 Hello and welcome to Noon Conferences hosted by MRI Online. In response to the changes happening around the world right now and the shutting down of in-person events, we have decided to provide free daily Noon Conferences to all radiologists worldwide. Today we are joined by Dr. Mark Gosselin, he was a professor at OHSU Diagnostic Radiology and Division Chief of Cardiothoracic Imaging for 15 years. He left the department in 2016 to take a job with vision radiology where he is the head of cardiopulmonary imaging. He started his academic career at the University of Utah in 1997. Reminder that there will be time at the end of this hour for a Q&A session. Please use the Q&A feature to ask all of your questions and we will get to as many as we can before our time is up. That being said, thank you so much for joining us today Dr. Gosselin, I will let you take it from here. All right, thank you so much for your invitation. Morning slash afternoon everyone, I'm in Portland, Oregon so it's 9 in the morning. I'm going to talk to you today a bit about imaging approach to pulmonary hypertension. And for as far as, let me get this set up here, there we go. I don't really have any relevant disclosures for the talk and I want to send a shout out to Dr. Kapal Alada, pulmonologist at OHSU who shared some of the slides and a fair bit of information with me on this topic. The objectives are briefly reviewing the classification as well as some current therapies for pulmonary hypertension. We're going to then focus on what pulmonary hypertension looks like on a radiograph and on CT as well as some other information about potential etiologies. I'll talk a bit about contrast dynamics and how that can help you identify some physiology of the cardiopulmonary system. And we'll kind of focus a little bit or want to make sure that you take home point is in your report, if there is pulmonary hypertension, to try to identify those people who may have a post-capillary etiology because this therapy is different, okay. So we'll start off, introductory patient, 67-year-old, progressive dyspnea and recurrence can just have heart failure episodes and you see a PA and lateral radiograph, heart size may be a little big. The right ventricle here looks a little big. You can see in the CT scan there is evidence of septal thickening, hydrostatic edema slash congestive heart failure kind of appearance with ground glass, small effusions. And then what you notice here on the heart is that there's thickening of the right ventricular free wall. It shouldn't be more than four millimeters. This one clearly is. And there is actually straightening of the intraventricular septum. So it does look like the patient has some evidence of pulmonary hypertension. What's the possible diagnosis? What would you put in your report? And we'll come back to that. So let's start off. Pulmonary arterial hypertension, well how is this defined? Clinically it's defined by doing some interventional test. Usually it's a right heart cath that remains the gold standard. Main pulmonary artery pressure is greater than 25 at rest or 30 millimeters of mercury with exercise. Now the capillary occlusion pressure and left ventricular endiastolic pressure should be less than 15. But I did put a little star because people with pulmonary hypertension that do not really have post-capillary abnormalities, this may be elevated still. So I'm not sure that's a strong criteria. And lastly, the pulmonary vascular resistance greater than three woods. Now woods unit is a measurement of the pulmonary vascular resistance. Now what are some normals? You can see what the normals look like. The severity of the pulmonary hypertension, usually when you start getting 25 to 40, they call it mild, 41 to 55 is moderate, but severe is over 55. So these are sort of your, there are the clinician's criteria on how to grade the degree of pulmonary hypertension. Now a quick definition, pulmonary hypertension simply just means there's an abnormally high pressure in the pulmonary arteries. And the whole circuit is set up where you have your arteries and arterioles, the capillary bed, and then the venous and the venules. And anywhere along the line, you can have an abnormality that causes the pulmonary artery pressures to rise. For the post-capillary, usually that's going to be left heart failure, either systolic or diastolic, or some mitral valve or aortic valve disease, often stenosis. There are some unusual diseases such as venous occlusive disease or extrinsic compression that could do it. If the abnormality is more in the capillary level, we usually start thinking about primary pulmonary problems inducing the pulmonary hypertension. Usually that's through hypoxia. Sometimes it's obliteration, but usually it's hypoxia. Some common ones would be any parenchymal disease that causes a chronic hypoxia, airway diseases do, and of course sleep apnea. And then there's the pulmonary arterial hypertension, note the arterial. This indicates a pre-capillary process, and that's usually the autoimmune associated pulmonary hypertension, idiopathic or primary pulmonary hypertension, chronic thromboembolic disease. But once you say pulmonary arterial hypertension to the clinician, that's inferring that this is a pre-capillary. Pulmonary hypertension is the general term that just says the pulmonary artery pressures are high. The heart cath, like I said, remains the mainstay for evaluation. Okay. How do you organize it? There are different ways. The anatomic one is very commonly used, and it's probably the one I'll use here most of the time. There's pre-capillary, capillary, and post-capillary. The physiologic, because I love physiology, is pulmonary arteries have increased flow. You have an ASD or a VSD. You have a greater amount of flow. Over time, pulmonary hypertension develops. You have a chronic hypoxic state, hypoxia in the lungs. What does it do? Induces a pulmonary vasoconstriction over the long term. The changes of pulmonary hypertension and right heart failure start to occur. Vessel obliteration. You eliminate enough of the vessels, and you start to develop pulmonary hypertension. But you have to eliminate a lot, because remember, you can take out a whole lung and not develop pulmonary hypertension. And then the last one is pulmonary venous hypertension. And that's usually, again, the left heart failure, causes the higher pressures. The world health symposium classification, if you're interested, it's pretty similar. It goes into the pre-capillary, post-capillary, and primary lung disease, or the capillary causes. This also includes chronic thromboembolic disease, and then the last category is for things that we're not really sure how the mechanism is. Sickle cell, sarcoid, that sort of thing. Because I got this from the internet. It's the types of pulmonary hypertension, and again, it's this circuit. If the disease is predominantly pre, that's where we call that pulmonary arterial hypertension. If it's predominantly lung slash capillary, and then you have your post-capillary, and you usually think about heart. What are the consequences? Well, of all of these consequences, it all comes down to a final common pathway. Obviously there's a progressive distal material narrowing. There's intimal thickening, medial hypertrophy. You get thrombosis and plexogenic changes within the arteries. And what's important is, it's not uniform. It's very patchy. There's a loss of capacity to dilate and recruit other vessels, and the gas exchange is obviously going to be impaired. And in the heart, the right heart progressively thickens and may dilate. You start to develop tricuspid regurgitation, which almost invariably is going to cause righty atrial dilation. Pathogenesis, when you look histologically, starts with a vasoconstriction. Over time, you get vascular remodeling, obliteration of some of the vessels through in situ thrombosis, and these things called plexiform thrombosis. This is a nice histological example. This is a normal pulmonary artery, arterial. And you can see what happens over time is that it really thickens out and also develops these in situ thrombosis and plexiform lesions. These are the alveoli, and in this case, they look normal. So this looks like it's a precaculary cause. Think of primary pulmonary arterial hypertension or autoimmune associated pulmonary hypertension. Well, that's a nice little drawing here or diagram that Gopal used. I thought it was cute. Dysmion exertion, one of the earliest ones, fatigue, chest pain, palpitations. It's important to know, though, that once you start seeing things like presyncope, syncope, pitting edema, cites, you're getting pretty advanced at this point. Pitting edema, both lower extremities, often indicates right heart failure. We always associate it with left heart failure. But in reality, left heart failure is probably one of the most common causes. But in reality, bilateral pitting edema, you think right heart failure. So when you're actually evaluating these patients, what are they looking for? Well, first, diagnose it, right, the presence. And then once you figure it out, well, I think this is pulmonary hypertension or at least that's a contributing factor. You try to identify the severity. You look for any underlying causes, and then you use the imaging and other laboratory values to guide therapy, such as medical, the surgical. Is this post-capillary? Do you do some cardiac intervention? But one of the most important things, and this is for us too, and as a radiologist, is this more likely a pre-capillary or a capillary level, or is this post-capillary? Post-capillary requires different therapy. Also, post-capillary does not respond well to the various medications that I'm about to go over. If you increase the arterial blood flow, but the problem is over on the other side, such as mitral stenosis, you can put a person into acute right failure. So imaging, I got some question marks here, and I'll explain why. So a lot of this is gonna start changing a little bit. I'm gonna tell you some things that are not commonly taught. I'll try to be transparent with it, and you can decide for yourself. Thoracic imaging, to me, radiograph and CTA, for us, is the workhorse. It gives you a great deal of information, not just anatomically and possibly deologies, but also some physiology in there. The, really, the gold standard is right-heart cath still. They assess the pulmonary pressures, output, wedge pressures, and then they usually try a vasodilation trial, intravenous flow and or nitrous oxide. And if they respond, that's a pretty good prognosis, and that they'll probably have a favorable response to calcium channel blockers or some other medication. If they don't respond, that's not so good. Like a patient with scleroderma, they tend to be more difficult to treat because they don't tend to respond as much. Now, everyone gets an echo. It's a grade C, actually, in use for pulmonary hypertension. So everyone will get it. But the echo does not really detect the right-heart changes as well as the left. And it's an indirect measurement using tricuspid regurgitation. It can be helpful, but the VQ scan. A lot of people still recommend it looking for chronic pulmonary emboli. But I think it can be useful if you are trying to detect, say, an AST or a VST, because you'll see the material go into the systemic. But I'll go into that at the end, why I think that the VQ scan has a limited role here. And cardiac MR. Well, if you're thinking of congenital diseases, subtle VSTs or so, that may be helpful. I like the cardiac MR more than I do the echo myself. But these are the imaging that we use. But again, the workhorse, CTA, radiograph, right-heart cap. Current therapy, and this is for pre-capillary. You have your basic ones of oxygen, diuretics, calcium channel blockers. And then you have the directed therapy. And these therapies go along different parts of the pulmonary capillary endothelium. And then this induces changes of the endothelium and the smooth muscles. You've got the price of the cycling, the endothelial, and the oral phosphodiesterases, like sedentifil. If these ways fail, then you start looking at the surgical options down here. And this is how these directed therapies work. This is a nice slide given to me by Gopal. And you have your endothelium, which is more of an antagonist. Kind of reduces vasoconstriction, reduces smooth muscle proliferation. That's the goal anyway. And then you have your other two, which is the nitrous oxide and prostacycline, which actually induces vasodilation. And it reduces proliferation of the smooth muscles. Now, let's shift into the imaging. We're reading a radiograph or a CT. What can you offer the clinician? First of all, for dyspnea of unknown origin, this is one of the hallmarks that I learned early on in medical school, was the persistence or recurrence of symptoms means a diagnosis is being missed. So whenever you see in a report or you find that this is a persistent or it's a recurrent or chronic dyspnea or something along those lines, this should be sort of a red flag. Take a close look at the lung, take a close look at the pulmonary arteries, take a look at the heart. Is the right heart wall thickened? Is it greater than four millimeters? Is there a dilated right atrium that might signify tricuspid regurgitation? What's the size of the pulmonary artery? Is there intraventricular septal straightening? That's not a good sign. Look at the intraatrial septum. That's a weaker one that will be bowing to the left. And then take a look at the contrast dynamics. Is there a transient or an eruption of contrast present? Or is the contrast refluxing into the IBC? The latter should be another red flag that there's poor forward flow. Now, if you diagnose it or you have known pulmonary hypertension, what would you be looking for? Well, first thing I do, I look at the left heart. I look for post-capillary causes. Is the left heart myocardium thin? Is it dilated? Yeah, look at the pulmonary arteries here. Is there evidence of chronic thromboembolic disease? Lungs, is there ground glass, fibrosis present? And then if I still don't see anything, then I kind of dive a little deeper. Is there anything that looks like an ASD, VSD, PFO? And then you can look for some rare diseases like pulmonary capillary, hematosis, or being an inclusive disease. But these are people, when you know they have pulmonary hypertension, this is sort of what I look for. Now, let's start with the chest radiograph. I still love the chest radiograph. I know I'm an older guy, but I look there. What is the size of the pulmonary artery and right ventricle? Now, the right ventricle chamber, you don't really see usually on an AP or a PA unless it's really big. At that point, the heart usually kind of rotates because the right ventricle, when it enlarges, has nowhere to go and it rotates and kind of splays out. But I find the lateral projection is quick. Take a look at the retro sternal area. Is it greater than a third of the way up the sternum? That's probably right ventricular hypertrophy. Is there evidence of lung disease? Is there evidence of chronic pulmonary venous hypertension? Now, what does that look like on a radiograph? I'll get into that. Now, are there any associated findings? It's very obese patient. Well, you probably got sleep apneas or tips, presences or evidence of prior cardiac surgery. So, patient with emphysema pulmonary hypertension. Well, how do you know? Well, you look at the pulmonary arteries. This does look a bit big. I don't use measurements because people are like snowflakes and we have internal controls within us. The pulmonary artery on end should be the same size as the bronchus. And in this case, oh no, that pulmonary artery is a little big, isn't it? It's much bigger, it's bigger here. Then you look at the lateral projection. Well, you look here, the right ventricle's a little bit big, but the whole heart seems kind of squeezed down. Why is it squeezed? Well, the lungs are hyperinflated. There's very severe obstructive pulmonary physiology here. And how do you tell if the lungs are hyperinflated? You count ribs. If you do, I want you to stop. People are like snowflakes. Don't count ribs. Look at the lateral if you can. The diaphragm will help you decide. The diaphragm really should have acute angles and have a nice curve and go all the way down posteriorly. That's normal. When the diaphragm begins to flatten, that's not normal. Okay, that means there is end residual volume that's much higher and the pressures are higher and it compresses the heart and it pushes down. So when you see the sternum and the diaphragm angle starting to approach 90 degrees, or in this case a little bit more, and the diaphragm is flat, no matter if it's down here or if it's up here, that's obstructive pulmonary physiology. In this case, it is much more crowded in the lower. There's increased branch angles of the vessels, but if you're not sure, you just say there's severe obstructive pulmonary physiology. Now, how do you get pulmonary hypertension physiologically from emphysema is that it's predominantly, it's multifactorial for most of these, but it's predominantly you obliterate enough on the pulmonary vessels. Once you eliminate the alveolus in emphysema, that's what happens, you destroy the alveolus, you've also destroyed the capillary bed with it. That means that these areas that have little perfection also have little oxygenation. So you're maintaining a relative VQ match down here where the vessels are still open and the alveoli are normal. Well, this is where the oxygenation is taking place. So you have to obliterate enough the vessels before pulmonary hypertension. That's why it's so late stage, but the VQ remains relatively matched. There's a confounding here that the surface area is affected and I won't get into that. Chronic bronchitis on the other hand, that's also listed as COPD. Well, that is more of an airway disease where there's thickening of the airways, the read index, remember from medical school how it's greater than 0.55, it actually causes decreased ventilation, but you're still perfusing those areas. So essentially you have more of a shunt and a shunt causes hypoxia. So between chronic bronchitis and emphysema, which is more of a dead space in vessel obliteration, which one of these will develop pulmonary hypertension earlier, well, chronic bronchitis. You get a generalized hypoxia, vasoconstriction and pulmonary hypertension and corpulmonary are part of the picture chronic bronchitis. Hence they called blue bloaters, they're hypoxia versus emphysema, pink puffer because you have a relative preservation of the VQ match. And this patient, how about this? It's a radiograph, yep. She has a central line in, she's actually getting prostacycline infusion for pulmonary hypertension. And you can see here, you got your thoracic aorta, aortic pulmonary recess, and main pulmonary artery, definitely enlarged here. So she has pulmonary hypertension, but she also has an extensive amount of lung disease, ground glass for sure. And she's got the commas, the cysts, she's got a number of cysts here in her lungs. And she's got a scar here from an open lung biopsy. So we know this is chronic. So what is the primary problem here? Well, one would assume that she's got some sort of lung disease that gives you chronic on glass and cysts, in this case, LIP, and she's developed pulmonary arterial hypertension from it. And that's her CT. Now, this isn't quite straightforward. It is chronic hypoxia. It's gonna be a big factor, but all of these autoimmune diseases, her churrogrins or SLE, I can't remember, I think she had features of both. Autoimmune diseases are an independent risk factor for pulmonary hypertension. And they in general don't tend to respond as well to the medications that the pulmonologists use. This person, Hayorta, main pulmonary artery, for way too big, right ventricle is here. It's a bit dilated. She may have a little pericardial infusion there, aureo-sine, but the lungs look good. But boy, that chin indicates what is the probable etiology here. Sleep apnea, chronic hypoxia. So again, chronic hypoxic state, vasoconstriction, long enough pulmonary hypertension. This pulmonary artery is markedly enlarged. She had severe pulmonary hypertension. Treatment, aim it at the hypoxia. Now, this is an example of a post-capillary etiology. This is a patient with mitral stenosis. This patient has pulmonary venous hypertension. How can you tell in a radiograph? Well, what you do is you see the vessels here, the arteries in the veins and the upper lobes are a bit larger than the lower lobes. It's not dramatic here. I actually use the lateral most of the time because I find the anterior segment vessels tend to be the largest in patients with sephalization, much more than the posterior. These vessels down here should really be the largest veins in arteries. Yet, you look and it's like, nope, these are bigger. So this is sephalization. So it's not just that it's upper lobe and it's not just that it's veins, it's arteries and veins. And on the lateral, you see it's usually the anterior segment of the upper lobe that have the largest. Once you see sephalization, you say, all right, well, this is going to be a post-capillary problem, probably hard. And then you look here, the right ventricle is clearly enlarged. This is how you get that ventricular heave or the sternal heave because the right ventricle sits right behind the stern and it crawls up there as it gets hypertrophied. And then you see the left ventricle and then whoops, there's the left atrium, kind of this bulge here, right there. That's actually a little dilated. That tells you the etiology is mitral stenosis. This is why the patient has pulmonary hypertension. Another patient had mitral stenosis, had a mitral valve placed. This is a tricuspid anuloplasty. How can you tell an anuloplasty on a radiograph for CT? Well, it's incomplete. It's an incomplete ring. A valve prosthesis is a complete ring, anuloplasty incomplete. Goes around, tightens it up, tells you that patient had regurgitation, in this case, the tricuspid valve from pulmonary hypertension. Well, she had this repaired five years ago, but look at the arteries and veins here. See the size, look at them down here. This is cephalization. Is she in pulmonary edema? No. She did have a calf to follow this up and her pulmonary artery pressures were minimally elevated, but things were back to normal. She's not having episodes of congestive heart failure. Well, why is this still here then? Well, it turns out in many patients, once you develop cephalization, it tends to be more permanent. And autopsies have shown that the veins in the lower lobes and arterioles, the venules on arterioles, are sclerosed and fibrose down. So, the adage that early pulmonary edema is a reflection of cephalization in the acute setting is unlikely to be true. That's a myth. Take a look for yourself. I mean, you know, to believe me, we see a lot of people who are in pulmonary edema. This patient's in congestive heart failure. Take a look at the vessel sizes. This is ground glass, septal thickening. This is the same patient after treatment. Take a look at the vessel size. There's no change. These things don't change quickly. When you have increase in pressure, get the uncuttered pressure. The fluid comes out and that's how you get your adema, all right? Another patient. Pulmonary arteries are markedly enlarged. Pulmonary hypertension. Look at the right ventricle, holy mackerel. It's way up there. So, this patient has pretty advanced changes of pulmonary hypertension on the radiograph. Ideology? Well, this one's a shunt. How do you know? The vessels are large here, just like sephalization, but the difference is they're large here too and they're all about the same size. So, they're all dilated. And over time, these will start to sclerose down and thrombose down and narrow and these will get bigger centrally, the so-called pruning, okay? So, shunt vascularity looks different than sephalization, although it is subtle and I've put it up here for you. And the key is both will have large vessels in the upper lobes but look at the lower lobes. If the vessels are smaller as they are here, then that's sephalization. That means there's reduced pulmonary flow and that's indicative of a left heart or a post-capillary cause. If they're the same size, then you start thinking shunt. So, lower lobes is sort of your key between the two. All right, quick break. This is a fun study. This is from the Canadian Medical Journals from a number of years ago. They call it in the wells, nodding off events per lecture. You can see some of the risk factors they found. I love the tweed jacket one, 2.1 odds ratio. You're going down, monotone. I think they're gonna have to redo in the study and just say, okay, what is gonna be associated with these web lectures and nodding off? I'll bet you the monotone is the big one. Okay, let's shift. Radiograph, now we're going to CT. Spiral CT. All right, supporting evidence. Yes, is the part of the pulmonary artery is large. Is there contrast? Reflex into the inferior vena cava. What's the right heart look like? Is there hypertrophy? Is there mosaic lung attenuation? Mosaic lung and I'll get into that. And that's usually a later stage finding. And also another little subtle one. If you have a person with pulmonary hypertension, take a look to see if you have large bronchial arteries. So bronchial artery hypertrophy, tend to see it in the setting of pulmonary hypertension and in the setting of bronchiectasis. Okay, normal CT, you commonly may see a transient interruption of contrast. I'll go into what that is. You don't tend to see any contrast reflux. The intraventricular septum is almost always bowed to the right, okay? Intraatrial is usually midline or maybe bowed to the right. And the pulmonary artery diameter is often less than three centimeters. Now again, I don't measure much. So just take a look at the ascending aorta at the same level and the pulmonary artery, main pulmonary artery. Are they about the same? That's pretty good. I don't usually use the three centimeter rule, but if I see someone who's about 3.5 centimeters or higher, even if it's kind of similar to the aorta, I'm suspect because 3.5 centimeters is getting up there. So to me, that's a little bit more of a specific number rather than three centimeters, which I think is a little too sensitive. Now contrast, what's transient interruption of contrast? It's a brief interruption of contrast that occurs in the column of blood, all right? So you inject the contrast going to the SBC, right atrium, right ventricle, pulmonary arteries, then into the left atrium and the left ventricle into the aorta. When the scanner gives the instructions, take a breath in, what happens? Well, the huge negative pressures in the lung suck in the blood from the IBC and the supragenic cava. Two thirds of the blood return are from the inferior vena cava. And now there's no contrast there. So this comes in and dilutes the blood and decreases the contrast. This used to be, and I think some people still call it, poor bolus or something along those lines. But it is actually seen relatively commonly, especially in people with very good forward flow, pregnant patients with increased blood volume, and there's a variable change in the decrease in density. But it's a pretty good sign if you see it that this is a relatively normal cardiopulmonary flow. So the key is, you see it all at the same level and there's no expansion of the pulmonary artery, so it's not an embolus. You look at the right heart chambers and the preceding images and you'll see that it might be low density, that's the inferior vena cava diluting. And you will see the hyper dense contrast coming in the supragenic cava. That's how you know it's not a late bolus or something. If there's no contrast in supragenic cava, then it's probably a late bolus. This is an example, normal heart. You can see the contrast within the right ventricle, but look what's happening here. It comes coming up from the inferior vena cava, floods in, and then you start to see the pulmonary arteries. Notice how they go unapacified to unapacified. This is not a poor bolus. This is transient interruption of contrast. How do you know? Well, contrast is still coming in the supragenic cava. And then it kind of makes its way through and then it goes into the aorta and the center eruption of contrast just kind of goes through the circuit. Now, quick case example, how did you use it? Now, a 40 year old was referred when I was at OHSU for pulmonary hypertension. They had an outside echo that said, hey, the pressures in the pulmonary artery are estimated at 60 milligrams, 60 millimeters of mercury, sorry. And it came for workup. So they got a CTA. And then when I read it, it was like, well, wait a minute here, this looks normal. The right ventricle wall is thin. There's intraventricular septal bowing to the right. And what's this? Contrast, no contrast, and into the pulmonary arteries. That's transient interruption of contrast. So to me, the echo is probably wrong because this is a normal, this tells me that this person is taking all of the IB contrast from the superior vena cava and letting it fill in the right atrium. It's also able to accommodate all of the unopacified blood coming from the inferior vena cava and just moves it right through the circuit. So the peripheral pulmonary vascular resistance or pulmonary pressures are likely to be normal. And the patient underwent a right heart cath and it was completely normal. The echo is wrong. So what about the opposite? When you start seeing hypervent contrast going into the inferior vena cava, well, that tells you most likely that the contrast is coming in and when the person took a breath in, it cannot, it didn't, it can't accommodate that unopacified blood from the inferior vena cava. In fact, it's having trouble accommodating the contrast coming in. And it tells the contrast to go weight down in the inferior vena cava until it can accommodate. So that's a sign that there's poor forward flow. I'll get into the exceptions after, but this is actually a very useful sign. I actually do use it quite often. There's usually also excellent pulmonary artery pacification. So if I see a CT angio in someone and the pulmonary arteries are beautifully pacified and there's no transient interruption of contrast, to me, that's a little bit of a red flag that I wanted to spend a little bit of time looking at the right heart in for any contrast reflex. This is a patient with dilated right ventricle, big dilated right atrium. Whenever you see a right atrial dilation, what are you thinking of? Tricuspid regurgitation. Notice also how the heart is shaped. Normally it's diagonal, but when the right heart enlarges, it rotates and looks more horizontal on the CT. So, because that's where it goes. The left ventricle looks normal, intraventricular or compressed, the intraventricular septum is straightened and you have a bit of hypertrophy involving the right ventricle and free wall. So this is a patient with chronically elevated pressures from pulmonary hypertension, has tricuspid regurgitation, has enlarged right atrium and there's the reflux of hyperdense contrast into the inferior vena cava. So another example, a lot of hypertrophy here and then a fair bit of contrast reflux into the inferior vena cava signifies there's poor forward flow. When you see contrast reflux, you wanna look at a couple of things. One is take a look at the pericardium. Does it appear thick and calcified? Could it be constricting the right heart, causing the reflux? Two, look at the pulmonary arteries. This is again a sign of pulmonary hypertension. Is there, is the diameter large? Is there evidence of chronic thromboembolic disease or an embolus for acute heart strain? And third, look at the heart. Myocardial failure is a common one to give this. This is an example of someone with a poor EF of 10 to 15%. Here are some of the changes when you see it. You identify the contrast reflux. Well, that's not normal. You look in and say, well, the myocardium is relatively thin. And you also notice that there's not a lot of a pacification of the left heart or the thoracic aorta. That tells me that, boy, this blood is not moving very well forward. The right atrium is dilated, tricuspid regerge. Now, how could you tell this probably was someone with a poor ejection fraction? Anybody know what that structure is? That's the moderator band. Look how clear and sharply defined the heart is. When you look at a CT angio and the heart looks like it's gated, but this is not a gated study, what does that kind of tell you? Well, the heart is just pumping very much. It's not moving. So a very clear looking heart or myocardium should suggest either A, they're really bradycardic or B, the contractility is severely reduced. Anyone can see here constricted pericardium. Yeah, there's calcification. It's squeezing the right heart and it's actually pushing the contrast back into the inferior vena cava. It can't expand to allow the contrast and the IVC blood to come through. There's a little bit of a correlation. It's rough, but when I see contrast, hyperdense contrast, refluxing down to about the diaphragm and it's not heart and it's not pericardium but pulmonary artery, that does seem to correlate with the pressure of about 40 millimeters of mercury. There's often some straightening and bowing too when you start having higher pressures like 67 or so. This is a patient with pulmonary artery pressures 35. There's some contrast reflux down to the diaphragm. Not a lot of intraventricular straightening. Cath showed pulmonary hypertension 35 millimeters of mercury. This is a patient with chronic thromboembolic disease. There is a lot of hypertrophy and there's a lot of reflux down below the diaphragm. There's also straightening of the intraventricular septum. These features on a CT, you'd say, hey, this is strongly suspect for severe pulmonary hypertension, in this case, secondary to thromboembolic disease. Another patient with reflux, excuse me, into the inferior vena cava, which looks pretty dilated, doesn't it? And into the paddock veins, right atrium is dilated, trying to cuspid regurgitation, right ventricular hypertrophy, this is chronic, intraventricular straightening, high pressures, likely about 70 or more, and compression of the left ventricle and poor forward flow into the left side. Go a little higher and you're like, oh snap. Looks like a big embolus. Except one thing, that was chronic changes, right? So this thing had to have been there for a while and then you can also notice, hey, you know, there's some blood vessels here, oh snap. This is gonna be a tumor, right? It's gonna be a tumor. And in this case, it was a pulmonary artery intimal sarcoma. Interestingly, once they removed it, look what happened to the heart. Again, the dynamic change. You start to see the decreased dilation. You are seeing transient interruption of contrast starting to return, suggesting that the pulmonary artery flow is now reestablished and there's good forward flow and the intraventricular septum is convex. So these are dynamic changes. Okay, here's your exceptions. You will see transient interruption of contrast commonly in people who have a large cardiovascular capacity, say a pregnant patient. And you will see IBC reflux with normal pressures in heart and pericardium and those who are generally petite or have small cardiovascular capacity. It's like a kettle of water. You pour the same amount of water in and if the kettle's small, it'll overflow. If the kettle's big, it won't completely fill it and you'll have decreased contrast to pacification. For pediatric patients, we give contrast based on what? Based on weight. Then at 18, we're all the same. No, that's not how it works. So when you see this, if you see IBC reflux and it's a small looking heart, it's a petite person, that may be normal. So one size does not fit all. So patient with pregnancy associated contrast, interruption of contrast, this is it. Again, you can see the hyper dense contrast coming in the spherovina cava. There is the mixing from the inferior vena cava and into the pulmonary arteries. So about 32% or a third of the CTAs and pregnant patients are indeterminate, mostly because of transient interruption of contrast. They have an increased cardiovascular system. They have a more hyper dynamic system. They probably are people who need more contrast in plus minus a faster rate. Smaller statute individual had reflux of contrast, but there was no elevation and pressure. The heart was normal, pericardium was normal. This is someone who is basically a smaller keto. And when they gave the same amount of contrast, it simply overflowed into the inferior vena cava. Now, when you're taking a look at a patient with pulmonary hypertension, after going through all of these other ancillary findings, you start to go, okay, well, what's causing it? Is this a pulmonary disease or airway disease? Is it cardiac or intrinsic? And I kind of caution you, more than one may be present. 54 year old with scleroderma, well, scleroderma in itself, right? Autoimmune associated. So that's factor one. Number two, you can see that she does have pulmonary hypertension. The heart is in fact now horizontal. The right ventricles enlarged. There's a hyper dense contrast reflux into the inferior vena cava. She's got the dilated esophagus, that's commonly seen. And then you look at her lungs and she's got a great deal of ground glass opacity, your regular dysroclura, little bit of traction bronchialexis. And the findings here are consistent with fibrotic NSIP. And that induces a hypoxia. So she's got chronic hypoxia and she's got also the related factor of scleroderma. Well, she also had another thing. She has an ASD. So she's gonna be a really tough one to treat. Special one here, usual interstitial pneumonitis. Interstitial diseases have become very hot over the last few years. And I've gotta mention this because I say this about pulmonary fibrosis, especially UIP. There are three complications that you should always be looking for and every one of them. One is any new nodule, which will be a lung cancer until proven otherwise. Evidence of ground glass like here, without fibrosis, that's just an acute deterioration. But the third one, it's quiet. Pulmonary hypertension is insidious now, people. It's just the people, they'll notice a little bit more pitting edema, a little bit more dysmean exertion. They come into the, see the condition a little more often. But with UIP, the pulmonary artery does tend to enlarge and they are very predisposed to developing pulmonary hypertension. And so that gets treated. That needs treatment to help reduce the amount of symptoms and hospital or outpatient visits. So whenever you're looking at anyone with pulmonary fibrosis, nodule, ground glass without any fibrosis and pulmonary artery that's getting larger, okay? Pulmonary arterial hypertension is a very common complication for it. Another patient with pulmonary hypertension, very severe right ventricular hypertrophy. Well, there's a small PDA. That's kind of small though. But take a look. Anybody see something here? Atrial septum looks good. Look what here. We got a membranous defect, VSD. And that was the main abnormality for this person. Another person who came to, this one I was at the University of Utah and a lot of people who had borderline cardiopulmonary problems, the minute they landed in Utah, they couldn't have trouble breathing because of the altitude and go off to the hospital they went. And that's what this guy did. He's got a big pulmonary artery here. He's got evidence of pulmonary hypertension, his right atrium, which when you see the right atrium going to about the level of the hyalum, yeah, that's probably dilated. And that suggests tricuspid regurgitation. And you just kind of look and the vessels look a little bit odd here. Big pulmonary artery, bronchial artery hypertrophy. See all these little bronchial arteries all over? Bronchial artery hypertrophy. Very severe right ventricular hypertrophy straightening of the ventricular septum. And the diagnosis, the person had a huge PDA. And it turned out the patient had a history that born a premature infant and had a PDA that never closed. He didn't know about this until he came to Utah and then he had trouble breathing. Chronic thromboembolic disease, that's one that most people look for, pretty severe. How can you tell chronic clot? Well, from say a lymph node. A lymph node, hyaluronic lymph node will have a very smooth inner border and more of a lobulated outer border because it's outside the pulmonary artery. Chronic thromboembolic or the chronic thrombus or murals thrombus will have a smooth outer border along the pulmonary artery, but it'll have a more lobulated inner border. Remember the lymph nodes within the hyalum aren't always these nice round things. They're kind of a morphous and sort of form along the branch points. Mosaic pattern. Now the mosaic perfusion pattern in most of the time we think airway, but pulmonary hypertension actually gives it. Remember it's a patchy sort of obliteration of the pulmonary artery. And so it's not surprising that you would get this. You would get an expiratory scan. There would be no air trapping. Then you go, oh shoot, this is pulmonary arterial hypertension induced. You can see the areas here of increased flow. They're not ground glass now. This is increased flow. And the vessels are larger here. And of the areas of decreased flow, the vessels are more attenuated and less in number. This is a very common scenario for all cases of advanced pulmonary hypertension. Literature kind of makes it sound that this is a sign of chronic thromboembolic disease. It can happen with any of the advanced pulmonary hypertension because remember it's a final common pathway. What does that mean? Well, let's look at it. There's a patient who's been diagnosed with chronic thromboembolic disease. There are, have pulmonary hypertension. They have a large right ventricle. Lungs look clear. This is the VQ scan. This is the ventilation. And you can see there are multiple perfusion defects. That's how the person was diagnosed. This was the CTA that was obtained a year later. Hmm, there's no thickening. There's no mural thrombi. There's nothing here to suggest chronic thromboembolic disease. They do have a little pseudo-aneurism from their prior pulmonary arterial or swan placement. Loomed it out, cut a pseudo-aneurism. And then here is what the person looks like. This is mosaic perfusion. You can see there's areas of increased flow here. The wider areas, decreased flow here. What we did was we did a quick 3D on it. And this is what it looked like on our kind of three-dimensional little fun scan of this. This can be done without contrast. The areas that brighter are increased flow. The areas darker, decreased flow. Well, look at the pattern. Look at the VQ scan. This is not a surprise. It's exactly the same. So any mosaic perfusion that you see, regardless of the etiology, is going to look like a high probe on VQ. And that brings me to the thought of we still recommend VQ scans. And it's probably reasonable if it's mild pulmonary hypertension, sure. But if you have a patient with advanced pulmonary hypertension, well, the VQ scan is probably gonna look high probe just based on this physiology. And it's not necessarily pulmonary chronic thromboembol disease. So let's finish up. Here's our patient. Now that we're done, what do we say about this person? They have pulmonary hypertension. They have evidence of recurrent congestive heart failure. They get small effusions. They get septal lines. Normal left ventricular function and echo, whatever that's worth. This is interesting. Capillary wedge pressures were not increased. Does that change anything? What would you say? Well, this person turned out to have pulmonary venous occlusive disease. And that was actually, unfortunately diagnosed on autopsy. Why was the pulmonary capillary wedge pressure normal? Quick note about the wedge pressures. With pulmonary venous occlusive disease or capillary hemanginotosis, the disease is just right past the capillary bed, the very tiny little venules. They develop intimal thickening and sclerose down. The wedge pressures reflect, and you gotta have a continuous column of blood for that, which is why it's not very useful in diffuse ovular geometry or DS. The wedge pressures reflect the pressures in the veins of the same or greater diameter. The disease is located here. So the pressures for wedge pressures can be normal in the setting of pulmonary venous occlusive disease. Left ventricle function is normal because the disease process is at this area of the circuit. 28-year-old female, recent diagnosed pulmonary hypertension. I show this just because it's the only case I've ever seen it. You can see some ground glass nodularity, central lobular, kind of funny, kind of funny. Noedema, normal left ventricular function. This goes along with pulmonary venous occlusive disease. I think they're on a spectrum myself. This is pulmonary capillary hemanginotosis. It's that proliferation in the same area around the capillaries and the post-capillary venues. So that's my summary or a talk on pulmonary hypertension. Remember, multiple ideologies lead to a common pathologic and physiologic consequences. Imaging role, recurrence or persistence of symptoms. Is there pulmonary hypertension? Is it there or not? Ideology, try to help it out. Is it primary lung? Is it primary heart? Is it intrinsic thromboembolic disease? Or is it more than likely a combination? And the most important thing if you're evaluating anyone with pulmonary hypertension with ideology, do you think this is post-capillary? The treatment is completely different and these people tend to respond well and can get quite sick with acute heart failure with the traditional pre-capillary, pulmonary arterial hypertension medications. Thank you so much. It was a pleasure and this is my email. I got two of them. Feel free to email me if you have any questions or if you'd like some other information, papers or just wanna chat. I got the time, all right? Thank you very much. Perfect, thank you so much. We do have a few questions in the Q&A feature if you don't mind opening that. I just wanted to thank everyone for participating in this new conference today. Remind you that it will be made available on demand on MRI online.com in addition to all previous new conferences. And we also want to just remind you that tomorrow we will have Dr. Steven Jay Pomerance with us on a conference on how to assess ligaments on MRI part one. You can register for that and all others on MRI online.com as well. Dr. Gossin, if you wouldn't mind just opening that Q&A and answering the questions there. Yep, and I got time. So I'll just keep talking until you guys are tired of hearing me. First one is how reliable is contrast reflux into the inferior vena cava as an indicator of pulmonary hypertension, the absence of other signs? Not too reliable. I gave the exceptions. Is a small patient. If there's no right heart hypertrophy, the pulmonary artery is normal in size. I don't tend to worry about it. I just blow it off. To me, it's helpful in the setting of pulmonary hypertension because it can help decide how severe is this. Next one. How to differentiate your pulmonary hematosis case from subacute HSP. Oh, that's a good one. Subacute HSP, to me, the central lobular nodulary looks a little different. It tends to be a more uniform, bit more in the upper lobes. Pulmonary hypertension is not necessarily a major problem with HSP unless it gets very severe and fibrotic. So to me, it really should have the fibrosis there. And capillary hemangemotosis does not induce fibrosis in general, except at the very capillary and venial level. So pulmonary hypertension, central lobular nodularity, I would be favoring more unusual causes, or if there is evidence of a fair bit of fibrosis, then you can start thinking of NSIP, HSP kind of deal. Who qualifies for continuous reflux? Or what qualifies continuous reflux? I sometimes see, and I know you have seen it, where the reflux of contrast looks like it's there and then it's unopacified and then there's some hyperdense contrast more distally. And when it's discontinuous like that, I don't put as much stock into it because it turns out when you watch closely on ultrasound breathing, there is this kind of to and fro with the inferior guinea cava, even in the normal patient with breathing. So if I see this discontinuous, I don't tend to put as much stock into it. I have to see a continuous column. And again, it's useful if there are other evidence of pulmonary hypertension. If there's no other evidence of it, I don't tend to worry about it as much. Who called me, sir? Sir, my name is Mark. What are the minimum imaging requirements in cardiac CT as in the number of slices in a CT scanner? What are the minimum number of imaging requirements? I'm not sure I understand that. We're talking more about the cardiac CT. I'm not sure I understand that question. I'll move on to the next. If you want to rewrite it, I'll try again. How do you distinguish TIC from thrombus? Good one. Yeah, thrombus. Not going to be at the same level. Two, the vessel is often expanded. Three, the right ventricle on the preceding images will have a continuous contrast column. So remember, if you're seeing some unopacified blood or something that looks like thrombus, is the vessel expanded, looking to the side? Is it also unopacified at the same level? Okay, yeah. Next, take a look at the earlier images down low. Is the right ventricle have unopacified blood? If it does, yeah, that's transient eruption of contrast. I also put a little note in there. If I see it and it looks like, you know, this is pretty severe transient eruption of contrast. It's easy just to say it's indeterminate. But I just say, look, in the setting of transient eruption of contrast, that's a very good physiologic sign that this person is normal. And it's unlikely that there is a cardiopulmonary significant embolus in that setting. I mean, there still could be a small embolus, but it's certainly not causing any right heart strain. Pulmonary counter-analysis with the imaging fix not seeming other conditions. Yep, I've addressed that one. How do you differentiate tumor thrombus from, or thrombus from tumor? Good one. One, there might be chronic heart changes, like I mentioned, right ventricular hypertrophy, dilation, severe TR. Two, this is big. The distal pulmonary arteries from the thrombus will be constricted. Over time, these vessels constrict in an acute pulmonary embolus. It does not constrict. Now, this brings up a myth about the Western Mark sign. Oh, there's decreased pulmonary flow distal to a pulmonary embolus. Absolutely not. Absolutely not. The Western Mark sign is a sign that there is chronic thromboembolic disease or chronic occlusion. Tumor thrombus, by definition, really is there for some time, usually. And changes of a pulmonary acute embolus will be expansion of the pulmonary artery at that level. And the pulmonary vessels may be unopacified, but not really constricted. With chronic or a tumor thrombus, tumor thrombus will expand, but you have this constriction distally, the so-called Western Mark sign. Three, look for any signs of enhancement. And if you're not sure, redo it. Unenhanced CT, then enhance it. Did it enhance? If it did, that's probably a tumor thrombus. In the end, if you're not sure, suggest a biopsy. Okay. Can standard axial images on any thoracic CT be considered adequate for basic evaluation of heart chambers? I think so. I always comment on the heart chambers. I think so. If the left ventricle looks big, the right atrium looks big, there's, you know, whether it's a pacified or not, I tend to comment on it. I think you can, at least you can get an estimation. I think that's reasonable. Okay. If you're not sure, it's borderline, don't mention it. With patients with poor EF, how do you time contrast injection? Oh man, that's a good one. If you're thinking about the thoracic aorta, you gotta wait longer and you gotta go delays. I don't know how, I think you almost have to put the cursor on the left or on the thoracic aorta. For most of these patients, they really, they may not have known cardiac ejection fraction issues. And again, to me, this is helpful diagnostic information when I see this very nice contrast enhancement of the right heart and pulmonary arteries, but not much in the left. I spend a fair bit of time commenting that this person's got cardiac issues that need to be addressed. They have poor forward flow or they have pulmonary hypertension. One of the two, as I look at the scan for the ancillary findings. If they're really interested, it's a, well, we wanna know if there's a left ventricular thrombus now, then you say, well, we gotta do this again, but we're gonna have to put the cursor on the thoracic aorta. Okay. Let's see what else. Have you come across physiologic prominence of the right ventricular alfaltract and pulmonary artery in young individuals? Yes, for sure, especially younger females. That's why I don't use the size alone. But again, I'm gonna say this. Once I start seeing 3.5 centimeters, I think you gotta mention it, but I've definitely seen the prominence and I blow it off, especially in the playing field. If I see other findings of the heart chambers or IVC reflux or something, I may mention it, but I've definitely seen it. What is the feature that is suggested about venous-inclusive disease? The main feature is gonna be this. Persistence symptoms and recurrence of congestive heart failure in the setting of a heart that looks normal and the pulmonary pressures are going to be elevated. If you scan them, you may see evidence of congestive heart failure, the septal lines, you may see the little central lobular nodularity. Again, it's an unusual disease, you're not gonna see it very much. But to me, it's that setting of heart failure and they often can get diagnosed, in my opinion incorrectly, as having so-called diastolic heart failure. And again, when I hear that, I at least think about it. Is there evidence of heart failure here? Yes, pulmonary hypertension, yeah. Okay, what was the wedge pressure? It was normal. Oh snap, you know what? I think this patient has something that needs more investigation like pulmonary venous-inclusive disease. Again, you may not even see this in your career. I haven't seen too many, but that's when I start thinking about it. Oh, careful. Okay, all right on. What is your thought about having straightening of the septum and reflexive contrast without dilated pulmonary artery? All right, straightening, that's when I start looking very carefully at the pericardium and I start, because to me it's probably gonna be pericardium or you could have an acute pressure increase in the pulmonary artery. That would be the sign of like acute heart strain. And if there's no pulmonary embolus you can see, then there's some sort of pulmonary vasoconstriction which has occurred. What I've seen in it is the IV drug abusers. They get this acute onset, tachycardia, shortness of breath. You do the CT angio, you see the right heart strain, the straightening of the septum, but there's no emboli in the pulmonary artery is normal. In that setting, I just say, look, there's probably some injected debris that went into the lungs and induced a cascade of pulmonary vasoconstriction elevating the pulmonary vascular resistance, giving right heart strain. Try pulmonary vasodilator therapy like Sedentifil. And invariably that usually works. So, okay, acute versus chronic thrombus. Acute thrombus will always expand or I shouldn't say always. There is no 100% in medicine, right people? It usually expands the vessel. And the vessel distally will be what? It will be normal in size. Chronic thromboembolic disease. It will, over time, constrict the pulmonary arteries. That's why they get smaller. And they tend to be more eccentric and mural. And again, use that sign. If the outer aspect is smooth and the inner aspect is lobulated, oh, that's gonna be a mural thrombus. And that would go along with chronic. If you see something that looks relatively constricted and there's constriction of the distal vessels in that segment or in that supply, mention the possibility of chronic thromboembolic disease. Again, the Western Mark sign is not a sign in the acute setting. That is a sign of chronicity. That's a myth. Okay, on chest radiograph, I often see prominent indistinct vasculature in the lower lobes. Normal with normal. Is this a normal variant indicative pathology? When I see indistinct vasculature in the lower lobes, but normal in the upper lobes, especially if it's symmetric, to me, I like your terminology, indistinct pulmonary vessels, the margins of blur, it's kind of a ground glass. That to me is a sign of pulmonary edema and congestive heart failure, especially, especially through septal lines. It could be some other ground glass producing process acute hypersensitivity, viral infection or so, but usually I, or DIP, if it's chronic, usually I think about pulmonary edema. That's how you diagnose pulmonary edema is the vascular indistinctness, plus or minus septal lines, usually perihiler, lower lobes. And it is not looking for enlargement of the hyalum. I don't use the term vascular congestion. I don't know what the hell you're talking about. Prominent pulmonary, no, I don't say that either. If I see sephalization, I don't usually use that term. I just say there's evidence here of chronic pulmonary venous hypertension and that's not necessarily a pulmonary edema. It's the vascular indistinctness and the perihiler and lower lobes, that's pulmonary edema. Hopefully I answered the question. When measuring the main pulmonary artery on CT, where should I measure at? I generally measure the main pulmonary artery at the horizontal portion. I put a cursor on it, if it's like 3.2 centimeters, I look at the ascending aorta, it looks the same at that level. I blow it off, I don't even mention it. If I measure 3.2 in the ascending aorta is 2.8, I mention it. If I see 3.5 or greater and it's the same as the aorta, I at least mention it, even though I know it's the same as the ascending aorta, but that to me is starting to get too big. So that's where I measure. Main pulmonary artery horizontal. How to decrease transient interruption of contrast? Oh, good one. There's a couple of ways. One, give a higher volume faster. Two, don't happen to take a breath in. Don't happen to take a breath in because the flow of the veins is not continuous. It is our breathing that causes the increase in flow and it goes in concert with our breathing. So if a patient is lying down, don't have them take a deep breath in. Just hold it and you're likely to decrease the amount of interruption of contrast. If you get a lot of contrast, interruption, to me again, that means it's probably not gonna be in a significant cardiopulmonary embolus anyway, but if you wanna redo it, try doing it with the patient in expiration or no breathing at all. And that has actually worked pretty well. All right, let's see, what else? Oh, a thromboembolasm in corona. So coronavirus, yeah, this is becoming hot. I looked it up. I can't find that they're necessarily hyperquagol. The coronavirus does affect the blood. To me, it actually seems, if anything, that these folks would be more likely to bleed rather than clot. When a patient has severe acute lung injury from coronavirus, the risks of DVT and PE appear, this is early again, to be the same as if they had ARDS without coronavirus. So I know the blood's involved. If anything I've noticed, they tend to bleed a little bit more. I've only seen one person with severe acute lung injury and coronavirus. And let me tell you, I see it every night. I see five to 10 cases of it every night. I mean, I've got the teaching file of this thing. And this one patient had been in the ICU for weeks. They had it really bad. So that doesn't tell me anything. See, some people would point that and go, see it could be from hyperquagol. It's like, no, well, you take a look at your diffuse alveolar damage patients, your ARDS patients, and they have a very similar. So I haven't found that it's hyperquagol. I haven't seen any increase and I see a lot of it. But that's anecdotal. We're still learning about it, something you may come out. All right. How to differentiate fibrosin mediastinitis with chronic fibrosin mediastinitis? That one to me is more of soft tissue, right? Outside the pulmonary artery constricting it. So the pulmonary artery looks constricted, but again, I would go to that same rule of thumb. It's not in books. Nobody really teaches this. Is that the soft tissue component, if it's in the mediastin, whether it's nodes or fibrosin mediastinitis tends to have a lobular or you're more irregular outer wall, but the wall along the pulmonary artery is smooth. Chronic thromboembolic disease being intraluminal tends to have a smooth outer wall, but a lobulated inner. So try that, that helps, but I'll tell you, sometimes that can be really tricky with some of those lymph nodes at the hyalumet that bifurcation. I've seen that miscalled a lot. So it is tricky. Where do you keep the ROI and CT to a pacify both chambers in a cardiac CT along with the pulmonary arteries? Well, personally, I would actually put it in the thoracic aorta and just make sure that the contrast is going in long enough. I would assume it's going to be fine. If they have poor outflow, poor cardiac output, we at least know it got into the left ventricle. If they have good output, there's a risk that you may have a little less a pacification of the pulmonary arteries, but especially if they're hyper dynamic, if they're normal people like pregnant patients, I probably just put it on the pulmonary artery. It'll be fine, but you can always redo those things, but it can be tricky that whole pulmonary artery, capillary, pulmonary, venial and left ventricle to aorta, that circuit has a lot of places where things can go right. And sometimes we may not be able to anticipate that. What volume of contrast usually administered? Yeah, I tried to get that changed a while back while I was at OHSU. That was really difficult actually. You could go based on DMI or weight and do it just like pediatric patients. Some of the technologists may not like that, but you could try that out, give it like a 30 day trial and see how that works. Because again, bigger patients need more volume and smaller patients really don't require it. So if it's a petite older woman or an older man, you don't probably have to give as much, but if it's a big person, you probably need to give more. So you could try out and say, let's take the pediatric criteria and why don't we just keep doing it into the adulthood? And each of these patients usually has some sort of weight attached to the requisition or in their chart where you can do a quick calculation. Try it out for 30 days at your institution, see how it works. Pulmonary, capillary, hemangiotosa, multiple central lobular, but the imaging feature is constantly seen with other infections. So yeah, I think the biggest thing here, infections are transient. And often when you have central lobular nodularity, there's usually some airway thickening and probably some terminal bronchial or the so-called budding tree filling. Capillary, hemangiotosis, the other thing I've noticed about those nodules, look at the central lobular nodules again. They look sharply defined. Now, look at an infectious-related central lobular nodule. They're very fuzzy, almost like a hypersensitivity. To me, hypersensitivity, central lobular nodules, are a little bit more confusing with the infectious. Capillary, hemangiotosis looks very sharply defined. And then other ones, summary of protocol for pulmonary embolism in your department. Well, I reach for a lot of folks now so I don't really have it, but the protocol before was, I forget the contrast that we used to give, changed a few times, and Dr. Foos now takes care of that. But I think we used to give around 100 cc's of contrast. And it worked most of the time okay, but again, we ran into problems with transient and eruption of contrast with the bigger patients. We would scan through at about, I forget, it was about 1.5 millimeters and overlapped them. And we always got coronal and sagittal reformations, which I found very helpful when looking at the lungs, more than the pulmonary arteries. If there were any questions, well, we would redo it or try something else. And that seems to be it for the questions. If you have any others, always feel free to email me. And thank you so much for spending the morning slash afternoon if you're in the East Coast with me. And take care. Thank you so much for your time today, Dr. Hassan. We really appreciate it. Thanks to all of you for participating in this new conference. Again, it will be made available on demand on MRIonline.com in addition to all previous new conferences. Please call us on social media at the MRI online for updates and reminders on upcoming new conferences. Thanks again and have a wonderful day. Take care.