim Barkley as well thank you for your kind words uh Teresa hey uh is that Teresa I wonder if it's Teresa from can West um be great if this is you um what dose of Lidocaine uh do you use in cats with vtac so uh that is a hard question as befits board certified criticalist the the not with that bareny thank you I think um it's a tough question so the standard dosage for a dog is 2 milligrams per kilogram given once and repeated up to three times in a 15minute window as needed for controlling vac whatever control is deemed to be uh defined as and uh in a cat it's recommended to use a quarter of that so 05 milligrams per kilogram and to only repeat it once you know to me that that is appropriate and is totally empirical and uh and that's the best that we got uh thank you Teresa an abuser thank you for your kind comment H Katrina likewise uh Masa thank you Britney thank you Allison thank you folks please Oxana and VJ thank you so much um I'm going to to wrap up with uh one more word of thanks and hand the microphone over uh to um Dr Laura and uh to our sponsors who made it possible uh to do this tonight so one last thank you a sincere thank you to you all uh to Liz and Tim and to Nestle Pina thanks so much Dr cot uh on behalf of cavm and everybody in attendance Oops I meant to turn my video on I am here hello uh thank you so much for the great uh lecture this evening it's really greatly appreciated um and uh if everybody could stick around just for a couple of extra minutes we've got Dr hartney here from Purina he's going to do a quick presentation as well thank you I'm just going to try and share or do I need to Dr cot you might have to stop your screen share perfect sorry about that no worries okay can you see the I can yeah looks great perfect thank you thank you so much for that lecture Dr cot that was um really great content I love seeing some feline content as a uh cat lover and I always preferred feline medicine um I am going to switch to speaking about a a diet that is only available for dogs um but still really really cool um Innovation um so our newest Innovation from Purina uh is the diet cardi care which is excuse me it is a um really a breakthrough Innovation to how we approach uh nutritionally managing um heart disease and dogs particularly mietus mitro valve disease so if anyone wants to stick around for the next 10 minutes or so I'll just summarize um this new diet cardio care um so momus mitro valve disease is the most common form of heart disease that we see in dogs representing about 75% um of heart disease in dogs and it is a Rive disease so Progressive um reduction of heart function uh which does potentially lead to full-on clinical congestive heart failure in about 30% of dogs and um so what the uh researchers took an approach to developing cardi care that was um using something called multiomic studies to take um a molecular level approach to develop a cardiac protection blend of nutrients which is not just something that we would feed a dog once they are in heart failure um but it's a novel dietary approach that um we can use to initiate dietary therapy um in preclinical stages of momus mitro valve disease so I'll briefly go through kind of the approach to developing this diet so the first study um was this multiomic study so they use metabolomics and transcriptomic which is um basically looking at metabolite and RNA transcript differences between dogs with heart disease and dogs with healthy Hearts um so taking this kind of molecular level approach to investigate where can we use nutrition to intervene um and how can we um potentially help these dogs um earlier than when they are in heart failure uh so the major findings of um these studies were that dogs with heart disease have altered energy metabolism in the cardiac tissue so decreased fatty acid oxidation and moving more towards glycolysis and ketolysis for ATP production and this is significant because about 90% of ATP production in the heart cells comes from fatty acid oxidation that's the most efficient form of energy production for heart cells to function and if they're not doing that as efficiently and they have to move towards glycolysis or ketolysis they're not functioning as as well and that's going to potentially lead to that Decline and progression um also not surprising surprising ing the other two um major findings were dogs with heart disease had increased markers of inflammation and oxidative stress stress which we would kind of expect to see so um those initial studies um then led to the development of what we call the cardiac protection blend of nutrients and so this um I will summarize briefly here what that is so the first thing is MCTS or medium chain triglycerides and this is important because this is what we're um kind of taking this unique approach to providing a source of fat that the heart cells can very easily get into the heart cell and very readily use as a form of ATP production so a very readily available form um of fatty acids for the heart cells to use so more efficient utilization of this type of fatty acid versus longchain triglycerides um so we're providing them an alternate energy source which could potentially be very impactful in maintaining their their cardiac function there's some other nutrients you would expect to see there so particular amino acids like toine we um are all aware of that's important for heart muscle contractility lysine and methionine are precursors to carnitine formation so you might expect to see carnitine in there well lysine and methionine are what the body uses to make carnitine carnitine is an important um transporter to get those fatty acids Into the Heart cell so that's going to help support that fatty acid metabolism as well um fish oils from um omega-3 fatty acids sorry from fish oil sources um we're well aware that those are going to be beneficial to reduce that inflammation um but they have other benefits with heart disease as well potentially um anti-ar rhythmogenic anti thrombotic and the levels in cardiio care are a therapeutic level so they're going to be just as high as a diet like the joint diet or the skin diet um so very good levels of Omega-3 in this diet as well vitamin E is an extra antioxidant to help with that oxidative stress and magnesium is also an important nutrient um for heart function so that cardiac protection blend of nutrients was then kind of put to the test with a dietary intervention trial um so that was study two where they took dogs in preclinical so Stage B um mitro valve disease and they did a six-month trial where they um were fed either a control diet or a diet very similar to the control diet but with the cardiac protection blend added to it for 6 months um and at time 0 3 and six months they did evaluate um kind of things that we use to to Mark progression of mitro valve disease so um using echocardiography they looked at um left atrial enlargement mitro regurgitation um and any kind of progression of staging and so that study um did show that the dogs on the control diet had um significant um left atrial enlargement um worsening of mitro regurgitation and um some dogs progress from stage B1 to B2 versus dogs on the cardiac protection blend um did not have those same um changes in terms of left atrial enlargement mitro regurgitation and dogs in B1 all stayed in B1 in that six month trial period so um these were uh very promising results in this um kind of proof of concept pilot study um which did lead to um making the commercially available cardio care um and then just to kind of Bring It all full circle they did repeat the um metabolomic study by taking the dogs in that dietary trial and um taking serum samples at time zero and then at six months and um basically looking at those metabolite differences in dogs on the cardiac protection blend versus a control to see um did we see any evidence of um impact at again a mo more molecular level um and they did see that as well so dogs on the cardiac protection blend had improved fatty acid utilization um decreased markers of inflammation and oxidative stress versus the dogs that had been on the control diet for that six-month period um so really um cool research that led to the the development of this um this diet and so really how it works is that cardiac protection blend is providing um improved fatty acid utilization and cellular metabolism reducing oxidative stress and inflammation um and that's going to potentially impact these dogs longer term it is also optimal um protein content to maintain lean body mass taking into account a lot of these dogs may be suffering from sarcopenia with older age um potentially even cardiac heia if they are in congestive heart failure and it is also o moderate sodium restricted which is um going to be the recommendation currently from the ACB IM for dietary intervention so um this diet is appropriate for dogs that are in clinical congestive heart failure um but where we would recommend starting dietary intervention is earlier so in B1 when you hear the heart murmur um this is where we can start with nutritional intervention and so this diet is a complete and balanced adult Main formula so if there is an otherwise Healthy dog in the household this is phenomenal nutrition so it would be beneficial to feed this to an otherwise Healthy dog um or if you're thinking of some of those Cavaliers who are in stage a you know as long as they have um finished growing you can absolutely start them on this before they even develop a heart murmur considering their um genetic predisposition to developing mitro valve disease you might also be thinking well what about some of other cardiomyopathy dogs um all of the research on this uh diet really did focus on mitro valve disease but all of those cardiac protection nutrient principles are going to apply to other forms of heart disease so absolutely other cardiomyopathies cardiovascular disease in general or conditions benefiting from moderate sodium restriction are also indicated for using cardio care so um thank you very much for joining the lecture tonight thank you to Dr kotay and the cabm um and if you want to learn more about cardi care it is available to order you can reach out to your local territory managers if you have questions or want further information thanks so much uh Dr hartney and thanks again to Dr cot and to everybody for participating uh this evening uh the contact information for both of them will be included in the email I send out with the c certificates so if you've got um any follow-up questions uh you'll have their contact information uh lots of thank yous uh coming in here uh in the chat box great talk thank you so much um uh oh somebody has a question for you it looks here what about a 17-year-old dog in early kidney disease would it be safe I'm assuming that's a diet question yeah so Edie kind of comorbid ities you'll have to take those on a patient by-patient basis generally with kidney disease we often have to prioritize the kidneys so sometimes we have to look at different nutritional priorities and what can we intervene with diet and um what can we intervene with other forms of U medications or things like that so um I would say if you do have specific cases with comorbidities we do have our um Veterinary Resource Center which we offer free nutrition consults for specific cases because that might be a different answer depending on the patient um the owner's priorities uh you know just kind of like other lab results things like that so um please reach out to our nutrition Resource Center to get a nutrition case consult for specific patients that's great thank you uh okay I don't see any other questions coming in the chat box so um I think we'll be signing off 99116 that's great timing for Wednesday night it's not too late uh and I just wanted to mention too that our next um upcoming sessions are on March 23rd and 30th um following the Pet Care pathway through anesthesia and Dentistry case scenarios uh two it's a full day session split into two Sunday mornings with Dr Britney riby and Dr Jessica Pang and then on April 6th Dr Bigby is speaking again on extraction of the maxillary fourth preer and MERS and dogs um and those uh sessions are on our website my cat is about to jump right up here uh those sessions are on our website so if you want you can uh find those on our website to register if you're interested in those sessions and I think that's it I'm just double checking to see if there's any other questions there's my cat uh no it looks like we're good so that's it for this evening everybody thank you so much for participating and uh we'll see you all next time have a great rest of your evening bye thanks LZ bye everybody