April 22, 2024

#118: 6 Steps To Solving Acute Respiratory Distress. With Dr Rob Webster.

#118: 6 Steps To Solving Acute Respiratory Distress. With Dr Rob Webster.
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Season 1

You know that feeling when the ‘not breathing well’ patient gets rushed to your crash bench, and you stand there with your stethoscope trying to look like your planning, but actually, you’re just panicking... You have to do something, but what? Where do you begin?!  This is exactly why I loved this conversation with ECC specialist and Director of Animal Emergency Australia, Dr Rob Webster, about the 6 steps that will help you localise the problem in the respiratory distress patient. Because once you localise it, you have a DD list, and you have a plan. Dr Rob guides us through the first minutes of assessing the respiratory distress veterinary patient and shows us how to quickly assess breathing patterns and sounds to help you pin-point and fix the problem. Trail our clinical subscription for free at vvn.supercast.com to access the show notes for this episode and to listen to all 500+ of our clinical episodes. Get help with your tricky cases in our ⁠⁠⁠⁠⁠⁠Specialist Support Space.⁠⁠⁠⁠⁠⁠ Connect with us through our online ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Vet Vault Networ⁠⁠⁠⁠⁠⁠⁠⁠k⁠⁠⁠⁠ for episode highlights, clinical resources, discussions, questions and support. Subscribe to our weekly newsletter ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠ for Hubert's favourite clinical and non-clinical learnings from the week.  Join us for a snow conference in Japan or in Wanaka with Vets On Tour: email vetsontour@gmail.com for details. (And tell Dave I sent you for your 10% discount!)  Topic list: 5:49 Step 1: Evaluate respiratory effort. 11:31 Step 2: Is the breathing noisy? 20:22 Step 3: Is the chest wall intact? 28:16 Step 4: Is the breathing fast and shallow? 36:27 Step 5: Fast and shallow, but with nothing abnormal on lung imaging. 38:01 Step 6: Non-respiratory causes.

 

There's a reason why B for breathing is right up there in the AB CS of CPR, right?And it's the same reason why most of us, when faced with the acute respiratory distress patient, develop some acute breathing.Issues of our very own.You know that feeling when the not breathing well patient gets rushed out the back and you stand there with your stethoscope trying to look like you're just planning but actually you are just panicking and the little hamster wheel in your head is spinning and spinning and the voice in your head shouts do something you idiot, But what?
Where do you begin?This is exactly why I loved this episode with ECC specialist and Director of Animal Emergency Australia Doctor Rob Webster about the six steps to localizing the problem in the respiratory distressed patient.Because once you localize it, you have a DD list and you have a plan.
Here's a story about this episode.Less than a week after recording this, I was on shift and this gorgeous little Dashan puppy was rushed in with very severe respiratory distress, complete with those purplish mucous membranes that makes you go Oh no.So I panicked and then I stopped and I said to myself, let me use Rob's 6 steps and by step three I knew exactly where the problem was and I had a pretty solid idea of what it was without even touching the patient.
It was a rack bait pup with a hemothorax by the way, and we saved him.So listen carefully and write these steps down so you can memorize them or sign up to the clinical podcast where we first published this episode to Get full access to our lovely show notes for this episode and for the more than 500 other episodes that we have on there.
If you have not yet checked out our subscriber only clinical podcast, well, why the hell not?I can only assume that you've not heard about them.So let me tell you more.For our clinical podcasts, I interview specialists and ask them all of the questions that I've accumulated over my 20 RDA career about their topic of expertise, all of the stuff that I used to or still get stuck on.
So it's updates on what's new, or sometimes it's a revision of the important things that you've long since forgotten.You're not going to find these podcasts if you search for them on your podcast player because access to them is through a paid subscription.But once you sign up for them at vvn.supercast.com, they will show up in your podcast layer of choice.
So if you like what you hear in this episode and you do want to check out our full feed of clinical content, go and try it for free for two weeks at VVN.That's VVN for vetvaultnetwork.supercast.com.It's about taking a certain set of steps with each patient with respiratory distress that will get you to that localization as quickly as possible, but also be able to short circuit that kind of panic that we get because we know if this patient's not going to be stabilized quickly, we're going to lose them.
Rob Webster, It's been a long time.Welcome back to the Red World.Thank you, Hugh.It's great to be here today and talking about something near and dear to my heart, which is respiratory distress.Oh.Why is it near and dear to your heart?Because it's one of those presentations that requires a very accurate and fast assessment in order to stabilize the patient.
And it's one that requires a little bit of clinical examination.And what I see is these days when a number of people, especially through COVID, have not had as much of an opportunity to work with men, people are reverting to the diagnostic tests before they've localized the salt, the source of the respiratory distress.
And because of the nature of this presentation, the patients are very unstable.And if you go looking in the wrong area of the respiratory tract, you can quite quickly compromise your patient and not actually reach the right diagnosis.And so I love things that you can utilize some clinical skills to point your diagnostic tests right at the right direction.
And I love things like respiratory distress where we can make a difference very, very quickly.And so, you know, localizing where the problem is in the respiratory tree ticks all of those boxes.First, it's an emergency condition.And 2nd, it's one that some physical examination or just knowing what to look for can really help expedite that diagnosis.
Yep, that's exactly what I.Wanted to try and achieve with this episode we talk about.I know when you talk about to to Jill Madison and the diagnostician teachers, they say you should avoid pattern recognition.I kind of feel like this is one place where pattern recognition is super useful, where they come in and almost, if you'd seen it enough times, almost subconsciously, you go, you've got a breathing problem.
But I know I'm going to start with your heart or I'm going to start with your upper respiratory tract or want to check your pill space.Am I right?With that, yes, that that's what we want to do.And it's really it's, it's about taking a certain set of steps with each patient with respiratory distress that will get you to that localization as quickly as possible, but also be able to short circuit that kind of panic that we get because we know if this patients not going to be stabilized quickly, we're going to lose them, you know, and if we do the wrong thing, we're going to lose them.
And so we've got a high stakes presentation.And what we want to be able to do is stabilize that patient, reach a diagnosis and be able to give their owners the right treatment options and the right prognosis as best we can.And so recognizing the pattern through an effective physical exam, that's for Jill and the diagnostician, you know, the the clinician diagnosticians to to remember is that we are doing it.
This is all about physical examination skills.We can hopefully, hopefully get this answer OK.I've heard you do a talk on this, so you have a fairly structured approach to this topic.So I'm not sure where you want to begin, but is it a a good place to start to say, well, let's recap the potential broad picture causes of respiratory distress because as you say, you come in with that patient, it has some you recognize.
Oh, it's not breathing.Well, something's wrong with the way it's breathing.I haven't put it into place yet, but starting from nose to diaphragm.It in.Broad groups.Is it worth outlining?What are all the things that can cause respiratory issues?It, it definitely is, Hugh.
But if we could today, let's talk about it in the way it was first presented to to me by Steve Haskins, my my mentor, because it really changed the way I thought about this because that's what I used to think.I used to think, well, everywhere from the nose to the diaphragm could be involved.
Let's let's figure that out.And then I remember this conversation started with Steve one day when, you know, I'd, I'd just managed a patient with respiratory distress.And I think Steve said something along the lines of, you know, you should be able to figure out where the problem is with just six steps.
And then he said something like, you know, I'll take 6 steps from the doorway of the consultation room to the consultation table.And if I take each of those steps and then use my stethoscope on that patient, I'll know where the problem is.
And I thought to myself, wow, that's all I need is 6 steps.And I've got a solution for this and it really helped me approach it.So, you know, there's a few things we could do.We could go through what which I'd like to do is go through our six steps and then supplement that by putting out on your app the actual algorithm or the stepwise process in writing that you can follow.
And then probably some videos of these different patterns, which can then help people that are listening actually, you know, get the visual aspect as well as the audible aspect that we're going to talk about today.OK, great.So for anybody who's thinking what app, So Rob's talking about that Mighty networks, the the vet vault network on those clinical spaces.
So once we get through this, I'll make sure notes that'll be the the written aspect to recap all of this, and then we will share videos on there as well.So when you listen to this, take a moment at some point and go look at the videos to cement it for yourself.Cool.All right, six steps.I love 6 steps simplified for my simple brain.
Thank you.And as an emergency vet with a simple brain, that's exactly what I thought.And so Steve said, and and we've got to remember I'm speaking from southeast Queensland.And so we also have ticks and snakes.And so Steve says, take your first step into the room and look at the patient on the table.
And the first thing to do is, is have a look.Are the respiratory efforts decreased?You know, look at that patient.And is that patient barely breathing?You know, are they breathing very slowly or are they breathing with very little respiratory effort?You know, and this is a really simple one, but this is important to rule out some of our neuromuscular junction problems.
And certainly especially in Southeast Queensland, we see this with snake bite patients, some tick bite patients, especially if they're cats, and some other, you know, less common toxins like tetrodotoxin and also sometimes things like myasthenia gravis.
But you look, you look at that patient and you go, you're not breathing enough.This is the step #1 and you can picture that from the consult room door.You know, we, we know what approximately the normal respiratory effort looks like.
Step number one is, look, if it's only if the patient's only breathing 12 * a minute, there's something wrong.And if the patient is not expanding their thoracic, you know, their rib cage very much when they're breathing, there's also something wrong.And so step number one, are the ventilatory efforts decreased?
We'll share a couple of videos of this.But if this is the case, the way to quantify that is having a look at the patient's carbon dioxide level, which measures the degree of hypoventilation, and then start looking for neuromuscular junction, neurological problems, or muscular problems that could be leading to hypoventilation.
So when you say not breathing enough, so we're talking shallow breathing.So the because you sort of expect the really sick patient can sometimes be, you know, I want to say panting.I know it's incorrect, but a big movement of the chest is is expected.So if you go you're really sick, but you're not, your breaths are really shallow.
That should Alert me to something.Can they have an increased?Rate of respiration, but with a an inadequate depth of breadth.So can they go yeah.Or are they generally just slow There's.Going to be a whole group of the ones coming along.OK, because step number one is breathing too slow or breathing, you know, what looks like tiny effort, you know, So it's not, it's not too fast.
It's generally, geez, that patient's not breathing like it should.It's not breathing enough.OK.So your neuromuscular junction problems, they're not going to be fast either.It's going to be too shallow and too slow, a combination of the two just in a OK, all right, thanks.I just need to clarify that.Cool.
OK, we'll get to breathing too fast and too shallow coming up a little bit.But they want that won't be a neuromuscular junction problem.And this step #1 is really very simple to rule out.And it's very rare that it actually is step number one, right?
But we can, we can make that determination from the doorstep.And then we take step #2 though, Hugh, because step #2 is like, well, if the patient's, you know, it's, it's not not breathing enough.Holy hell.This patient is breathing really loudly.
And this is very important because the patients I'm talking about in step #2, you can hear them from the consult room doorway.And in actual fact, some of these patients, you'll hear them as they walk in the door out the front and, and they are patients with very noisy breathing.
And in effect, very noisy breathing equals obstructive breathing.And the noisier it is, try and remember the noisier it is, the more of the minute volume or the more of the of the air moving in and out of the lungs is affected by turbulence.
And so the loudest form of breathing you'll hear is the upper airway obstruction, because everything, all of the air getting to the lungs is moving past this upper airway.And so when there's an obstruction of the upper airway, you'll hear a lot of turbulence.
And effectively what we'll have is we'll have an in a prolonged inspiratory effort and a lot of noise.And that's the first form of very loud breathing to mimic it yourself, you know, place one finger over a nostril and try and breathe in with maximal effort and you'll hear and feel what these patients are trying to do.
They're trying to get a lot of air past a fixed obstruction.And so the inspiratory phase will be prolonged and there'll be noise the whole way in.And one of the the classic breathing patterns that we'll we'll publish as a video is a patient with laryngeal paralysis.
And these patients with laryngeal paralysis, you can often hear them from the car park as they come in.And we've got to alleviate that obstruction to help settle them down.So, you know, I, I don't really want to try and mimic the sound of an upper airway obstruction, apart from suggesting that people put one finger over a nostril and breathe in as hard as they can.
And that is your upper airway obstruction.Long inspiratory phase.A lot of strider in the in the breathing pattern.The the laryngeal, because it's easy enough to picture it with a nose.
So your your bulldog with the completely blocked nose is dying of heat stroke.As you say that that's sort of an upper.But if you go a little bit lower down to to the larynx as well, that and I like like it instinctively makes sense because I, if I try and memorize this, these things in the panic state of my patient can't breathe, I find it harder to go find the facts.
But if I think about it instinctively, exactly as you say, if all of the air, if I've got a liter of air that needs to get into my lungs, to fill my lungs, but it all has to go past my collapsed larynx, it has to take longer, right?That inspiration, the time of inspiration has to be longer because a liter still needs to get in there and I'm going to have to really suck it in like, and then I can puff it out.
So it makes sense, almost sense instinctively.It it does, it makes sense.And the other thing to remember in all of these breathing patterns is that the patient doesn't adopt A breathing pattern to maximise their oxygenation capability.
What they're trying to do is that the biggest drive of breathing is the ventilatory drive to increase the Alveola ventilation or the respiratory minute volume, and they adopt the pattern that minimizes the work involved in doing that right.
They want to minimize the work involved in maintaining their respiratory minute volume.And so exactly as you said in slightly different words, when you've got an upper airway obstruction, you minimize the work involved by having a prolonged inspiratory phase and then a very fast expiratory phase.
And and that's the most effective way at minimising work involved with this particular problem.And you'll see as we go further down, particularly with pulmonary parenchymal disease, it'll change the the pattern.But again, this pattern and if you could do your your in that your little example there was perfect Hugh Yeah, that is exactly the noise that we're going to be that we're going to be hearing, but it's very, very fast.
So OK is that?Kind of like when you're doing your your your burpees in the morning.Oh, I, I, I feel, I, I, I don't get to hear it.
Apparently it does sound quite distressing.But anyway, you're embarrassing me.We'll now move on the the next sound of noisy breathing, which is still step #2 right.We, we, we're only one step into the consult room here.The breathing is really noisy now.It's either going to be noisy in the way that we've just described or it's going to be reversed.
We're going to have an ex spiritual dyspnea and difficulty breathing out and we're going to get that with the structures in the lower airway and it's going to be and a fast breathing with a pronounced expiratory effort is going to be associated with lower airway obstructions.
They're rarer than upper airway obstructions, but we're going to see this with dogs and cats with bronchoconstriction or say intrathoracic tracheal collapse or even mass lesions associated with the lower airway.
So we'll have the opposite.Inspiration is easy, but expiration is prolonged and difficult.So basically this loud breathing patient that we're here with, our second step into the consult room is either going to be breathing like inspiratory dyspnea or expiratory dyspnea.
If I have a Yep foreign body or something in the in the lower Airways, let's say so I once had AI think I told you about that carrot like went all the way down to the bifurcation.Is that going to be an expiratory effort more than inspiratory?Does that count as a Mass Effect in the lower Airways or is it not low enough?
Does the trickiest.Still, you said that that counts to kill collapse.It's generally no below the at least below the tracheal bifurcation.Your carrot is still like and that what a horrible upper airway obstruction to try and do is still going to be inspiratory.
The inspiratory and, and a complete obstruction is, if we think about it, in the upper airway can be expiratory as well.But because of the dynamics of the airway, as you breathe in, you have negative pressure around that upper airway view.
Everyone imagines a carrot stuck in there.So we'll suck the airway down, but as you breathe out, you've got positive pressure and you'll push the air out past the carrot, right?Makes sense.So different once we get past that tracheal bifurcation, you know, once we're past the bifurcation, say we've got an obstruction in one, even then we've got an obstruction in one main stem bronchus we've we've opened up half of the lung for breathing in.
But the typical expiratory obstruction is actually going to be down around the bronchioles.So you're blocking multiple Airways as you breathe out.OK.Thank you.OK, so our loud breathing patient is the first one to exclude.
We're going to look for obstruct and basically the layout of the breathing, the more certain you are is that something's obstructing the airway.If it's on inspiration and extremely loud, it's the upper airway.If it's on expiration and extremely loud, it's very pronounced lower airway the quieter it gets on.
Expiration, the less of the lower airway is obstructed.It's a spectrum and you'll hear everything from loud wheezers to wheezers that you hear on your stethoscope.But the pattern is the same, prolonged expiration and loud noise on expiration.
So that's step #2 is noisy breathing.Step #3 is we'll take another step.This breathing is not overly loud.The next thing we're going to do is actually look at the patient and we're going to say we're going to ask ourselves, is the chest wall intact?
You know, sounds pretty simple sometimes, you know, the owner says, we'll have a look at this side and we see a massive hole in the chest on the other side.But the other thing that we'll see in these patients, because we're now on the chest wall and plural space, the other thing that we'll see is sometimes flail segments of chest.
So the chest might be open, there might be a flail segment of the chest.But the other thing that we might see in this patient while we're still looking from a distance is very pronounced paradoxical abdominal movements.So on inspiration, the abdomen opens up a whole lot.
You see a big pronounced expansion of the abdomen on inspiration and then it sucks in on expiration.And we're looking at those things that that really pronounced paradoxical movement is often there because you've got a plural space disorder.
And we can't, because of this plural space disorder, we can't actually expand the rib cage.So the only way we can breathe in or inspire is by displacing the diaphragm down into the abdomen, which pushes the abdomen out.So you know to to evaluate the chest wall and pleural space where you know looking at the patient, have we got a flail segment or a hole in the chest?
Have we got a really pronounced abdominal component?And now's when we first put our stethoscope on the patient's chest and we go, are the breath sounds quieter than I would expect for the amount of effort.
Because all of these things answer the question around chest wall and plural space.You know, if we've got a hole in the chest wall or we've got a flail segment that says that the chest wall is not working very well, If we've got this marked abdominal component to the breathing, it says, geez, maybe the diaphragm is having to be displaced out into the abdomen to generate any inspiration.
And we put the stethoscope on the chest and ask ourselves, are these chests sounds quieter than we expect?And if they are, that certainly makes us much more concerned about a plural space disorder.And that's our third step into the consult room.
Hopefully it's a small consult room here because now we're beside the patient because we have had to put our stethoscope on the patient's chest.OK, so just to clarify again on the paradoxical abdominal breathing.So with plural space disease, you lose the ability to use your chest wall, expand your lungs.
So you're going to have to start doing belly breathing to put it in the in the yoga and the meditation, you have to start using your abdominal muscles to do the job for you.Yeah, OK.Absolutely.Because you've got this, this, you know, whether it be fluid or air or abdominal organs in between the plura and the chest wall.
So the chest wall has far less ability to expand.And this goes to the extreme hue with a tension pneumothorac.So let's just touch on this right now because this is one that does need to be recognized very, very quickly.
If that patient has just had a trauma or for any reason you're concerned about attention pneumothorax, what happens is it's a dynamic process and every time the patient tries to expand the the chest wall, a small amount of air leaks from the airway into the plural space with a one way valve.
So very quickly we build up positive atmospheric pressure in the pleural space, which further collapses the lungs and collapses the major blood vessels which are feeding blood back into the heart.And so the picture of very severe tension pneumothorax is really exaggerated breathing efforts, but very little chest wall movement.
And people will describe these chest walls as barrel like because they're completely full of air, not like how not to be confused with our patient in the beginning, the abdomen will be, you know, they'll be trying to move their abdomen and it'll look paradoxical, but effectively you're going to have this patient with a barrel like chest gasping for air.
And the gums will be both, you know, sometimes cyanotic, but quite often very, very pale because we're not even getting much blood flow back to the heart.And you can't hear any chest sounds here.And if if we get that presentation, I'd suggest in many cases move straight to emergency thoricocentesis.
OK, makes sense.Attention, everything is going to be a tear in lung tissue or a tracheal tear or something like that.That's going to be the cause.Anything that causes A1 way valve effect, which is not uncommon, of course, because as, as the patient breathes in, we have negative plural space pressure, at least to start with.
So we're actively trying to suck air from the airway into the plural space, but it can't go back the other way.So it's a, it's a, you know, every single breath makes it worse.OK, cool.OK, so remember we've had three steps.First step is have a look at the patient and they may not be breathing enough.
They probably got lower mode in your own disease.Second step is the very loud breathing patient has either an upper airway obstruction or a lower airway obstruction.And of those patients probably 80% or upper and 20% or lower.Third step of the patients where there's a sign of a pleural space disorder and that might be problem with the chest wall, diaphragmatic paradoxical movement, but most importantly chest sounds that are quieter than what we'd expect for the effort of breathing that's going in.
And those patients were either going to move directly to a emergency thoracocentesis if we suspect A tension pneumothorax, or we're going to, you know, get an X-ray or an ultrasound of that pleural space to see if there's something there that we need to drain.OK.So we're three steps here I.
Wanted to give you a quick update on our specialist support space if you haven't come across it before.We created a space where you can interact with a group of specialists to give you case support on those tricky case conundrums that you face in everyday practice.The space is housed on the same app where our subscribers get their show notes, which is a super nifty tool where you can upload photos or videos or even chat live to the specialist if the case requires it.
The idea with this is that you have a direct, guilt free line of communication with somebody who can help you out with those cases that you can't refer or you don't want to refer, but you just need a little bit of extra brainpower to help you make decisions or to check your thinking.We started off the space with support in medicine and emergency and critical care, but in the last couple of months we've added support in dermatology, veterinary oncology, as well as support specifically for those tricky diabetic cases.
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It is a paid space, but we've kept it as affordable as possible at about $15.00 a month.That's one $5, not 50.And for this, you can ask as many questions as you want and expect a same day turn around time.We've put the link for the space in the show description wherever you're listening to this.
So if you feel like you can sometimes use a little bit of extra help, go and check it out today.Step 4 is the pulmonary parenchymal diseases, right?And of the actual respiratory diseases, this is the last group.
And when you said before, Hugh, about breathing fast and shallow, that's the breathing pattern that typically these patients with step four will exhibit because they've got pulmonary parenchymal disease.And So what happens?
It costs them effort to expand the lungs and there's not much trade off in expanding the lungs because a lot of the alveoli have either got fluid in them or have got edema around the entrance to the alveoli.So we can't really recruit anymore alveoli by an increased inspiratory effort.
And So what we find is that these patients will double or triple their respiratory rate but not put any effort into inspiration.And so they'll be breathing like it's not actually panting, although many of these patients will pant in between.
But if we're going to be semantic, panting is just the Dead Space moving in and out to keep them cool.And generally, a patient that's panting is going to be breathing too fast to count.OK.So that's that.
Yes, yeah, you can't count that.And I find a vet will say, oh, it was 80 and you're like, really?Is it 80?It seems a lot faster than that.You know, panting is exactly as you said.So the little stress patient or the, you know, the the patient that's that's hot will be panting too fast to count.
But what we'd call a restrictive breathing pattern is this patient that's breathing fast and shallow.And it's more like gotcha.I've heard it also described as no gap at all between expiration and inspiration.
Yeah right, that makes sense cuz it's a normal breathing pattern.You'll have a breath out, pause and start breathing again.Whereas these guys are there's no time to rest because you've got to fill those few alveoli that are still working.That are still working.Yeah.And that's where this breathing pattern comes down to.We can't recruit the other alveoli for because without a ventilator we can't expand them.
And so we breathe many more times per minute to try and recruit them, you know, to to try and aerate them 60 times rather than 20 or 30 times.So can I put that in my own words as well please?So if you've got shit in your alveoli for fluid or blood or anything that's filling the parenchymal space so you can breathe as deep as you want, but it doesn't help because that extra air that you're trying to breathe is not going to go anywhere beyond the the upper respiratory tract.
So what you need to do is cycle faster through your respiratory cycles to fill those functional LVL.They're the ones that still have air and you may as well empty them and fill them quicker to get that oxygen flowing in and out of there to get it into the bloodstream.That's right.Makes sense, yes?Although, remember, the patient's not prioritizing oxygenation.
None of these strategies might be the best for oxygenation, but they're the best for increasing minute volume.OK.Yeah.All right.Thanks.And so these patients to do any, we, we could just draw a line there.And I tend to suggest to a lot of vets that you know, we, we know this patient's breathing hard and fast.
We listen with the stethoscope and the chest sounds will generally sound loud and what we hear is adventitial sounds.So abnormal sounds, crackling or wheezing.And you know, what we could easily say is for these patients, it's very likely they've got lower airway disease, meaning disease is interfering with gas exchange.
So they're either fluid in the alveoli or interstitial edema or inflammatory infiltrates in the terminal bronchioles preventing recruitment of the alveoli.And your best bet here is, you know, maybe stick an ultrasound probe on or take a chest X-ray to try and determine what disease process it is.
But if we're going to be purists around our physical examination, we should hear faint crackling noises when we've got fluid in the alveoli because of the popping sounds as the alveoli do open.And on the other hand, we we could hear faint wheezers if our problem is a little bit higher up in the terminal bronchioles.
But I find that's a very academic description and it's very easy to, to get confused.You know, basically what we've got is increased lung sounds.So they're much quieter than the sounds we'll hear with airway obstruction because there's very little air moving in and out of the alveoli.
But they're certainly abnormal sounds, and they've been described as crackles, wheezers, popping, just just abnormal sounds.OK, great.OK.So those four steps here, they're they're really all of our respiratory diseases that we're going to be able to diagnose and treat.
We've got, you know neuromuscular junction patients not breathing enough, upper airway obstruction or lower airway obstruction, plural space disease or pulmonary disease, you know, in four steps.By the time we've put our stethoscope on that patient, we should have localized where the problem is.
There are two more steps I'll go through that are far less important, but these are the ones on physical exam.And I'll add a note for our less, you know, less aged challenged colleagues who are now using ultrasound as part of a physical exam rather than a diagnostic test.
And it's a really interesting concept that, you know, it'd be great to have a debate on in some time.But I like to think of fast scanning or you know, point of care ultrasound scanning as being an extension of a physical exam rather than a specific diagnostic test.
Because I would say here that you can use your stethoscope to listen for reduced lung sounds and a plural space problem, and you can use your stethoscope to listen for fluid in the alveoli.But a point of care ultrasound is more sensitive and more specific then a stethoscope here.
And so you know, you place your ultrasound on the chest and there's no glide sign, you've probably got a pneumo, there's a big patch of black fluid, you've got a pleural effusion.And equally your lung rockets or B lines indicate that we've got pulmonary parenchymal disease.
And that test is very easy, non invasive, and can really add to the localization of this problem.And so now I would say take 6 steps into the consult room and stick your, you know, use your ultrasound when in doubt and you should be able to localize between upper airway obstruction, lower airway obstruction, neuromuscular junction problems, plural space disorder, and pulmonary disease.
OK.Can I recap those quickly in my simplified language?So number one, I can't see you breathe, and you should be thinking if I can't see you breathe really almost at all, you've got to be leaning towards again in there, maybe putting an ultrasound on it.But you got to intubate me and breathe for me.
If I can't see you breathe, consider intubate and breathe for me.In terms of actions we need to take, stop me at any time, if I'm getting it right #2 Your breathing is too loud.I can hear you from a distance without a stethoscope.I can hear you and those ones potentially you got to start thinking, well, you might be obstructed.
So maybe intubation is going to be life saving for you if it's bad enough #3 I can see you breathing really obviously, sometimes really in your abdomen.But I can't hear you breathe even with a stethoscope.I can't get lung sounds.And potential action is maybe you should stick a needle into my chest and get some crap out of my little space.
And then #4 your breathing is too fast and too shallow.It's quite obvious it's in your chest, but it's too many and too shallow.And then when I put my stethoscope on you, I can hear weird stuff and you should give me some oxygen and ultrasound and then X-ray me to go figure out what's wrong with your parenchymal tissue.
Does that make sense?Yeah.So we're all the way down the respiratory tree now with four steps and there are two very brief extra steps, which I'll quickly mention.The first one is when we're looking at this patient, they're breathing generally too fast and too shallow.
It's one of these pulmonary parenchymal diseases, but you went a little bit further and you X-rayed it or you put your ultrasound probe on it.There's nothing wrong with the lungs.And we've still got this terrible breathing pattern.The next thing is that we go, well, are you actually hypoxemic?
You know, is there a problem with your breathing?And ideally you evaluate the level of hypoxemia with an arterial blood gas, but you know that that's often problematic in a patient respiratory distress.And so the other thing that we can do is is we put a pulse ox probe on the patient and you know, have a look to see if there is very obvious hypoxemia.
And we see that this patient is hypoxemic.And so we've got a patient with signs of hypoxemia.None of the other signs of the respiratory tree involvement seem to be causing this hypoxemia.Our fifth step is to go right.
Is there a chance that this patient could have a pulmonary thromboembolism?Right.So pulmonary thromboembolism isn't an uncommon diagnosis.It's a very sudden onset of respiratory distress.And the thing about pulmonary thromboembolism is that you've got severe breathing problems and hypoxemia.
They respond to oxygen therapy.We can't find another cause of the respiratory distress, but then we've got to go looking for a disease process consistent with a pulmonary thromboembolism.And if we can find a disease consistent with pulmonary thromboembolism and no other cause for this breathing difficulty, generally we make the conclusion that this is likely a pulmonary thromboembolism causing the breathing difficulty.
So that's that's step #5 everything sounds normal, looks normal, can't find a problem, but the patient is absolutely hypoxemic.Then it could be a pulmonary thromboembolism.And the final step is step number six.Everything looks bad but the patients not hypoxemic.
We can't find the problem in the respiratory tree.Then we've got to look at non respiratory look alikes.What I would warn everyone to do is go back through these the first five steps before even thinking about a non respiratory look alike because I've seen a few patients die over the years where a well meaning veterinarian and one of them was me for sure thought, well, this is a, you know, non respiratory look alike and we got it wrong.
OK, so you know, make sure you don't have a respiratory condition before you think, geez, this could be something else.But the common things that will make patients breathe fast and shallow and not be related to the respiratory system are things like hypotension and pericardial tamponade that will leave the areas of the brain that Dr. respiration.
You know that those those areas are often hypoxic because oxygen delivery is compromised and the only thing they can signal is fast breathe, fast breathe.And so you know, hypotension, hypovolemia, pericardial tamponade are certainly causes for rapid breathing or equally hypothermia, acidosis and anxiety can do this.
And so, you know, The thing is, there are other things other than the respiratory system that can cause rapid, shallow breathing and look like respiratory distress.Look for those things once we've ruled out a primary respiratory problem because we know if you're not getting, you know, adequate arterial oxygenation, you you're on a very limited time for survival.
And so make sure it's nothing compromising that oxygenating ability of the lungs before going and evaluating the patient for these respiratory, non respiratory look alikes.Would anemia fit in that number six as well that in the same basket?
Yes, yeah, absolutely.Because, you know, there's not enough hemoglobin to carry oxygen to the tissue.So at a tissue level, the body is hypoxic as in not, you know, inadequate oxygen delivery.And that will drive both the respiratory center to increase respiratory rate, but also catecholamine release which will also increase the respiratory, right.
So yeah, definitely a non respiratory look alike.So the brain's going, hey, I'm not getting enough oxygen, breathe faster, even though that's not really the problem.That's the body's response to say, well, yes, somehow oxygen's not getting to the tissue level.And what I can do about that?
One of them is by breathing more.Yeah, stimulate the respiratory center, stimulate the sympathetic nervous system, which in turn stimulates a faster respiration.OK.Cool.OK.Can I step back?Back to #5 so you talked about thromboembolism and go looking for causes, diseases that would potentially 'cause that.
So what are we looking for?I want to say sepsis go.Yeah, sepsis is is a cause, but it's unusual.Usually the septic patient, especially in dogs presents with, you know, pretty classic science of systemic inflammatory response rather than, you know, straight out respiratory distress in dogs.
There are I think 5 big diseases consistent with thromboembolism and the first is immune mediated hemolytic anemia.The 2nd is a hyperadrenocorticism, so Cushing's disease, the third being diabetes, the 4th being cancer of any type and the 5th being protein losing nephropathy and to a lesser extent protein losing enteropathy.
Because especially with protein losing nephropathy, quite commonly you lose antithrombin, which is a small protein, so it gets out through the glomerulus pretty easily.And if you don't have enough antithrombin, you you very quickly develop a pro thrombotic state.
So in dogs there's really the big 5 and in cats it's usually heart disease or cancer.OK.Cats heart disease or cancer?And in looking for any thrombo, you know, anytime where concerned about thromboembolic disease, you've really got to be able to demonstrate there's a primary disease consistent with thromboembolism.
It's very rare that animals develop primary thrombotic disease.OK, great.Those are so useful, Rob, 6 steps.I think it's a super super useful and it's a critically a visual picture in my head.Especially if you've seen these.Most of us, if you're not a brand newbie, you've seen these, but actually now linking that mental picture that you have with these very defined, clear steps really helps to clarify it for me at least.
Cool.And that's how I found it.When Steve said about it, it suddenly seemed very clear.And I went from, you know, the patient came in in respiratory distress.And I would get a little bit of my panic on to then I was like, OK, you know, I know this is going to be one of these places, let's work through it.
And it made a lot better for me.Great.Stuff.Magnificent.Thank you so much.

Dr Rob Webster