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Hey everyone, it's Mark. Again. We're gonna

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move on to the next block here, which is

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we're going to talk about the Imaging approach to pulmonary hypertension.

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Now pulmonary hypertension is something that is

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often overlooked. So

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no disclosures for any of these talks and I want to acknowledge Dr.

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Kapole a lot of for a lot of the helpful information

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that's on the clinical aspect of

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pulmonary hypertension.

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So

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first and foremost with these talks, I want to

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encourage and increased awareness of pulmonary hypertension.

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And then we'll kind of go through some of the classification in this talk as

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well as some of the physiology and pathologic

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changes that occur and then kind

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of get an understanding that your report really towards the

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end and the impression you really want to know if this

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is more of a post-capillary etiology versus one

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of the others.

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Okay, so let's start off. These are two patients with radiographs.

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They have main pulmonary artery low bar

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pulmonary arteries are enlarged. There's some lung disease in this

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patient.

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And this is pretty I mean, it's it's pretty advanced.

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Both Radiology reports did not mention anything about

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pulmonary hypertension again. It's often overlooked.

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And it's often overlooked clinically too because it's a very quiet process.

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So what is the definition of pulmonary hypertension? Well the

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right heart cath pulmonary artery pressures

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are greater than 25 millimeters and mercury has sustained

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elevation at rest or a sustained elevation

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over 30 with exercise often in

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the setting with normal pulmonary capillary wedge pressures.

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And Pulmonary vascular resistant measurement of

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three Woods wood units are a measurement of pulmonary

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vascular resistance. You can see with the normal numbers

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are for pulmonary artery pressures usually 12 to

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16. It's a much lower pressure system than the

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systemic.

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And the severity you can see is kind of gauged between these numbers

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usually greater than 55 is fairly severe.

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Now, how do you organize it? There's different ways to organize it

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the one I'm going to focus on today.

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Is the anatomic because I think that one in the end is probably

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the most practical.

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Just as a side note, when you say pulmonary hypertension

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that just means there's elevated pressures in the pulmonary artery when

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someone says pulmonary arterial hypertension. They're

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actually referring to elevated pressures from

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pre-capillary vessels, you know the post

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So the anatomic is precapillary capillary and

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post capillary post capillary being different. I really

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kind of like the physiologic but you know,

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it's just more for your understanding.

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Does this person have increased flow say from a left to right

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shunt asd/vsd over time? The increased flow

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causes the dilation of the pulmonary artery and the

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pressure's elevate.

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Does this patient have a chronic hypoxic state, you know

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chronic bronchitis would be you know, an example

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trachea bronchial some of those over time

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the hypoxia induces a vasoconstriction in the

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pulmonary arteries that becomes longstanding and pulmonary artery

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pressures Elevate and you get pulmonary hypertension.

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Do you destroy enough anatomically of

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the capillaries and vessels so that your vascular bed

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doesn't have quite the amount of

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flow and the pressures increase now that one,

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you know, you can remove a lung in that developer hair retention, but

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a nice example, that might be like emphysema.

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And the last one is pulmonary Venus hypertension chronic

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pulmonary venous hypertension left heart failure mitral

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stenosis that sort of thing.

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And that's the post capillary cause and that's actually one of

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the most common causes for pulmonary hypertension.

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Just for completeness the World Health symposing classification

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is here. It's roughly similar to

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what I just talked about. You know, there's pulmonary material.

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There's Venus hypertension is the most common you can see

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it is by far and away the most common we're always looking for

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chronic thrombolic disease turns out that's one of

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the least common of all the causes.

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And then there's a whole bunch that we just don't know.

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How the pulmonary hypertension functions or how it

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develops?

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So anatomically we're looking

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at this circuit, right? We're looking at

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the circuit.

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So you have the pulmonary artery here pulmonary veins

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here in the lungs the post capillary pulmonary

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hypertension is these are some causes which I

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mentioned mitral stenosis systolic dysfunction venal occlusive

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disease.

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Then you have the capital that usually goes along with the

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lung diseases, you know hypoxic induce lung

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disease is sleep apnea. That's sort of thing.

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And then the pre-capillary that's usually the thrombogenic

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arteriopathy also called chronic thrombolic disease

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and the idiopathic pulmonary hypertension

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or primary pulmonary hypertension.

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So what happens in the setting of pulmonary hypertension?

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Well, you start to develop that basal constriction and

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then you get a vascular Remodeling and thickening of

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the intima and eventually you develop inside youth rhombus.

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This tends to be a very patchy process. This is

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a histologic.

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Example of pulmonary hypertension. This is a normal

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so that you can see you can see that pulmonary arteries intimal thickening

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the insights you thrombus so

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called plexiform lesions.

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Now this can happen with a lot of different causes.

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So these multiple causes of pulmonary hypertension

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lead to the final common pathway.

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And you get this Progressive patching. I'm going

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to underline patchy here. It tends to be kind of patchy in

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the lung distal arterial narrowing and then

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eventually you develop occlusion of that pulmonary artery.

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There's a loss of capacity to dilate and

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recruit other pulmonary vasculature.

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And you start to lose that gas exchange

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and develop hypoxia and dysmian exertion.

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Eventually, you start to develop right ventricular hypertrophy and

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then failure. That's more advanced.

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The signs and symptoms early, they're quiet. They're

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quiet. Clinically. They're quiet radiographically. They're

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subtle.

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So, you know just like systemic hypertension they may be

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asymptomatic. But eventually they'll start to developing some dismu when

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they exercise and fatigue.

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Later stages you start to develop things like chest discomfort

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or pressure. Maybe some palpitations, maybe

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some syncope.

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And then in late stages you get that pinning edema

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on the lower extremities and maybe even

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ascites that's really Advanced the pinning

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edema again in the elevated jvp. That's a reflection of

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right heart failure not left. That's right hard failure.

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Okay. What is the goal? Well goal number one?

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Is it there?

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I mean, that's the first thing you got to find it.

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Then you try to judge. It's severity look for any

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underlying causes. Okay, and then you try

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to guide the therapy. Is this a medical therapy cardiac requires

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surgery.

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Try your best to decide for these etiologies

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whether you think it's probably capillary / intrinsic pulmonary

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or lung versus the post

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capillary causes because that requires a

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different therapy.

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The evaluation through Imaging well radiographs and

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CTA chest radiograph CTA. These are very big. This is

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where it's usually going to be found and you can deduce a lot of information

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from them.

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The echo is used often. It can

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be misleading.

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but

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the VQ scan is still recommended. I'm not a big fan of

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it and I'll kind of explain why because even if

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you get it and it's high problem, you're still probably going to do a CTA.

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Cardiac Mr. For you know, very specific problems

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now.

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I usually kind of consider the radiograph CTA and then right heart

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cath because those are the kind of the big ones in the right

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heart cath. You can assess pulmonary artery pressures directly not indirectly

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like Echo you can assess the capillary wedge

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pressures cardiac output. You can even do a pulmonary angiogram at the

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same time looking for chronic thrombolic disease. The other

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thing it can do is it can trial of

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nitrous oxide or some you know, some other pulmonary

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artery basil dilator and see if they

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respond and improve by lowering the pulmonary pressures a

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favorable response usually indicates improve

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survival.

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Okay.

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Some of the therapies for the pre-capillary causes not

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the post you can kind of see them as they go down early kind of

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more advanced and then this is more.

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very Advanced heart lung transplant, that's extreme,

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but

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So finish up, what can we offer the clinician

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for dismay of Unknown Origin identify subtle

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findings of pulmonary hypertension. Now, that's

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you know, maybe there's some early thickening the right ventricle. The

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pulmonary artery is dilated. There's interventricular straightening,

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you know these sort of things.

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For known pulmonary hypertension what can you offer the clinician?

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Well try to estimate it's severity based on

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contrast Dynamics degree of pulmonary artery

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dilation and right ventricular hypertrophy interventricular straightening

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that sort of thing.

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Then try to assess you know, what the etiology

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is is this a lung disease is this chronic thrombolic

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disease or does the patient have a

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post-capillary Cause?

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So summary.

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It's often overlooked. That's the first and foremost

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increased awareness putting this into your

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search pattern on these radiographs and CTS.

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The definition is a sustained pressure of 25 millimeters of

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mercury at rest and 30 with exercise and there

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are different ways to organize it. I might

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suggest the anatomic pre-capillary capillary

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and post capillary and remember post capillary causes

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require different therapy.

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So with that I will stop and we will

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move on to the next level.