¶ Intro / Opening
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¶ Podcast Welcome and Guest Bio
Welcome back to Pete Script. I'm Zach Hodges, a pediatric ICU fellow from UT Southwestern in Dallas.
And I'm Alice Shanklin, a Critical Care Fellow at Children's National in Washington, D.C.
Alice, please remind our listeners what we do here at Pete Script.
Absolutely. Pete's Crit is an educational pick you podcast. We're looking for the best bedside and basic science teaching spiels around the country and the world, and we're recording them and putting them on the internet.
And we have a very special episode today. Alice, please tell us what we're talking about.
Yes, this is chapter one in the Pick You Textbooks. This, but we're doing it a few years in. The fundamental topic of cardiopulmonary interactions. It does not matter your role when you are resuscitating a patient. This is the thing that matters. Who is doing this topic with us?
Alice, I think we have the best guest with us today to talk about this topic. We have Dr. Bradley Furman. Doctor Furman completed his training in pediatrics, followed by fellowships in cardiology and genatology at the University of Minnesota.
where he actually went on to found the first PICU at that program. He served as the chief of critical care in the University of Minnesota as well. His career next took him to the Children's Hospital of Pittsburgh where he served as the associate director of the PICU. He then moved on to be the Division Chief of Critical Care at Children's Hospital Buffalo and the and later in his career the physician-in-chief at El Paso Children's Hospital.
His career in the pediatric critical care exceeds forty years. He has many peer-reviewed publications with a research career that is focused on cardiac and respiratory physiology. And he, of course, is a co-author of Ferman and Zimmerman's Pediatric Critical Care.
Yes, the doctor Furman. Let's get right to the interview.
¶ Dr. Fuhrman's Career and Mentorship
Well, welcome back to the podcast. We are so very excited to be speaking today with Dr. Bradley Furman. Dr. Furman, welcome to the podcast.
Thank you. I'm glad to be here.
To get things started, Doctor Furman, will you please share something with our audience about yourself and include something you enjoy outside of medicine?
Well, I've always thought that I wanted to be a pediatrician'cause I wanted to play with kids and uh I have to admit that I was sort of uh tricked into going the pediatric route because I started out thinking that I wanted to give kids lollipops and balloons in the office and I ended up taking care of very, very sick kids and the th none of them wanted balloons and lollipops. They just wanted to be left alone. Um, but I did drift into intensive care and I've been very happy with that.
I actually w I was thinking about this and I don't really have a hobby, but I am a napkin artist. So I will sit down with the problem and scribble on whatever paper is nearby and I actually play with that a lot. Sometimes I spend hours doing that. So I would call that my hobby.
Oh, that's lovely. I've never heard anybody call it that before, but I could totally picture what you're doing. Now, doctor Ferman, will you share with us a key mentor or a decision that you made early in your career that was important in your development as a physician or as a physician scientist?
Okay, well you can't imagine how old I am. But when I was a pediatric resident, uh I discovered that there were kids just too sick for me to take care of them. And there really were only about three or four programs to train pediatric intensivists in the country. So I instead designed my own program and I did some pediatric cardiology to learn the heart and some neonatology to learn the lungs.
and I forged my own pathway to be able to become a pediatric intensivist. The person who supported that was a guy named Russell Lucas at the University of Minnesota. and his understanding and letting me do that, um, modifying his program so that that would fit in was very helpful to me. So that that was a big adventure to me.
Oh wow, that's amazing.
It is remarkable to have the foresight of putting together different fellowship programs and it you trained in neonatology and cardiology and giving yourself the skills necessary to take care of this newly being born specialty in pediatric critical care. That's remarkable. As you reflect back over your career, you certainly have had a very impressive one. What makes you personally most proud? What do you feel like had the greatest impact?
I think clearly what what I've done that had the most impact was my training of fellows. and the development of the textbook that I worked on with Jerry Zimmerman. I think our effort to make it possible for people to learn critical care And to sort of define the scope of critical care, because we did this very early, I think those are the things I'm most proud of.
¶ Reflecting on Failures and Career Advice
And on the other hand, we mentioned many of your successes, but another key point that I and many of our listeners can learn from are failures, their favorite failures. As you reflect over your career, is there a a favorite failure, so to speak, or instance when a situation didn't go to plan, but you feel like you or the team around you certainly learned something?
Well I can certainly tell you one that didn't go to plan. I decided as I was getting older and had felt that I was not as fast on my feet, I decided I would Try to become a pediatric department chair, and I did that for about six years and that was the worst job I ever had.
Oh, no.
I believe that it's a tough job. It definitely seems like one.
Yeah, it's hard and I I I don't want to try to make you too sympathetic to your own chairs, but for me that was the worst job I ever
Especially looking back to still feel like and be able to say that. That's powerful. To speak for Picky Fellows in general, we're extremely grateful for the fact that this is a field and in order to have a field you need research and all of these things and excited to participate. When you think about the fake pick you fellows who are in training and listening today, what advice would you have in terms of career building, thinking about life?
I think the most important thing to advise people is to follow follow your own path. Don't let somebody else tell you how you're supposed to function, what you're supposed to become. Some people will start out thinking of Pediatric critical care one way and end up thinking about it another way and life accommodates all kinds of changes in direction. So I would just recommend following one's path.
Wise words and words that apply to almost every situation. Alice, I I'll have to hate to bore you with this, but I almost say it every single week. I really uh enjoy the mentorship we get from all of our guests all around the United States. It's one of the best parts of this project. Doctor Furman, our last introductory question before we get into our topic today. Any relevant conflicts of interest to talk about before we move into our conversation?
I don't think so. I do have some conflicts of interest, but we won't touch on those areas.
That sounds great. Alice, you want to give us our first case?
¶ Cardiopulmonary Interaction Fundamentals
Yes. All right, Dr. Furman. We've got a six year old admitted for a minor elective surgery. She is in good general health. Understanding that hopefully these things are inconsequential, what are the interactions between her breathing and circulation? What's happening in everybody?
Okay, so for all normal people, there are interactions between the cardiovascular system and the respiratory system. when you think about your blood volume, most of your blood volume at any one time is sitting in venous or capillary areas, sinusoids in various parts of your body. And those constitute your working blood volume and they create pressure by virtue of the fact that they're filling that compartment.
Which is called the mean systemic filling pressure. And that is the pressure that forces blood back toward the heart. The pressure that opposes that is the right atrial pressure. We always think well if you've got a high right atrial pressure, that's a lot of uh blood volume and it'll be helpful to you. But in actual fact that's a back pressure. to the PMS or mean systemic filling pressure that actually propels blood toward the heart.
The um heart it sits in the juxtacardiac fossa, which is the membranes of the mediastinum and the pericardium, is sort of adjacent to the pleural space. And the pressure that's in those spaces impacts the pressure in the right ventricle. So when you breathe in, you reduce the pressure in your pleural space. That's how you get air to come into your lung. And that is transmitted to the right atrial pressure.
So, in a normal, spontaneously breathing person, inspiratory pressure improves the gradient from the mean systemic filling pressure to the heart and increases venous return. The lungs are the ultimate source of the right ventricular inflow, and resistance to flow through the lungs is affected by a number of different things. The inflow pressure is pulmonary artery pressure, because your right ventricle can squeeze and can elevate the pressure on the right ventricle so that it ejects forward.
The outflow pressure for the lungs is the left atrial pressure. In between, the pulmonary vessels run adjacent to the alveolus. And the pressure in alveoli can squeeze down on the alveoli. So the interaction of those three forces helps to create a vascular resistance, a resistance to flow. And those characteristics can be modified during breathing. So if you cough, for instance, you raise your alveolar pressure, and that constricts pulmonary blood flow for a period of time.
Lung volume also influences pulmonary vascular resistance. If you have a relaxed breath at the end of expiration, you're sitting at your functional residual capacity. and if you blow more air out so that you get below functional residual capacity, that increases the vascular resistance to flow through the lungs. On the other hand, if you take a really deep breath and you get way above functional residual capacity that also increases pulmonary vascular resistance. It's least at FRC.
It's important to keep pulmonary vascular resistance down because that creates back pressure to right ventricular ejection. And if you have high resistance to flow through your lungs, then your right atrial pressure and your right ventricular and diastolic pressure are elevated. And those act backward again to reduce venous return to the heart. So vascular resistance becomes very important for
Some other influences on pulmonary vascular resistance are things like your pH. Acidosis increases vascular resistance in the lung, your PCO two, high PCO two increases vascular resistance in the in the lung and alveolar PO two because alveolar hypoxia causes vasoconstriction. So as you breathe the various combinations of Pressures that push blood through the lung, lung volume, PHPCO two and alveolar PO two all act to influence pulmonary vascular resistance.
Pulmonary vascular resistance also modifies the filling of the left heart because if your right ventricular and diastolic pressure is high, that shifts the ventricular septum toward the left ventricle and it makes the left ventricle smaller. So it's less receptive to inflow. The ventricular wall tension that you need to use to make your heart contract, that wall tension is also influenced by juxtacardiac pressure.
So say for this normal child, she needs a pressure systolic of about one hundred and twenty to get blood to pump across her aortic valve through the aorta and then out of the thorax. that hundred and twenty, if she gets a boost by having a high juxtacardiac pressure, then she doesn't need to generate as much wall stress in her left ventricular myocardium to hit an outflow pressure of one hundred and twenty systolic. So those things all kind of change over the course of respiration.
Doctor Furman, this was a great overview of the fundamentals, I would almost say of first year of critical care fellowship. And as you were going through this, I I just imagine you reading me the chapter in your textbook and your review articles that you've had over the years. Certainly insightful, just for our listeners, just to kind of tie these fundamentals in. mean systemic feeling pressure. That's the pressure pushing blood essentially into the heart.
right atrial pressure. It's essentially the pressure that's resisting, not necessarily resisting, but maybe uh back pressure pushing against the mean systemic feeling pressure, maybe preventing blood flow into the heart. When you start looking at the right ventricle, the main afterload to the right ventricle is the pulmonary vascular resistance and you've detailed a number of considerations for for pulmonary vascular resistance.
you got into the considerations of the PVR and many things that contribute to left ventricular filling. And then you even mentioned how interthoracic pressure can affect LV cardiac output.
¶ Spontaneous vs. Positive Pressure Ventilation
Will you tell us how spontaneous breathing affects the right side of the heart?
Okay.
This is the spontaneously breathing patient. Yes. In inspiration, the pressure in the pleural space goes down, that drops the right atrial pressure a little bit and encourages venous return to the heart. It also, on the left side of the heart, reduces the pressure surrounding the left ventricle, so it increases the afterload to ejection of blood.
If you take a really deep breath against a closed glottis, that's called a mueller maneuver, then the pressure can get quite low in the pericardial space. And the pressure then that you need to generate inside the ventricle, a hundred and twenty or so, is additive to the pressure drop across the left ventricular myocardium.
So let's say you did a Mueller maneuver and your pericardial pressure fell to minus thirty, and you want to eject blood into the aorta at one hundred and twenty, then you need a hundred and twenty plus thirty is a hundred and fifty. generated across the ventricular uh muscle to be able to do that. And that's a stress on the myocardium. So normally we breathe with over relatively narrow bounds.
When you talk about positive pressure breathing, which is the next thing this little girl is going to face, she's going to go to the OR and she will be intubated for her procedure. And there's some things that will immediately change for her. And this is where people usually think about heart lung interactions is during positive pressure ventilation, even though you have those same kinds of interactions when you're spontaneously breathing.
But in positive pressure ventilation, alveolar pressure goes positive, the lung expands, pleural pressure goes up in inspiration. When the pleural pressure goes up, adds to the right atrial pressure and impedes venous return. You know, I'm not sure I said it correctly early on. When you take a deep breath spontaneously, you encourage venous return to the heart. When the ventilator gives you a positive pressure breath. it opposes Venus return to the heart.
The positive pressure also changes the alveolar pressure, which is the pressure surrounding pulmonary capillaries, so it tends to compress them and increases pulmonary vascular resistance. On the left side of the heart, the rise in juxtacardiac pressure reduces the amount of wall tension that the left ventricle will have to generate to get its pressure up to where it wants to eject. So in positive pressure ventilation in this child, say she had an airway pressure that went up to twenty five.
Stad centimeters of water went up to twenty five. and her pleural pressure then went up to some positive number, like positive fifteen. Then to get up ventricular ejection at a hundred and twenty, she'd only need to generate a hundred and five With her myocardium. So it reduces the wall stress on her left ventricle. So you can look at the heart lung interactions as being favoring or opposing venous return on the one end and on the other end favoring or opposing left ventricular ejection.
This is of immense clinical importance, especially when you start talking about kids that are critically ill, just to restate what you've already said so well, negative pressure or spontaneous breathing helps facilitate venous return to the right side of the heart. But it opposes left ventricular ejection. On the other hand, when a patient's intubated or otherwise receiving positive pressure ventilation,
Those positive pressure breaths increase intrathorac pressure, oppose venous return on the right side of the heart, but it does support L V ejection. Do I have that right?
That was that was much better than I said it. That was terrific.
I cut you off. Please, please continue.
No, I think that's the the important thing. So what you would like to know when you're about to change the pressures that you're using to ventilate a patient. is whether you're going to predominantly get impediments to venous return or augmented left ventricular output. That's what you'd like to bet on. And the way that I think about that is that under normal circumstances Positive pressure ventilation will have more of an effect reducing inflow to the heart than on ejecting blood.
But if your big problem is left ventricular ejection, then it works the other way around. And you get more of a benefit by reducing afterload on the left side than the effects you see on the other side.
¶ Clinical Application and Predictive Challenges
It can work either way. And one of the big rules about being and attending and talking on rounds about heart lung interactions is try to explain what has just happened. Don't try to predict what's going to happen. Because sometimes you just can't put your arms around all the different variables.
This is fantastic. I'm not sure if there's a more high yield ten minutes that anyone should listen to before they walk into the ICU for the first day of their first year PQ fellowship. Alice, I'm not sure if you feel the same way.
I feel the same way, and I'm not sure if there's a more high-yield teaching point for us going into our third year, then you better do your teaching points about the things that just happened because you're going to be eating your
That's right. Anything else to add before we move on to our next case?
Well if I could just brush up one more point having to do with the difference between effects on preload of the right side of the heart and after load of the left side of the heart. Remember that the PMS, this mean systemic filling pressure, that's normally around seven millimeters of mercury. And if you raise or lower right atrial pressure by a millimeter of mercury, that may have perhaps a fifteen percent effect on Venus return to the heart.
On the left side of the heart, you're trying to eject at about 120 millimeters of mercury. So a one millimeter change in juxtacardiac pressure is peeing in the ocean. Doesn't have any real effect on the left ventricle at all. That's if it's normal. So what you expect are inflow effects. What you actually get will depend on the overall condition of the patient, including how weak the left ventricle is and how much help it needs.
And to reflect on something you've already said, the actual pathology in the patient's gonna drive the effects of these cardiopulmonary interactions. And we'll certainly explore that more with our cases coming up. Alice, we wanna give us our next case?
¶ Cardiopulmonary Interactions in Sepsis
So we've got a two-year-old girl who's an X26 weaker. She is in the pickup with pneumonia and concern for septic shock. On exam she's dehydrated, she's got poor peripheral perfusion. She's also tachypnic with moderate to severe work of breathing, and we are going to talk about her cardiopulmonary interactions. What are the clinically relevant interactions that we should expect in her immediately when she's spontaneously breathing, but she's in respiratory failure and likely in septic shock?
Okay, so this is a patient who you started out by saying is presumed septic. And sepsis in and of itself has a number of effects on the body. feed into your heart lung interactions. The first of those is capillary leaves. So she may have started out two days ago, she may have had a normal blood volume, but today she probably doesn't. And what that leak has done is that it has taken fluid out of her reservoir. so that they're no longer very full and hermine systemic filling pressure is reduced.
One of the tricks to living with all these reservoirs is that they are regulated. So the venous reservoirs are under neural and humoral control that are designed to keep them around this magic number of seven or so. So a normal person, if they lose blood volume will pretty quickly shrink down their compliance vessels in their spleen and in their liver and in other vascular compartments, and they restore their immune systemic filling pressure.
Those reservoirs may not be full anymore, but because they've increased tone, they now have a good pressure to push blood back to the heart. One of the things that happens in sepsis is that this regulation is impaired, so they no longer respond appropriately to neurohumeral control. So PMS will be low in a patient like this. The other thing is that a patient who's in shock will have abnormalities of acid base balance.
and you didn't tell me that this patient had metabolic acidosis, but there's a good chance that she did. And the metabolic acidosis has an adverse effect on pulmonary vascular resistance, which raises the right ventricular and diastolic pressure, causes the right atrial pressure to go up, and opposes venous return to the heart. The rise in right ventricular and diastolic pressure also shifts the ventricular septum toward the left and makes the left ventricle less receptive to filling.
The patient with sepsis also will typically have derangement of their left ventricular contractility and of their left ventricular diastolic function, so the left ventricle won't fill as well or eject as well. Those are all from being in shock. Then she's got the problem that she's having trouble breathing, and because she's having trouble breathing, she has increased inspiratory forces and probably increased expiratory forces.
And that means that when she's spontaneously breathing, she has reduced or negative juxtacardiac pressures. And those may encourage filling of the heart. But they will also have negative effects on the other side of the heart, on the uh on left ventricular afterlode. Her respiratory distress actually will cause her to have more forceful diaphragmatic contraction, more forceful diaphragmatic descent.
And when the diaphragm comes down, it squeezes the venous reservoirs in the abdomen and encourages blood from the spleen and liver to flow back to the right atrium. So that will favor her preload, the fact that she's in distress. Her left ventricular afterload is affected because when she's struggling to breathe, she may generate a lot of negative Juxtacardiac pressure and have trouble ejecting, especially if she's got a compromised left ventricle.
So her work of breathing poses both advantages and disadvantages to her circulation in general, but they will be predominantly disadvantageous. Predominantly uh disadvantageous on the left side of the heart.
I was just gonna say you expertly walked us through many of the considerations for the septic patient, the relevant cardiopulmon interactions, just to review those quickly. They'll have capillary leak, they'll be hypovemic as I just mentioned. they're going to have decreased mensystemic filling pressure. They may be acidotic and have derangements in their pulmonary vascular resistance. They're going to have impaired LV filling.
the uh strong negative spontaneous breathing that may be impairing L V systolic function. really sepsis is a total body dysregulated response and it's really awesome to hear how it interacts with every cardiopulmonary interaction.
And what I like what we've done with this case is we've got sepsis, probably a propensity towards increased pulmonary vascular resistance. And you've got a kid who's working to breathe so hard that they're squeezing their splenctopatic vessels into the RA and they're exaggerating the gradient between the mean systemic pressure and the RA pressure to fill it up. And so this case truly has everything and it's not uncommon. Right. And see it often. Yep.
¶ Respiratory Distress and Oxygen Debt
And we cut you off. Please continue.
Yeah, uh what I was gonna say is that obviously you don't wanna make things worse by creating positive pressure in the juxtacardiac space, but We haven't yet hit the worst things about her sepsis and respiratory distress, and the worst thing is that she's got a really high oxygen consumption because she's working so hard.
We have all watched patients who are struggling to breathe. And normally when you're breathing, I'm sitting here breathing a couple times a minute, and I spend about 3% of my cardiac output on that. The diaphragm uses about three percent of my oxygen uptake. When you're in respiratory distress, that changes dramatically.
In fact, your oxygen consumption becomes enormous. And if you've watched a person who is in severe respiratory distress, every muscle in their body, from their nose to their toes, is working hard to breathe. So they really require a lot of cardiac output and they just have a limited amount of cardiac output to spare. So that steals from the cardiac output that they would like to send to their brain and to their viscera and makes them susceptible to brain failure and visceral failure.
It also sets them up for cardiac arrest. If an animal in the wild is shot by a hunter and they start bleeding profusely, the way they die is they have a respiratory arrest because they can't keep their muscles working effectively. So just looking at you, I can tell you're both in top physical condition. My guess is that you could each do about 20 chin-ups.
If you think back to the time when you actually invested a lot of your self image in doing twenty chin ups, the twenty first chin up is a real bear. You just can't pull yourself up, you can't make the muscles contract because they're at the limit of their oxygen reserve. And the result is you just go limp. You can't shorten those muscles anymore. Well that's what happens to the muscles of respiration in a person who is really badly distressed.
They have an oxygen debt, they build an oxygen debt, then they reach a point where they just can't do it anymore and they go apne. And that's when they have an arrest. So the big trick to this transition in somebody who's really sick with sepsis, the transition from spontaneous breathing to intubation, the big trick to that is you want to prevent and arrest.
So it's almost a prophylactic measure, and then you can worry about the effects that positive pressure breathing have on the circulation at your leisure.
Sure. Such great stuff.
¶ Assessing Fluid Responsiveness
Don't let them tire out to the point of cardio.
That's right.
I feel like when we're talking about cardiopulmon interactions at the bedside, quite commonly is when we're talking about optimizing fluid status. We mentioned many things so far about how the septic patient has many reasons to be hypovolemic and giving IV fluids is certainly cornerstone to sepsis treatment.
Will you share with us what parts of the physical exam can give us insight into the patient in front of us, their ongoing cardiopulmia interactions, and perhaps which physical exam findings that you'd like to use to guide fluid resuscitation?
Yeah, that's a treacherous area. That's another place where it's much better to look back on the situation than try to guess in advance. If you know that the patient is poorly perfused and they perhaps they're sweaty, they're struggling, they feel cold and clammy, then you know that you want to give them fluid. But you don't know whether that's going to benefit them or not.
There's some literature in adults that only about half of patients who are critically ill in shock will respond to fluid resuscitation. Telling which ones will and which ones won't is largely guesswork. There are some tests that are designed to try to look at that. I think the best one is you take the patient who has been lying in bed at about a thirty degree head up angle.
'Cause that's the way we like to position them. And you flatten the bed and lift the legs. Mm-hmm and if holding their legs up for fifteen or twenty or thirty seconds improves their apparent cardiac output, their pulses, their blood pressure if they have an arterial line, then they probably will respond to a fluid push. At least transiently.
Whether it will stay in the vascular compartment or not, that again is a guess. You don't really know whether it will benefit them long run. But there aren't too many other things you can do. Sometimes if a patient has wide blood pressure swings with respiration, you're tempted to say, well that means they will accommodate more fluid, but that's a guess, and personally I don't think it helps you that much.
I've certainly read about the passive leg raise and I r really wish that I would think about it more at the bedside. I imagine the youngest patients probably not as effective as would be an adolescent who has more blood volume in the lower extremities. Alice, do you use this in your practice very much?
No, but I I was on call on the CICU most recently and A lot of kids you're wondering if you should give them fluid and I push on a lot of livers in recent cardiac surgery patients and these babies are just looking at you like geez lady. So I think that pushing on a liver is what I do and I recognize that
Unless someone is at a very like deep plane of sedation, that will probably stress them out to do. And so it's sort of you push it like right next to a strenotomy and it's like, yes, the blood pressure goes up.
So how about this? Next time we're in the picky and we have the cardiologist, the nephrologist, the intensivist all at the bedside trying to decide fluid about just raise the legs. We'll see how that goes. Uh I'm only kidding.
Um well they can laugh at you, but sticks and stones will break your bones, names will never hurt you.
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¶ Podcast Outro and Disclaimers
And thank you for listening to this episode of Pete's Crit. Please remember that all content during this episode is intended for informational and educational purposes only. It should not be used as replacement for medical advice. The views expressed during this episode by hosts and our guests are their own and do not reflect the official position of their institution.
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Thank you again for listening and goodbye.
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