The first question actually refers to Dr. Grayson's talk, and I guess to some extent to mine. It basically says in RV infarction, people are taught to load 500 or 600 cc's of normal saline. It says per hour. Is that right? Jim, I'll give you first crack, and then I'll go with my response, and David, you can chime in as well. Sure. Sure. I think the issue is really the end point, and in an RV infarction, it is important to maximize the RV preload, and I think a number of the speakers have mentioned that the RV, you know, you can exceed actually the optimal RV preload. So the issue is to get volume in rapidly and to what I would use as a CPP. The rate at which you do that is, of course, dependent upon the clinical scenario. Generally, we would pour it in, of course, in a hypotensive patient after an RV infarct. Certainly they can probably tolerate that if that, in fact, is the issue. Yeah. I think I agree with most of that. I guess if there's anything to be learned is that there is a limit. I actually prefer in this context more of a bolus. So you want to evaluate at certain steps. So you might well give 500 cc's and see what happens, and then 500 cc's more and see what happens, and I agree with you. You follow the CBP. Once that CBP begins to plateau, begins to go up quickly, then you're in trouble. And also on the other end, you'd like to look at the physiologic effect of your fluid resuscitation. If your patient is looking better and perfusion looks better and is making urine, then you're doing the right thing. If the patient doesn't look better and the stroke volume slash cardiac output, if you're measuring that doesn't look better, then you should think a little bit about whether that's really what you want to be doing. So David, both of you, just a great talk. David, you want to talk a little bit about the effects of the peak and plateau pressures on mechanical ventilation, on heart-lung interactions? I think everything will have to do... Any high pressure or any high volume will affect venous return first to the right atrium and then blood return to the left atrium, depending upon volume status. The higher the pleural pressure, and depending upon a patient's intrinsic lung mechanics, whatever pressures the ventilator needs to insufflate the lungs to achieve a set volume that what the clinicians decide is important will limit venous return to the right heart. This is a really important concept because it turns around 180 degrees the normal physiology of breathing and circulation. So when you and I take deeper breaths, and this is one of the hidden gems of exercise physiology, I always ask this on rounds, who here goes and does exercise, and everybody raises their hand. I said, okay, who here gives yourself a thousand milliliter bolus of saline or ringer's lactate before you go exercise? And nobody raises a hand. I said, well, why is this? Why are you able to raise your cardiac output so much during exercise without the benefit of intravenous fluid? And this is sort of mysterious. Nobody kind of intuitively gets this. And one of the big reasons is that as we breathe more deeply and more forcefully and more often during exercise, we actually pull a lot of venous blood back into the right atrium as our pleural pressure becomes much more negative and it happens faster. So there's no increased circulating blood volume, but the flux is faster. Things are moving around the circuit more quickly. We turn that on its head when we put somebody on positive pressure ventilation. And let's say you or I, when we go out for a jog, our pleural pressures become negative 20, negative 25, negative 30 centimeters of water. All of a sudden, somebody's got stiff lungs because of pneumonia or pulmonary edema or interstitial lung disease. And we start insufflating and peak airway pressures are positive 30 centimeters of water. But that's going to limit venous return a great deal. That's going to have effects on cardiac output. And then the effects of lung volume. When we insufflate the lung to larger than functional residual capacity, we're going to cause compression of some of the intra-alveolar pulmonary vessels. The degree to which we cause that compression will depend on the volumic state of the individual. So if the patient's relatively uvolemic or hypervolemic, there will be less compression of the intra-alveolar vessels. If the patient's relatively hypovolemic, there'll be more. But that will also slow venous return through the pulmonary circulation and into the left atrium. So both positive pressure in the pleural space, inside the thorax, and larger lung volumes during insufflation will tend to limit cardiac output. And mostly as a result of impaired return both to the right atrium and the left atrium. All right. From the audience, we have a question. You have a massive pulmonary embolism that happens right in front of you with cardiac arrest. What do you do about fluids? Who wants this one? All right, David. So aside from giving tenecteplase, I mean, I think, and we'll talk about this, well, I probably would tend not to give fluid, right? If you believe that the primary reason for shock and death in cardiac, and rather in pulmonary embolism, is obstruction and acute right heart failure, right? The physiology will lead us to believe that loading fluid, which will increase, theoretically may increase return to the right atrium and right ventricle, could potentially worsen overall cardiac output. Because the right ventricle is going to be pressure overloaded. And you have McConnell's sign echocardiographically, where you have a bowing of the interventricular septum from the right ventricle into the left ventricle, thereby further limiting left ventricular stroke volume, because left ventricular end diastolic volume is going to be smaller because of the constraints within the pericardium and now the enlarged pressure overloaded right ventricle. I think there's a lot of chance you're going to make that situation worse by loading fluids to the person with acute pulmonary embolism. The bottom line is we actually don't have a lot of good empirical evidence to help us make decisions. There are some animal models that suggest that this is the physiology. When you give animal models large obstructing pulmonary emboli, fluid loading tends not to be helpful. But in the absence of good clinical evidence with good monitoring, I think you have to take it on a case-by-case basis. I think fluids should not be your first choice, but if you have monitors and you want to give a small bolus of fluids and you show that that improves hemodynamics in an individual patient, well, then you should give fluids to that individual patient. But we lack robust data from population-based studies to help us make decisions. Yeah, I think that's just right. To me, you can be forgiven for giving a couple of hundred cc's of fluid while everybody's running to the patient, but the open pulmonary vessels, the ones that aren't obstructed, won't benefit from the increased fluid, and the ones that are closed won't help. So it's really obstructive. I think it's really not a fluid-responsive state in general. The question is, with regards to volume and RV dysfunction, if the RV is already enlarged with poor contractility, say poor TAP-C and non-collapsible IVC, would you still titrate volume challenges to CVP alone, assuming the CVP doesn't look as bad as the echo? Jim, first crack, and then I'll get in there. Sure. So can you restate the question again? So in the way- If your RV is already bad, is CVP the thing to titrate to? Assuming you have a CVP that's not sky-high already, would you still titrate fluid to a CVP, or would you use some other things as well? Yeah. I think CVP monitoring is useful in these situations because at the end of the day, a lot of us do a lot of empiricism, right? But usually, we usually shoot for the mid-teens with the hope that you're maximizing the preload sensitivity of the RV. But again, people are often very preload insensitive when their RV has already begun dilated. And so I think it's important to look at the CVP, not only to try to figure out the target, but make sure it doesn't go too high, as we talked about. And you shouldn't forget about inotropes as well. RV failure and maximizing the preload is certainly one way to improve RV failure. Then we can talk about afterload. But one of the things that are quite dramatic, actually, particularly with RV infarction, is a combination of debutamine and fluids can really turn somebody around. So you shouldn't lose sight of that issue. Yeah, I think that's a really good answer. And one thing I will mention, and that sort of goes to a lot of what both of you have said, is that what can be useful is looking at the position of the ventricular septum. David and Cliff both talked about how that septum moves over and begins to impinge on the left ventricle. How do you know that's happening? Well, you do a focused echocardiogram. You try to figure out where that septum is. And when it starts moving over the left ventricle, that's another indication that you may be at the limits of fluid administration. I thought, Steve, I would just probably also mention something that Cliff mentioned during his talk, and I'm sure David feels the same way, is systemic blood pressure. People often forget about the systemic blood pressure for the management of the RV. We see it a lot of this because everybody's vasoplegic after cardiac surgery. And getting the systemic blood pressure up is really important for RV performance. And the points were made that RV perfusion occurs both during systole and diastole in contrast to the LV. And so you should never forget about dealing with the systemic blood pressure and making sure that it's high enough. Yep. Okay, we're going to get to two more questions. There will be plenty of time for questions later, hopefully, and afterwards. So two questions. One question is, talk about the difference between how you'd manage acute and chronic right ventricular failure. Nothing like a simple short question. Well, that's like the difference between acute shock and acute on chronic shock. I think the principles are still the same. You want to obviously optimize RV preload, and often you need to use inotropic support. The reduction of preload, particularly in chronic heart failure, is primarily done with diuretics. Because stiff lungs obviously are non-compliant lungs, and because of the sensitivity of the RV to impedance, it's really important to get the lungs as dry as possible. And sometimes the wedge pressure doesn't completely reflect that, particularly in chronic heart failure, because the lungs are just chronically soggy. And people forget about the fact that one of the primary managements of acute on top of chronic RV failure, particularly when it's from the LV, is the diuresis and diuresis. So yes, and as you just mentioned, sometimes in acute heart failure, there's a need to support the systemic blood pressure and think about coronary perfusion. That's somewhat less of an issue in chronic RV failure, except as you mentioned for acute on chronic. All right, last question. Why is positive pressure ventilation so effective for pulmonary edema? And on the other hand, why are patients who are extubated with underlying heart failure sometimes go into pulmonary edema? So I'll start with the easy part. I'm going to go with the first part, and I'm going to leave the second part to you guys. So the reasons for positive pressure ventilation effective for pulmonary edema have to do with both preload and afterload. So positive pressure ventilation decreases venous return, thus decreasing your left atrial pressure and helping with oxygenation. Similarly, if you think about, say, the aorta goes from inside the chest to outside the chest. So if you increase the pressures inside the chest, and the pressures outside chest remain the same, you're actually decreasing the afterload. So positive pressure ventilation, particularly CPAP and BiPAP in acute pulmonary edema can be very effective, and as a matter of fact, the first thing to do. Now, it's a little more complicated when you extubate somebody with heart failure. I'm going to leave that to my heart failure doc. Good luck. Well, I was going to try to loop in David and some of his thoughts. Yes, David, you too. Microphone. You know, it all goes back to first principles, right? I mean, it has to do with increased venous return. And if a patient has a stiff or poorly contractile left ventricles, and the increased venous return raises the left atrial pressure, that will change the Starling relationships in the pulmonary venous bed leading to pulmonary edema. And, you know, the other thing, a hidden part of this, and it's controversial exactly how much this plays a role, but one of the principal things that positive pressure ventilation does is relieve the work of breathing from the respiratory muscles, right? So if you have wet lungs, if you have sick lungs, for whatever reason, airways resistance is high, respiratory system compliance is low, the work of breathing is elevated, and the respiratory muscles have to work harder in order to insufflate the lungs. When you relieve that work, even with pressure support breathing, the respiratory muscles will consume less oxygen in the smaller part of cardiac output. If you change that fundamentally by taking a patient off of positive pressure ventilation, and you impose that work again on the breathing muscles, they're going to demand a higher cardiac output, and VO2 and VCO2 may rise to levels that the myocardium may be unable to sustain. So I think it has to do with venous return, I think it has to do with congestion within the pulmonary vasculature, and it has to do with VO2 and VCO2, and the ability of the myocardium to sustain a given VO2 and VCO2. Yeah, and you also have to think a little bit in some settings about ischemia, for the reasons that you just stated. You weren't using any energy to breathe, now you're using a lot of energy, and you can sometimes unmask ischemia, and you try to extubate somebody. We're thinking about, and in some contexts, measuring left atrial pressures during extubation attempts can be useful, because if the left atrial pressure skyrockets, you know you have that sort of problem. So all right, thank you for the first. We're going to go on to the second set of talks. There are some unanswered questions, particularly about mechanical support. We'll have a chance to talk about that later, and there will be other sessions. So we're going to go on to the recorded talks.

right ventricular failure

fluids

positive pressure ventilation

pulmonary edema

management