Transcript
- Well welcome everybody.
Thanks for joining us for Focus on Undifferentiated Shock.
My name's Chris Pennell
and I'll be hosting today's webinar today.
Our guest speaker is Dr. Cameron Bain from the
University of Pennsylvania.
We'll be doing a second webinar with Dr.
Bain on Tuesday, July 1st at noon entitled Lung Pocus
and Critical Care, and we'd love for you
to join us for that one too.
You can sign up for that webinar@sonossite.com slash
behind the scan webinar.
With that, let me introduce Dr. Cameron Baston.
Cameron Baston is a clinician advisor for Penn Health Tech
and an assistant professor
of clinical medicine in the Department
of Medicine at the University
of Pennsylvania's Perelman School of Medicine.
He serves as an associate program director for the pulmonary
and critical care medicine fellowship
and as a doc director of clinician performed ultrasound
for the Department of Medicine.
He has an interest in helping create low cost medical
devices in the resource limited critical care setting
and works with several organizations on POCUS
and critical care education,
a mechanical engineer epidemiologist,
critical care physician and medical educator.
He spends about two thirds of his time caring
for critically ill patients
and the remainder working on education innovation
and health technology.
And with that I'll turn it over to Dr.
Basten to get started.
- Hi, my name's Cameron Bain.
I'm a pulmonary and critical care doctor at the
University of Pennsylvania.
Today I'm going to talk to you about POCUS
and undifferentiated shock.
The way we're going to do this, we're going to break it down,
we're going to start with a brief review of shock in general
and then I'll start talking about the way
that I use ultrasound to differentiate the
etiology of shock.
Once we have that, we can really start leaning into how
to narrow that differential as we go forward.
And then I'll talk about some of the next steps, things
that people want to do once you've figured out what type
of shock your patient has.
When we do this, we're going to
start with the definition of shock.
I'll get into the etiology and our traditional
windows into the body.
So I really like this original definition of shock,
that it's the clinical expression of circulatory failure
that results in inadequate cellular oxygen utilization.
And the most common reason that we have that
and the thing that we tend to recognize is
someone's blood pressure.
If they have arterial hypotension
and signs of tissue hypoperfusion,
and that could be a bunch of different things
that we'll get into, then we say they have shock if they
just have low blood pressure, they don't have shock
and then wheel and all had these original categorizations
of shock where you had hypovolemic shock, cardiogenic shock,
obstructive shock and distributive or low resistance shock
and they, they broke these down.
And I feel like these really help us know
what therapies are indicated
to help our patient get better tissue of oxygenation.
That said, we now have a more sophisticated understanding
than just macrocirculation.
If you look at the blood vessels with dark field microscopy
as seen here in the sublingual area, you can see
that sometimes the problem is not just low blood pressure,
it's actually edema, preventing diffusion
of oxygen across gradients
or other disruption, hemodilution constriction, tamponade,
something else causing a problem in the process
of getting oxygen to the cells.
Even when oxygen does get to the cells though
sepsis poisons the mitochondrial processes.
And so that means that sometimes the problem is not
sufficient cardiac output, not sufficient oxygen delivery
to tissues, but truly just that at a cellular level,
the tissues have been poisoned.
Ultrasounds not going to help us reverse that process,
but what it can help us do is make sure
that enough oxygen is being delivered to the cells.
And this brings us back to those
that etiology symbol we have for our shock states.
And so if we start thinking about these
and have in our head a pretest probability, knowing
that distributive shock,
primarily septic shock makes up most of what admissions
to the intensive care unit are, we can start thinking about
what patterns of ultrasound findings are going to let us know
which shock state our patient is in.
Before we get into ultrasound,
let's talk about our traditional windows into the body,
and that's inspection, auscultation,
palpation, and percussion.
We also get to go a little beyond that
and think about whether we're seeing altered mental status
signs of encephalopathy
or if we're seeing oliguria hyperemia
or modeled clammy skin as a way to see signs
of hypoperfusion beyond just our inspection.
We can also look at lab values with both lactate
and central venous saturation, giving us a clue as
to whether or not the patient has adequate oxygen
delivery to the periphery.
And thanks to the andro to shock trial,
we also should be thinking about capillary refill
as another indicator of whether
or not somebody has sufficient delivery of blood.
But now we can get into the really exciting part of this.
How are we going to use POCUS to figure out
what etiology of shock they have?
And the place we tend to start is the heart.
This review in New England Journal talked about the idea
that if you think about these four shock states,
there are typical patterns to echocardiography of the heart
and we think about distributive shock
as usually having normal cardiac chambers and preserved IL
and comparison to hypovolemic shock
where you have smaller chamber sizes
and you have high contractility, cardiogenic shock
of course tends to have large ventricles, poor contractility
and obstructive shock depends on which etiology
of obstructive shock you're talking about.
But they all should have a dilated inferior vena cava
whether or not you have a compression of the right ventricle
or an expansion of the right ventricle
depending on the etiology.
So let's talk about how to do this.
We're going to be able to look at the left ventricle,
the right ventricle and the atria.
And when we do this we're going to look for patterns
and we have an overfilled heart on the left
where you can see a dilated left atria, a dilated ventricle.
You can see in the middle the normal pattern
of normal sized left atria, normal sized, left ventricle,
normal sized rv, and on the right an underfilled heart.
And that's where you have a small end diastolic diameter
and we'll get into that in a little bit
more detail in a second.
When it comes to the left atrium, we can look on ultrasound
and we can see whether that left atrial volume represented
here by the left atrial diameter measured at end systole is
normal or abnormal and normal is dependent on
height and sex at birth.
But if you look at four centimeters as a general rule,
that's too big, you can also think about it relative
to the other chambers of the heart with this rule of thirds
where the left atrial diameter should be about the same
as the left ventricular outflow tract,
which should be about the same
as the right ventricular outflow tract.
This picture representing somebody
who has a dilated left atrium,
we can look at the right ventricle
and we can get information about the right ventricle from
any of our traditional cardiac windows.
In our peroneal long axis view, we're again using that rule
of thirds to see whether the right ventricular a flow tract
is greater in diameter than the LVOT
or the LA in the peroneal short axis view.
We can talk about the crescentic shape of the RV
and the apical four we can talk about whether it's bigger
or smaller than the left ventricle.
And the same thing is true in our subcostal view.
So here's going into detail
and giving you examples about that.
Here's a peroneal long axis view
and you can easily see here
that the right ventricular a flow tract is bigger in
diameter than the LVOT
or the left atrium that is abnormal In this view.
You can see the peroneal short axis view, you can,
you can see that the right ventricle is pressing the
interventricular septum into the left ventricle,
changing the shape of the RV from a crescent to more
of a oval.
And here in the apical four chamber view,
you can see on the left a normal heart with the ratio
of RV diameter to LV diameter,
that should be less than two thirds.
And on the right you can see a severely dilated right
ventricle, a severely dilated right atrium
and the intraventricular
and intraatrial septi are being pushed into the left side
of the heart representing increased pressure.
The normal ratio of the RVD LV being less than two thirds,
but we allow people to get
to one-to-one when they're critically ill.
It's important to remember that when you're looking
for pericardial tamponade,
the subcostal window tends to be our best.
And you can see the hand position needed to scan this
as well as a view you might get of a patient
with a large pericardial effusion
as the pressure in the pericardium increases,
the first thing that happens is you get IVC plethora.
This is the most sensitive finding for tamponade physiology
and then right atrial collapse
and then right ventricular collapse
where your sensitivity decreases
and your specificity increases as
that intra pericardial pressure rises.
So let's start to put this all together.
If we think about our etiologies of shock, hypovolemic,
cardiogenic, obstructive and distributive,
what we see in our cardiac views is now in the second column
of this table, small hyperdynamic chambers
for hypovolemic shock, large impaired function
for cardiogenic shock, typically obstructive shock showing
either the air artifact of a tension pneumothorax,
a clot in transit or right ventricular dilation
and impaired function in massive PE
or a pericardial fusion in tamponade.
In distributive shock, it might be hyperdynamic
or in the case of septic cardiomyopathy,
it might be impaired.
So the next window into the body
that we have is venous filling.
And we'll look at two different ways to look at this,
but I do want to offer that there are more
and more sophisticated approaches.
This is a review in that showed using spectral doppler
and the patterns of spectral doppler in different organs
of the body to talk about filling pressures.
But I'm just going to talk about evaluating the inferior vena
cava and the internal jugular vein.
So when you're trying to get your IVC, again,
you're starting with the transducer laid against the
subcostal region,
and you want to get this view that allows you
to see the IVC longitudinally, the hepatic vein starting
to drain into the IVC to confirm
that it's not the aorta liver on both sides of the IVC
and you can see the right atria
as the IVC drains into it really nicely.
In this picture interpreting this
is a little bit tricky.
So in the spontaneously breathing patient,
we think about the size
and the percentage that it collapses.
As visual representatives of the CVP
originally we would assign specific
and precise CVP values to different patterns of IVC size
and collapse, but we moved away from that
and now we use the American Society
of Echocardiography recommendations
where we basically say if A IVC is small
and collapsible defined
by less than 2.1 centimeters in diameter
and collapsing more than 50% in a spontaneously breathing
patient, then we assign the right atrial pressure of three.
If somebody has a large
and un collapsible IVC so greater than 2.1 centimeters
and collapsing less than 50%,
we assign them the estimated right atrial pressure of 15
and everything else, any other combination of size
and collapsibility, we assign the
right atrial pressure of eight.
We also tend to follow their guidelines that say
that if a patient is on positive pressure ventilation,
we assign them a right atrial pressure of eight regardless
of what their IVC dynamics look like.
As we do this though, I want to make sure
that we're not inappropriately narrowing our differential
to only thinking about their volume status.
Because IVC plethora is a non-specific finding.
Many things will cause a large non collapsing IVC
and that includes tamponade physiology as we just mentioned,
as well as multiple different times of cardiomyopathies
or pericarditis, massive PE or tricuspid regurgitation
and IVC thrombus is are rare,
but in my institution sometimes seen phenomena
where the IVC will be large even though the patient is
relatively hypovolemic.
Beyond that, even IVC collapse is non-Pacific.
We've all seen the patient who's got severe dyspnea
and their intrathoracic pressure swings are so great
that their IVC will collapse regardless of
what their intravascular volume status is.
And similarly, you can have something externally compressing
the IVC such as a mass or 10 societies causing a small
or collapsing IVC in a patient whose volume status,
which they have an elevated right atrial pressure.
So here's an example of video like this
I tend to use for teaching.
You can see the IVC in the longitudinal view,
you can see it draining towards the right atrium.
You can see liver on both sides
and you can see a hepatic vein starting to go into this
and you might look at this and say, oh,
this IVC is about two centimeters
and is not collapsing at all.
But you also, if you have a keen eye, can see
around the heart an koic space.
And when I rotate my transducer, I'll see that
that brings me again to a large pericardial effusion.
So when we think about the IVC
and the internal jugular vein, we get to see patterns
of these that correspond.
If you have an IVC that's not achievable
and many times in our critically ill patients,
we can't see the IVC because of ileus
or bowel gas or surgeries.
So if we think about plethoric, I vvcs, as you can see here,
large unchanging, normal IVCs or flat IVCs.
We have a correlating internal jugular pattern
where high on the neck,
you can see here a dilated IJ much bigger than the carotid
not changing with respiratory variation.
Here you can see a normal IJ where even just
above the clavicle you have a triangular,
a trapezoidal shape that changes in size with respiration.
This represents a normal right atrial pressure.
Or here you can see somebody who just
above the clavicle has a completely collapsed IJ
that only expands during exhalation.
So if we put that together into our table,
now we've got our third column thinking about
our etiologies of shock.
We can think about the fact that a hypovolemic
or hemorrhagic shock patient should never have a plethoric
IVC absent one of the confounders that we just talked about.
Instead their IVC or their IJ should be flat.
Cardiogenic shock patients tend to be volume overloaded,
so they tend to have plump IJs
and IVCs obstructive shock patients.
Similarly, the blood has to back up somewhere.
So if a obstructive shock patient is evaluated,
they should have a dilated neck vein and a dilated IVC
and distributed shock patients.
It depends on what phase of resuscitation they're in
prior to resuscitation.
These both these vessels are flat and then normal
and then plethoric if they are resuscitated.
Great. So that's our venous filling.
Let's talk about the pulmonary window as a way
to get an idea of what's going on in shock.
The first thing we can do is we can look for pneumothorax
and we do that primarily through lung sliding.
And if you look at these two videos, one done
with a linear transducer
and one done with a phased array transducer,
you can see the glistening shimmering artifact at the level
of the pleura that's highlighted here in the white box.
I'll offer that if you're a computer nerd like I am,
you might see this and say each pixel's just going black,
white, gray, black white, gray, black, white,
gray over the course of a respiratory cycle
and the presence of this finding
of this shimmering artifact known
as lung sliding rules out a pneumothorax at the place
of the transducers being held
with a greater confidence than a chest x-ray interpreted
by a radiologist.
Sometimes that lung sliding artifact is difficult to see
or if you have a patient
where their lung's not moving very much.
For instance, somebody who has bullous emphysema
or has low tidal volume ventilation, you can look
for the lung pulse.
And what you're seeing here is in the M mode imaging version
of evaluation for lung sliding, you can see a break
in the horizontal lines highlighted by those white arrows
or here on this longer spectrum.
And this allows you to see
that every time the heart beats in the chest,
it causes the two layers
of pleura to move against each other.
So even though there's no phasic variability of the pleura,
there's still aphasic variability
and that allows us to rule out pneumothorax
with the same confidence
as seeing respiro phasic lung sliding.
So if we put these together, we have lung sliding the
presence of beelines, which cannot be seen.
If there is a pneumothorax
and lung pulse, we start to get a pretty robust set
of indicators to rule out pneumothorax in a patient
with undifferentiated shock.
There's only one finding described in the literature
as ruling in pneumothorax
and what it's seen here, it's referred to as the lung point
and what you can see is that there is no lung sliding in the
pleura on the left hand side of the screen,
but there is lung sliding in a phasic pattern on the right
hand side of the screen.
This suggests that we're seeing the bottom edge
of the pneumothorax.
I'll offer that.
You can see this finding,
although it's described
as being a hundred percent specific in patients
who do not have pneumothorax, if they have a history
of thoracic surgery, for instance in my center
with a large number of lung transplant patients,
we frequently can find a lung point in a patient
with no pneumothorax.
It's also not very sensitive.
If we think about the size of pneumothorax, that tends
to cause tension physiology.
It's circumferential large pneumothoraces
as seen here in this chest x-ray
and that means you're never going to find the point
where the lung re adheres to the pleura.
The next step of my lung evaluation
with point-of-care ultrasound is is looking for B lines.
And what I'm looking for is whether there are these vertical
hyper coic artifacts and what their pattern is.
You'll also notice that on the left we have a smooth pleural
line, perfectly smooth white line with beelines coming off
of it, whereas on the right you have a little bit more
of a jagged plural line.
These are referred to as an irregular pleura
that irregular pleura suggests that it's an inflammatory
or infectious etiology of the beelines as opposed
to purely a volume overload etiology in comparison
to the smooth pleura here,
lung ultrasound is useful not just for the presence
of cardiogenic or non cardiogenic pulmonary edema,
but also for the detection of pneumonia.
So if we think about focal beeline patterns
as being present in our pneumonia patients
or potentially a consolidation as seen here
with a small pleural effusion in this patient
with strep pneumo pneumonia
or the dynamic air broncho Graham seen here
where you can see these white lines moving
with a phasic pattern in a patient who's got pus
in the airways.
These things all make lung ultrasound a better diagnostic
tool for pneumonia than plain chest x-ray
beyond just the pneumonia you can evaluate
for whether there's a closed space of infection like mima.
If you look closely at this image,
you can see the consolidated lung,
you can see the hypoechoic pleural effusion surrounding it
and you can see a couple of loculation connecting
that can consolidated lung
to the diaphragm on the right side of the screen.
That suggests pretty strongly
that this is going to be an exudative effusion.
The absence of loculation does not mean
that it's necessarily going to be translative,
but the presence of loculation was found
to be very predictive of an exudative effusion.
So now we've got our fourth column in this
table pulling this together.
We can think about whether we're seeing a diffuse ALINE
pattern as we should see in a hypovolemic patient,
a diffuse bline pattern as is present in a cold
and wet cardiogenic shock patient.
Or we can see the specific patterns of obstructive shock,
either the absence of lung sliding in pneumothorax,
the ALINE pattern of pulmonary embolism
unless you happen to catch the area of infarcted lung
or the ALINE pattern of tamponade
where you have clear lungs,
elevated neck veins in a distributive shock patient.
Again, you might see ALINE patterns or a pneumonia pattern,
but gradually as they get fluid you may see a beeline
pattern start to appear
as you get capillary leak into the lungs.
Pulling this together, there's a few other windows
that we can use to get some ideas of what form
of shock a patient's in.
We can do a DVT examination
and this is an example of a free floating thrombus in a vein
and you can see that you want to check all of the zones
of the lower extremity in order to have the confidence
to say that you've truly ruled out DVT.
Again, the absence of DVT does not mean
that PE is off our differential,
but the presence of DVT certainly raises our
pretest probability.
We can do skin and soft tissue ultrasound
looking for infections.
On the left you can see a video showing the irregular
borders, posterior acoustic enhancement
and hypo coic space of a abscess.
And on the right you can see the cobblestone pattern
that typically is seen in cellulitis
evaluating the gen genital urinary system.
We can see here the hydronephrosis of a patient
who had an obstructing urinary stone
and on the right you can see a distended bladder
with debris inside of it.
In a patient who had an untrained UTI effectively acting
as an abscess just looking at free fluid in the abdomen can
help us because if we see
what we see on the left ated hyper coic fluid, we start
to worry that this too is an infected space.
Again, an anti coic fluid does not rule out infection
and you have to do a paracentesis
and that's where ultrasound really leans into its strength
as procedural guide seen here doing real time ultrasound
guidance of a paracentesis in a patient
with a very small pocket.
Alright, now we've gotten through the first couple sections
and we can put together this pattern
of the ways in which different POCUS findings correlate
with different etiologies of shock.
Beyond that, we can start narrowing it down
and saying what things are different as we go from one form
of shock to another.
So the idea that if you find impaired function
that could be present in septic cardiomyopathy
but it makes cardiogenic shock think
higher on my differential.
Similarly, if we see a clot in transit
or rv PE is suddenly surged up if we see a pericardial
effusion, we have to think about pericardial tamponade.
We want to think about the pattern of filling pressures
and how those fit with different forms of shock.
If I have a patient who I'm worried about hemorrhagic shock
and I see a plump I have, you see
that moves down my differential.
And conversely, if I see a patient
where I'm thinking about obstructive shock,
but I see a flat IVC
or IJ that moves down my differential,
the lung ultrasound pattern can be helpful,
especially if we're trying to identify a pneumonia
that might might have been missed on our chest x-ray.
And then other findings such as free fluid in the abdomen
in a trauma patient, the presence
or absence of plural effusions DVDs
or a source of sepsis can really help us figure out which
type of shock we're dealing with.
So let's take this on a bit of a test run.
I'll show you some images and we'll practice figuring out
which form of shock these images would boast
appropriately be lumped into.
So if we look here, we have a pararenal long axis view in
the upper left hand corner, a longitudinal view
of the IVC in the right hand corner
and a lung ultrasound view at the bottom.
And if I look at this, I say, oh man,
I see a large left atrium
and a large fight right ventricle, I see a dilated LV
and I see a plump unchanging IVC and beeline pattern.
So when I put this together, I might think big rv,
big LV, plump IVC beelines, that's cardiogenic shock
until proven otherwise.
If I see this pattern of findings,
a dilated right ventricle, a dilated right atrium, a plump
or plethoric IVC
and an ALINE pattern, putting that together, I think man
that works with pe, an obstructive physiology of shock.
If I see this, a hyperdynamic heart both left
and right ventricles hammering away as hard as they can in
that apical four chamber view on the left, a flat IVC,
you can see it draining into the right atrium with almost
invisible diameter during inspiration
or a consolidated lung
as seen in this lung ultrasound showing a small pleural
effusion surrounding it to me that says normal
or hyperdynamic heart flat IVC consolidated lung,
I'm thinking about septic shock
unless I have a reason to not.
So where do we go from here? Now we've got a way
to figure out which form of shock we're in.
Let's talk about what we do next.
And this is where we're going to talk about izing,
our assessment of shock and the perhaps the most commonly
used protocol is the rush protocol.
And this can be thought of as an evaluation of the pump,
the heart, the pipes, the IVC, the aorta
and the deep veins and the tank, the pleural cavity
and the abdominal cavity
or this is sometimes thought up as high map
where you have the heart, the IVC Morrison's pouch,
the aorta and the lungs.
And this starts with a parasternal long axis view.
You can see that being acquired here.
And then you can move to an apical four chamber view
because as I like to tell my trainees, one view is no view.
You should always get two views of the heart
before committing to your interpretation of it.
A view of the IVC looking to see whether that's big,
small collapsing, non collapsing Morrison's pouch
and the other chambers in the abdomen with the understanding
that Morrison's pouch is the most sensitive
of those chambers for free fluid.
An evaluation of the aorta to look for aaa, an evaluation
of the lungs, primarily looking for pneumothorax as a source
of obstructive shock.
You can include other things such as ectopic pregnancy,
which as an adult pulmonary and critical care doctor,
I'm very rarely looking for evaluation of DVT trying
to figure out whether
or not I need to move PE higher on my differential.
Beyond that, we can get into this interesting skillset
of spectral doppler, interrogation of the aortic valve
and this allows us through VTI evaluation to look
for whether we are in a low output shock state
or a high output shock state.
And so we think about this using that VTIA measurement
of the diameter of the left ventricular outflow tract
and a in our minds a typical normal range.
And this one study from C in chest a couple years back
talked about the idea that if we have a VTI range
of less than 14, that's a low output state greater than 22,
that's a high output state
and we need to think about that
normalized to the heart rate.
If somebody's heart rate goes up, we expect
that each stroke is going to be smaller.
The challenge here is when we think about all of our forms
of shock, cardiogenic shock, obstructive shock,
hypovolemic shock and distributed shock prior
to resuscitation, these should all be
low cardiac output states.
But the difference is that once you've resuscitated a
patient with distributive shock,
they go into a high cardiac output state, they have shifted.
If we think back to those original couple slides from a
space of inadequate blood delivery to tissues
to now there's adequate blood delivery,
but unfortunately the cellular mechanisms
or the microcirculation has been poisoned,
we can use this serially
and this is where the real power comes in
and we can change ourselves from
thinking why are they in shock?
We've already established that too, is what I'm doing
to them helping the shock.
And so we can think about a hemodynamically unstable patient
who start in this low cardiac output state for all of them
and then we do something, we either add inotrope or fluids
and we see whether that improves our cardiac output
as measured via L-V-O-T-V-T-I.
If we want to get an actual cardiac output instead
of just L-V-O-T-V-T-I, the equation's here
for calculating stroke volume using that diameter
of the LVOT
and then we can multiply that by heart rate
to get a cardiac output number.
I'll offer that measurement errors in this get magnified
because you're thinking about a radius squared value.
So we can also just look at the VTI
and scale it over time normalized to the heart rate.
Here's an example. We have a patient who's got a VTI
measured through that aortic valve of 11 that's low.
This is a patient who's in a low cardiac output state
and then we can look at them
after the intervention of adding epinephrine.
And what we can see is they have improved their VTI they're
now, they now have a VTI of 15, they've moved closer
to a normal cardiac output it.
One of the questions that's often asked is, can we use POCUS
to answer whether or not a patient is going
to be fluid responsive?
And the answer to that is it is better than a physical exam.
But I want to highlight as this graphic shows from DeBaker
that while we may still be on the part
of the Frank Starling curve, we're adding additional fluid
to the patient, improves cardiac output.
We also could be on the part of the curve
where there is steep increases
with permeability of the capillaries.
So while we're improving cardiac output,
we're also causing more leaking into the lungs
that EVLW vascular lung water,
which can cause more harm than benefit,
especially if we already have adequate oxygen
delivery to tissues.
That said, there's a few different ways we can look at this.
One is this idea of the underfilled left ventricle
and this is really referring to LV and diastolic diameter
and a excellent study of VIN etal in 2017 looked at this
and said, Hey look, if you look at fluid responsive
patients, patients who improve their cardiac output by 15%
or more with bolus compared
to not fluid responsive patients,
the fluid responsive patients have a smaller LV
and diastolic volume.
The thing is that any 2D echo indicator we're using
to look at fluid responsiveness is going to depend on them
having normal diastolic function
and normal valvular function.
Also, it's going to be disrupted
by any atrial arrhythmias such as AFib.
If we're looking at the RV measurements to decide whether
or not somebody's fluid responsive, we have to assume
that they have normal RV function and normal RV afterload.
That said, when you take all these together
and you compare them to clinical indicators alone,
as was done in this study by Jack asking cardiologists,
do you think this patient has an elevated pulmonary
capillary wedge pressure versus echocardiographic
indicators, the ones that we just described,
they are superior to physical exam alone.
Then we might ask ourselves, which indicator should I use?
And this is where I'm going to go back to that study
by Ian Etal from the blue journal
where they compared a bunch
of different echocardiographic indices to see whether
or not somebody was fluid responsive.
And I love this study, it's incredible
and it's worth reading in detail,
but buried in the supplemental tables is this one which I
think is just gold.
And this is the idea that instead
of having a single threshold value for any indicator,
we want to have a recognition of whether we're trying
to maximize that indicator's ability
to be sensitive or specific.
And you can see here a comparison
between pulse pressure variability,
the change in max velocity through the aortic valve,
the change in size of the superior vena cava
or the change in size of the inferior vena cava.
And you can see that when you optimize this for sensitivity,
you get very different values than our normal thresholds
versus when you optimize it for specificity
and then you have this gray zone between the two.
And that's the area where I should not change my pre-test
to post-test probability.
I do want to close by saying while we spend a lot of time
and money trying to figure out
how we can predict fluid responsiveness in our patients,
I've started to care a little bit less than I used to.
And if we think about the classic study
that was released a couple years ago
where they tried randomizing people
to a more restrictive fluid strategy versus the standard
fluid strategy, they found no difference in mortality
or any of their other outcomes.
Admittedly, this is probably a reflection of the fact
that our standard of care has made it so
that the difference in amount of fluid received
by the restrictive versus standard group was a difference
of only a liter and a half,
which is relatively small compared
to when we look at historical norms.
And this clover's subgroup analysis shows
that the practice is already changing.
And when we really try to push people
to be in a restrictive versus liberal fluid group,
again we see no real difference in outcomes other than the
fact that the restrictive fluid group got more vasopressors.
But we see a difference in fluids of about two liters.
Again, making it so that I feel as long
as you're within a range of appropriate fluid values,
I'm a little less concerned in most patients, those patients
around the edges where I think another leader really will
hurt them or will they really be hurt
by the escalating vasopressors that are on.
Those are the patients where we want to think about, hey,
can I use POCUS in order
to differentiate their fluid responsiveness status?
So pulling this all together, I like to think
of point-of-care ultrasound as an important
part of the workup for shock.
It augments the ability of our physical exam to see
what someone's etiology of shock is
and a little bit of whether or not they're adequately perfu.
We can use advanced techniques such as VTI
to help us track whether or not our interventions are
improving or worsening our cardiac output.
And we can remember that patterns
of point-of-care ultrasound align
with certain clinical etiologies which can really help us
combine this with our history
and physical to create a meaningful illness script.
Thank you so much. Really excited to get
to answer some questions about this
and see how people are using POCUS in the field.
- Alright, thank you so much Dr. Bastin. We do have Dr.
Bastin here on the call to answer questions.
So we will go ahead and start the the q and A section.
Now, Miriam Jamil says,
how do we interpret IVC diameters in intubated patients?
- This is a great question
and something that I really enjoy talking
about when I'm in the hospital.
You, if you ask the American Society of Echocardiography how
to interpret the IVC for an intubated patient,
they'll tell you you can't
and you should just assume that the estimated right
atrial pressure is eight.
And I'm not trying to disagree with that.
It's, it's the standard that's been used for all
of the studies that have been done using echo
to do things like right atrial, sorry,
like right ventricular systolic pressure calculations.
But I think we can get a little bit more sophisticated in
our interpretation when we're talking about critically ill
patients in a medical intensive care unit
or really anywhere.
And that that means, what I mean by
that is we know the direction of error.
So positive intrathoracic pressure,
when somebody's on positive pressure ventilation, whether
that's bipa or
or invasive positive pressure ventilation should cause blood
to pool in the abdomen.
The obvious C should become plump, should be bigger
and should collapse less than we're expecting.
And so if I see a collapsing IVC,
that means something to me.
That means that this person doesn't have enough blood,
even when augmented
by the positive pressure ventilation does not have enough
blood to maintain their IVC as plethoric.
On the other hand, if I see a plethoric IVC in an intubated
patient, I don't know what to do with that.
I, I go back to my,
this should not affect my pre-test probability.
Now if we go back to that IGN atal paper though,
they did look at this in intubated patients
and what they specifically said is
that you should have different thresholds
and that's where that one table that they pop up in
in the supplemental table C, they have,
whether you want to maximize sensitivity
or if you want to maximize specificity.
And again, they're like, if you want to maximize the
specificity of this, then you unfortunately have
to use a change in IDC diameter of 3%.
Which gosh, that's so subject to measurement error that I,
I don't really end up using it all that often.
But they say if you have a,
if you want to maximize sensitivity, you can use that 22%.
And so, and so again, it's a, with the knowledge
of the directionality that the error should be moving based
on positive pressure ventilation,
we can get really useful information
about inciting etiology.
This all goes out the window if the patient is
interacting with the ventilator.
Spontaneous breathing on top
of positive pressure ventilation makes it really tough
to know what the pressure swings are looking
like and how to quantify them.
And then I just go to,
this should not affect my pretest probability
of either etiology or vine responsiveness.
Awesome. That great question.
- Awesome. Yeah, we've got another one here.
As a beginner using pocus,
how do you trust your skills enough to make a judgment
to change management?
- Another great question.
I, I'll tell you,
I very much remember the first time I picked up an
ultrasound and looked at it
and I was like, this is definitely a molar pregnancy.
All I see is snowy day and a polar bear.
I have no idea what's going on.
And I, I think that the hardest part right now is we're in
this transition time where there's certain areas
of concentrated expertise, p places where you have lots
of faculty who know what they're doing
and can help supervise
and areas where there's just not somebody to help you out.
The the thing that I remember is early on in my career,
somebody told me, anybody who's serious about getting good
at this keeps a portfolio of their scans.
And I think that's the best advice I could give
for a beginner is don't make
clinical decisions based on this.
When you start, make your clinical decisions based on the
illness scripts, physical exam history that you trust,
but as you develop your confidence
and you have this portfolio that you can compare
and you can go back and be like, oh, I thought that this,
this ended up being hemorrhagic shock
but my ultrasound showed this.
I need to learn how to put that together better.
This is how you get to the point
where you can trust what you're scanning.
So just a, just another reminder like call out
for building a portfolio for finding somebody to trust
to help you overread it and gradually
building up that confidence.
- So, alright. Let's see.
Do you have any other kind of tips
and tricks that you use when you're,
when you're scanning using pocus?
- Yeah, I mean I think, I think this was really focused on
this idea that shock is an isolated etiology and,
and we all know that that's not what happens
and that people come in with multiple
overlapping types of shock.
So when you have your patient who has known heart failure
and is septic
and you're trying to figure out which is the driver
for this, you know, this is, these are times
where sometimes you can use an ultrasound
to spare your patient the right heart cath.
That would probably give you the answer.
And what I mean by that is you get
to see what's driving first.
And the VTI is a great example of this.
When I have a patient who's got a
known heart failure produced ejection fraction
and they come in with what looks like sepsis
and I'm trying to figure out whether their hypotension is
primarily driven by pump failure or if it's driven by sepsis
and distributive after load reduction.
I like to be able to see two things.
Number one, have I seen their ejection fraction improve
from where it was before?
'cause if I think about it, you know,
gram negative broad sepsis I like to say is a great
after load reducing drug.
It makes it so easy
and you'll see people's ejection fraction augment in the
setting of their sepsis.
And you can say, all right, this plus maybe a central venous
saturation of a central line.
This points me towards the distributive state is what's
driving this person's hypotension.
And then the real power of ultrasound is that I get
to repeat my scans iteratively
and I get to say, all right, now 24 hours
of antibiotics later, let's see where we're at.
And I can say, oh my gosh,
now their ejection fraction has decreased
from yesterday to today.
I think we might be moving into
that post volume overload cardiogenic state that happens
after somebody sepsis starts to resolve 24 hours.
Being a little bit fast for that, but the,
the whole point I'm trying to make is don't scan once
and then lock your differential in there, scan,
do an intervention and see how it changes over time.
That gives you the, both the, the opportunity
to see whether the lab values are tracking in a direction
consistent with the ultrasound.
And if not, gosh, that narrows my differential
and to see whether or not my interventions are moving things
in a direction that appears to be more towards homeostasis
or away from them that those,
that's one quick thought Chris.
- Awesome. And we have another question coming in.
In a patient with a low ef, do you have a lower threshold
to start pressors over fluids
and unspecified shock even if you have some space fio two
wise on the vent?
- Yeah, this is a, this is a question
that I feel like is a callback to, to the fact
that when we look at patients
and how much volume they receive, anybody
who carries a chart history
of heart failure gets less fluids
and, and that makes sense, right?
We know that they're more vulnerable to volume overload
and likely to have volume overload occur with a steeper,
you know, extravascular lung water, water will appear at,
with a steeper curve on that kind of frank starling
and inverse frank Starling curve
that we talked about earlier in the talk.
So yeah, I, I want to be more careful.
That said, when we look back at these patients
as a large cohort, they tend
to probably get under resuscitated
and this is where ultrasound wins.
Again, I get to look at them
and say, my main fear from giving these people fluid is it's
going to spill into their lungs,
but if they have no B lines, then I can say I'm not afraid
of that right now and give them small boluses
and then check again.
And if I get to see in real time those B lines appearing
before they become hypoxemic,
I can get them adequate resuscitation, whatever that means
with the gray scale about it, without having
to worry about the damage that gets caused
by significant volume overload.
I get to watch really closely.
Just because a patient has a low ejection fraction does not
mean that they don't also have the potential
to benefit from fluids.
It just means that you want to be checking more frequently.
And again, I think of ultrasound as being
a little more rapid,
a little more accurate than my pulse oximeter in knowing
when I've started to have water spilling into the lungs.
And gosh, the first time you do a lung ultrasound,
it seems like it takes forever.
But as you get used to this hand positioning
and just where the pro goes, the dance that you do,
it's literally a 62nd test
and you do that while you're also checking cap refill,
you're in the room, you're bonding
with the patient and their family.
It's bringing us back to the bedside.
It's making us feel the connection with clinical care
that got us into this industry to begin with.
- Great. No current questions at the moment.
We can wait around for a little bit more.
Like I said, you can put those questions down in the q
and a box at the bottom or the side of your screen.
Cameron, any other things that you want
to talk about when it comes to undifferentiated shock?
- Yeah, well I'll offer the, the kind of cool thing
that I'm thinking about right now
and I'm curious if anybody wants to take this
and make a a project out of it.
I deal with a lot of patients where their IVC is collapsed
because of that false positive I talked about of
intraabdominal hypertension because of tens cytes.
And I'm trying to figure out in these patients whether their
IVC is collapsing
because they're relatively hyperbolic,
whether they're in a distributive state
or if it's collapsing because of the fluid on the outside.
And then the thing
that I think is interesting is I am fascinated
by these disparities when,
when the POCUS findings don't match up to this simple story
that we, that we learn about.
This is what all volume overload looks like.
This is what distributed shock looks like.
This is what cardiogenic shock looks like.
And when you have somebody who has elevated neck veins,
but a totally flat IVC in the presence of ascites
or in the presence of intraabdominal bleed, this is
where I start thinking, oh man,
is this intraabdominal hypertension?
How else do I get signs
of volume overload in the SVC while signs
of volume under load and the IVC?
So I like this, this thought process of saying, Hey,
let me start to do these combinations.
This is all separate from the people
who have gotten much more specific in their ultrasound
interrogations and they're able
to put spectral doppler on organs like the kidneys
and the liver and start to say, Hey, am I seeing a pattern
of resistance in the renal arteries consistent
with Anasarca Arena sarka?
Am I seeing a pattern in the hepatic veins consistent
with regurgitation in the absence of a valvular pathology?
All these start pointing you towards more subtle
and technical indicators of volume overload.
You can put these together into a scoring system that's
described by some people as veys.
I don't use veys in most of my shock patients
because mostly I'm trying to figure out etiology of shock,
fluid tolerance, fluid responsiveness,
and then is my intervention making things better or worse?
- Alright, that is fantastic information.
It looks like we don't have any more questions coming in.
So Dr.
Bain, thank you so much for being here
and thank you so much for the incredible information
that you shared with us today.
We really appreciate it.
- So happy to be here, Chris. Thanks so much for having me.
- Awesome. Well once again,
we'll be doing a second webinar with Dr.
Bain on Tuesday,
July 1st at noon entitled Lung Pocus and Critical Care.
And we would really love it if you joined us for that.
You can see the webinar QR code here.
If you go ahead and scan that, that'll take you
to sono site.com/behind the scan webinar.
Thank you all so much for joining us today,
we really appreciate it and we'll see you at the next one.
Thanks again, Cameron.
- Bye.
When treating critically ill patients, shock is frequently identified, yet the underlying etiology is elusive. Recognizing and interpreting POCUS findings is crucial for rapid diagnosis and proper treatment of these time-sensitive cases. Join Cameron Baston MD to learn how to use POCUS to differentiate the etiology of shock.
What You'll Learn
- Identify the components of shock with POCUS: cardiac, venous filling, pulmonary, and others.
- Recognize and interpret the pattern of POCUS findings in case study examples to narrow the shock differential.
- Apply the appropriate treatment in clinical shock scenarios.
- Appreciate growing applications and advanced POCUS techniques in shock cases.
Cameron Baston, MD, MSCE, is a clinician advisor for Penn Health-Tech and an Assistant Professor of clinical medicine in the Department of Medicine at the University of Pennsylvania's Perelman School of Medicine. He serves as associate program director for the Pulmonary and Critical Care Medicine fellowship, and as director of clinician-performed ultrasound for the Department of Medicine. He has an interest in helping create low-cost medical devices in the resource-limited Critical Care setting and works with several organizations on POCUS and Critical Care education. A mechanical engineer, epidemiologist, Critical Care physician, and medical educator, he spends about 2/3 of his time caring for critically ill patients, and the remainder working on education innovation and health technology.
This educational webinar is intended for healthcare professionals and not for patients or consumers. The material is provided for general educational purposes, as a reference and a supplement to professional experience, education and training, and should not be considered the exclusive source for this type of information. This educational webinar is not intended to recommend any device for a particular indication or to provide indications for use for any device. At all times, it is the professional responsibility of the practitioner to exercise independent clinical judgment in each particular situation. Fujifilm assumes no responsibility or liability for any misuse of the information imparted in this webinar. This educational webinar does not supplement, replace, or supersede device labeling, including instructions for use, which accompanies any FUJIFILM Sonosite product.