“Cardiopulmonary Interactions” by Jordan Rettig for OPENPediatrics

“Cardiopulmonary Interactions” by Jordan Rettig for OPENPediatrics


Cardiopulmonary Interactions by Dr. Jordan
Rettig. Hello, my name is Jordan Rettig, and I’m an
Attending Physician in the Division of Critical Care Medicine at Boston Children’s Hospital. Today, I’ll be discussing cardiopulmonary
interactions with particular attention towards positive pressure ventilation. So I want to just start by illustrating the
differences between a positive pressure breath and a spontaneous breath. So if we look here at our graph, we have pressure
and time on the x-axis. And if you look at the mechanical breath,
I just want to highlight the fact that as we look throughout the course of the inspiration
and expiration of that breath, it is all positive pressure. Whereas, with the spontaneous breath, you
see there is an element of negative pressure. And that’s very important when we want to
discuss the effects on cardiopulmonary interactions. So I would like to start off by talking about
some cardiac basics. So we need to talk about cardiac pump function. The components of pump function are preload,
afterload, myocardial contractility, and heart rate. Honestly, when we’re talking about positive
pressure ventilation, we’re going to be affecting preload, afterload, and perhaps contractility
because we’re going to be affecting afterload. We’re likely not going to be affecting heart
rate with any of those maneuvers. But it is important to realize that cardiac
output is a component of stroke volume, which is made up of preload, afterload and contractility
times the heart rate itself. So when we look at cardiac performance, I
just want to go through the basics of this because this is an essential physiologic framework
for how we discuss how ventricles are functioning. It’s important to note the caveat that this
is a model of the left ventricle. The right ventricle does have very similar
interactions, but obviously different anatomy. And this is, again, meant to be a framework
for us to discuss how we are going to mitigate various elements of this with positive pressure
ventilation versus spontaneous breathing. So if we start at point A on this graph, this
is mitral valve opening. And the distance between point A and point
B, where the mitral valve closes is, essentially, filling. And so this is where the heart should be in
its most relaxed state. And this is where the preload comes in, and
the heart fills up getting prepared to eject its stroke volume. If you go from point B to point C, that’s
the point from the mitral valve closing. You get isovolumetric contraction and the
aortic valve opens at point C. Most importantly, I want to point out between
C and D. Between C and D is the period of ejection. And if you look at our diagram here, you’ll
see that the distance between C and D corresponds to the stroke volume. So there are a couple important elements here. Obviously, filling, which has to do both with
diastolic compliance, as well as with preload. And then we want to talk about ejection, which
has to do with inotropy and afterload, and ultimately determines your cardiac output. As we go through this talk, we’re going to
discuss how positive pressure ventilation is going to affect these relative relationships,
and so it’s important to keep this as a framework for how you think about cardiac performance. Let’s talk specifically about preload, afterload,
and contractility. So to be granular about it, when we look at
that same graph somewhat simplified, I want to point out here that there are two dashed
lines on this graph. The dashed line at the bottom that’s slightly
curved is known as the end diastolic pressure volume relationship. And this basically signifies how the ventricle
relaxes. The vertical line dashed line represents the
end systolic pressure volume relationship. And this is a combination of afterload and
how well the heart muscle squeezes against that afterload. If you look at the gray box– this is the
normal ventricle. And again, this is a model of the left ventricle,
but this can generally be applied to both sides of the heart. The gray box represents the normal myocardium. So if you look at the bottom dotted line,
you have a normal end diastolic pressure volume relationship. If you look at the vertical dotted line, you
see that in the gray box you have a normal ejection and a normal end systolic pressure
volume relationship. What I specifically want to talk about, though,
is afterload, and that changes the end systolic pressure volume relationship. So if everything remains the same about myocardial
relaxation, about the diastolic relationship, for the same given preload, your stroke volume
is going to depend on how much afterload you have. The gray box is normal. This box shows what happens when you have
increased afterload. And increased afterload or increased systemic
blood pressure definitely will reduce your stroke volume. If you imagine the area from C to D defining
your stroke volume, that area is smaller. Likewise, If you decrease the afterload–
that would be the green box. And when you decrease the afterload, you notice
that the area from C to D is larger. The stroke volume is larger. What this indicates is that for the same diastolic
conditions and the same preload conditions, afterload is going to directly affect your
ability to maintain your cardiac output. This is important because positive pressure
ventilation will affect afterload. If we look at preload– so again, looking
at our dotted lines. In this particular example, the vertical line
that represents the end systolic pressure volume relationship maintains the same because
we’re assuming the same amount of afterload in this patient. We’re assuming the same blood pressure. And if you look at the bottom dotted line
that’s slightly curved– this is the end diastolic pressure volume relationship. This relationship looks normal. If you had a heart that didn’t relax as well,
you would see a different shape to this curve. But the point of this is that under the same
conditions, under the same diastolic relaxation, if you have normal preload, you’re in the
gray box. If you have decreased preload, you’re in the
green box. And what that means is that in the same ventricle,
under the same conditions, with the same systemic blood pressure, if you acutely decrease venous
return, you are going to decrease the distance from C to D, which is the stroke volume or
cardiac output. Likewise, under the exact same conditions,
if you increase the venous return, for example, by giving a fluid bolus, then you’re going
to see the blue box, where you’ve actually increased the preload. You have increased the area from C to D, and
therefore, you’ve increased the stroke volume and cardiac output. Preload. So as we mentioned before when we started
talking about preload, one of the major components that are involved in cardiac output is preload,
and therefore, how much blood you’re able to eject from the heart. One of the things that happens during positive
pressure ventilation is your ability to get venous drainage may be compromised. This diagram is actually an example of what
happens during negative pressure, or spontaneous breathing, as we like to call it. So systemic venous drainage, which is the
broken arrow, depends on a driving pressure between the extra thoracic great veins in
the right atrium. This is a very fundamental physiologic concept. What we’re talking about here is the hydrostatic
equivalent of Ohm’s law. Flow is driving pressure over resistance. If you remember that through this talk, a
lot of what we say will become very logical. So the idea here in this diagram is that during
spontaneous breathing, the pleural and right atrial pressure falls because your intrathoracic
pressure is becoming negative, and therefore there’s less pressure in the right atrium,
and it’s easier for blood to return. Additionally, as you’re taking a breath in,
your intra-abdominal pressure and your pressure in your extra thoracic great veins is going
to rise. So you have the combined benefit of decreasing
the right atrial pressure with negative intrathoracic pressure, and you also have an increased abdominal
pressure. So if you think of it in terms of flow is
driving pressure over resistance, when you’re spontaneously breathing, your body is well
set up to actually augment your venous return. We can also say this in a different way. Systemic venous return is the mean systemic
venous pressure minus the right atrial pressure over the resistance in the systemic veins. For those of you who prefer graphs, this might
be more logical. The idea still is that flow is driving pressure
over resistance. The question becomes, though, when we introduce
positive pressure ventilation, how do these changes happen? Because what we talked about in the first
two slides was that we were talking about this in terms of negative pressure ventilation
and spontaneous breathing. Now, this is a diagram showing aortic flow,
pulmonary artery flow, and vena cava flow. And what we note, if you look at the bottom,
is that on initiation of positive pressure ventilation, all of these things go down because
all of what I said before is now the opposite relationship. So when we have negative pressure in the thorax
generated by spontaneous breathing, the right atrial pressure falls, the abdominal pressure
rises, and you get better venous return. When you introduce positive pressure into
the thorax, you are going to increase your right atrial pressure, and it’s going to be
harder for that venous return to come in. So right from the beginning of positive pressure
ventilation, you may see a decrease in cardiac output due to the fact that you don’t have
as much venous return. So when we think about right atrial preload
and positive pressure ventilation specifically, we need to think about the physiologic changes
that are going to happen acutely in our patients. And as we prepare for getting those patients
ready to tolerate positive pressure ventilation, there are some maneuvers that we like to do
in the ICU. To begin with, we like to give them volume. We like to make sure that somebody is euvolemic. We like to choose sedation agents carefully. Because if you make somebody very venodilated
in addition to the fact that you will have an increase in intrathoracic pressure, you’re
also going to venodilate them. And so they’ll have less of a driving pressure
in terms of venous return. And there’s also going to be an increase in
RA pressure due to a change from negative to positive pressure, as we mentioned before. On initiation of positive pressure ventilation,
we do need to remember that there is a decrease in the systemic venous return due to venodilation
and an increase in RA pressure due to change from negative to positive intrathoracic pressure. That is the take home. So one of the things I want to talk about–
so we’ve spoken about right atrial preload. And I think we understand the concept. Flow is driving pressure over resistance. When you move from spontaneous breathing,
negative intrathoracic pressure to a positive intrathoracic pressure, you are going to create
increased right atrial pressure, which is going to be an impediment to getting venous
return. Afterload. So now that we’ve talked about the preload
and the fact that the preload may be affected by positive pressure ventilation, I want to
take a minute to talk about the afterload. If you recall where we started this lecture,
we said that there are a couple of ways to augment cardiac output. One of them is with preload, and one of them
is by mitigating the afterload. When we think about the right ventricular
afterload, it’s a little bit different than the left ventricle. The left ventricle has an afterload that is
basically defined by your blood pressure, for lack of a better phrase. When we think about the right ventricle, we’re
actually talking about afterload in terms of the pulmonary vasculature. So what we want to do is we want to mitigate
pulmonary vascular resistance. So I want to talk about mitigating right ventricular
afterload. So we just talked about the fact that preload
can be adversely affected by mechanical ventilation or positive pressure of ventilation. Because we talked about the relationship of
once you introduce positive intrathoracic pressure, you’re going to have a higher right
atrial pressure and less likely to get venous return. But I do want to talk about afterload because
I think, traditionally, people think that mechanical ventilation or positive pressure
ventilation is bad for the right ventricle. And often, they think that because of the
relationship between the decreased preload and positive pressure in the thorax. I just want to be careful, though, to articulate
that right ventricular afterload is equally important in the right ventricular function. If you recall where we started this lecture,
we talked about the components of cardiac function, and we talked specifically about
preload and afterload, and how you could actually increase cardiac output if you mitigated afterload. What this essentially shows is that, overall,
in the lung, if you were too atelectatic or you’re too overdistended, you’re likely to
have elevated pulmonary vascular resistance. So if you have a patient that actually needs
recruitment or requires positive pressure to allow their lungs to be open, in some ways,
even though you might be impairing their venous return to their right atrium, you are likely
going to be augmenting the afterload of the right ventricle in so far as you’re going
to be reducing it, and actually making cardiac function better. If you look at this graph, it describes the
relationship of the alveolar and extra-alveolar vessels, but the total relationship is quite
clear. When the lung is atelectatic, you have high
pulmonary vascular resistance due to hypoxic vasoconstriction. And when the lung is overexpanded, you have
high pulmonary vascular resistance due to mechanical compression. So essentially if you look at RV afterload
and mechanical ventilation, the goal of mechanical ventilation is to restore functional residual
capacity. On induction, sometimes we do consider recruitment
maneuvers, which is putting a relatively high amount of pressure into the lung to begin
with in order to restore volume to reach functional residual capacity. But we must balance the effects of preload
and afterload because you are hearing, in fact, a mixed story. As stated before, the preload may be adversely
affected. But if you titrate your ventilation correctly,
the afterload may be mitigated to increase cardiac output. So the clinician is constantly going to have
to balance between those two relationships. When we think about left sided preload– so
we just talked about the right side of the heart, and now we’re going to shift to the
left side of the heart. Pulmonary venous return is essentially the
mean pulmonary venous pressure minus the left atrial pressure over the pulmonary venous
resistance. Again, this is a derivation of Ohm’s law. This is flow is driving pressure over resistance. In most cases, this is actually determined
mostly by the right ventricular output. Unless there is a specific issue anatomically
with the left ventricle or with the function of the left ventricle, for the most part,
what the right heart puts out will be equivalent to left ventricular preload. There are a couple of relationships that are
important, though. And this is where in the conceptual physiologic
framework we can use charts and graphs to sort of talk about cardiac output. But in the actual practical patient, we do
have to address the fact that there are intraventricular relationships. And so what happens on the right side is inherently
going to dictate what happens on the left side. What happens on the right side traditionally
is associated with venous return. And what happens on the left side is traditionally
associated with cardiac output. But the truth is, both sides of the heart
depend on both preload and afterload to dictate their function. So when we talk about transmitted or intraventricular
relationships between the right ventricle and the left ventricle, we want to talk about
the fact that if you have decreased right ventricular preload, you will inherently decrease
left ventricular preload because the blood to the left ventricle is all coming through
the pulmonary circulation. So essentially, if you have poor venous return
to the right side, you’re going to have a low cardiac output state. The other thing is if you have increased RV
afterload, it will diminish the ability of the right ventricle to pump blood through
the pulmonary vasculature. And this is where we really talk about targeting
functional residual capacity with our ventilator strategy. Again, getting back to previous slides, we
want to mitigate the relationship of pulmonary vascular resistance and lung volume. So we want to target functional residual capacity
in order to make sure that the right ventricle doesn’t have additional afterload. Some situations where you can get additional
afterload include pulmonary hypertension, and other pulmonary vascular disease. But in general, if we have a patient without
pulmonary vascular disease, we can often successfully mitigate the afterload with our positive pressure
strategy. The other thing that is worth noting because
it does come up with patients, and it can be quite disconcerting for clinicians is you
can get increased right ventricular filling. Now, I know that for the majority of this
talk, we’ve spoken about briefly spontaneous breathing, but we’ve shifted focus into positive
pressure. I do just want to say that as you approach
a patient, and you’re trying to figure out why they might have a low cardiac output,
and you’re trying to figure out the origin of their respiratory distress, one of the
things that’s really important to consider is actually somebody who has obstructive lung
disease or restrictive cardiac disease. Because there is an intraventricular dependence
here, where if you can imagine increased right ventricular filling– so if somebody is really
gasping for breath, and they’re generating huge amounts of negative intrathoracic pressure,
remembering that flow is driving pressure over resistance, they’re going to get a lot
of venous return each time they take one of those massive negative pressure breaths to
overcome the distress that they’re feeling. The problem with that is that the right ventricle
is actually a lot less, sort of, stiff and muscular than the left ventricle. And the intraventricular septum does tend
to bow at some points. And so if the right ventricle acutely gets
filled with increased venous return because of large negative intrathoracic pressure,
what can actually happen is the right ventricle can bow into the left ventricle. And bowing into the left ventricle functionally
makes the size of that ventricle smaller. And it makes it less compliant. And it makes it harder to fill. So what ends up happening is while you may
have more than adequate preload, under those conditions the left ventricle isn’t able to
fill, and what you’ll see is actually a decrease in cardiac output. So to summarize this particular section–
and I know we’ve said it a lot, but these relationships are very important. So if you look at this graph again, when you
augment preload and imagine the curve from C to D, you see stroke volume in cardiac output. And you can see readily how under the same
conditions of the myocardium, adding preload will allow you to augment your cardiac output. I also want to talk about left ventricular
afterload because this is a really important concept moving forward for positive pressure
ventilation. So left ventricular afterload is essentially
generated by the Law of LaPlace. And when we talk about afterload, what we’re
really talking about is left ventricular wall stress. And I want you to remember this not because
this is a physics lesson, or because we expect somebody to know the Law of LaPlace at the
bedside. What I want you to remember is the relationship
of left ventricular afterload has to do with wall stress. And when we talk about the various changes
that happen in the thorax, the difference between spontaneous negative pressure breathing
and positive pressure breathing, I think it’s going to make a lot more sense how this can
mitigate afterload. And once again, back to our diagram here. We talked about preload. We’re talking about afterload now. And if you look at the end diastolic pressure
volume relationship, which is the horizontal line connecting the points D, you see that
increased afterload results in decreased cardiac output, decreased stroke volume. So let’s talk more specifically about LV afterload
in mechanical ventilation. So we talked about right atrial preload, and
we talked about how mechanical ventilation may not be good for that. We talked about right ventricular afterload. And we talked about how ventilating to FRC
might actually decrease pulmonary vascular resistance, and therefore, decrease right
ventricular afterload. So let’s talk about the left side now. So on the left side of the heart, initiation
of positive pressure ventilation acts as what we would call a left ventricular assist device
because it decreases left ventricular wall stress. That’s the Law of LaPlace. That’s why we brought this up in a prior slide. Because understanding the concept that left
ventricular afterload is defined by wall stress makes this a little bit more intuitive. So basically, what happens is, if you imagine
in the thorax, when you generate a spontaneous or negative pressure breath, the thorax is
pulling outwards. And it creates more wall stress on the left
ventricle that’s then trying to contract. If you imagine a positive pressure breath
where the pressure is coming inwards, you can imagine that that inwards pressure decreases
the wall stress, and actually allows that ventricle to contract better. So even though there are some adverse effects
on preload, one of the great benefits of positive pressure ventilation is to mitigate left ventricular
afterload. So we consider positive pressure ventilation
when somebody has diminished cardiac function and cardiac output because, if you remember
back to where we started this lecture, when somebody has decreased afterload, they can
actually acutely have increased stroke volume. So the other caveat to this, though, is attention,
strong attention, needs to be paid to when we discontinue positive pressure ventilation
in those patients who have left ventricular dysfunction because you cannot underestimate
the fact that we have provided this left ventricle with an afterload reduction by causing positive
pressure in the thorax. When you acutely remove that, if the left
ventricular function has not changed from where it was, you may actually have an acute
cardiac output failure. You may actually have an acute left ventricular
failure. So you need to be very careful about how you
add and remove positive pressure ventilation for a variety of reasons, but particularly
when you’re removing it in the case of left ventricular dysfunction. This is also further exacerbated by excessive
negative intrathoracic pressure. So as we spoke about before, a lot of negative
intrathoracic pressure definitely helps venous return. But when we talked about the intraventricular
relationship, what we also discovered is that excessive venous return can cause bowing of
the septum. It can cause an acutely enlarged right ventricle. And it can actually cause a smaller, less
compliant left ventricle, and therefore, decreased cardiac output. If you imagine this scenario of extubating
somebody in the ICU, particularly a child, who you may not be able to have fully awake
and cooperative at the time of extubation– if they start off with left ventricular dysfunction,
and then additionally get extubated, and have a laryngospasm or respiratory distress, or
anything– crying– that would prompt them to take large, big breaths, suddenly, not
only is their left ventricle missing its assist device to mitigate the afterload, but you’re
then having that adverse intraventricular interaction of the RV becoming acutely dilated
with large venous return as a result of big negative pressure breaths. And so you have sort of a double hit for losing
your cardiac output. So it turns out that while positive pressure
ventilation can be a very effective way to support the ventricle, as you remove it, you
also have to be extremely careful that you don’t suddenly induce a state where the patient
would acutely lose cardiac output. Clinical Examples. So let’s talk about some specific examples
because I know these concepts can be a little bit confusing to talk about abstractly. So we’re going to talk about some patient
examples that are fairly common in our practice, and I think help illustrate some of these
points. So I want to talk about obstructive disease. I’ll tell you as an intensivist, this is one
of the scariest patients we see in the emergency room. This is a patient who is in acute status asthmaticus,
has bad obstruction, and there’s a question about whether or not you want to manage his
airway, and there there’s a question about, is this child going to have a significant
life-threatening event beyond what has brought him in? And so I want to use this opportunity, as
this is a common disease, to reinforce some of the concepts that we’ve discussed earlier
in the talk. So I want to talk first of all about dynamic
hyperinflation. So I’m talking specifically about the lungs. This is not about cardiac function, but they’re
very much related. So if you think about somebody with an obstructive
pattern, if you look at the flow diagram in letter A, what you’ll see is somebody who
has obstruction. They breathe in, and they breathe out. And these are spontaneous breaths, so you’re
going to see positive and negative pressures. But they never quite fully exhale. And as they don’t fully exhale, if you look
over at letter B, what you can see is the lung volume starts to go up. It starts to stack. And that’s the physiology of obstructive disease. They become hyperinflated. If you look at C and D, that would be a normal
patient. If you normally exhale, your lung volume returns
to its normal state, and you don’t become hyperinflated. So I want to think about hyperinflation in
the context of our asthmatic patient, and how that might affect cardiopulmonary interactions. So there’s blood pressure variation with inspiration
and expiration due to intraventricular dependence. We’ve talked about this before, but I think
having seen these patients, this will really bring the concept home. During inspiration, we have increased venous
return, increased RV preload, bowing of the septum, and decreased left ventricular compliance. The decreased compliance, remember, comes
from the fact that you have this big negative intrathoracic pressure, which is adding wall
stress to the left ventricle. The decreased filling leads to a decreased
blood pressure. And this process is reversed during expiration. For those of you who have been reading classic
physiology will recognize this phenomenon as pulsus paradoxus. So what we see here is with an arterial blood
pressure and time, when somebody goes through inspiration, and therefore, the right ventricle
enlarges, there is an adverse intraventricular relationship, and the left ventricle has worsening
function due to increased afterload of the negative intrathoracic pressure, you see that
the arterial blood pressure goes down. During expiration, this is reversed because
those relationships are reversed. So again, pulsus paradoxus can occur– really,
because this is a cardiopulmonary talk, it’s fair to add that there are a couple scenarios
where this can also occur independent of acute obstructive disease. And one important place to talk about this
is restrictive cardiac physiology because that will exaggerate the impact of the intraventricular
septal dependence that we have been talking about throughout this talk. So if somebody has a restrictive cardiomyopathy,
or if they had, potentially, a pericardial effusion, or other things, we would see an
exaggeration of this phenomenon. But mostly what we see in our patients is
with obstructive pulmonary physiology. So they have increased work of breathing,
which generates increased negative intrathoracic pressure. This increases the LV afterload. And basically, you’re also at the same time
having these adverse intraventricular relationships. So that’s a good example of why it’s important
to understand the differences between preload and afterload, and how the right and left
side function differently. I want to talk about another case which is
perhaps a little bit less of an acute situation sometimes, but certainly something that we
come across, and actually one of the best uses of non-invasive or positive pressure
ventilation. And this specifically, I’m talking about muscular
dystrophy, but I think you could generalize this to most neuromuscular disorders that
are accompanied by myocardial dysfunction. So essentially, the pathophysiology specifically
for muscular dystrophy is kind of interesting. So there’s restrictive lung disease, which
in and of itself is a little bit of a problem, and might require management with chronic
ventilation. There’s also obstructive sleep apnea. There’s hypoventilation largely associated
with the muscular disease, and there is a cardiomyopathy. So this is really, I think, one of the most
poignant examples of why you have to be particularly careful about your cardiopulmonary interactions
because these patients have both heart disease and lung disease. And understanding how your intervention is
going to mitigate each one of those things either positively or negatively is very important. And likewise, when you take away the ventilatory
support, you want to know what to anticipate in terms of their lung function and their
heart function, and how that might manifest itself clinically. So I think one of the most important things
to consider here is looking at a failing ventricle versus a normal ventricle. So in fairness, when I started off this talk,
I didn’t just talk about afterload as a way to mitigate cardiac output. I also talked about preload. And I said if you give volume to somebody,
or if you have good venous return, you’re probably going to maintain your cardiac output. Well, the trick there is that we had said
the entire time that that would depend on a normal end diastolic pressure volume relationship,
as in the myocardium relaxes normally. When you have cardiomyopathy, when you have
neuromuscular disease, often the myocardium doesn’t relax normally, and it doesn’t squeeze
normally. And so those relationships are off. So if you look at this graph in particular,
what we see on the top curve is a normal ventricle. And what you see is change in pressure and
change in stroke volume. And what you’re really seeing is that when
somebody has, basically, low preload state, by giving them preload, you do see an acute
change in stroke volume. As they get more and more volume resuscitated,
that relationship doesn’t hold quite as well. But what you will notice, if you look at stroke
volume and preload in the failing ventricle, you don’t really see a dramatic response to
preload. And that has to do with the fact that the
myocardium isn’t compliant. The end diastolic pressure volume relationship
is not intact. And therefore, one of the only ways to support
a ventricle like this is really not through mitigating preload. Don’t get me wrong– if you deprive that ventricle
of preload, you will have problems. But adding additional preload doesn’t necessarily
solve your problem. This is a ventricle that’s going to need afterload
reduction and careful inotropic management. So when we think about this, again, going
back to our graphs, I want to highlight here that there is a relationship not just between
afterload, but also with inotropy. And they’re completely related insofar as
they create the end systolic pressure volume relationship. Just to orient ourselves again, the end systolic
pressure volume relationship is at point D, and is the linear line. The curved line on the bottom of the graph
is the end diastolic pressure volume relationship. So this graph is meant to illustrate a couple
of things. So the end systolic pressure volume relationship
is mediated by afterload and also by inotropy. This is why we use things like epinephrine
in the ICU when somebody has a failing ventricle. So if you look specifically at the scenario
with the figure on the right, what you’ll see is there’s a decreased inotropy. And what you can imagine in this end systolic
pressure volume relationship, the gray box is normal. The blue box is decreased inotropy. Likewise, on the left side, you can see increased
inotropy. So I’ll encourage you to remember that when
we’re talking about the end systolic pressure volume relationship, it’s mitigated by inotropy
and afterload. So when you’re in a low state of inotropy
insofar as what I mean by that, your ventricle isn’t squeezing well. If that occurs, one of the ways you can mitigate
that is either by adding an inotrope, or you could mitigate the afterload. So again, when we think about that– going
back to our first diagram. If you decrease afterload you’re going to
end up on a different part of the slope for the end systolic pressure volume relationship. So you can imagine– going back one– if we
look at the decreased inotropy, and then we imagine moving forward if we decrease the
afterload in a state of decreased inotropy, we could, in fact, end up with a relatively
normal stroke volume. And that, in fact, is the entire goal of why
we put people with muscular dystrophy and cardiomyopathy on positive pressure ventilation. We do it because it actually helps us to mitigate
left ventricular afterload, which in a low contractility state, in a cardiomyopathy state,
is going to maintain your cardiac output. The caveats are obvious here. If you use a lot of positive pressure ventilation,
you’re going to adversely affect preload. So you need to be cognizant of that. You also have to be aware that if you acutely
take away the positive pressure ventilation, that left ventricle is going to have immediate
afterload. And in the context of somebody who has cardiomyopathy,
they may not be able to cope with that. So you have to be thoughtful, particularly
in the floor setting and in the outpatient setting of how you quote unquote “sprint somebody
off” of non-invasive because while their lungs may tolerate it, their heart may not tolerate
it. Negative Pressure Ventilation. So I want to talk for a minute, and I want
to end on a concept that sort of turns everything on its head. I want to talk about negative pressure of
ventilation. And I really do think that once you understand
cardiopulmonary interactions, you’ll be able to go and flip over to negative pressure ventilation. And that’s a good test to see if you’ve understood
the fundamental concepts of this lecture. Because if you can explain negative pressure
of ventilation in the context of the right-sided and left-sided interactions, you really have
understood and mastered the material that we’re trying to present here today. So just a quick word about negative pressure
ventilation because it’s not really that common, and it’s possible that a lot of people haven’t
heard of it. In fact, we don’t use it commonly at all at
Boston Children’s Hospital right now. It is still around. It was something that started off as the original
mechanical ventilator, as many of you recall– the Drinker ventilator– and now has come
back in various forms. It’s not yet totally practical. It really flies in the face of a lot of our
physiologic assumptions about positive pressure ventilation in cardiopulmonary interactions. And it makes it difficult for us to figure
out exactly how to integrate that into practice. It is, however, more physiologic. Because remember where we started this talk,
the very first slide where we illustrated the difference between the positive pressure
and the negative pressure breath. In a lot of ways, all of the interactions
that we’re talking about would just maintain as normal if we used negative pressure ventilation. There would be no difference between using
a device and not using a device. And invariably, that would be more physiologic. It does, however, depend on what goal you’re
trying to accomplish. So it is preferred in some diseases where
venous return is vital. And it is preferred in neuromuscular diseases
because you can sort of imagine not just in terms of physiology, but in terms of relative
patient comfort, the negative pressure ventilator that has been developed is actually a shell,
a cuirass that fits over the chest. And it doesn’t involve a mouthpiece or a facial
interface that could potentially be distressing to a patient. And so in a lot of ways, it’s more physiologic. In a lot of ways, it could be more comfortable. People could talk. They could eat. They could wear glasses. They could really function normally in terms
of their face, and their mouth, and everything else. However, there are some obstacles. But again, we’re here to talk about cardiopulmonary
interaction so we’re going to stick to that topic for now. So basically, how does it work? And we’re going to talk a little bit about
biphasic cuirass ventilation because it’s not fair to ask you questions about cardiopulmonary
interactions if I haven’t told you how the device works. So the pressure applied within the cuirass
acts uniformly over the thorax. It works like a shell over the chest. And the lung expansion is also uniform, so
it ventilates all areas of the lung. There’s a negative pressure that gets generated
within the chest cuirass for an inspiration or a continuous inspiratory assistance. If you think of it in terms of positive pressure
ventilation– if it’s continuous negative pressure, that’s analogous to continuous positive
airway pressure or CPAP. If it’s something that synchronizes with the
patient’s respiratory effort and provides bilevel level pressure, that’s analogous to
BiPAP, or biphasic positive pressure ventilation. A positive pressure within the cuirass induces
expiration if you want to be in that biphasic mode. So basically, there is a sensor at the level
of the nose of the patient, and you have negative pressure. And then when the patient starts to exhale,
you get a burst of positive pressure, which creates a bilevel difference. But in general, you’re maintaining a negative
pressure, much as you would maintain some degree of positive pressure whether you are
on CPAP or BiPAP. So as we talked about, CNEP, Continuous Negative
Pressure, is analogous to the CPAP. There is a control mode and there is a synchronized
mode. And that’s important to know because this
is coming. This will be in your patients. And each one of these things definitely has
a different interaction with your cardiopulmonary status. Advantages include skin integrity, thermoregulation,
ability to monitor pressure. But potential adverse effects on cardiac output. What do I mean by that? Let’s talk about this specifically. Let’s go through it in terms of the framework
that we’ve used for the rest of the talk. So I told you at the beginning that right
atrial preload was going to depend on venous return. And we talked even further about that by saying
it really depends on flow is driving pressure over resistance. And so what we really want to know is the
difference between the pressure in the great veins and the pressure in the right atrium. We talked about the fact that during positive
pressure ventilation, the right atrial pressure definitely increases. It makes it harder to have good venous return,
and therefore, makes it harder to have right atrial preload. And again, that’s the common reason why most
people say that positive pressure ventilation is bad for the right side of the heart. If you imagine negative pressure ventilation,
though, we’re talking about negative intrathoracic pressure. This is analogous to spontaneous breathing. And when we talked about spontaneous breathing,
if you recall, when you take a breath in, you generate a negative intrathoracic pressure,
which reduces your right atrial pressure. And at the same time, your intra-abdominal
pressure increases, giving you a better driving pressure. So your flow is increased because you have
a higher driving pressure and less resistance. Negative pressure ventilation would accomplish
that well. So if you have a patient who is particularly
dependent on preload, a kid who has a dysfunctioning right ventricle, or somebody with a very stiff
right ventricle, or somebody specifically with pulmonary hypertension who’s very sensitive
to preload, this might be a good modality for you to use. Because the opposite of positive pressure
ventilation, negative pressure ventilation is going to augment your preload. But let’s talk about one important fact is
left ventricular afterload. So in all honesty, I had started to make an
argument about negative pressure ventilation used in chronic patients, many of whom have
neuromuscular disease or neuromuscular weakness from chronic illness. And we talked before about positive pressure
ventilation. And we specifically talked about left from
ventricular wall stress. And we determined that wall stress is, in
fact, what afterload is. We also further said that left ventricular
wall stress was mitigated by positive pressure ventilation because as you induce the positive
pressure in the chest, the wall stress went down, the left ventricular afterload went
down, and your stroke volume would go up. Unfortunately, the opposite would be true
in negative pressure ventilation. Remember when we talked about the obstructive
patient, or patients taking deep gasping breaths that were generating large amounts of negative
intrathoracic pressure? As they generated those large amounts of negative
intrathoracic pressure, their left ventricular wall stress increased. And as that happened, the ability of the left
ventricle to provide stroke volume and cardiac output went down. So negative pressure ventilation, while it
may augment the right-sided preload, which in theory should provide you with more cardiac
output– practically speaking, you have to be careful because it will increase your left
ventricle afterload. And depending on what your patient has, whether
they have predominant right-sided dysfunction, left-sided dysfunction, global dysfunction,
or no dysfunction might decide whether or not you think this is an appropriate modality. But in the very least, I think it’s a great
way to illustrate the cardiopulmonary interactions. And I think it’s a good check. Because if this makes sense in the context
of the rest of the lecture, I think you’ve mastered the concepts. Review of Key Points. So I would just say the take home points. And we repeat these because they’re so very
important when we take care of patients. Positive pressure impairs right atrial preload
as compared to spontaneous breathing. That’s why we talk about positive pressure
ventilation potentially adversely affecting the right side of the heart. However, if we are able to target functional
residual capacity, if we use positive pressure ventilation to do lung recruitment in a patient
who is otherwise atelectatic, we may be able to mitigate pulmonary vascular resistance. And therefore, we might decrease right ventricle
afterload. And if we do that, ultimately, the output
from the right side of the heart will be higher, and you will potentially have more cardiac
output. So it’s a mixed story on positive pressure
ventilation in the right side of the heart. But I would argue that if you’re careful with
your volume status and you’re aware of the issues of preload, you can successfully use
positive pressure ventilation to ventilate to FRC. And you can actually result in an overall
very happily functioning right side of your heart. On the left side, left atrial preload depends
largely on right sided conditions, which is why I say that mitigating the right ventricular
afterload by ventilating to FRC will ultimately increase your cardiac output. Left ventricular afterload is reduced by positive
pressure of ventilation. It is absolutely essential to remember that
positive pressure ventilation is, in essence, a left ventricular assist device, which can
get you out of trouble if somebody has an acutely dysfunctional left ventricle and low
cardiac output state. But be aware that if you acutely remove that
therapy, you’re going to increase that afterload, and you may find yourself in an acute low
cardiac output state as you remove positive pressure ventilation. So I want to thank you guys very much for
listening to the lecture. I hope this was informative, and I wish you
well in your patient care. Please help us improve the content by providing
us with some feedback.

6 Replies to ““Cardiopulmonary Interactions” by Jordan Rettig for OPENPediatrics”

  1. just WOW , very informative, clear and concise regarding such complex topic.
    thanks dr.jordan .. thanks OPENPediatrics.

  2. This is probably my 4th time watching this lecture and I learn/relearn a concept every time. Great lecture – thank you!

  3. I'm a clinical educator in Respiratory Therapy and am adding this to the viewing links I give my new orientees to PCICU, with a strong recommendation to watch it multiple times. The segment at the end on negative pressure ventilation is also excellent in thinking about Glenn and Fontan physiology. Thank you.

Leave a Reply

Your email address will not be published. Required fields are marked *