Download Oh-no-the-heart-failure-cat

Oh no the heart failure cat! What now? – Rachel James
Summary
In this webinar, Rachel James gives advice based on her clinical experience in practice on how to
diagnose and manage heart failure cats. She highlights the difficulties faced in managing the
dyspnoeic patient and places emphasis on the importance of an appropriate environment and
avoiding stress in these patients.
Rachel explains that cats are often challenging patients to diagnose because they are easily stressed,
often tachycardic in the clinic, even if healthy, and they may present with no heart murmur.
Furthermore, there are no licensed treatments for the heart failure cat and only limited amounts of
information in the literature.
At the start of the webinar, Rachel considers the mechanics of heart failure and the cause of
dynamic murmurs that can be auscultated in heart failure patients. Rachel describes the different
cardiomyopathies encountered in cats, explaining that 85% of cats with heart disease have
hypertrophic cardiomyopathy. She clearly explains the differences between the two clinical forms of
hypertrophic cardiomyopathy; obstructive and non-obstructive forms.
Rachel explains her diagnostic approach to the heart failure cat, starting with a thorough clinical
exam before focusing on the heart, using auscultation recordings to explain what to listen for in
auscultation. She discusses the use of echocardiography, ECGs, blood pressure and radiography in
these patients and the importance of keeping the patient calm throughout the whole process. For
example, she explains that thoracic radiology is important in diagnosing heart failure, but will ideally
only perform x-rays in a stable patient. In the unstable patient, she advises only performing a brief
ultrasound examination to assess left atrial size, look for pleural and pericardial effusions, and
thoracic masses until the patient is more stable.
Finally she runs through many of the drugs used for treatment in cats with heart failure, providing
insights from her extensive personal experience.
Key Points
-
-
-
There is no licensed product for the treatment of heart failure in cats, all treatments are
prescribed using the cascade.
Hypertrophic cardiomyopathy (HCM) is inappropriate myocardial hypertrophy of a nondilated left ventricle that is occurring in the absence of an identifiable stimulus – in order to
diagnose HCM we need to rule out hyperthyroidism, hypertension, acromegaly and renal
disease.
There are a number of genetic mutations which predispose cats to HCM, particularly in the
Maine Coon and Ragdoll breeds, resulting in a wide phenotypic variance in disease which
makes determining effective treatments challenging.
Diagnostic investigations for heart disease cats include clinical examination and auscultation,
ECGs, echocardiography, radiography and blood pressure assessment.
It is very important to minimise stress in dyspnoeic patients and avoid sedation wherever
possible. This might mean it is not possible to perform radiography until the patient has
been stabilised.
-
Emergency treatment for the heart failure cat involves draining any pleural effusion, and
treatment with furosemide at 1-2mg/kg followed by a 1mg/kg dose hourly for two to three
hours.
Keywords
-
Hypertrophic cardiomyopathy
Dyspnoea
Systolic anterior motion of the mitral valve
Obstructive HCM
Non-obstructive HCM
Venturi effect
Dynamic murmur
Gallop sounds
Ausculation
Echocardiography
Radiography
Transcript
Thank you very much Wendy, thank you so much to webinar vet for inviting to me to come and
speak on what is a very favourite topic of mine – the cat in heart failure, what on earth can we do
now with them? I think as a foreword I would like to say to start with that I think cats with dyspnoea
are incredibly difficult, they are one of the most difficult clinical challenges that we face in practice
and they are not easy. So unlike dogs which can be helpful in heart failure when they have got fast
heart rates and you have got tachyarrhythmias etc. and we often have murmurs, we can have cats
that have very severe heart disease that have no murmur whatsoever and have no history of a
murmur, and they may have a gallop sound, they may not. Trying to decide a tachycardic cat vs. a
normal cat is very difficult because they are all tachycardic in the clinic. So these are a real clinical
challenge and what I hope to do tonight is to go through what I look for when I am looking at these
cats, what I personally do in clinic and how I treat them.
Ok, so what do we mean by heart failure? How are we going to diagnose heart failure in the cat and
then what on earth are we going to treat them with? Unlike dogs where we have a good body of
evidence based medicine now for treatment, in cats, things are really tricky. We still don’t have a
licensed product for the treatment of heart failure in cats so we are having to use the cascade and
go on treatments that yes are licensed in dogs, but not in cats at all. So the advice I am going to give
you tonight and the information I am going to give you is based on my clinical experience of having
treated cats in heart failure for the last 15 years or so – far too old these days!
So, thinking about our heart, we always think in very simplistic terms of the heart that it has got to
pump blood out, but we also have to remember that the heart has to be able to receive blood, it has
got to have that elasticity to be able to receive blood easily. So we are very familiar in dogs when we
talk about systolic failures, so the inability of the heart to pump blood out correctly. But we are less
familiar with the idea if diastolic failure, that inability of the heart to relax well enough to receive
blood. So when that left ventricle becomes very very stiff and tight, it then becomes difficult for the
heart to receive that blood, and if it can’t fill there is nothing for the heart to pump out. And when
the heart is unable to do this we then get the clinical signs associated with heart failure.
So those of you that listened to my last talk will remember my fantastic drawing skills and my ability
to draw superb diagrams on a computer, obviously incredibly proud of this one. So this is our normal
heart, so this is my little population of people that are sat on the mountain and they require water
that is pumped from this reservoir in to the heart and the water is pumped up the mountain and the
people are happy. These people at the bottom of the mountain, they live by this large lake and if the
water isn’t pumped out of the lake then the lake floods and these people drown.
So in very simplistic terms, when we have systolic failure, the heart is unable to pump enough water
up the mountain and these people die of dehydration and these people, because the pump has
failed and they are not able to get water in to the pump because it is full and can’t pump it out, then
these people drown. And it’s, you know in very simplistic terms, like that.
So when we are talking about heart disease in cats we are talking about cardiomyopathies. So
different to the vast majority of our dogs. So 85% of our dogs with acquired disease have valvular
heart disease, cats get the cardiomyopathies, so a problem with the muscle. And the vast majority of
these cats, well over 80% and in some papers as many as 85%, that cardiomyopathy is classified as
hypertrophic, so we have this hypertrophy in the left ventricle. Then we have got other pigeon holes
that we can put these cats in, we have got this one – restrictive cardiomyopathy, we are going to talk
about all of these later, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy
and then we have the favourite one at the bottom, the unclassified. And how do you class a
cardiomyopathy as unclassified? There is a discussion point in its own right.
Ok, so on to hypertrophic cardiomyopathy. Now how do we define this? HCM is inappropriate
myocardial hypertrophy of a non-dilated left ventricle that is occurring in the absence of an
identifiable stimulus, i.e. haven’t got hypertension, we haven’t got acromegaly, we haven’t got renal
disease, we haven’t got hyperthyroidism. So all of those things we have to exclude.
So this is the list that we will work through. So aortic stenosis, making sure there is not a thick
stenosis there, so a problem with the size of the aorta or the aortic valve. That we haven’t got
systemic hypertension so we don’t have primary hypertension or diabetes or Cushing’s. That we
don’t have any metabolic disorders that could induce hypertrophy, such as hyperthyroidism, the
classic change. And I think that it can be very difficult in these hyperthyroid cats to differentiate
between their cardiac disease because they’re hyperthyroid and cardiac disease because they have
concurrent hypertrophic cardiomyopathy. In a lot of these cases it is sometimes extremely difficult
to get their thyroid disease stable and you just about get them stable and you think oh that’s great
and they are taking their felimazole etc. and it is all good and then the disease changes and they
destabilise. Sometimes it can be very difficult to then say well their thyroid level has been stable for
a while now, has their heart disease resolved or not. In my experience, it is very rare for those cats
with primary hyperthyroidism with cardiac changes, it is rare for those cats to progress in to heart
failure unless we do something to them – i.e. we anaesthetise them for a dental and we put them on
fluids but then we give them a little bit of a volume overload that with the stress etc. that just kicks
them in to heart failure. So it is rare with just primary hyperthyroidism to have heart failure itself.
Certainly we have acromegalic cats and obviously cats with renal disease as well.
So these photos, thanks very much to Phil Fox for lending me these slides. These are some beautiful
slides from Phil showing the really variable phenotypic variability we have with this disease. And one
of the biggest problems that we have when we are researching in to this disease and treating cats
and doing research projects with them, is that we still don’t have a very good way of classifying
these cats. So we say they have HCM but there is probably a very different genetic variation, let
alone the phenotypic variation from one cat to another. So we may well have one cat that a specific
genetic mutation that causes it to have HCM and that genetic type may well have a very different
long term prognosis to another cat with HCM that has a different genetic fault. And we are very
much trying, in the research world, to try and identify these cats and try and group them in to how
they are going to do prognosis wise without any treatment. And then when we are trying to then
add treatment in to these cats and see how they do, if we could group them to say well, if you have
a cat with this specific type of HCM and we can then group them in a similar group then when we
give them treatment we can then judge the treatment as successful or not. It is trying to compare
apples and pears with a lot of these different cats.
So with HCM we talk about the two clinical forms. So we have the obstructive form which is the form
that gives us the nice murmur that identifies them. In humans if we look at the data it is around
about 25% of humans will have the obstructive form. When we look at cats, you know if we look at
the number of papers that have been published about cats, it is around about 40 to 42% of cats.
Interestingly in dogs, the vast majority of dogs that have this disease have the obstructive form, but
this is a rare disease in dogs. Then we have the non-obstructive form, and these are the tricky ones
because we maybe don’t have a murmur with these cats at all until maybe later on when we get
valvular insufficiency or we just get gallop sounds with them.
So HCM, the obstructive form, why do we get a murmur? And we have all been in this clinical
situation, when we are based in the consult room, we have a stressed cat, it is a difficult cat to
handle maybe, it is very difficult to auscultate, it is very wriggly or it might be aggressive etc and we
go I am sure I heard a murmur there, yep I definitely heard a murmur. You have to sedate the cat to
do anything with the cat and when the cat is sedated there is no murmur there at all. I remember
this as a new graduate thinking I am sure I heard a murmur in that cat, and this is why that situation
occurs. So we have what we call dynamic left ventricular outflow tract obstruction and that
obstruction is caused by abnormal movement of the anterior mitral valve leaflet in systole. This is
what we call this systolic anterior motion of the mitral valve. Now cardiologists, as many people are
aware, love abbreviating everything, we can have entire sentences as abbreviations, so systolic
anterior motion of the mitral valve I will now call SAM because it is easier. Typically with this
obstruction we get turbulent blood flow in the left ventricular outflow tract and we get a concurrent
eccentric jet of mitral regurgitation which traditionally occurs along that posterior wall of the left
atrium.
So if we look at the mechanisms of how this occurs, now we don’t know for sure how it occurs, these
are some of the theories that have been put forwards. So when we have severe hypertrophy of the
left ventricle, then we get abnormal papillary muscles, and it may well be that these abnormal
papillary muscles are malaligned now with regards to the septum, which then allows the mitral valve
leaflet here, the anterior mitral valve leaflet, to become displaced. And this according to various
researchers etc. who have done their PhD with this, have looked at this, and they really think that
the vast majority of this occurrence is due to these abnormal papillary muscles. The second theory is
that we get mitral valve malalignment, this might be a degree of mitral valve dysplasia that
predisposes these cats to getting systolic anterior motion of the mitral valve. Whichever way it
occurs we then often end up with this Venturi effect, and the best way to consider the Venturi effect
is when you are standing in the shower and you put the shower on, all of a sudden the shower
curtain sticks to your leg, and that is because of this Venturi effect. What happens when we have
this anterior mitral valve leaflet is that it is sucked or pushed in to the left ventricular outflow tract
here, causing this severe narrowing, and in effect an aortic stenosis, and we then get this curling of
eccentric jet that occurs around the posterior wall here, in to the left atrium. The mitral
regurgitation that occurs is usually fairly minimal, the major problem is severe turbulence. The
higher the heart rate and the more stressed the cat is, the more severe this obstruction will occur.
So you might be in the consult room and the cat may have a heart rate of 160 and it may have a
grade 1 or 2 systolic murmur that’s loudest over the sternal border. If you then hit the table hard,
and it always advisable to warn the owner that you are going to do that when you do it, and you
then increase the cat’s heart rate, you can maybe increase the grade of that murmur to maybe a
grade 4 murmur at a heart rate of 180 or 190. That is very classical for this disease. So this is what
we call a dynamic murmur and it can be very difficult for owners to appreciate that their cat may
have a murmur on some days and it may not have a murmur on others depending on its level of
stress and its heart rate. That is sometimes difficult for owners to get the concept of, especially
owners will often say ‘well what grade is this murmur?’ and you can go ‘well when his heart rate is
slow he may have no murmur or a very low grade murmur, when his heart rate is high his murmur
grade is high’. Owners often say ‘well is it a 2, is it a 3, is it a 4?’ and it is very difficult with these cats.
So again, these photos from Phil Fox, thank you very much for lending them to me. Hypertrophic
cardiomyopathy, the typical features of this disease are disproportionate hypertrophy of the septum
and this myofibre disarray or malalignment. Now we believe that we have this arteriosclerosis which
is a small vessel disease, interestingly if you take the left ventricle and it is hypertrophied, if that
hypertrophy is due to physiological change due to exercise and training then we get proportionate
coronary artery hypertrophy as well so we get a perfect between the number, quantity of coronary
vessels, and myocardium. However, if we get pathological hypertrophy, so the hypertrophy occurs
due to a pathological process, that then does not occur. And so then we have less coronary
vasculature per amount of myocardium. That puts the myocardium at massively increased risk of
hypoxic episodes and true infarcts.
So hypertrophic cardiomyopathy in our clinical cases, what do we see? Well we know it is the
commonest acquired heart disease in cats. We have identified three genetic mutations, one in
Maine Coon and one in Ragdoll cats. There are blood tests to look for these genetic mutations but
we know it is not the whole story. So we know that Maine Coon cats can have this genetic mutation
and yet they are completely phenotypically normal, i.e. they don’t have HCM, and equally we can
have cats with HCM but they are negative for the mutations. So unfortunately, a nice simple blood
test doesn’t work. HCM is rare in dogs. We know that we get excessive left ventricular hypertrophy
without dilation. We don’t know what the cause is but it is most likely to be genetic. The left
ventricular hypertrophy we know can affect the free wall or the septum or both. The extent and
distribution of the left ventricular hypertrophy is highly variable, and the extent and distribution
doesn’t necessarily correlate with prognosis either. All we do know is that left atrial enlargement
varies depending on the severity of the diastolic dysfunction and that left atrial enlargement is a
good prognostic indicator.
So the clinical presentations, again they are extremely variable and they range from the
asymptomatic cat with a heart murmur to a cold, recumbent, dyspnoeic cat. Again there doesn’t
seem to be a correlation with how they present and how they do. I think there are definitely, from
the research work that I am going to talk about later, it does appear that we do seem to have a
subset of cats. So we do appear to have these younger cats that can suddenly present at young ages
with a profound heart failure, they can be cold and recumbent and in a very poor state and very sick
cats. With correct treatment these cats can do extremely well and live for years on medication.
Equally we can have some of these older cats that present not too badly but they don’t respond to
treatment anything like as well as these younger cats. So it does seem we do have a couple of
different populations already from the research work we have been doing just recently. These cats
will often have an increased respiratory rate at rest, but these changes can often be very subtle, and
it can be very difficult for owners and vets alike to pick this up because these subtle changes are
going to be apparent at home and when the cat comes in to the clinic and it is a bit stressed they are
often going to have an increased respiratory rate, so it is looking for the changes in respiratory
pattern, and whether they have got changes in body position and whether there is dyspnoea or not.
Unfortunately, these cats often present at a very late stage, and one of the key things that I am very
passionate about is trying to echo these cats very early on, so that we can educate the owners about
the changes to look for changes we would see at a subtle point so that these cats present earlier
when they are just about to go in to heart failure or have just gone in to heart failure rather than
when they are extremely dyspnoeic. These cats will often present with acute onset lameness or
paralysis if they have got a clot. We see cats that will present with intermittent episodes of collapse
or syncope and indeed I saw a cat only yesterday, an 18-month-old cat that presented with a couple
of episodes of syncope, and that indeed was HCM. Unfortunately, we also have number of these cats
that will present with sudden death, often they have never shown any clinical signs at all of heart
disease, the owners just find them dead. I think that the sudden death scenario with this disease is
probably a lot more common than we think it is. Especially in the practices, as you all know, there is
often a notice about a missing cat etc. and I do wonder whether we have an increased number in
this population, just literally sudden death and not returning home.
So when we are taking a history from these cats, we want to take a good general history, we want
their vaccination status, worming status, virus status etc. We want to know their appetite and
drinking habits, have these changes recently? A third of cats that present in heart failure will present
with vomiting. Great, a vomiting cat. Respiratory rate, have they ever panted, have the owners
noticed this? Coughing, now years ago I would have gone nah, coughing in a cat is usually a sign of
respiratory disease, I don’t think that is true. I believe there are a subset of cats out there that will
cough because they are in heart failure, and I think it is probably more common than we think it is.
Now exercise intolerance, how do you tell in a cat? Now cats will often have subtle changes in
behaviour when they are just going in to heart failure, and you have got to really observe. The owner
will often come in and they will go ‘well he seems to be sleeping a bit more, he is not going outside
as much as he used to, he seems to be hiding a bit more than he used to, he doesn’t seem to be
playing as much’. Subtle signs but the behaviour changes are there if you have got an owner that
notices.
So, general clinical examination, the body condition score etc., the normal clinical examination in a
cat that we should perform every time. If we focus on the cardiovascular system. Mucous membrane
colour, you do have a number of cats that will present quite pale but it is not always reliable.
Femoral pulses, I am a big fan of femoral pulses, I want to know, are they bilateral, what is the
quality of them like, are they regular, do I have a pulse deficits, do they match, are they the same,
have I got the same strength of pulse in each femoral artery? Have I got cold extremities? Have I got
evidence of any thromboembolic disease? I want to feel that apex beat, I want to put my hands on
that cat’s chest and feel the heart. Does it feel big, how does it feel? Have I got chest compressibility,
always very gentle with this but could I have a chest mass there? Chest percussion, sometimes I do,
sometimes I don’t, if I am really thinking I have got a pleural effusion but most cats don’t enjoy
percussing their chest. And auscultation, are the heart sounds as I would expect for this individual?
Have I got a cat that is stressed and it has got a heart rate of 120? Oh my goodness, I am worried.
Have I got a cat and it’s got a heart rate of 260, yeah I am worried. Have I got heart sounds that are
really muffled? Absolutely that is a concern. So always, are my auscultation findings appropriate?
So when we are thinking about HCM, many cats will have auscultatory abnormalities but they are
subtle and difficult to hear. It is very important when we are auscultating our cats that we don’t just
listen on the sides of the chest, that we actually put our stethoscope on the sternum, literally on the
sternum, just to the left and just to the right. And that is where we are going to hear these dynamic
murmurs the best, that is where they are going to be the loudest. Gallop sounds are often there,
particularly in severe hypertrophic cardiomyopathy cases. Occasionally we will have crackles in the
lungs, but if you have got those you have a very sick cat. Dull lung sounds and dull heart sounds are
common with pleural effusion. Don’t forget that a lot of these cats with heart failure will often have
a pericardial effusion as well, secondary to their heart failure, which will muffle their heart sounds.
So here is the technology, let’s talk about these gallop sounds. Gallop sounds are something that we
hear in cats and they are quite common. Why do we get them? Well we get them because we have
literally such a stiffness in the ventricle, it is very difficult for these cats to fill their hearts with blood
from the atria so we get these very stiff hearts, so we are literally getting a sound as the heart if
filling that is just juddering and saying I can’t fill any more. So those atria are trying to contract and
push blood in and the ventricle is going no, can’t take any more. So these gallop sounds are, in my
experience, pretty much 99% pathological when I hear them in a cat but they’re quite difficult to
hear. So these are sounds from Jens Haggstrong’s book which I would fully recommend to everybody
and I could certainly send the link to webinar to tell you where you can get hold of this book. But
Jens has put together a fantastic book of all the different heart sounds that you would commonly
hear in our patients. Now these gallop sounds are made by a simulator. We start off with them very
slow, and they are there and they come and they go. So we starting at very slow speed and then we
go to medium speed and finally we go to cat speed. So hopefully technology is going to allow us to
play these. So here we have a gallop sound at a slow rate, and the gallop sound is gone, and it is back
again. Half speed gallop sound present. Gone. Back again. Cat speed. Gone again. And back. Ok, so
those gallop sounds, if we can hear those in a cat, we are happy with them, that is a good marker to
say we have cardiac disease and maybe the only marker that we have.
So when we are auscultating cats, sometimes we get a whole host of information about the cat and
it is sometimes very difficult for our brain to process it. So when I am auscultating my cat I really
want to break things down and say ok, because I get overexcited as a cardiologist when I hear a
murmur and I say ‘oh the murmur is great’ and then I forget to take a heart rate. So whenever I am
listening to a cat, I am going to say, ok what is my heart rate? Get a heart rate. Then I am going to
see whether I have got a murmur or not, yes or no? Then I am going to say have I got a gallop sound
or not, have I got abnormal sounds or not? And I am going to say have I got an arrhythmia or not.
Those are the bits of information I want to get from my auscultation and if I try and listen for them
all at the same time that can be really difficult and you will miss something. So it is always easier to
say ok, what is my heart rate, have I got a murmur, have I got gallop sounds, have I got an
arrhythmia? And listen to all of those things. In this particular one there are a few of these findings
that we are going to have, and this is a real life case that came in to the clinic one day. Ok, so that
cat, the first thing that I would note is that we have got quiet heart sounds, those are definitely
quiet, we have definitely got a gallop sound. Have we got a murmur? I think that, that is a very
difficult judgement to make with that heart sounds. I think we have, but I would say it is difficult to
make that call. The most important thing to take away from that is that we definitely have gallops,
we definitely have muffled heart sounds in that cat and we definitely know that cat is breathless. We
can hear its increased breathing rate and effort.
Ok, so on to ECGs. A large number of cats with myocardial disease will have abnormal changes on
their ECG. We get morphological changes due to chamber enlargement, yeah absolutely but that is
not the most important thing. We have a lot of conduction abnormalities with these cats, so a high
proportion will have changes. And we also have a high number of arrhythmias that are occurring,
ventricular arrhythmias including ventricular tachycardia, we can see atrial fibrillation. If you see
atrial fibrillation in a cat it is very bad news, it is bad. So atrial fibrillation in a cat, we know we have
got problems.
So this is a little cat, Benny, who came in to the clinic, and this is his ECG. I know that everybody
always hates ECGs but if we run through this we can say is it fast is it slow? Probably about normal
for a cat. Is it regular? It is certainly it is regular. Have we got a P wave for every QRS? Yep, certainly
looks like it. A P here and a P here and a P here. And have we got a QRS for every P? Yep, certainly
looks like it. But the ECG doesn’t look normal. And you know it doesn’t look normal because when
you turn it upside down it look more normal, so you are looking at it going this is not a normal ECG,
so what is wrong? So we can certainly see that our lead 2 should be upright, it is negative. And this is
a very classical pattern, when we have got positives in lead one, negatives in lead 2 and negatives in
lead 3. This is a conduction abnormality that we see with cats with myocardial disease. So we have
got a regular rhythm, it is a sinus rhythm, we have got a heart rate of around 155, we have got a P
for every QRS and a QRS for every P. The other finding that is really important with this ECG that we
can see, we’ve got out P, we have our QRS and we’ve got this real elevation of our ST segment here,
well above baseline. And that really signifies to us that we have probably got a degree of myocardial
hypoxia. Now that is not proven definitively in cats but that is what we suspect it is. So we have got
these changes here on our ECG. And as we said we have this conduction abnormality which is a left
axis deviation.
And that particular pattern is very common and we call it left anterior fascicular block. Now there
are lots of theories about why we see this conduction disturbance in these cats and people have
proposed in humans that we have these anterior and posterior fascicles that pass through the
corresponding papillary muscles, and if one is blocked then ventricular activation begins at the other
papillary muscle and moves across the myocardium. Whether this is a true finding in cats, we don’t
really know. What we do know is that when we see left anterior fascicular block, then it is very likely
that the cat has myocardial disease. And you know, 20-30% of cats with cardiomyopathy will present
with this ECG pattern.
Blood pressure. I think blood pressure is really important in cats. I think that it is something that we
are getting much better, as a group of practitioners, at taking blood pressure. And I think blood
pressure in our clinic is extremely common, all our patients will get blood pressure taken pretty
much at most visits. Traditionally we have always done forelimbs in cats but I think that there are a
number of cats that don’t like their legs being touched and are much happier with their tail. And as
long as you always record on each visit, the size of the cuff and where you have taken it from, the
blood pressure will always be comparable between visits. It is really important to use the correct
technique and be patient with these cats, have them in a quiet room, give them time to acclimatise,
do everything the same way each time with them. It is amazing when I look back at my patients how
consistent the blood pressure is, until we get a problem. So with any cat that we are diagnosing
HCM, we need to take a blood pressure to rule out hypertension in those cases, so we can make a
diagnosis. But I think the other important thing is the number of heart failure cats that are actually
hypotensive, it is actually a lot more common than we would give it credit for. And these cats, we
need to monitor their blood pressure. It is amazing, some of these cats will present and when we
measure their systolic pressure directly with Doppler, it will be around 75-80mmHg.
Now echo. This is the gold standard for making a diagnosis in cats with cardiomyopathy. It is really
important to have the correct environment and if you have that, you don’t need to sedate cats. This
is a picture of a little cat that came through one of the clinics that I visit. This was a very nervous cat,
we had two people very gently, we have got one handler here just very gently holding on to the leg
and supporting it and stroking the cat at all times, and then we have got a second person here very
gently just holding those back legs out of the way. The cat is not being pinned down at all, it is lying
down and being encouraged to lie down. If you have got that quiet environment without dogs
barking and people shouting and doors banging etc. in my experience the majority of cats are very
happy to have an ultrasound performed. This cat we can see has ECG cables attached, and again
these are attached to little pads, and these cats are often very happy to tolerate these ECG pads and
it’s not a problem for them.
So what do we find with these cats with cardiomyopathies. The left ventricular hypertrophy is often
asymmetric, and that is very classical. The basal septum is frequently affected and that big septal
bulge is common. We need to be careful because a lot of older cats will get that basal septal
hypertrophy as almost a normal old age finding so we need to able to differentiate those two things.
The classical change that we get consistently in these cats is these changes in the papillary muscles.
They are often hypertrophies, they are often hyperechoic, they are often irregular and patchy
papillary muscles, that is very common. The left ventricular hypertrophy, how do we say definitively
this is HCM? Well if we have got an ECG and we can be sure that we are in diastole, end diastole,
then we can say that if the wall measurements anywhere along those wall segments are greater
than 6mm then we have definitively got HCM. Now we often compare in different conferences
whether that should be 5.5 or 5.0, for me personally looking at the cat 5.5 would be my cut off, 6
and I would call it. But really at the end of the day, it is about how severe this cat’s diastolic
dysfunction is and how big the left atrium is that is key. I think two dimensional measurements are
really important and I think that using M mode in these cats can be really tricky because we have got
luminal obliteration, we have got asymmetric hypertrophy and sometimes it is very difficult to know
whether you are well aligned or not when you are in M mode. So some cats you can’t run an M
mode particularly well, and then we are going to run 2D measurements. The left ventricular lumen is
usually small, or normal, very rarely enlarged until we get to end stage. And the left atrial
enlargement is very variable, and that is mild to severe depending on the severity of the diastolic
dysfunction. And as I talked about earlier we can have this obstructive component as well.
So let’s get on to some videos and see some. So this is a cat with pretty severe disease, we can see
that we have got some severe asymmetric hypertrophy, we have got this enormous round left
atrium, we can see that we have got high left atrial pressure because this left atrium is bulging. So
this is a cat that is in congestive heart failure and this is a cat that we need to treat. We can also see
very subtly that we have got a very small amount of pericardial effusion here as well and that is not
uncommon in these cats with heart failure. This is how we would measure wall thickness. So we can
see at end diastole here and we can measure this septal bulge which in this cat is 6.3mm.
And these are a number of videos that we have got with various different cats. I know it is very
dangerous playing lots of different videos at the same time. But we can see with these cats the
variation in the different changes to the papillary muscles. So these are right parasternal short axis
views of the left ventricle in short axis. And we can see in this cat here that we have got these
hyperechoic lesions here and these very moth-eaten papillary muscles, again here we have got
hyperechoic papillary muscles and this bright endomyocardial border, and these papillary muscles
here are very large and tall and hypertrophied. So, a big variation phenotypically in this disease.
When we get SAM we get this classical, if we use colour flow Doppler, this is the left ventricle, this is
the left atrium, this is the aortic outflow here. We can get this severe turbulence occurring just as
this anterior mitral valve leaflet is pulled in to the left ventricular outflow tract here and this
eccentric jet of mitral regurgitation at this posterior wall of the left atrium.
Here is an echo loop of a cat that has got severe asymmetric hypertrophy, we have got SAM
occurring here because we have got this turbulence occurring in the left ventricular outflow tract
here and we have got this jet, this eccentric jet around the posterior wall in this left atrium. So the
left atrium here and left ventricle. So this pattern is very classical for these cats with HOCM (so
hypertrophic obstructive cardiomyopathy).
If we zoom in we can see that this is the left ventricular outflow tract here, this is the left atrium, this
is that anterior mitral valve leaflet that we can see in systole that’s curved upwards and we can see
this severe narrowing. These are mm markings here so we can say that this gap that we have got
here in the left ventricular outflow tract is about 3 or 4 mm because of this obstruction. So it is a
severe obstruction that occurs in these cats.
If we look at this in a short axis M mode, so this is the left ventricle here in short axis, this is the open
frog mouth view here with the mitral valve leaflet here and we cut through this, and we can see that
in systole when the anterior mitral valve leaflet should be closed, we can see it lifting up towards the
septum very beautifully here. If we zoom in then we see this anterior mitral valve leaflet lifting up
very clearly here in systole.
So what happens when we get this obstruction is that we get this dynamic left ventricular outflow
tract obstruction. And we get these classical dynamic envelopes on Doppler. So this is us looking
down the left ventricular outflow tract with Doppler. And we can see at the start that the valve is not
obstructing so much here, that we have got normal flow, and then as the valve obstructs, as we
progress through systole and we get more and more obstruction and the narrowing becomes more
and more severe so the blood flow through that obstruction gets faster and faster and faster until
we aa velocity of about five metres per second with such severe obstruction. We this classical shape
we get is classical for this dynamic left ventricular outflow tract obstruction due to SAM.
We can also see dynamic right ventricular outflow tract obstruction, this can cause a right sternal
border murmur. We don’t know the exact significance of why this occurs but it seems to occur in a
much higher frequency in those cats with left sided disease. Very rarely is it severe enough to
warrant treatment but we do hear this right sided sternal murmur. And it may be that’s all we hear
in these cats, we don’t hear a left sided murmur, we just hear the right sided one.
This is what this looks like. We have the aorta here, the left atrium, the right ventricular outflow
tract here, and we get this really turbulent jet as we have these high turbulent velocities. When we
look with Doppler, we can again see these dynamic profiles, where we can see the blood accelerated
at almost 2.5m/s in this cat, with normal being around 0.7 or 0.8. So, HCM.
So with dilated cardiomyopathy, Paul Pion who set up VIN, he discovered in the 80s that this was
secondary to taurine deficiency in the vast majority of cats. And this was prior to taurine being
added to cat food. Taurine is an essential amino acid for cats so if it’s not enough in cat food then
they become deficient. It is now actually incredibly uncommon, I very rarely see cases of it. The most
common time that we see dilated cardiomyopathy is usually the end stage of another myocardial
disease that might be a metabolic abnormality, toxicity or infection or maybe end stage of HCM, or
other cardiomyopathy. The features are very similar to those that we see in dogs.
We tend to see dilation of all four chambers, we see poor myocardial contractility and we often see
AV valve insufficiency. The changes don’t tend to be quite as dramatic as those that we see in dogs.
So this is a cat with dilated cardiomyopathy, this is the left ventricle, this is the left atrium and this is
the aorta coming up. A bit of an atypical view due to the fact that this cat was not the most
cooperative. We can see this very big, rounded, poorly contractile ventricle. If we do our end point
septal separation on M mode, so we take our M mode, we can see that we have got a big gap
between the top of the E wave and the septal wall.
On to restrictive cardiomyopathy, this is when we see a non-hypertrophied left ventricle, but we see
a very very enlarged left atrium. The theory is that we get a severe fibrosis of this myocardium, this
might be focal or diffuse. That might look on echo that we get these bright areas within the
myocardium itself or within the endocardium. We get profound diastolic dysfunction in these cats
and that is why we get the big atrium.
So here is a cat with restrictive cardiomyopathy and we can see we get this big septal bulge, not
septal bulge but we get this hypertrophy in the mid-ventricle and we get this luminal obstruction
and we get more dilation at the periphery. If we use colour with this cat then we can see we get a
mid-ventricular obstruction here, due to the changes within the myocardium.
So thoracic radiology, really imperative for diagnosing heart failure but that said I don’t like to X ray
dyspnoeic cats unless I absolutely have to. So I would use ultrasound in these cats and when I am
looking at ultrasound in an emergency situation, I want to answer the questions has my cat got a big
left atrium – yes or no? Has my cat got a pericardial effusion, yes or no? Has my cat got a pleural
effusion, yes or no? Has my cat got a thoracic mass? If I have got a dyspnoeic cat and the answer to
all those questions is no, then it is highly unlikely that I have got a cat that is dyspnoeic because of
heart failure and I would probably reach for the steroid bottle in an emergency situation or I would
go and take a chest X ray. If I have got an answer of yes to those questions, then my pleural effusion
I need to get drained, my pericardial effusion is very likely to be secondary to heart failure, if I have
got a big left atria I am going to treat the heart failure, get my patient stable and then I will take a
chest X ray, 24 or 48 hours later when I have got a stable cat. When we look at these chest X rays,
cardiogenic pulmonary oedema in cats is very variable. There was a beautiful study written up in
JSAP where they looked cats with heart failure, or supposedly heart failure with lung patterns, and
they found that there was not particularly great correlation between the cardiologists themselves,
the diagnostic imagers, interns and residents. So it can be very difficult to tell with these cats, is that
lung pattern oedema or is it something else? A classical example in cats I have seen that look like
they have cannonball masses, you would think that they have mets everywhere, and actually it is
just areas of pulmonary oedema, so they are difficult. The classical triad of signs we would look for
would be an interstitial / alveolar infiltrate, cardiomegaly, pulmonary venous congestion. But don’t
forget with cats, a lot of these cats don’t have significant luminal dilation so their hearts on chest X
ray may not look particularly spectacular, especially when compared to dogs, so they are tricky.
The majority of our cats that we see with congested heart failure will obviously have a significant
interstitial pattern. So this is a cat with heart failure. We have got a really big heart with this cat and
an increase in interstitial pattern here. And post furosemide treatment we can see that we have got
a significant reduction in cardiac size.
Akiyama came up with a beautiful analogy a few years ago when he presented at BSAVA. When if
you think of a cat’s heart when it looks like a boiled egg, that’s a normal heart, when it looks like a
strawberry, that’s an abnormal heart. Even when a cat’s heart doesn’t seem to be that big, if you
have got that change in shape you need to be concerned. So this classical left ventricular
enlargement, when we get these very tall hearts in these cats, is something that we are very
concerned about. We get this left atrial enlargement and left auricular appendage enlargement
here. So left atrial enlargement here, left auricular appendage. We get this classical Valentine
shaped hearts, these very wide hearts. We can see in this cat that we have got this enlargement
here as well.
So, treatment of cats. First and foremost, don’t stress a cat, you want to do the absolute minimum
for these cats when they are very breathless because they will not only threaten to die, they will die
if you stress them. So we want a very brief echo, if they have got a pleural effusion we want to get
that drained. We want to give the furosemide, 1-2mg/kg initially, if you can get an IV line without
stress great, if not give it intramuscularly. Get it on some oxygen and leave it alone in a quiet, dark
area with that furosemide on board. Then give that cat 1mg/kg of furosemide hourly for maybe two
or three hours until we get respiratory rate under control. Nitroglycerine cream? Absolutely, an
eighth of an inch. If we have got a hypotensive cat and it doesn’t have a really loud murmur so
maybe no murmur or soft gallop sounds and it is a really hypotensive flat cat then I have certainly
used IV pimobendan extremely successfully. If we have got a loud murmur in these cats then we
have probably got severe hypertrophic obstructive cardiomyopathy and therefore I would be really
cautious about using pimobendan in those cases, those are really a judgement call for a specialist.
But if we have got a cat, it is a low blood pressure, it is very dyspnoeic, and it doesn’t have a loud
murmur, then I would be more confident to give pimobendan. I have used it in cats extremely
successfully, obviously it is not licensed but it works very well in those hypotensive cases.
So our treatment options. We have got furosemide, and ACE inhibitors, and beta blockers, and pimo,
and spiro, and aspirin… What are we going to choose? Let’s go through some of these.
So furosemide, it is the most important drug in cats without question. It is one of the few drugs that
we know works. We don’t need to do a trial because we know it works. It is extremely potent but
always be careful, never give a bigger dose than 2mg/kg. Remember that these cats are relying on a
high pre-load, so high pressure forcing blood in to that heart to get that heart filling. If we take that
away with too much furosemide too quickly then we are going to send these cats tachycardic and
hypotensive. But we can use 1mg/kg hourly thereafter to control respiratory rate, I really don’t feel
comfortable with more than four doses but sometimes we need to. But remember that cats are
really really sensitive to furosemide, or the vast majority are, compared to dogs. And we will get
severe, profound hypokalaemia with these patients, and if we are having to use reasonable doses of
furosemide, you need to start supplementing with potassium. Don’t wait until they become
hypokalaemic, because a cat that wasn’t eating, when it’s hypokalaemic it’s really not going to eat,
so we need to be on top of that potassium level from the start and be aggressive with it. Giving
potassium, usually I use Kaminox, it works very well, Tumil-K, if only, I wish it was back on our
shelves, but be aggressive with your potassium, if you give too much they will pee it out.
ACE inhibitors, lots of theoretical benefits, there is no evidence based medicine yet to say that it
works in cats. Personally I think that it works very well. Again, always careful with left ventricular
outflow obstruction cats, so these cats with a very loud murmur, we need to be careful. Phil Fox did
a trial that he presented years and years ago at ACVIM where he took four groups of cats with heart
failure secondary to cardiomyopathy, he gave a quarter of them an ACE inhibitor, a quarter of them
furosemide, a quarter of them had atenolol and he said ok how did they get on, and a quarter had
diltiazem. Ones that just had furosemide did ok, ones with the beta blocker and furosemide did
worse and the ones that did best had the ACE inhibitor and the furosemide.
Be careful on your dose. If we have a hypotensive cat we need to be very very careful with using ACE
inhibitors at a big dose. We are very familiar with ACE inhibitors, we use them a lot, we feel very
very comfortable but they are a potent drug and if your cat is relying on its RAAS system to maintain
its blood pressure and its blood pressure is only 90 and you give a big dose of an ACE inhibitor, you
can plummet that blood pressure and send that cat in to hypotensive and tachycardic. So be careful,
start off with a low dose and increase carefully, watch the renal function.
Pimobendan. The retrospective studies of pimobendan have been quite promising, but again be very
careful with cats that have got significant left ventricular outflow obstruction. They do feel better on
it, they do feel good on it but just be, case selection I guess.
Spironolactone, this is an aldosterone antagonist, we really think that a lot of cats with
cardiomyopathy have a lot of fibrosis, if that is true then the spironolactone having its anti-fibrotic
effect should be beneficial.
We looked at, we have just presented the results of this SEISICAT study, this was the safety and
efficacy investigation of spironolactone in cats with congestive heart failure secondary to
cardiomyopathy. This was a double-blind, randomised, prospective, placebo-controlled, multicenter
clinical study. I was the lead author on this study.
And what we did was we took a population of cats with congestive heart failure secondary to
cardiomyopathy, we looked at the safety of spironolactone, the pharmacokinetics of spironolactone
and the efficacy.
Now, the first and most important thing to say with this is that this was a pilot study, we looked at
20 cats. We showed the spironolactone was well tolerated, we showed that it was safe, we showed
that the pharmacokinetics appeared to be similar to those in dogs and predictable. Once a day
dosing was very adequate in cats with a dose rate of around 2mg/kg. Once daily with food. We did
see a significant difference in the survival of cats in the cats that there had been given
spironolactone, furosemide and ACE inhibitor, compared to those that had only been given ACE
inhibitor and furosemide. But, although there was this difference in survival and it was quite a
profound difference in survival. In the treated group we didn’t have any cats die in the entire length
of the study which was 60 weeks with cats with HCM. In the placebo group, none of the cats in the
placebo group made it to the trial at all, they all died within the study. So there was a big difference.
But unfortunately, despite our randomisation and also the way that we stratified these cats, there
was a slight difference between the two groups. So we need to be careful when we are interpreting
the results. On the face of it, it looks like a fantastic drug, but until we get a bigger study we can’t say
for definitive reasons that it is definitely the drug to use. But I think that there is enough evidence in
this study that it is likely that spironolactone will be beneficial in these cats and therefore I would
always use spironolactone in cats when they are in heart failure.
As we said before, potassium supplementation, it is really important. Hypokalaemia will certainly
lead to weakness and anorexia and arrhythmias. As I say, Tumil-K.
Now atenolol, heart rate control it is very good at. I personally don’t like using the tablets because I
think that the dose that we get with those tablets is not small enough. I think you can give cats a
much smaller dose of 1mg/kg twice a day and that is often enough to maintain heart rate in the level
that you would like it at. And if you use the syrup you can titrate up very easily. It certainly will
reduce left ventricular outflow obstruction, but the study that was performed by Cast and Shaver
and others didn’t show a benefit of using (sneezes – pardon me) when the study that Cast and
Shaver and other used, when they looked at a five year study looking at the use a atenolol in cats
they didn’t show a long term benefit to the use of atenolol. So, is that because their case selection
wasn’t sensitive enough? I don’t know. I suspect there is a subset of cats that do respond well to
beta blockers but equally there is a subset that don’t. Never ever use it when you have got an animal
in heart failure, only ever use it in your non-heart failure cats or you stable heart failure cats and
always titre up very carefully.
Diltiazem, this is bizarrely the only licensed product for these cats, it is supposed to have positive
lusitropic properties. However, diltiazem has a very variable pharmacokinetics in cats, some cats will
get a therapeutic dose from the normal dose range, and other cats if you give them the normal dose
range will not have any therapeutic range at all, so it is very variable from one cat to another. You
can see side effects with it. It is a useful drug to control heart rate in certain individuals, but it does
need dosing three times a day and that is difficult for owners to do. In a recent study there was no
effect on survival time in cats with severe hypertrophic cardiomyopathy and heart failure when
diltiazem is used.
So clopidogrel, this is useful to try and prevent thromboembolic disease in cats, it inhibits platelet
aggregation. It appears relatively safe. And the FATCAT study that has just been published showed
that there was a benefit to survival with cats using Plavix over that of aspirin. In those cats they also
had a longer time to repeat thrombosis compared to the cats given aspirin. So we know this works
quite well. Unfortunately, it tastes absolutely foul, it makes metronidazole look positively tasty. They
will drool for up to half an hour if you don’t get the tablet down. So unless you have got a very good
owner who is very good at tableting, always use gelatine capsules with this drug or alternatively
wrap the tablet in butter and help the tablet slide down.
I still use aspirin, but I use low dose aspirin, so a quarter of a 75mg tablet every three days. It does
work. We sometimes see gastric ulceration and GI upsets but generally I think that those are
minimal side effects now at that low dose.
And, hopefully, just about run to time. I would be delighted to have any questions. Thanks for your
attention and I will wait to hear. Thank you very much.
Wendy: Excellent, thank you very much for that Rachel, great presentation as always. Let me just
have a look to see if we have any questions, sorry I am still navigating this new software. Excellent. I
think most people have got used to the new software so that’s great. I think most people have
managed to connect ok. And I think that one of the highlights for me was listening to those heart
sounds, Rachel. I think you and I got quite excited earlier with the technology. I didn’t realise quite
how sad I am. But anyway it made me very happy so we have got a few questions come in. Chris has
asked what stethoscope did you use to capture those beautiful sounds with?
Rachel: Well the first was one that Jens Haggstrong lent me, the second one is a new stethoscope
from Cruise, the thinklabs, and it is a fantastic electronic stethoscope, it is really good. I think it is
getting close to now where vets in practice will be able to record at work and then email heart
sounds to cardiologists and go what do you think of this? It is a fantastic stethoscope. I have been
working with Cruise with it and I love it, it is absolutely superb.
Wendy: Excellent, thank you very much, and just a reminder to everyone if you haven’t already
voted in the RCVS election, all you vets and RVNs out there, you have got less than 24 hours. That is
my little plug. Back on to the questions. Michael has said great webinar, and he has said I am
treating a cat, presented yesterday, with acute onset diabetes mellitus and has what I initially
thought was neuropathy in the hindlimbs, he also has severe osteoarthritis in the stifles. He is
responding to insulin and corrective fluid therapy. He has weak femoral pulses, especially left hind.
His mucus membranes are poorly oxygenated, heart rate of over 180. I suspect he has significant CV
problems, and he question marks HCM. Do you have any suggestions for treatment and further
investigations?
Rachel: Absolutely, I think Chris Little published a paper a few years ago in JSAP which showed that
diabetes mellitus has a high incidence of cardiomyopathy in cats. I can’t remember the exact details
of the paper. But my own personal experience of cats with diabetes, I do think that they do get
cardiomyopathies. Whether they get HCM or not depends on the cat itself. Certainly I would use ACE
inhibitors. The biggest problem you’ve got with these cats is that using fluids that you want to
correct and help the cat correct its pH and diabetes, but that again is giving the cat preload so it right
on the edge of heart failure. If you give fluids then that fluid is going to accumulate in the cats lungs.
So you want to try and reduce your fluids as much as you can and ideally get them off fluids as
quickly as you can. Ideally get these cats eating. And then be very careful with the low dose diuretics
to try and improve reduce your pulmonary oedema. And then using ACE inhibitors. I think that ACE
inhibitors are very beneficial in diabetic cats. And depending on your cat’s blood pressure depends
on how much should be using.
Wendy: Excellent Rachel, we have got a few more questions come in so are you ok to hang on for a
little longer? Excellent. Correct answer. Let me have a little look. Heather has asked I have a cat
which presented with chylothorax that was hyperthyroid at diagnosis with cardiac changes on echo.
From what you have said, does this mean that the cardiac changes are unlikely to be secondary to
hyperthyroidism and he has gone in to heart failure, if this is what is causing the chylothorax?
Rachel: Yeah, absolutely. I think that is a really good point. I think that when we see chylothorax with
cats in heart failure then yes I think that it is very likely that it is the heart failure. And the
hyperthyroidism is not helping and it is probably adding to it but I would say in my opinion that it is
very likely that is heart disease with hyperthyroidism over the top. Obviously you have got to correct
that hyperthyroidism. I think that in many cats that have got hyperthyroidism and heart failure, you
need to be very cautious on the amount of felimazole you are using in these cats, and just give half
the normal dose that you would start with and just see because they are often very sensitive.
Wendy: Super, thank you. We have a question from Robert and I am not sure exactly what it relates
to or if it will make sense to you. Robert is asking what about morphine, now I am not sure if that
relates to anything in particular before?
Rachel: I am not sure, in response to sedation maybe?
Wendy: Yeah, Robert if you could perhaps type in some more details about that question please so I
can ask it again. I didn’t see at what point that question came in so I can’t relate it to a particular
point, sorry about that Robert. We have another question here, have there been any trials using
Upcard, the new loop diuretic for dogs?
Rachel: Not that I think that have been officially published. Personally I have used Upcard a number
of times in cats. I do think like dogs there are a number of cats that become resistant to furosemide.
And even a number of cats that I think present that come in and just do not respond to furosemide
as you would like and yet they do respond extremely well to torasemide. Before upcard came out I
actually used to use torasemide syrup that you can get formulated and I think that is still something
that is a good choice to use in cats that cannot use tablets. And unfortunately you due to time
constraints I didn’t go in to using liquid products in cats. I am a great fan of using liquid products in
cats, they work very well. I use atenolol liquid, I use furosemide liquid and I use spironolactone
liquid. And you can put all of those in the same syringe as a cat cocktail and that can work extremely
well for the cat. So yes, torasemide I certainly use in cats, I tend to use it twice a day in cats rather
than once a day. And I think it does work spectacularly well, but again you do need to be careful with
your potassium levels.
Wendy: That is super, thank you so much for that Rachel. Really great presentation from you as
always. So excited with those sounds. It’s great. And I think you mentioned about perhaps doing
another webinar for us soon covering murmurs, now that we can hear those heart sounds.
Rachel: I think that would be just so much fun. Just to do an hour of heart murmurs. It would be
brilliant. I would be delighted to do that.
Wendy: That’s brilliant. Thank you everybody for your patience with the new software, hopefully it is
going to be a great move forwards for us. I know Rachel is very excited about the sound function but
there are other functions to hopefully make it a better experience for you all. Robert has just typed
in more about the morphine question so you’re not quite released yet Rachel. Here we go, Robert
says, morphine not recommended for use in cats. Has been recommended to quieten hyperstressed, dyspnoeic cats in acute CHF.
Rachel: Yeah, to be honest I don’t tend to sedate my cats, I tend to try and put them in a really quiet
non-stressed environment and let them settle themselves. I think morphine in cats, it can make
them hallucinate and make them stress and panic more. I can’t actually remember the last time I
sedated a cat. If I do sedate a cat it is usually with butorphanol rather than morphine but again it’s
not something that I really do with cats. If I have a cat that I can’t get near and that I have got to
drain a pleural effusion with it’s a really stressed cat and it is dyspnoeic, and if I don’t drain its
pleural effusion it is going to die, I tend to use a box to pre-oxygenate them with. So I put them in
the box, pre-oxygenate them with maybe 15 minutes of time just filling that box with oxygen and
leave them in there with a high flow rate going through and then I will literally just switch on
sevoflurane or isoflurane (ideally sevoflurane but iso if you haven’t got it) and those cats are gassed
out very quickly and then you have got your cat asleep, it is well oxygenated, it gives you some time
to get that effusion drained, get an IV line in, get the cat stable before it wakes up. And I would
rather do that for the really awful stressed ones that I can’t get near rather than give them sedation
and potentially make them more stressed. But I think the secret with cats is all about the
environment, it is getting them away from the dogs, it’s keeping them quiet, it’s keeping them in a
quiet safe environment, often in a darkened room and they are, you know, much much better.
Wendy: Excellent, thank you very much for staying on and answering those questions Rachel. I think
that is it for now. Rob has said thanks, very helpful for your previous answer on his question. So you
have answered everyones’ questions, unless you are very quick on a keyboard I think we will start to
draw this webinar to a close.