Hello, Thank you for joining us today. I'm Shelly Gunther, sonographer and clinical marketing manager at Clarus. I'd like to welcome you to today's live webinar, and what a way to end our 2024 webinar series.
Joining us today are esteemed guest speakers doctors CERN Boyen and Serge Chalo. Now today's topic is pulmonary hypertension in crisis. Can pocus save the day?
We'll have a lively debate about pocus and whether it's a game changer for diagnosing pulmonary hypertension in the unstable canine patient. Now, before we start, I'd like to thank the vet Cho and Nav C for inviting you all to join us here Today you're among just under 2500 veterinary medicine enthusiasts who registered for today's popular event. This webinar is race approved thanks to the vet show, so please do stay on for the full session to qualify for one CE CPD credit and by participating for 50 minutes or longer, you'll receive an email from the Vet show in the coming week to redeem your educational credit.
Now, after the main presentation, I'll do some live scanning with my dog Mabel, a six year old Wheaton terrier, and at any time during the Webinar, you can use the Q and a box at the bottom of your screen, and doctors Boyen and Chao will be able to answer questions during the live Q and a session after the presentation. So I'll be your host today, and I'm really looking forward to this presentation. I always learned so much from these two doctors.
Now I'll set the stage by sharing a paper I came across. It's a nice study from the frontiers of veterinary science that describes the value of focused cardiac ultrasound, or FCU to diagnose pulmonary hypertension and assess its severity. In this study, the authors talk about how moderate to severe precapillary pulmonary hypertension is typically associated with clinical signs and negatively impact survival and how prompt recognition of PC PH might benefit affected dogs, resulting in earlier intervention and possibly improving their quality of life.
Using focus cardiac ultrasound assessments. Examining five different parameters, they conclude that moderate to severe pulmonary precapillary pulmonary hypertension that's a multiple can be detected with good accuracy by non cardiologists. Now we just like to put out a quick poll before we get started just to figure out where everybody's at and get to know our audience a little bit better.
And what do you see as the key advantages of using ultrasound in your practise? Is it for improved diagnostic accuracy? Are you even doing ultrasound at your practise, or are you just looking to increase referrals?
Just give you a couple of more seconds to complete the poll. 321. All right.
Most people are using ultrasound, which is fantastic. And, most of you are looking for improved diagnostic accuracy, so this is gonna be great for you, so stay tuned. All right, So now I'd like to introduce our guest speakers for today.
Doctor, Son Boyen is considered a leading expert in all things veterinary Pos. He's the winner of the 23 2023 Jack Marrow Scientific Achievement Award. Advances in point of care Ultrasound.
The co-founder of veterinary emergency and critical ultrasound Working group. VECC US. He's co-lead on the veterinary pocus.
Consensus statement documents co developer of the Calgary pleural lung and ultrasound approach to the pleural space and lung and primary. Author of the original 2004 small animal fast Exam. He is currently employed as full professor at the city of Calgary, where he continues to do research and develop focus techniques.
Doctor Serge Shaloub also joins us from the University of Calgary, where he's been a faculty member of veterinary medicine since 2021. Doctor Chao was the recipient of the 2021 and 2013 Canadian Veterinary Medical Association's Teacher of the Year award and 2015 University of Calgary team Teacher of the Year Award, the 2017 Carl J Norden Distinguished Teacher Award and is a 2024 3 M National Teaching Fellowship recipient Recognising Canada's outstanding teachers. He's also authored and co-authored numerous scientific articles and book chapters on veterinary pocus.
So, as you can see, we are in very good hands today. Gentlemen, I will hand the presentation over to you. Thank you so much, Shelly and hello, everyone.
Welcome back. It's exciting to be here. I'm Serge.
I'm sir and sir what are we gonna be talking about today? Kidneys. No, we're not gonna talk about the kidneys.
We did that once. That was enough. Once is enough.
When it comes to the kidneys, we're gonna focus on pulmonary hypertension and how we might use pointy care. Ultrasound to help us come to a suspicion or a suspected diagnosis of pulmonary hypertension. Wait.
Pulmonary hypertension with pointy care. Ultrasound. Who?
Well, let's go through and see if we can sort this out and whether it truly is helpful or not. OK, well, triage. We got a dog coming in.
It's piccolo. Seven year old female spayed French bulldog comes in for acute collapse. I'm looking a little less stressed than usual.
I don't know. You look both confused and stressed there, but also came in with a three week history of cough, exercise, intolerance and increased effort. Breath.
OK, well, that's already concerning. I'm starting to run in the opposite direction. But, you know, hearing you talk over the years, I know we shouldn't do a full physical exam that last two hours.
Drink or coffee? We should do something called A a what? Now?
Exam. So we're going with the triage exam, and, we'll come back to that. We'll, talk about triage, Po, But let's talk at our triage exam to start with, OK?
What do you think of our initial vital sign? Well, that heart rate would be great if it was a cat once again. Is it a cat?
Look at it. Does that look like a cat to you? I mean, it does look like an alien from outer space.
So this is 168 and the dog. We are worried. Respiratory 48 temperature 38.
Well, temperature is OK. That respiratory rate is a little high, you know, But, seeing that this dog is anxious and definitely effort way more important, definitely seeing an increase in effort. Oh, I'm a little worried here, all right.
And so you should be. We'll look at the mucus memories. Refi time.
They both look OK. Yep. And strong from old pulses.
Happy. 000, here it is. We got a grade two out of six left systolic heart murmur, harsh lung sounds of crackle.
CERN. You know what? My preliminary thoughts just thinking about this.
Hold on. I think this is getting me to get some chess rads. Send it to the cardiology service.
It's 4:30 p.m. Anyways, on a Friday I'm out of here.
I'm gonna be home for dinner. OK, so let's wind this back. What did we teach you 20 years ago?
When you were a vet student, Stable or unstable? Is this dog stable? Did you teach me that?
I'm pretty sure I did. Do, the dog would be unstable. Respiratory.
All right. So I would agree with you. And in that case, do you want to send it somewhere away from your resuscitation area to a specialist in a different room or a different area of the hospital?
That sounds like maybe a bad idea. This is a bad idea. Let's bring the machine to the patient.
We do not want to get rain gras in this patient. We could stress this patient. In essence, don't make the walking dis Nick the walking dead.
Is that a song? No. No.
Ok, well, OK, wait a minute. All right, let's back it up. You said unstable, right?
Unstable. Don't take X rays. Don't stress it when it's unstable.
Ultrasound for the assessment of our patients is very valuable. So we have respiratory distress. I think you and I agree that that's one of our primary problems here, right, I would agree.
We've got respiratory and the other big thing that we noticed If we if we look at the little summary down here. We had a history of sudden collapse. So syncope is another big differential that we want to work up.
So hold on. Syncope probably has 622.6 different differentials that it could probably talk about for the next 48 hours.
Actually, no, I would say not that many syncope has a number of differentials, as you can see here. Not as many as you usually go through When you, talk about your internal medicine cases, but yeah, syncope. We can have multiple different causes, as you see here.
Cardiac vasovagal, situational or cough induced what we call tussive collapsing trachea. In that sense. Y, hyper hypertension, cardiac, intra canals, a pericardial fusion heartworm and, of course, neurologic conditions.
Potentially, this was a seizure, so that makes a lot of sense. Respiratory distress. Though.
You and I love this, I I like it because it's relatively simple. There's, like, three categories. Yeah, So we're gonna start big.
There's lots of, smaller categories. When you think about, we're gonna think about cardiac, pulmonary and plural space as our big causes. Of respiratory distress.
And then we'll narrow those down as we start to gather a bit of information. You know what makes me really excited here on all of these lists or on all these lists? We cannot blame the kidneys, huh?
We are the kidneys. We are, 0, 3040. I give All right, OK, in all seriousness, though.
But obviously it's not the kidney's fault. Now I'm thinking about clinical signs for pulmonary hypertension. Are there any any defining clinical science?
Something that's a go to and a for sure thing. Yeah, So if you go back and you think about those differentials we had one of the big ones we were working up with syncope and not everybody associates. Pulmonary hypertension with syncope.
Those two things don't always correlate. Good point. So let's look at some of the literature out there.
Then you can see this is a study by the creo of Belgium. If we look at this study here when they get a severe pulmonary hypertension, they had 29 or 30 cases in this case. And if you look at the number that syncopy they had 16 of these cases had syncope, So actually, more than 50% of these patients had syncope, but not 100% not 90% like 50%.
So that that's kind of the tough thing. And I wonder if that's the reason why we don't always associate it with, pulmonary hypertension, Is that it? A lot of other things can cause syncope.
So let's look at, other things here that we could talk about here. So other clinical science. We have two studies here talking about different things.
So syncope in that first study, the clinical features outcome of 25 dogs, syncope, 64% with cough and just a little over half. Yeah. So, again, what was the most common cause reported in that particular study by, JB M syncope.
And if we look at another study, another one by the crew out of Belgium, they've done a lot of work on pulmonary hypertension. This is sort of one of the, go to centres for pulmonary hypertension in our veterinary patients. You can see again.
Then, once it got severe, they only had 10. In this case, it were severe, but they still had or 20. Sorry, but they still have eight cases of syncope out of 20.
So close the picture. You see, so syncope is definitely a common sign seen with our patients that are coming in with pulmonary hypertension, something we should definitely be thinking about. Patient comes in with syncope.
Pulmonary hypertension should be on our list of differentials, so pulmonary hypertension syncope should be thought as together. So let's think about the classification of pulmonary hypertension. It's not as simple as we previously thought.
Yeah, this is where it gets complicated, and this is a nice paper. This is a very common, comprehensive, consensus paper that came out by JIM. And you can see that if you look at the classification, it's defined as an increase in pulmonary vascular pressure, so that's pretty easy.
Increased pressure in the pulmonary vascular makes sense to me subgroup into six, and this is where it gets quite complicated. You have to think about the six pulmonary hypertension left, heart disease, respiratory disease, hypoxia, pulmonary thromboemboli, a big one that we tend to look for in the IC U and our critically ill patients. Parasitic disease.
A bit unique to are veterinary patients compared to people, but, diver and and strong. And then disorders that are multifactorial are unclear. So six big groups.
But there's a way to make this a little bit easier when it comes to thinking about pulmonary hypertension. Because this could be a bit overwhelming when we're thinking about six. Yeah, let's divide it actually, into two broad categories.
Precapillary and Postcapillary. I know Shelley was talking about that in that paper. And both are issue of increased pulmonary hypertension.
It's an interesting way to think about it, because when we think about postcapillary pulmonary hypertension, what are the main groups that we're going to see in there? Yeah, So we're thinking about those with left sided congestive heart failure or those that are unclear that still have signs of increased, pulmonary wedge pressures or increased, capillary pressures. So these are ones that are going to be left sided heart failure.
So this is a nice way to think about that postcapillary. We're thinking about problems on the left side of the heart right now. Probably the most common group is gonna be the precapillary pulmonary hypertension.
And that's gonna be all those groups, except for group number two And in here, we have a normal pulmonary tear wedge pressure. And there's a lot of different causes which have already outlined lung pintal disease. I think that's a big one.
We tend to think about hypoxia thromboembolic disease, parasitism, et cetera, et cetera. So lots of different things. So, CERN What I'm thinking at this point is we stop already.
We stop again, and I think it's time to do that rectal exam which denied me during that triage exam, you know, and maybe do AC T MRI right now, eight o'clock at night. So did we decide our patient was stable or unstable? I can't remember.
So our patient was very unstable. We had respiratory distress. We had tachycardia.
We didn't have a patient that looked very good. So we are actually going to come back and talk about working up pulmonary hypertension in the unstable patient on the menu. We're going to talk about the approach to pulmonary hypertension on triage.
Thank you. Triage being the big word there. What pocus can do for us with pulmonary hypertension?
What changes will we see with point of car sound? And then we'll talk briefly briefly on treatment and prognosis, because you saw how many categories There are. You can see that that, prognosis is gonna vary tremendously depending on the underlying disease.
So we're not gonna spend a lot of time on treatment and prognosis, but we will touch briefly on it, particularly with regards to Piccolo. So you're telling me that point of care ultrasound is gonna save today Live to pocus, pocus the limb? Here we go.
Absolutely. Look at that. It's no hocus pocus.
This stuff is real. So let's go ahead and talk about it. So, like you said, we don't We wanna do a whole bunch of different tests.
This patient is unstable right in front of us. We want to do Min Meg database. What do we got?
So part of our minimum database is pretty common. We're gonna get cysto, systolic, Doppler blood pressure, 100 and 26 millimetres of mercury. In the case of Piccolo, we're gonna put an ECG on, as we saw it as one of the causes or participant underlying, contribution to syncopy.
We might have an arrhythmia. Sure. So ECG makes sense.
There's our ECG. What are we looking at? We're looking at here.
Tachycardia. It looks pretty regular to me. Just fast and nothing else spectacular here.
Correct. And then we're gonna get a minimum emergency, blood work. We often look at the blood work.
Maybe we've got an insulin or something that's causing our patient to be, sync or collapsing. So we do want to get that minimum, blood work. But while that's being drawn and run, it's gonna take a few minutes.
What else can we do? Well, that's the thing. I didn't think this was an ECG lesson.
We wanna do pocus to po pocus, to live lives to po. How to that the for the walking dead, my friend. All right, so it is true that point of care ultrasound is an extension of the triage exam Focus, or also in the general is an extension of the physical exam.
When it comes to point of care sound, we use it differently. We've talked about that in multiple other episodes, but in this sense, we want the, minimum windows to find the underlying problem. We want to use a triage focus, not take too long to see what the problem is.
Stabilise the patient and then complete the, ultrasound evaluation. Just like we did with a second physical or something along that line, Right? It's all about pret test probability.
We have a patient with syncope. We should think that pulmonary hypertension is in there. So if we think about point of care ultrasound, we wanna rule in or rule out pulmonary hypertension.
The big question I have for you is, you know, in all the webinars we've done, you know, it's a little more obvious, you know, hit by car, painful abdomen. Well, duh. We're gonna go for the abdomen, respiratory distress, high heart rate murmur, et cetera.
But we're gonna go for heart and lungs, you know? What order should we start in in this case? Good question.
And, when we're looking at this patient, let's come back to Pre-test Probabilities in our patient looks as part of that triage exam. So we're gonna focus on the big things that are most life threatening. And if you looked at our patient and we look at Piccolo, what do you think was the most life-threatening concern?
00, I got this. Respiratory distress nailed it. Nicely done.
So that is a big one. That we want to assess for sure. But we also do have and know that we might see cardiac changes.
We talked about it with pre, with our, left sided congestive heart failure. We got crackles. We got to have a murmur.
So we do want to check that heart as well. All we do have the concerns for pulmonary hypertension. We wanna check the heart for that, and then we do have the abdomen, and I'm not saying we should ignore the abdomen, but our patient does not indicate that we have a life-threatening intraabdominal problem at this time.
So we're gonna start with that which is the most life threatening. Therefore, we're gonna start with the respiratory and then move through the system. Yeah, I love it.
So, for reference, people can go back to our previous clear talks regarding pleural space and lung ultrasound. Plus, we actually had a couple of them, but essentially, we're using lung and pleural space borders that we're finding using. Point it there, ultrasound, and we're gonna use our, border to border approach.
So we're gonna use the plural lung ultrasound, the Calgary plus approach. So we're gonna start right behind that front limb and go through the, different details here in this video. Yeah, that's right.
So we start right behind that front limb, and we consider that our cranial border at least the most cranial that we can go to And we know there's one there, so there's no guesswork and the probe is perpendicular to the rib. So we got our nice classic bat sign to find that plural line and looking for lung sliding. And then we're simply gonna slide caudal until we hit that Caudle border.
That's the curtain sign. Really nice thing to assess for pneumothorax or other pathology looks normal here. So we're gonna slide dorsal till we come off the lumbar hypoxia muscles.
Then down till we just see the lung again. That, by using our borders is the most sensitive spot to find air. For example, in the standing or sternal patient, that's our caudal dorsal site.
Caudal dorsal. We didn't count a rip to get there. We just use visualisation of ultrasound and just figure out where our landmarks are.
OK, so from there we're gonna start scanning the lung in a big S shaped pattern. Going border to border to border to border, looking for lung surface pathology. Biggest ones being bee lines and consolidations.
Absolutely. So we just simply jump, a rib forward from that, Caudle dorsal site to hit the front lamb come down to mid thorax and that, behind that front lamb. And then we slide Caudle again looking for surface pathology till we hit the curtain sign.
Yeah, So we're gonna just separate the fur here, as you see, and there's our curtain sign a second time. Yep. Now we're gonna follow that curtain sign Cranial eventually until until we get down to the Peric cardio diaphragmatic window.
So, essentially the lowest part for external standing animal. We're pretending this animal sternal standing. We're gonna get the diaphragm, the actual diaphragm here with the heart in the same window.
And the reason why we can do that is because there's a mediastinal triangle of fat between the heart and the diaphragm. A little hard to see here because our patient isn't lateral and the heart has fallen to the other side. But we have the heart and diaphragm the same window.
Then what? And we're gonna actually scan between the plural border and the ventral lung border. So we actually turn the peal parallel.
And we scan from lung ventral lung looking for pathology in the lung, like you see here and then down to the ventral border to look for pleural effusion. So we're using our borders, and we're assessing multiple different regions in a very rapid manner. Any standing patient, we imagine our patient is standing in this case just easier to show it in lateral.
And we look for different pathologies in a very, very short period of time. Yeah, so on that patient, we saw a very nice clean surface. We didn't see any bee lines.
Those beautiful light Sabres that we don't want to see. That plural line looked nice and smooth. And this is Piccolo.
Whoa, sir. And this looks completely different. Yeah, this is actually quite interesting.
If I look at these four different images, I'll ask you a few questions. Do you see vertical white rays of sunshine from the heaven increased in numbers. I don't see rays of sunshine, but I see an increased number of light.
Sabres. Yes. OK, so terminology is a bit controversial right now.
Let's just agree to call them vertical vertical artefact. Vertical vertical artefact. All right, so you can see vertical white moving artefact.
Agreed. And what do you think of the plural line in this case, is it very smooth and regular in all our images? Or is it starting to get a bit thickened?
Irregular, or we start to see some consolidation. Well, I mean, it's thickened and irregular, and most of these images that we're seeing here it's really looks gnarly and on the top right image. We can actually see a partial consolidation.
That's actually quite concerning there, sir. These lungs are definitely not normal. I I'm quite worried.
But you know what? Hold on, Hold on. Piccolo had a heart murmur.
He's a breed dog. I see a whole bunch of beelines Boom. It's congested.
Part be. Let's bring up the pros. Now let's wind this back here.
This is a very interesting thought process that it wouldn't be uncommon to jump to that conclusion. But let me ask you a question. Uncomplicated lefts sided, congestive heart failure.
Do you think that that plural line is smooth or irregular and thickened with uncomplicated lefts? Side congestive heart? You know what I think it's usually very smooth and we don't usually get consolidations.
That would be correct. So let's look at a couple of papers. We're starting to see this evidence on the veterinary medicine as well.
Let's look at a few of the papers that came out. This is one from the human literature, and you can see the guy acute cardiogenic pulmonary on the left, acute lung injury in the middle. And then they've got its tradition.
It's called Aspiration. Pneumonia in our veterinary patients on the right clinical course can be very similar between all three. Sure presence of bee lines can be very similar between, but this is where it gets interesting.
You look at the pleura in these three different disease conditions. We can see that with acute cardiogenic edoema. That plural surface tends to be smooth regular, and you don't see those sub plural consolidations.
Whereas in the acute lung injury aspiration pneumonia diseases with inflammation, we'll often see that we get a thick and irregular pleura and we start to get consolidation. Well, you know what's interesting too, sir, is because small dogs we usually about acquired left sided congestive heart failure from mitral valve disease. And that murmur should actually be much higher and again, Like you said.
Now that plural line wasn't smooth even though we had all those beelines. So maybe it's less likely congestive heart failure. Yeah, so less like the left side of congestive heart, right?
Do we still want to scan the right side of the heart? We come back and we look at syncope and some of the history we had with, Piccolo, and we can see that we still have pulmonary 10 and pericardial fusion on our list. So wait a minute.
You're telling me we should not rule out heart disease at this time? We can say it's unlikely left side of congestive heart failure, but we still should look at the heart. And not only should we look at the left side of the heart, let's also consider the right side of the heart Wait.
What? Let's consider the right side of the heart. And let's actually start with two different windows that we often look for a right Pernal short axis and a right Pernal long axis views.
What do we got here? Ok, well, all the way at the bottom, right? At the apex.
We're just seeing the left ventricle. So this is not really helping us. So the right side of the heart, No.
But as we start to move up, you'll see that we have the mushroom view, and then we see that we actually have the right ventricle, that little crescent shaped moon outlying and above that, interventricular septum. So we got that right ventricle starting to come in at the level of the mushroom just below the, this view. You know what's interesting is because I I don't feel like I usually look at that area.
I'm usually looking at that left ventricle, left ventricle and then getting the bla bla bla bla bla the fish mouth and looking for the whale in the Mercedes. Yeah, and it's interesting, because even if we go up from there and we get to that left atrial ratio, we can see the pulmonary main pulmonary outflow tract. Yeah, on that right side of the heart.
So that is something we're gonna come back to. So that left atriotic ratio and a little bit above that, we can start to see that, outflow track. We can also see like you said, the right ventricle at the level of the mushroom.
So things that we should think about and again, if you are interested. We did have a prior talk and, focused, cardiac windows in one of our prior clarus. Yeah, exactly.
Now, what's interesting is that most of the time when you and I teach labs, we concentrate on short axis windows. They are easier to get. But if you really want to look at the right side of the heart, what we should come down to is come back to that mushroom rotate 90 degrees and boom, get our four or five chamber view of the heart.
Yeah, A Absolutely. So as you look over here, you can see you got the right ventricle in the near wall because we're coming off the right side. So that's the right ventricle.
Alumin. We see here is the right atrium, and we got the left ventricle Lumen in the far field, and we got the left atrium, in the our field. So we get that four chamber view, a nice four chamber view here.
And this is very, very helpful when it comes to looking for pulmonary hypertension. Yeah. What's interesting is you could tell this is not a cardiologist getting this.
I mean, first of all, this is a micro convex term probe we've got rip in the way. We've got some shadows, but again for diagnostic purposes on triage, using pointing Caro that it's gonna be more than enough. But let's go ahead and show how we got these right parasternal short ais windows so we could see our probe is at a 45 degree so that it can cut the heart in short axis windows markers towards the elbow.
And we have a beautiful mushroom here. Yeah, And then from there, we're gonna keep the point of contact on the chest of the thoracic wall. The same, we're gonna keep our angles the same.
We're just gonna fan the probe or tilt the probe until we go across that fish mouth view that you see there and then we get that left atriotic, outflow track or left atriotic ratio and the outflow track. Yeah, what's interesting again? This dog is standing, sir, We're not using a fancy schmancy echo table right there.
We can do this on the flying emergency so that our short axis windows. And then what about our long axis windows? So from that mushroom, we're eventually gonna turn 90 degrees like you see here.
And when we turn our probe 90 degrees, you can see that we get that four chamber view. So we get the right ventricle, left ventricle, right and left atrium. And we achieve that by rotating our probe 90 degrees and getting that long access view.
So what's really interesting, sir, is what I'm hearing from both of us is we're not cardiologists, right? We're not, Radiologist, we're not gonna stop and do a whole bunch of fancy SMANCY measurements. We're gonna be eyeballing a lot of these changes like we were doing on the short axis.
Yeah, we've talked a lot about the short axis, but let's now look at what should we assess? Because we haven't done a lot of discussion on the, four chamber view. But let's go ahead and look at what we should assess them when we're looking at the four chamber view, especially when we're looking for right heart changes.
So one of the big things we want to do, we want to look at the right atrium and the left atrium, and they should be roughly this whole in size. So we should have roughly the same size, right atrium, left atrium, and the septum between them should be neutral, which means it's not curved either way should be relatively neutral and flat. And then we look at the size of the right ventricular Lumen.
And generally speaking, it should be about a third the size of the left ventricul. Lumen. So once we start to get larger than the third, especially if we start to get half the size of the left.
Ventricular. Lumen, we're really worried that we got some changes on the right side of the heart that are concerning, and the last one there that, right ventricular wall thickness for hypertrophy relative to the left ventricular wall. When it starts to get up to about half the size 50% the right ventricle gets to be about 50% the size of the left ventricle free wall.
Again, we worry that we have hypertrophy. Change is suggesting right sided heart. That's definitely a harder one to interpret.
In my opinion, I think the other ones are easier to visualise. I would agree. So let's go back to Piccolo and see what we got.
So we got normal there, and we're gonna have Piccolo coming in shortly. I'll just ask the questions real quick on this side. Left atrium, right atrium.
I'll ask you the question. Since we got them here. What do you think?
Are they roughly the same size as equal? Equal? All right, What about that intra atrial septum here?
Do you think it look neutral? Doesn't have a big hammock sticking one way or the other. Nice and neutral, all the neutral.
What about that left ventricular, right, Ventricular. What do you think of that? Right Ventricle is definitely smaller than the left.
All right? It's about a third. I'd say not.
Definitely not large than that. And that left vicar Free wall. We look at it here.
I just see if we get that. There we go. You see it in the far wall?
Here. We got the right left Var wall on the right. What do you think?
I think the the left one is way thicker. All right, so I think we're good. Now let's look at Piccolo.
All right, Here comes the Whoa. So let's ask him one question at a time. Oh, I'm a little worried about this.
So if I look at the two Atria, that right atrium looks like it's ready to be below. All right. So in terms of size, you would argue the right atrium is at least double the left atrium.
In this case. Definitely huge. All right.
Definitely concerned. What about that In atrial septum? Is it nice and flat like a two by four between the, septum and the, atria?
No, it's definitely curved towards the left atrium. I think you like to call that the, what do you like to sign? Because it looked like somebody could just right down there and have a nice nap between the, atria and that nice hammock curve there.
You don't want to bring back this key slope? No. No, we tried that once and didn't really work.
So we're gonna move on. Left bench. You got a Lumen size compared to the right.
What do you think? I mean, that right is almost if not probably bigger than the left ventricle. I would agree.
I think it's it's bigger than the left, Ben. Whoa! That's a problem then.
What about that right? Ventricular free wall compared to the left, is it less than half? No, it definitely is.
That Brent particular free wall looks thick. All right. I would think it looks about the same thing.
The left, which is So we've got four strikes when it comes to pick a wall, and we're looking at that right side of the heart. Wow. But let's also look at that short axis also right?
So the intraventricular septum should curve toward into the right ventricle. Semi circular shape. Yes or no?
We can see that in the normal dog. Hey, look at this beautiful rainbow shape to that, interventricular septum. Nice and curved.
The whole left ventricle is a beautiful circle. I come over and look at this one here, and whoa. Looks like somebody's jumping on my septum, man.
No, it looks like someone's punching it. Look at that. So we get a flattened, interventricular septum.
And if I look at that crescent shaped moon on the, normal dog and I look at it over here, that's like a half a moon. It's almost pack Manning It's huge. The full moon there.
That's a pretty big moon there. OK, so that makes a lot of sense now, C, I'm looking at this. I'm like, Great.
I think this looks abnormal. Is there a way for me to grade it with a score? That helps me better interpret what's going on.
I think it was brilliant that Shelley brought up that paper that she found at the beginning there because it fits so nicely to what we're gonna talk about here. The crew out of Belgium has done a couple of studies. This is one of their earlier ones.
This is a 10 point. They did switch it to an eight later. But we're gonna talk about the 10 point scoring system because it's really nice to pull everything together and you can see that scores higher than five had a, and less than two.
So if you had less than two, it ruled it out with a very high probability. If you had a score grade in five, it tells you you got public hypertension with a high specificity. So it's 90% accuracy overall.
OK, so yeah, let's go ahead and look at parameter number one so right. Atrial right ventricle. Enlargement, yes or no?
So score zero would be no enlargement. Score one would be one of the other enlargement. Score two is both enlarged.
I come back and I look at this two still images. I put them up here at Piccolo. You can see that.
We do have right? Atrial and right ventricle. Enlargement.
Boom. He gets a score too. Oh, my goodness.
I like this scoring system. It's very easy not starting out. Very good.
You can. Someone like you can add to 10. I'm sorry.
You can add to 10 with a calculator, so this tends to work well, so we'll look at the next question then, right? Ventricular hypertrophy. Well, again, if we look at Piccolo, I think we're pretty clear that we had right ventricular hypertrophy.
Yeah. So this one's a little bit tougher because it also includes the, prominent papillary muscles and the addition of prominent. It does take a little bit of practise.
So let's just say that we had the right ventricular pre wall was hypertrophy. So we're going to go with a score of one in this case. Yeah, so it wasn't zero.
We both agree with that. Correct. OK, all right, So now moving on forward with intraventricular septal flattening yes or no?
And I like this because it's truly binary. It's either there or it's not. It's not a degree of flattening.
Either it's flatten or it's not. So we get two because, as you can see in the image to the top, right, that, still image there. We've definitely got interventricular septal flattening.
Jeez, Louise, that's really getting concerning. So now, right. About what?
About rights sided, congestive heart failure sign? Yeah. So this is the one that they actually did a later study and said, You're still gonna be able to use the scoring system with or without the rights sided congestive signs.
But I like the congestive signs because they have been looked at. We usually see them when it's a bit more severe or an advanced form of right sided heart failure. But you can see here that what are we looking for?
We're looking for the presence of infusion or a distended, non compliant cove cava. There's still things that we can look for, and they did score them based on whether they had one or both of those present. So let's go ahead then.
We haven't looked at the abdomen. We said we would. Y Our patient's sufficiently stable.
Let's look at the abdomen and see what we find with Pallo. OK, so let's start with the kidneys. We're gonna go short axis.
Long axis, right kidney? No, no, there is, there is no place for the kidneys in triage. All right, fine.
So, looking for right sided, congestive heart fail signs again. We're looking for a abdominal effusion or sites, distended hepatic veins and a non compliant A Caio cava. Potentially a halo sign so we can see normal in the bottom.
Yeah. So we got a normal picture down here, and we got the gallbladder diaphragm, the Vedic cava down there. Very narrow.
Collapsing, bouncing and up here to the piccolo. We got What? What do you think about Vedic Cava?
You could fit your head through there, Doctor. So not moving much at all. Very distended with the gallbladder.
What are you thinking? The gallbladder. I'm thinking we have a halo sign.
Yeah, I don't know why you have a raccoon bounces through there but yes. So we got a halo sign. We got a thick No.
So we got this thickened halo sign. So we got the halo sign coming in. Very nice.
And what do you think about the abdominal fusion down here in the bottom left? You have abdominal fusion? Yeah, definitely.
Between the diaphragm and the where I can see some effusion, which is definitely abnormal there. And then you also start to see distended hepatic veins are also very good. We're starting to see, signs suggestive.
I would say at least two signs that do support the, evidence of right sided, congestive heart failure. You really don't want to change it to the raccoon? I sign.
OK, so let's go back to our scoring system. And again. Criteria number five is signs of bright set of congestive PRI failure.
And I think we can say an absolute score of two because there was a presence of the fusion and a distended non compliant, called of any cava. So that was concerning. So now that leaves us another category here, which, you know, honestly, I'm not very familiar with.
Are we gonna be looking at the pulmonary artery. Yeah, And I think this one this is where the crew out of Belgium and Claire Marva Chris goin and their crew and their contingent, had done a a bit of work. And I do think the pulmonary, artery is a great thing to look at when it comes to pulmonary hypertension.
Everything in here is good. With maybe the exception. Like I said of the right side to congestive heart failure signs in the abdomen, they tend to be a little less, specific, and we don't tend to see them as nicely.
But when it comes to the pulmonary artery, I do think that is something we should be looking for for pulmonary hypertension. OK, so how do we do that? We often start by finding the, whale driving the Mercedes that LAAL so we can do it in both short and long axis.
So here, we're gonna start the short axis. We have a well over here, which is left atrium and the Mercedes, which is our aorta. Perfect.
What do we do from here? And then we're actually gonna usually just fan a little bit until we, start to lose that, left atrium middle. You can see that over here on the right.
Now, we've started to lose that left atrium. We start to see that, outflow the main pulmonary artery A bit better. So here we go.
That's our aorta here. That's our main pulmonary. Here we see the pulmonic valves coming in, and we look at the ratio of that main pulmonary, artery compared to the aorta.
They should be roughly 1 to 1. What do you think here is? Which one's bigger?
The aorta and the pulmonary artery. The pulmonary artery? Definitely.
I mean, look at that length, even, I can tell you that. All right, So now this is one of our signs of pulmonary retention, because that pulmonary artery is much wider, more distended than that, the aorta. And that's pretty quick to do, because if you start getting confident getting that LAAO I mean, this just requires a bit of more fanning.
It's basically deflating the whale. Yes. OK, very cool.
So now let's go through the long AIS changes. Now this one's a little harder for me. Yeah.
So a lot of us can get a four chamber view. We can get that right ventricle, left ventricle. Right.
Atrium, left atrium. So you see that here? This is where we need to rock the probe to try and bring the Atria in a little bit better and, stay underneath that lung.
So we got to try and rock that probe a little bit more so that we can start to pick up. And you just see it coming in here on this view here, this normal patient we had, you see the pulmonary vein? Which one goes into the atrium, the vein or the artery?
The vein is gonna go, so it comes in in long axis. You can see it coming into the to the, atrium here, and then you can see it on short axis right here at times, and it tends to be circular, and if you get up here on a still, this is from a different patient. Just labels everything nicely.
This is what you're looking for. You're looking for that pulmonary vein going into the atrium and that pulmonary artery on short, a circular that's the right pulmonary artery on short axis. And that is our pulmonary vein going into the left atrium.
Ok, All right. You gotta stay below the lung. You gotta rock the probe.
You gotta try and bring in the atrium nicely without the lung in the way so that we can see that image. You may need to rotate a little bit more towards the five chamber. You between the four and the five to sometimes pick it up.
And this is that we see here. We also have a still image from, an article. If you want to read up more on that from cardiology here, 2016, the ENC.
But this is our, image here of Piccolo. And let's, look at that pulmonary vein then. Compared to that pulmonary artery, I can barely see the pulmonary vein compared to the big pulmonary artery.
Yeah, it gets squished and flattened between the right atrium and the, pulmonary artery, and therefore in the pulmonary artery, then is much bigger than the pulmonary vein. And you can start to see that here I like. That's why we included the cardiology image.
Just because you can still see it's not POY collapsed. I still see that pulmonary vein coming in And it is again pulmonary artery. Much, much bigger.
So I really like looking at this, four chamber view. It was the crew in Belgium that showed me how to do this. And claire Marva, actually, the cardiologist there, showed me how to do this when I was visiting.
I really like this having done that, in Belgium, I've taken that with me. That's a really, really nice skill to be able to do. So that is definitely more challenging again.
It takes practise. You got to get that poor chamber view and think about those little changes that we just talked about. But again, if we come back to our scoring and come back to Piccolo pulmonary RT R enlargement artery enlargement and the answer was an absolute yes.
And if you look at the literature this 10 point scoring system again, they've gone to an eight point as well, using the first four criteria. But it still holds true. It's still going to be accurate.
And in this case, we got a score of nine. We have a 90% accuracy that we are going to be dealing with moderate to severe pulmonary potential. That's the other thing we should do to emphasise here.
This scoring system works very, very well for moderate to severe pulmonary hypertension. It doesn't tend to be as discriminatory for the, less severe, but we're worried most about the most. Well, exactly.
And like we said, this we're talking about a patient population that usually is had come in for syncope. Right? So most of those patients are probably gonna have moderate to severe pulmonary hypertension.
Now, there's another way to look at this. And that's the eccentricity index for pulmonary hypertension. Take us through that.
Yeah. So this is another one. You did this on your your short axis window.
So you can see this is Piccolo on the left. Where we got, the, heart in short axis. Very distended, right ventricle.
But then we're gonna actually freeze this. And I've done so on the right and made two still images in end diastole and then Sicily. And it doesn't work a little bit better in Sicily.
You can do it in both, but it does tend to work a little bit easier in Sicily. So I, I do find it a little bit easier and a little bit more accurate in the in Sicily than dioli. And essentially, what we're gonna do is we're gonna get the width of the, left ventricle.
So the widest point and the, the height Essentially, and we're gonna compare the two, and we're gonna see how they look. And we should actually, if you look up here, this is the eccentricity index. We should have a value normally, of about 1.1 to 1 pretty close to the same.
And would you say that the two are the same? And this example down here with Piccolo? Absolutely not.
And once that gets to be more than one, before and in our case, we got 2.67. You can see that again.
Its sensitivity 67% but specificity of 95%. So, again, that eccentricity index just another means by which we can double check or measure to see if we're starting to see signs of, pulmonary hypertension or supportive of pulmonary hypertension. Yeah, see that?
That seems to make a lot of sense to me. And again, it comes in that short access window, so definitely something I think most people can do. So Whoa.
So Piccolo probably has severe pulmonary hypertension. We know he has syncope. Clinical signs.
What did we end up doing for him? Yeah, exactly. So we gave some tool for anxiety, came in pretty anxious.
We gave him oxygen, which is pretty standard. And then we used a When we start to talk about pulmonary hypertension, we want to address both the underlying cause. Try to find it and reverse it.
Because there are many, many causes that we said. But we also do a general, therapy. And a lot of our patients will benefit from specific T targeted, pulmonary arterial vasodilators like senna.
So we did start Senna, fill in, Piccolo, along with oxygen therapy and porn All Yeah, it's interesting. Saldana was actually created in humans to treat pulmonary hypertension, but of course, during trials, they discovered this multibillion dollar side effect which has made the company a lot of money. But hey, we still use it in veter medicine because it's relatively affordable.
It works and does not have that side effect in dogs correct in dogs so improved in hospital was a discharge, so we couldn't find a specific cause. We had an idea. But the reality is in talking to our cardiology service as well.
Proper idiopathic pulmonary hypertension. But what was interesting is on the lungs. What did we see?
Let's relate it back. Yeah. So then we started to see that thick and the regular, line.
And in this case here, we, actually did suspect that we might have had underlying pulmonary fibrosis as well. With Piccolo. So that's kind of what we were working with.
Unfortunately, we did not go further with our diagnostic criteria. We did, treat Piccolo. We did get piccolo home.
But again, overall prognosis in these cases, not that great. Usually under a year. So they will respond to slow down and fill therapy in terms of clinical signs.
But yeah, that's pretty much it and yeah, they declined referral. At that point. I think they just knew how serious it was.
So, in summary, what are abnormalities suggesting a right sided heart failure and pulmonary hypertension? Yeah. So we're gonna come back to the paper, and there's actually a couple three or four studies on that, bacteria that, pulmonary hypertension score now, But you can see one of the big ones.
Significant right. Atrian right ventricle enlargement. See that we should be thinking high on our list along.
Especially if it's got syncope and signs that are supportive of pulmonary pretension. We should be thinking, Oh, this could be a pulmonary hypertension. Yeah, an increased cave.
Cava diameter decreased collapsed index. And there was that big fat cave cava that's not changing with respiration whatsoever or other signs of, abdominal, infusion. So we might see that Hal or Ascites again, That one was a little less, specific.
And there are some studies. There was a study that was also looking at the, Colin Cava that didn't find it correlated well with, pulmonary hypertension. But the, other changes we're looking for in ventricular septal flattening for sure.
Would you see that? That's a definite, strong indicator that we could have pulmonary hypertension and pulmonary enlargement. Like we saw, on that long axis view.
Definitely think pulmonary hypertension in that case. So that is all we have today. Pretty awesome.
Yeah, That was it. So it was pretty quick. But we do have a chance now to take a look at our our volunteer puppy dog.
I believe Mabel is gonna pop in and we'll be able to maybe take a look at our dog scanning live. Sounds good. Take it away.
She Mabel is gonna pop in. She's popped up already, So I'm using the C seven vet scanner and let's get Mabel standing here. Come on up here, girl.
Turn a little bit. All right. I'm just gonna part theer here, and we'll just kinda get right under her right armpit.
Try to get the right parasternal view here. It's a tough one for me. Freeze.
I've got my voice controls. Activated here just so that, because I've obviously got my hands are tied up, You're doing pretty darn good by yourself there, Shelley. Look at that beautiful mushroom.
Great. OK, mushroom. Nice ventricle.
Nice crescent shape to it. That's all looking pretty normal. Good.
Yeah, and I can't use my pointer here. So just to point out structures, but I think it's fairly obvious here. There we go.
There's our intraventricular septum. There's our ventricle free wall right, Vicar. Free wall.
There's our crescent shaped right ventricle. That looks beautiful. Great.
So then if we want to just go, fan up a little bit higher here just to 00, nice job. All right. And I have our outflow track off to the left of the screen there that you just start to see, on the left side of the area there.
Yeah. And, between the pulmonary. Yeah, you go.
There you go. You can get the pulmonary valve is starting to come in a little bit there. So you've got a nice 1 to 1 ratio, for the pulmonary artery.
Nice job. Tiny tiny little rib spaces. OK, and then if I want to get my, long access, I'm going to rotate my scanner here.
And I'm just trying to make sure I stay within that rib space. We're done. Look at that left ventricle, Right ventricle.
There you can see the microvalve flowing into the left ventricle. That's the perfect long, long axis view. There has a lovely four chamber view.
I agree. I got the right ventricle in the air field left ventricle in the far field. That's right ventricles There.
There's our left. They look good. We got the mitral valve.
Just coming a little bit under the lung. That's our right tree up here a little bit along there, but, a tough one. Yeah.
In that rib space, Yeah, in that rib space with the dog in the standing position right off the back. You see that? That you know, that right ventricle was not enlarged.
I mean, that's already very hard to not think hypertension, you know? And one thing. One thing I know from from the human world is that when the heart is really enlarged, it's easier to see.
Yeah, totally. So, yeah. Yeah.
This place the tongue and gives us a larger, cardiac window to assess, path. This is true. Same thing with per car.
Such a good dog. She's getting good at this. Hey, like, why we're done.
Aren't gonna get something else. I know. She's like, Where's my Where's my cookie?
There you go. Ok, excellent. All right.
So thank you very much. Yeah, Like I said, I always learn so much when I when I have such good instructions. So, to our audience just a friendly reminder to stay on for at least 50 minutes, to qualify for that, C CPD credit.
And before we begin our live Q and a I hope you'll stay on for a couple of more minutes. Here we have a question for you. And this poll is an opportunity to learn more about the clarus vet scanners.
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We have quite a few questions. I can moderate this. I have to put my glasses back on.
All right. OK, so first question, what percent of syncope are caused by pulmonary hypertension? Yeah, it's interesting.
We actually, Justin and I were talking about these questions, and actually, I don't think that we know, you know, And the problem is, syncopy is already a tough thing to really truly identify. I don't know that I know the number. Yeah, No.
I'd have to actually see if there's a specific, sync paper. And then we can pull the incidents off of, some the research that's out there, but yeah, off the top of my head that I couldn't say what percentage of syncope is caused by pulmonary hy tension. But let me just flip that around from the standpoint of clinical value.
If I get a patient that comes in with respiratory stress at rest, and it comes in with a history of syncope, pulmonary hypertension is high on my list of differentials. For sure, it is awesome. What is the patho mechanism?
Pulmonary hypertension leading to syncope. Yeah. So, sir and I also were talking about that.
That was great. So I think it depends if it's precapillary postcapillary. I think at the end of the day is especially with the precapillary, there's gonna be less oxygenated blood, right?
So either that blood isn't getting to the lungs or the lungs isn't doing the exchange or whatever, cause. But at the end of the day, there's gonna be on the flip side, less oxygenated blood, which obviously can then lead to the syncopy. So That's the precapillary stuff.
Yeah, so exactly. Anything that can essentially decrease blood, oxygenation and generally to the brain can cause the syncopy. So if you've got underlying pulmonary fibrosis or lung disease that's contributing to your pulmonary hypertension, you're gonna likely have some oxygenation problems.
You also get decreased return of blood to the left side of the heart, and therefore you get decreased cardiac output that will also contribute to decreased oxygen delivery. So there's a multifactorial mechanism by which we can it and it does vary as, sort of said based on the underlying cause. So and if you've got left sided congestive heart failure again, then you can see how that can contribute decreased cardiac output as well and decreased delivery of oxygen to the tissues.
So you just think of it as all the different mechanisms when you're thinking of a pulmonary hypertension that can contribute to decreased oxygen delivery to the brain at both the level of the lungs and their function, as well as the cardiac output and its function. Yeah, All right. There's a question here about the caudal vena cava.
Is there a normal range of size? Yeah, so at minimum, we want to see a 25% change in, width of that cardio cave in dogs, 20% in cats with respiration. So that's normal.
And usually it's much more visible. So often again, it's more of an eyeball thing. We we see that change with respiration and change in diameter, and we're also gonna get a cardiac pulse.
And there's one of the heart beats we can actually see radiating on that cave cava and seeing that pulse on there. So those are the normal findings, and often when the coun cave is that distended, we lose that pulse, and we barely see any change in diameter. Yeah, and if it comes down to what's the normal size, it varies so much based on breed, too.
So if you said what is the normal size, it's gonna depend on the respiratory cycle, and we have looked at it. We actually did document the size in the study we did with the reference intervals, but we tend not to rely on rely so much on the size because there's so many variations that can affect in terms of abdominal pathologies. The degree of respiratory effort et cetera.
So we tend to use more because then it eliminates the size factor. We tend to use more of the change because that is relevant to all size dogs or cats. So we tend to use the change in diameter with the respiratory cycle than an absolute size to the Veni.
Cava. Not right now. There's one question here.
I think it's kind of mistyped, but I'll try to, translate that. Do these simpler measurements to measure the findings replace Doppler measurements enough to start treatment. So I think, yeah, does that make sense?
Yeah, it's a very good question because when we're looking at the actual, pressures and we grade the pressures across the, the tricuspid valve when we look for regurgitation. So we're looking at the pulmonary valve when we're looking for, regurgitation. We use the Bern equation, and we measure the, regurgitation for the pressures across that, pulmonary valve.
And what we find is, those are the ones that we use to cri criteria to grade it like the the The gold standard is to actually put a swan Gans in and measure your pulmonary artery pressure really invasive, not done. We rely on that, pressure gradient and Doppler to do that. And it gives us the severity.
Does it replace it? No. No.
Would I make a decision to start therapy and sildenafil based on the pulmonary hypertension scoring system and clinical findings that we can see with ultrasound? Absolutely 100%. So doesn't replace it.
No, not as accurate as it. No, but enough to start therapy with it. Yes.
OK, so does not preclude a referral to a cardiologist. All right, are there any variations when applying these scanning techniques for pulmonary hypertension to a cat or a horse or an exotic species like rabbit? Well, that's a great question.
I mean, to my knowledge, pulmonary hypertension is not really a common thing in a cat. Not not at least leading to Not that I know about honestly and horses, I have absolutely no idea. Or exotics also.
Yeah. I'm sorry. That's a big one.
Next. Yeah, yeah, yeah, yeah. That's a little outside our wheelhouse.
So a cat or a dog? There's a chance we'll have scanned it because we scan everything. But that, would you have clinical signs of pulmonary hypertension and diagnosis of pulmonary hypertension.
Without all of these changes, that's a good question. So I think in general, moderate to severe pulmonary hypertension is gonna lead to some changes in clinical signs. I think in general, but there's no doubt there's been situations where I've seen cases in clinic where, you know, we think it's pulmonary hypertension.
There's some mild changes. We can't really find anything else we treat for pulmonary hypertension and things do get better. So I can't say that everything fits all the time.
But I would say for the ones with moderate to severe pulmonary hypertension, likely there's gonna be changes in clinical signs. Yeah, and I. I would also second that and say that occasionally we'll see a dog coming in with a milder form that does have, syncope.
So we do see that clinical sign with that milder form that doesn't result in all the changes that we see on all, so the definitely the milder cases are tougher to correlate to the right sided heart changes and things that we talked about today they tend to be more obvious as Sir said when it's moderate to severe hypertension. Those are the ones that we really want to identify early and start treatment on because I think that's where our impact on outcome and prognosis is gonna be. Yep.
This question is, pertaining to Piccolo. Did the dog get some other medicine on the right side? Heart failure, except still no, via no, nothing.
So we had we had discussed working up for, pulmonary pereny disease. And potentially, that could have led some to some specific treatments, maybe slow down the disease. The reality is that the this is already set in.
Not much we can do, but maybe there's secondary airway infections, inflammation, et cetera. The reality is we didn't do anything else. But the dog actually ended up rallying and doing OK on Silda fill.
I think we got, what, 68 months? Yeah, I believe so. I'd have to go back and check.
That we got about six months. OK, would you generally see dry lung with pulmonary hypertension? Unless there is fibrosis, interstitial disease of an underlying cause.
That's a great question. So the in our case again, that's what raised the suspicion. Is this idiopathic or is there pulmonary peral disease that led to it?
Or are they two completely separate things? Right. So in general, I mean, right sided heart disease should not lead to any changes within the lung itself.
Yeah, and I think it depends on which group you're in because we see a lot of the If you look back at some of the groupings that you have for pulmonary hypertension, we see some that are secondary to decreased oxidation in the lungs. So you get vascular changes, so we will see rank lung changes that will result in pulmonary hypertension. And I expect those guys to have increased beelines.
But do all cases of or left sided congestive heart failure. Some of those guys are gonna have those beelines 100% so But if you said, do all patients, with pulmonary protect, have beelines. No, we will see some that have significant pulmonary pretension.
Grade four severe pulmonary pretension. Clear lungs that are perfectly normal lungs. So you can see what the underlying variation is.
How you get six groups. What you're gonna find depends on which group you're in. So we definitely have some that will get beelines frequently and some that won't have any beelines.
Mhm. This isn't really a question, but a follow up to the, exotic animal. Question.
It said most of these parameters. I somebody, obviously, that has experience, have found are relevant for ferrets and rabbits, but getting good views of guinea pigs are extremely difficult due to their small thorax rats. Huge problem with chronic chronic pulmonary fibrosis.
And I have seen the caudal vena cava and heart changes as well. Holy moly. That's so cool.
I know. Yeah. Thank you, Doctor Delaney for, contribution and input.
We appreciate that. Yeah, love it. Love it.
She says thank you, and I love your lectures. All right. Look at that.
I know what to do next time I'm presenting or in the morning. All right. How much time do we have?
One question How common is pulmonary hypertension in dogs? Probably not that common. So it's certainly not a high high on the list of differentials.
You know, even in school curriculum, and I teach heart disease here, and the reality is it it takes up a very small portion. The reality is also it's a vague condition. That's the problem, right?
A lot of dogs have it, and it develops late. It gets missed. They maybe get euthanized or have some other issues.
So I, I don't know what the true frequency is. I don't think it's that high. It's certainly not, You know, a problem that we see every week?
No, but I will also argue that I think with the advent of, things like the pulmonary hypertension scoring system and the applications of ultrasound that we're starting to use in general practise outside the specialty hospitals, I do think we are starting to diagnose it more frequently than we would have say, 10 years ago. And I don't know if it's necessary an increase in prevalence, but a greater knowledge of how to identify it and look for it, and having the ability to do so. Because even 15 years ago, we used to have to send everything that we suspected of having pulmonary hypertension to the cardiology service.
Now, I do think that it is something we can, at least suspect or refer in, and, maybe we're seeing it, with a higher ability to pick it up. So it's not truly an increase in incidence, but an increase in ability to identify. Right?
So, I, I think we're probably gonna run out of time here pretty quick. So, any questions we didn't get to, Shelly will email us to us, and we will respond to you guys, out there and, in the world with any questions that we didn't get to. Yeah, for sure.
And again, you're you're gonna all receive a copy of the webinar recording as well, by email this week. So just complete the closing survey to give us your feedback so that we can continue to bring you great educational content, like today. Now, I'd like to conclude by thanking Dr Boson and Doctor Shaloub and also thanks to all of our furry supporting characters.
And of course, thank you all so much for joining us today. I hope you had as much fun as we did. And, we'll be taking these new skills back to your practise.
And just remember, practise makes perfect Thanks and goodbye. Thank you, everyone
