Cardiopulmonary Interactions with Dr. Bradley Fuhrman -- Part 2

Welcome back to Pete Scritt. I'm Zach Hodges, a pediatric ICU fellow from UT Southwestern in Dallas. And I'm Alice Schenklin, a critical care fellow at Children's National Institute. Washington D C It's Alice, we have a very exciting topic today. We tell our listeners.

Absolutely. Today we are going back in on cardiopulmonary interactions, this time with a little bit more of a cardiac ICU focus, but I would still argue that this is the foundational PicU topic and that it will be relevant to your general pick. Zack. Who did you recruit today for this half of the episode?

We are so excited to be speaking with Dr. Bradley Furman today. Doctor Furman, who needs no introduction, but he completed his training at University of Minnesota in pediatrics, cardiology, and neonatology, where he went on to actually found the the original PicQ at that program.

He has held leadership positions in addition to University of Minnesota, at the University of Pittsburgh, at SUNY Buffalo, and at Children's of El Paso here in Texas. He has a rich research career based in cardiorespiratory physiology. And he of course is the co author of the textbook Pediatric Critical Care. Yes. Dr. Furman is one of the people that we have to thank for the field of pediatric critical care, and this is a phenomenal interview. Let's get right to it.

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. You've trialed some BIPAP, you've resuscitated a bit, and ultimately you need to intubate this child. How are the cardiopulmonary interactions going to change as we move from negative to positive pressure ventilation? Okay, the most important first thing that changes is the patient's no longer working to breathe.

if you get them through induction for uh intubation and they don't arrest during that and you have them on positive pressure ventilation, now their oxygen demand is down, their demand for cardiac output is down. So everything is already much better. The intubation and the initiation of positive pressure ventilation affects all four of your major heart lung interactions. On the right side preload, the increase in juxtacardiac pressure will have a tendency to impede venous return.

And certainly if you intubate a patient and you immediately pop'em up to an expiratory pressure of twenty and a peak pressure of thirty five There's a chance that impeded right ventricular inflow is going to be a big problem to One thing to keep in mind as you're doing that, you may be impeding their venous return, but not as much as you may think. So if you got an X-ray of this patient and they have a pulmonary white out.

And you think their lungs are very stiff. A very stiff lung does not transmit pressure well to the juxtacardiac space. I guess one way to look at that is that when uh Einstein was thinking about gravity and Newton was thinking about gravity, Newton was very happy with action at a distance. I mean he felt that the apple falling off the tree

didn't have to be pulled down with the string for it to fall. Einstein, on the other hand, he thought you needed to have some kind of a connection between the apple and the ground. And for him that was curvature space time, okay? But for us, the important thing to take from that is that when you try to increase juxtacardiac pressure by distending the lung, it is not action at a distance. The airway pressure doesn't just yell down to the juxtacariac space I want your pressure to go up.

It goes up because the lung expands and compresses the heart. compresses the juxtacardiac space. It's a direct transmission, physical direct transmission of the change in lung volume to the change in juxtacardiac pressure. So if your patient has really stiff lungs, they'll be very resistant. They won't see much of a change in juxtacardiac pressure.

If on the other hand it's a person with nice normal lungs and you intubate them and you put them on a high amount of P and a high positive pressure ventilation, their lungs will distend really nicely, their juxtacardiac pressure will go way up and that will impede their venous return.

Second major thing that changes when you initiate positive pressure ventilation is that the alveolar pressure goes up and that impedes blood flow through the lung, raises pulmonary vascular resistance. and backs up to increase right atrial pressure and oppose venous return.

You also are choosing what lung volumes you will ventilate at the If you ventilate the patient and next x-ray you get the lungs are really overinflated and you've overdone it, you're above FRC and vascular resistance will probably be elevated from that. You have a chance to restore acid base balance by blowing down the CO2 after intubation, and that can be a favorable effect on pulmonary vascular resistance. Those things all influence vascular resistance.

Preload is affected because everything you do that raises right ventricular and right atrial pressures in diastole will tend to shift the ventricular septum. to the left and that makes the left ventricle smaller and less receptive to fluid inflow. So it impedes venous return. And then positive pressure ventilation, if the lung will distend with the positive pressure ventilation, the juxtacardiac pressure goes up, and that facilitates emptying of the heart and systole.

So it may actually reduce the myocardial workload, the amount of work that the heart has to do to achieve the outflow pressure of 120 that it wants to achieve. So those things change very quickly. So managing the high risk patient going into intubation and the change in the cardiovascular physiology, gosh, I feel like that's the essence of a pediatric intensivist. And it certainly isn't one of the most high risk things we do. Alice, you may have a follow-up question.

Prior to this conversation, I would think about a peak pressure of thirty five and think I'm definitely decreasing the gradient between their mean systemic pressure and their RNA pressure and therefore decreasing preload. But after hearing you talk through it, I'm thinking maybe a better proxy is how overexpanded are my patients' lungs? What's my plateau pressure? Something like that, which tells you more about how distended the lungs are and less about the pressures you need to open them up.

Yeah, I think we're always guessing about lung volume until we get our first X ray. If a patient's lungs are real stiff, they may have a high plateau pressure. if it's an asthmatic and they have a low plateau pressure that doesn't assure you that they're not overexpanded. So it becomes difficult. But a lot of the heart lung interaction related to

Application of positive pressure ventilation has to do with whether or not you have really expanded or overexpanded the lungs. You want to get it just right.

Doctor Furman, you mentioned earlier in our conversation that sometimes it's more effective to reflect on what changes have happened in your patient's cardiopulmine interactions rather than trying to predict them. So if our patient that we're talking about here, say the predominance of her shock, secondary de sepsis related LV dysfunction, How do we think that intubation will affect her overall physiology, positively or negatively?

If her biggest problem was left ventricular dysfunction, it's definitely a positive effect. If you raise the juxtacardiac pressure, say you raised it from zero to twenty. then you get a boost of the intercavatory pressure during ejection, and the heart doesn't have to eject as hard as forcefully. The myocardial wall stress is a function of the myocardial radius. The wall stress in the myocardium is greatest at high ventricular diameter.

And the wall stress is influenced by how much the muscle has to add to the juxtacardiac pressure to get an intracavitary pressure that's high enough to eject blood. So if you get that wall stress down, then you reduce the myocardium's oxygen demand and convert an ischemic myocardium into one that's not so ischemic. Great. Certainly fundamental things that we do every day in the PICU, intubating that patient with possible L V dysfunction, trying to improve their cardiopulmonary physiology.

Alice, we have another update for our case. You wanna give that to us?

Sure. You've intubated your patient. This is complicated by hypotension. As you had anticipated, it improved with an IV fluid bolus. Chart review shows that this patient has a history of pulmonary hypertension and has only been off of oxygen for a few months. She's got pulmonary hypertension. How are we optimizing our initial ventilator settings for best cardiopulmonary function?

Yeah, that's a hard question. We know that there will be adverse effects on pulmonary vascular resistance if you let the patient be acidotic and or hypercarb. So you would like to avoid those things. There's a tendency to say, well, you know, the patient's intubated now. Let's not ventilate too hard so that we don't further damage the lung. Let's use a lung protective strategy.

Well that lung protective strategy may be disadvantageous in a patient who's got pulmonary vascular disease, and this patient may very well have pulmonary vascular disease. For the PO two and Mix Venus PO two, you'd really like those as good as you can get them. So you would like to get the lung well expanded. You'd like not to have atelectasis, you'd like to have good alveolar PO two because that's a major contributor to pulmonary vascular resistance.

So you may work harder in this patient to get normal blood gases than you would in a patient who where your only concern is not further destroying the lungs. You want to try to ventilate somewhere around FRC so that first x ray that you get. can be very important. You can get a glimpse of whether or not you have the patient over inflated, whether or not you have their lungs stretched too much.

Because you know that if you exceed their normal FRC by very much, you will see adverse effects on vascular resistance from that. Doctor Furman, this is all fantastic clinical information. This patient with pulmonary hypertension who has pneumonia maybe down the road will develop ARDS. At least initially, we won't necessarily allow permissive hypercapnia or even mild hypoxemia. We want this patient to have normocarbia, normooxia to try to minimize pulmonary vascular resistance.

You also mentioned targeting FRC. Will you remind us, go over the interactions between the the alveoli and the pulmonary vessels and how lung volumes affect that interplace? If you look at a uh microscopic section of lung, you see a bunch of alveoli, and at the intersection of several alveolar septi, you see something that we call a corner vessel. That's actually a vessel that's destined for another alveolus. It's going through the area in the lung, but it's on its way to another alveolus.

You also see some vessels that are in the septi between the alveoli that aren't at the intersections, but are just little vessels that are in the alveolar septum itself. When you inflate the lung, if you apply a lot of distending force and you stretch the lung, those corner vessels will get stretched widely open. Okay, so their resistance falls, but the vessels that are in the wall of the alveolus they get stretched and narrowed, and their resistance goes up.

In the aggregate, if you're much above FRC, the predominant effect you see is on the vessels that are in the alveolar wall that are getting stretched and thinned out. If you let the lung volume fall, on the other hand, those corner vessels no longer have radial traction to keep them open. So the resistance in those vessels goes up. The alveolar septal vessels they don't see much pressure or much stretch, so they relax their vasculars as well.

But because of the effect on the splinting open of corner vessels, if you let the FRC get too low, vascular resistance in the aggregate rises. So there's a U shaped relationship between lung volume and vascular resistance. It's least at the bottom of the U, it's least at FRC, and then vascular resistance goes up. as you exceed FRC or as you fall way below FRC. So you want to target a good lung volume on your first exercise.

That's exactly what I was gonna say. Just why it's so important to make sure you're adequately recruited but not over descended on that x-ray after you intubate these patients.

So doctor Furman, think about our patient who has pulmonary hypertension. Let's say in this case, her pulmonary hypertension is causing some RV dysfunction. Will you tell us how that might also affect the left ventricle? The primary effect is through what they call diastolic ventricular interdependence, and the theme to it is that.

If the right ventricle is expanding to larger than normal volume, the ventricular septum shifts over into the left ventricle. The right ventricle gets bigger, the left ventricle gets smaller. And the left ventricle then can't fill as effectively. It doesn't have the volume to fill effectively. So a high RV and diastolic pressure impedes filling of the left ventricle.

There's also a phenomenon of systolic interdependence of the ventricles. And the way to think about that is that the ventricle actually has one muscle cell. It's got a lot of cells and they're connected at intercalated disks, but they're all connected together. And the myocardium kind of wraps around these two ventricular cavities. So in the process of wrapping around there are right ventricular fibers that are attached to left ventricular fibers.

And if the right ventricular fiber contracts really well, then the left ventricular fiber benefits from that. If on the other hand the right ventricular fiber is dysfunctional, then the left ventricular fiber sort of pulls the fiber over toward the left ventricle, but doesn't contribute to intercavitary pressure. So there clearly is a relationship in systole between the left ventricular performance and the right ventricular performance.

In general, in the conditions that we deal with in pediatrics, both sides of the heart are kind of affected at the same time. In sepsis, neither ventricle is spared. So that systolic interdependence is not something that you need to separately think about in children. In adults with coronary artery disease, the two ventricular pumps may help or hinder one another, depending on who has good blood flow and who doesn't. Oh, interesting.

I was just gonna say it's such an important concept and it wasn't something that was very apparent to me when I was starting fellowship those first six months. I'm not sure, Alice, if you see it the same way. The point about remembering that the muscle is within the same cell and therefore very intimately connected. Yeah, it makes it so makes so much sense.

The other place that that comes into play, thinking about them both being inside the same space, is when you think about pericardial tamponade. In pericardial tamponade, you've accumulated fluid outside the heart. which reduces the ultimate filling volume of both ventrics. I mean there's just so much space that you can put ventricular blood into because the rest of the pericardium is full of either blood or inflammatory fluid.

When you then take a deep breath in, you reduce the pressure in the cardiac system, but you don't make new space if you have fluids surrounding the heart. So the heart can't actually respond to the fall in juxtacardiac pressure by increasing its volume. So it gets no added force of ejection by doing that. Also when you have inspiration in a patient who's got fluid around the heart.

And it encourages right ventricular filling. The septum shifts over to the left, and there's no room for the left ventricle to expand further. So between those two factors, breathing in when you have tamponade reduces stroke volume, it reduces uh the pressure that the heart can generate in the arterial circulation. So the left and right ventricles tend to be twin. They tend to work together. Oh I appreciate that. Do you have any other thoughts about this case before we move on to the next?

I think just to re-emphasize that overall intubating this kind of a patient is a good thing, even if you have to make some accommodations to the heart-lung interactions, because you do not want them to arrest. Your big mission is to maintain control of the patient.

So doctor Furman, your next patient is a fourteen year old male. He's admitted to the cardiac ICU with concern for myocarditis. His echo demonstrated moderate to severe LV dysfunction, LV systolic dysfunction. On exam, as you're looking at him, he's wet and cold. He has poor peripheral perfusion, has evidence of pulmonary edema.

And he has moderate to severe worker breathing, and he's only being supported currently by nasal cannula. So doctor Furman, what are the key cardiopulmonary interactions that are affected by this patient's LV systolic dysfunction and worker breathing and why? Okay, this is a patient. for whom I would guess prospectively that he's going to benefit from positive pressure ventilation.

His uh contractility being reduced means that his muscle is greatly advantaged. His cardiac muscle is greatly advantaged. It's working at high fiber lanes. The ventricle is probably somewhat dilated, and because of that he needs all the assistance he can get in ejecting blood. So giving him positive pressure ventilation, raising his juxtacardiac pressure.

will reduce how much force the ventricle itself has to generate to be able to get a systolic pressure up to 120 or so to get it out of the thorax. So the big thing there is the transmyocardial pressure gradient and you benefit that with positive pressure breathing. It's also important to recognize that the myocardium itself is oxygen limited. That is, when it's operating at high fiber length and high tension, it requires more Oxygen than a normal myocardium would

And by giving it that little boost, you take some of the strain off the oxygen supply demand situation for the myocardium. And again, intubating him could avert arrest. Absolutely. Our number one goal in all papers.

So Doctor Furman, you've mentioned earlier in our conversation it's not always clear exactly what's gonna predominate in the cardiopulmonary interactions, whether it's the right side of the heart versus left side of the heart, but this is an example of a patient in response to positive pressure. we would expect that the beneficial effects of supporting the LV is going to outweigh any mild reduction in right side of the heart filling. Would that be correct?

Yeah, I think so, and probably in a patient like this his filling pressures are high anyway. So they're going to be less susceptible. For the right side of the heart, for instance, that gradient between mean systemic filling pressure and right atrial pressure is pretty sensitive to mean systemic filling pressure. But the right atrial pressure is already so high that the mean systemic filling pressure has had to adapt to that. So that's probably already taken care of.

The other thing you get for intubating the patient and putting him on positive pressure breathing is you can now sedate him as much as you want. And by sedating him and easing his anxiety and eliminating his muscle work, he reduced the demand on the heart for cardiac output. So high risk of cardiac arrest during intubation, but once he's intubated, hopefully you'll be able to clear your lactate, relax the patient and get him better.

Fantastic. Alice, we'll get to our next case. I'm really excited about this one.

Yes. We've got a three month old girl with tetrology of philosoph she's in the CICU after her complete repair. She is intubated. The anesthesia team mentioned that she required a high CVP to maintain an adequate blood pressure. Post-op echo demonstrated good biventricular systolic function, but RV diastolic function was. Present. What are the key cardiopulmonary interactions that are affected by this patient's R V diastolic dysfunction? And why is that?

Okay, I think first of all the elevated right ventricular and diastolic pressure tends to move the septum, the ventricular septum toward the left ventricle and therefore impedes left ventricular Filling left ventricular inflow. This kind of patient probably also has some pulmonary insufficiency because they've probably had to do things to the infundibulum and maybe to the pulmonary valve.

That increases the load on the right ventricle and has the same basic effect that it moves the ventricular septum toward the left. The fact that you can see forward flow in the pulmonary artery and diastole. in a patient like this just means that the right ventricle is not very helpful to you. If it's not very helpful and you can't get a lot of blood into the pulmonary artery, then that reduces left ventricular inflow also.

So this patient is going to have several reasons to have impaired left ventricular inflow and an inefficient right ventricle. We had a previous episode on post op management of tetrology of flow, and I feel like a theme from that conversation was to what are your tets, right, Alice? They're gonna need Yes.

Yeah, water detects. They're gonna need to increase mensystemic filling pressure. Doctor Ferman, you mentioned forward flow in the pulmonary artery during diastole. I feel like I've heard that referred to as restrictive cardiovascular physiology. Is that correct?

That's my understanding of what the term means, yeah. I think it's a marker for bad R V dysfunction. I don't have anything really to add to it. But I would worry about that for a couple of reasons. I mean you just made a big incision in the right ventricle. And you may have cut across some of the coronary supply. There are a lot of reasons to be worried about whether or not the right ventricles an adequate pump and apart from their impact on cardiopulmonary interactions.

A devitalized right ventricle of ventricle we've cut muscle bundles out of is gonna need some support. And my approach with post op tetrads has been just not to rush them off the ventilator. To wait until they're good and ready and keep them full, keep their vascular bed full because you need to get flow over to the left ventricle.

Sure, so the theme of watering the tets or at least keeping them evolemic seems to be holding true here. And then by keeping them on the venture till they're ready, I assume that means ventilate them FRC, keep their normoxic, normocarbic, and just wait till they're ready to be liberated. Yeah, that's how I feel about it. Do you subscribe to the high tidal volume, low rate settings to maximize their time at FRC?

I would try to put more into the picture to see what the lungs actually look like on X ray, to see what the filling pressures actually are to see what the blood pressure actually is. I don't think a general rule would help me that much. Sure, very fair, especially on all the complexities of our post-op cardiac kids. Dr. Furman, anything else to add to this case before we move on to our final one? No, I don't think I have anything real to add. Fantastic. Alex, you want to give us her last case?

Yeah.

We've got a four-year-old boy with hypoplastic left heart. He's in the CICU immediately following his fontan. He's intubated and post-op echo demonstrates mild diastolic dysfunction, but ventricular systolic function is normal. How is the fontan circulation affected by these pulmonary interactions?

The big difference is that you can think of the right ventricle as an elevator. You know, blood goes into it and it raises the pressure to get it into the pulmonary circulation. You don't have that in the post fontan patient. So the pulmonary vascular resistance is the primary cause of back pressure to the venous return to the heart. So those things that affect pulmonary vascular resistance, the idea is to keep your vascular resistance as low as possible.

To me, that means maintaining good acid base balance, not using excessive airway pressures. keeping the patient sedate and comfortable, but it really does not necessitate getting the patient off the ventilator the minute he gets back from his operation because some of the effects

of positive pressure breathing are beneficial. You can then keep the patient really well sedated. You can work on all of his other problems until you have them under control before you uh let him try to breathe spontaneously. But I'm not sure that's all that different from other patients. It's just that the link between pulmonary vascular resistance and venous return is more direct because you don't have that right ventricular elevator.

Sure. So for learners, this patient, as you said, all the pulmonary blood flow is passive. So anything that increases their pulmonary vascular resistance, hypercarbia, acidosis, hypoxemia. you would assume I would assume they were they would have negative physiologic effects because they can't compensate by increasing their pulmonary pumping chamber, so to speak. Fair enough.

Dr. Farman, this has been such a fun, exciting conversation. I feel like as we've gone over these core concepts, I'm just thinking about where I was a year and a half ago coming into Critical Care Fellowship, everything that I've learned thus far and Every time I speak with one of our guests on the show, it just opens up a whole nother chapter for my next level of learning. And I really appreciate your time sharing this with Alice and me and with our listeners. We're very excited to share this.

One final open ended question. Anything else that you'd like to mention? This can be you can plug anything or maybe a resource for listeners or perhaps reinforce a couple of key concepts from today.

First thing be just to remind you that cardiopulmonary interactions are somewhat idiosyncratic. They depend on the precise circumstances of the patient. It's easier to explain what happened than to predict what's going to happen.

In general, you should expect cardiopulmonary interactions to have more of an effect on venous return than on afterload of the left ventricle. If you think about where your individual patients Vulnerabilities are whether it's left ventricular myocardium or vascular volume and leakiness, that helps you to decide whether or not they're likely to benefit from positive pressure breathing.

One of the most important things to keep in mind is that whether you think they're gonna get advantages from cardiopulmonary interactions, whether that's gonna help them or not. You still want to preserve their ability to have their heart beat, so you don't want them to arrest. That's your biggest threat. So I guess that's the way I would sum it up. Fantastic. Well, Doctor Furman, thank you so much for joining us today. Well, thank you for having me.

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Thank you again for listening and goodbye. So Alice, I feel like my bucket list has been checked off. The two biggest celebrities we could ever encounter. That's right. Zach, I have a question. Did you tell any of your cofellows that you were spending the evening with Furman tonight? You know what I did, but I'm not sure if they understood me completely. It's'cause you spend every evening with Furman, don't you? Uh

That's right, that's right, yes. Uh yeah, yeah, and just children just peeling it off pulling it away from me and and trying to spill juice and such on the on the on the pages every night. Listen, listen, I always with that book, but tonight you were with the real person. That's right. It's great to put a a face with a name, right? Really great.