Flow Patterns Arterial
Flow Patterns Arterial
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is a low resistance. So organs like brain and kidney will have low resistance in their vascular bed, so they allow more blood flow to come. And in this type of flow the spectral waveform is typically

a sharp systolic peak, followed by thorough/g diastolic flow throughout the cardiac cycle. And this is also called as a monophasic flow. This is as against the high resistance flow, which is typically seen in the extremities where the arterial bed of the muscle offers a lot of resistance to the blood flow. And because of that resistance, after the systolic peak

there is a early diastolic reversal and then there is a forward diastolic flow for a variable length. So the high resistance flow is also called as a triphasic flow because there are three phases in this spectrum. Coming to the venous spectrum. So this is a venous spectrum which is acquired with

free breathing.

causes or rear allows for opportunities anything that alters blood flow in this case it might be something that beats too too much blood flow right so in this case right here we see that there's here's the renal artery it's being

filled and then we see this artur venous malformation or AV fistula so it's big deal with an AV fistula over here we see we see the artery filling and then we see the vein and then there's IDC so what happens is if there's increased

flow through there it's police resistance notice that we're not getting much perfusion to the upper pole of the kidney so that's leading to steal syndrome so its path of least resistance so if there's a bridge that's open and

there's a one-way there's a road right there's there's a freeway and another side road it's going to take the freeway because it's a path of least resistance and therefore divert flow from part of the kidney and that part of the kidney

feels d please pressure so saying I'm not get enough blood flow so I'm going to send back some hormone angiotensin in order to increase the blood pressure so anything that can affect the blood perfusion or flow to the kidneys can

send back those hormones so it's not only stenosis but anything that alters the perfusion pressure aneurysms can do the tip can do the same thing right and so to any of those typically associated with various syndromes that we're

talking about and then in this case the AV official or AV malformation that we

they will have increased velocities during the inspiration. That

is because during the inspiration there is negative intrathoracic pressure which allows more venous return to come inside the chest. And opposite happens during the expiration, because expiration has a positive intrathoracic pressure that raises the venous return, and there'll be low amplitude or low velocities in the venous waveform. Now

if you move to the diaphragm, there are three openings in the diaphragm. The first one is at T12 level which allows aorta to enter into the abdomen. This opening remains unaffected during the diaphragmatic contraction during inspiration because it is behind the crura. The second opening is at T10 level which allows esophagus to go into the

abdomen. This opening gets narrow during the inspiration because of the diaphragmatic contraction, and it also pinches the gastroesophageal junction preventing the gastroesophageal reflux. The third opening is at T8 level which allows the IVC to enter into the right atrium. So this opening is in the fibrous tendon/g part of the diaphragm, so it remains widely open during the diaphragmatic contraction.

And because there is increased intra-abdominal pressure during the inspiration, there is increased venous return to the IVC during the inspiration. So in the IVC and hepatic vein there is increased amplitude or increased velocities during the inspiration, which is similar to the upper extremity and neck veins, and there is reduction in the velocity during expiration, which is again similar to the

upper extremity and neck veins. Now if you go down to the legs the story is slightly different because there is increased intra-abdominal pressure which raises the venous [INAUDIBLE] From the legs. So during inspiration in the leg veins there is actually reduction in the velocities, and there is increased velocities during

the expiration. So to say, the effect of respiration on the venous velocities is exactly opposite in upper and lower limbs. Now we'll go region wise in all the organs and see what are the normal

MI, and for standard stroke results in approximately 1mcg/ml

of CC, now this is an incredibly low serum level dose, but it works, and that just shows you how powerful this drug is. So if we're gonna duplicate that with an intra-aterial dose, we have to give something that is incredibly low. We've done some tests in the past, but we have done far less than we need to to understand

exactly how this process works. This is a dynamic flow model that was instructed years ago to illustrate the difference in various lytics, and how they are clot bound. There was a circulating reservoir, and blood flow would go down through this little chamber here where the clot was, and the lytic drug would go down through, and this illustrates how certain drugs are more bound to the clot than others.

But it also illustrates the speed of lysis depending on the degrees of concentration of the clot. The key thing to be aware of is if you notice that the speed gets faster, and faster. This is the time scale over here, the speed gets faster, and faster of lysis down to a certain level, and then when the concentration of the drug goes up, up, up, the speed of lysis slows down. And so therefore,

this has direct applicability to what we are doing in our field with trying to dissolve clot. Just getting in a hurry, and trying to put in more and more drug may be counterproductive for what we are trying to do. So the key thing is today, if you learn nothing else, note that Activase works worse when too much is given. Our natural tendency for most everybody including me, is that when

I'm in a hurry I wan to do more and more, and more, and hopefully speed things up, but unfortunately that's not the way this drug works. Also unfortunately, there's really been no dose ranging study for intra-arterial use of alteplase for anything, the legs or the heart or the brain. Years ago, back in the early 2000s I started a registry which was specifically designed to be a dose ranging

study for intra-arterial reteplase, and alteplase, but unfortunately we did not have enough participation to actually learn anything from this study, and to this day we still do not know the proper dose for intra-arterial use. Even in the trials that we have had including the IMS trials. We just made up numbers for how much we were going to inject, and we used that not knowing whether this was an ideal

number or not. This is an example of that previous flow model illustrating the difference between alteplase, and reteplase with the adherence

and

we are not able to go into this in great detail today but in many cases, the clinical question that faces us as imagers, is whether myocardium is alive or dead or in some kind of intermediate down regulated state in which it does not appear to function well but perhaps if flow is improved to that portion of muscle will regain function with time. And there are a number of techniques

that can be used to predict hibernation and Positron Emission Tomography or PET is probably the best known. But I would suggest to you that MRI is also equally good in many cases, and it has the same prognostic ability. And I would like to illustrate that with two cases both taken from the literature with the references as provided. Here is a patient who appears to have a large segment of dead muscle.

If you look at panel C, bottom left , this is a standard maybe perfusion study which clearly shows an arid area where there's very little perfusion. And when you contrast that with the MR perfusion in panel A, you again see an area that clearly is darker and appears hypo-perfused compared to the lateral wall. However, when we look at panel B which is the late enhancement

image, in fact we don't see any evidence at all of myocardial scarring in this region, and furthermore, when we look at the PET image which looks at myocardial viability in terms of energetics, we can see that in panel D the area that appears to be dead in panel C in fact lights up, suggesting that this is not an area that is dead, but is an area which is chronically hypoperfused,

and has effectively metabolically down regulated, gone to sleep or hibernated. And therefore this is an area which should recover if flow is adequately restored by bypass surgery. And then if you look at panel E and F which are static CT-frames prior to surgery, you can see in F that the septum is not really thickening normally. So there is an abnormal area

of wall motion which co-relates with the area of poor perfusion. However, when coronary flow is restored and the images are reacquired six months later, after surgery, you can see in panel H, that that area of the septum is now thickening entirely normally. So this is a very good example where both PET and cardiac MRI were in brilliant complete agreement, that this was not a segment that was dead,

but was a segment that was hibernating, and was highly likely to recover following revascularization. Here's another example from the same publication. Again in A we can see there's a perfusion defect by MRI in the septum, and yet in B we can see there's no evidence of scar that may account for such a perfusion defect. Panel C show us the MIBI, where there's obviously a large

apical septal defect. Yet in the PET image in panel D, there's a lot of metabolic activity. So again, both MR and PET are suggesting that the apical septum in particular, is not dead, but is not contracting normally because myocardial flow is inadequate. And the absence of late enhancement would suggest that this is is an area of myocardium that will actually recover normal function if flow can be restored.

So again, if you look at the static CT-images in panels E and F in the top right, you can see that the apical septum fails to thicken up normally during systole. However, six months later following bypass surgery, that area has entirely recovered with normal systolic thickness. So again, not an area of the heart that was actually dead, but an area that was hibernating, and

correctly predicted by MRI. So now here is an example from my own institution where a patient was found to have significant impairment

high resistance vascular bed of the musculature. So it will show a typical triphasic pattern which consists of sharp systolic peak

followed by early diastolic reversal and then forward diastolic flow. There are also changes in the waveform in the extremity arteries with age. In a smaller child there is less diastolic flow as compared to the older child and adult, and in premature baby there may be complete reversal of the diastolic flow and that may be related to the patent ductus arteriosus. Upper limb veins will show changes

with the cardiac phasicity and respiratory phasicity, so there is increase in the velocity during the inspiration and reduction in the velocity during the expiration. [BLANK_AUDIO] Lower limb arteries will show similar waveform to the upper limb arteries, and as you go down from proximal to distal, the forward diastolic flow amount gradually reduces, and at the level of the ankle or wrist, you may

not see any forward diastolic flow above the baseline. And this is still normal. As long as we have a nice systolic peak it is still considered a normal waveform. The lower limb veins will show exactly opposite changes related to the respiration as compared to the upper limb veins. So there'll be reduction in the velocity during the inspiration and increase in the velocity during the expiration.

[BLANK_AUDIO] Coming to the chest, ascending aorta is a large vessel, and as we saw it shows a plug flow, so the spectral waveform will be a sharp spectral line with clear black window. The brachiocephalic artery is similar to the common carotid artery, and may or may not show diastolic reversal, or a triphasic pattern. The superior vena

cava and the brachiocephalic veins are very close to the right atrium, so even without breath hold they will show the a, S, v and D waves. The amplitude of these waves will change with the respiration but they're are very clearly seen because they are closest to the heart. Moving to the abdomen. So abdominal

aorta shows plug flow, as we noted earlier, with a clear spectral

are higher in children especially in neonates, in brain and kidneys, the resistive index is higher than the adult. So after looking at normal waveforms all over the body, just one slide on typical abnormal waveforms. So this a normal waveform. Triphasic high resistance

waveform in the extremities. This is a biphasic with absent diastolic flow waveform. The difference between this and the upper waveform is that there is significant reduction in the height of the systolic peak. So this waveform with reduction in the systolic peak and absent for our diastolic

flow is typically seen in the distal obstruction. This is a classic parvus tardus waveform which is slow to rise and less to rise. So these waveforms are typically seen in the proximal vessel obstruction. This is a monophasic, high velocity, turbulent, continuous flow. There are high velocities,

and there is a turbulent flow because the spectral window is filled. So this flow is seen when there is no resistance offered distally, and this is the typical waveform of the arteriovenous fistula. The last waveform is called as a forward systolic and reversed diastolic, or to-and-fro flow sample in the pseudoaneurysm. So there is equal amount of blood going into the pseudoaneurysm and same amount is

coming back. This is as against this waveform which looks similar to this one, but the amount below the baseline is quite less. So this is a diastolic reversal which is typically seen in patent ductus arteriosus. So to summarize, each vessel has a characteristic flow pattern seen on Doppler waveforms that reflects its relative position

after meal. The RI is less in the parenchyma as compared to the portal/g. There's normally a smooth or slight variation in the amplitude

of the portal vein, which the cause is precisely not known but it may be related to the cardiac changes or the respiratory phasicity. Kidneys are one of the organs which draw a large proportion of cardiac output. They typically show a low resistance monophasic waveform, and there are changes in the amount of diastolic flow with the age. In smaller children, especially the neonates and premature

baby, the amount of diastolic flow is quite less, resulting into increased resistive index. So for a preterm baby the resistive index upper limit is up to 0.9, for the infants it is 0.6 to 0.8, and for the older kids and adults the normal range is 0.5 to 0.7. When you sample the resistive index in the kidneys, you should sample either arcuate arteries

or interlobar arteries, then it truly represents the true parenchymal perfusion rather than the central vessels. Coming to the ovary and testicular vascularity. So ovary typically has dual blood supply. The major artery comes from the aorta as the ovarian artery, and ovary

think we can do this and T car is the new term that it's been used for trans

carotid artery revascularization or some of you may know it as the Silk Road procedure and that's what I want to talk a little bit about so the proof of concept is in it has been long in the making

even though this is relatively new so can you do flow reversal and decrease your stroke risk and all of these very small studies look at the major and minor strokes extremely low compared to anything in the literature so it works

flow reversal work so if you can make flow in the internal carotid artery go backwards while you're intervening on a lesion that's the best flow reversal that you can have short of putting a plant on the carotid artery and yours

the t'car procedure as we now know it so you can barely see this little incision but you make a small incision at the base of the neck you can clearly do it under local anesthesia and you establish basically an arteriovenous

fistula so if here's the carotid artery arterial sheep here's a femoral vein sheath and obviously arterial to venous flow this is the direction it's going to go there is a little flow controller and you can

control the flow rates and there's a filter in here that will catch any ambala debris that comes out so what are the advantages of the procedure clearly you can establish symbolic protection before you cross the lesion

so if you remember the list of steps that create ambala crisc it's you have to get your filter through the lesion before you're actually protected here you have protection before you actually cross the lesion and you create flow

reversal or surgical back leading as we can think about that if you just put a clamp on the common carotid artery and open up the carotid artery you'll have flow reversal down the internal and here i think is probably the biggest piece of

this whole puzzle is avoiding the aortic arch and especially as we get to older folks that number that i showed you once you get to 75 or 80 the arches become more difficult more angulated more calcified and are clearly a stroke risk

This is just a little picture of the arterial sheath here for the device. So advantages again established embolic protection before you cross the lesion. Here is another really pictorial of what happens with embolic risk again looking

at TCD data. So placing the sheath there's essentially no risk there. The wire hardly has any risk. But as you go up here with predilataion stent placement and post dilatation you clearly have embolic risk before you

have before you've crossed the lesion with your regular transfemoral stent. But with the TCAR you really establish flow reversal. Again here's your endarterectomy but a couple of things that you actually avoid. There is no

filter so is no vasospasm. So those of you that have seen transfermoral carotid stent procedures with a embolic protection device vasospasm clearly happens. And if you get enough stagnation flow you can

clearly get thrombus above your filter which is even an bigger problem. DW-MRI has been performed on a lot of patients with TCAR and the percentage of new lesions seen in TCAR versus CAS vs CEA are clearly favorable

for theTCAR patients as opposed to the transfermoral stent patient. And in case you if you're keeping up with this literature there is clearly evidence now that neurocognitive decline is associated with some of these

asymptomatic new DW-MRI hits. So what happens here. Can we really prove this so these are a list of studies and cut to the chase here this is a endarterectomy trial or the endarterectomy arm of a stent trial I should say. The percent of

patients that had new DW-MRI lesions 17%. This is transfemoral stenting look at the numbers there. This is transfemoral with proximal occlusion the MoMA device that big device that I showed you. It's kind of intermediate here

because getting that device in is an issue. And then here is the initial TCAR trial proof and we are in surgical were in the surgical realm with the number of new hits that we're seeing. So clearly it works. Avoiding the arch is

the issue and if you look at predictors of cognitive decline in stent vs endarterectomy there's a big statistically significant difference here. And again predictors of cognitive decline seen in another

pictorial. So should all patients be

portal officially again these are the

most common type and they come in all sorts of sizes i'm going to skip through this they come through all sorts of sizes in theory native livers okay are more likely to form fish alize than transplant livers for some reason okay

theories behind that a transplant liver had basically has bad arterial flow anyway so that pressure of maintaining a biopsy tracks between the archery and the portal vein keeps it open and actually grows it and develops it that's

one theory another theory is that a native liver is usually more compliant and softer okay so it's more likely to just stay open when a liver transplant liver is actually stiffer ins and may may have an issue with helping out

closing closing a transplant but most likely it is compromised of the LP of the hepatic arterial flow so transplants despite being under constant imaging surveillance are less likely to find out your portal Fisher than natives for some

reason like I said they come in all sorts of sizes is actually a whole spectrum of them from a small little miniscule one that means nothing two big ones this seal all the blood away from the from the graft the top ones actually

are not detected by Doppler they're detected by detailed angiography the bottom ones that are significant or detected by doctor so what do we match you the bottom two is actually progression over two and a half months

so which ones do we treat we treat the ones that are symptomatic and they present usually with ascites and liver dysfunction one of them one of the other or both we also treat big ones so how do we

diagnose or how do we define big ones a big one is usually it there are changes in Doppler on the portal site or to realization of the portal flow it becomes pulsatile reversal of flow in the main portal vein that's signs of the

hemodynamically significant one and that's what those are the ones that we actually go after in addition to the symptomatic ones so symptomatic you get treated asymptomatic but significantly hemodynamically would still go after or

like I showed you on the other one rapidly progressing ones because the bigger they get the more difficult it is to treat them because you're going to take out more and more arterial territory and the artery is important

for their paragraphs and we usually coil them imaging it's the same on Angira and geography and and and CT you actually see a portal venous phase blush on an arterial phase angiogram basically that's basically the diet of the

diagnosis so to the side here you actually see a portal venous phase blanching on the CT early in your aterial phase of the graft the graft the liver is in the dark but the area that's under the influence of the portal vein

is already portal venous face because this shunting right there and that's how that's how you pick up a arterial coral fistula okay and you treat it by basically emboli Xena's much as possible the key is not to shut it down

completely if you shut it down completely without any repercussions that's great but the key thing is just to impede flow to reverse the hemodynamic effects by Doppler which is the RT realization of the portal flow

and and the reversal of flow in the portal vein and there's just some examples of embolization successful

than that it is not just pure steel and that's why we're kind of gravitating away from using the term splenic steal

syndrome and again it goes back to history and against a small world the Germans talked about splenic seal the screen is stealing blood from the liver the Japanese we're talking about there's too much flow in the portal vein and

they were actually talking about the same thing and I'll show you what's going on here celiac axis gives you at Baddeck artery gives you a splenic artery to the spleen but the spleen then dumps the blood into

the portal circulation the portal circulation goes back to the paddock artery okay in this in the case of too much portal flow hyperdynamic portal flow the hepatic artery actually slows down in a reflex response by what's

called the habber hepatic artery buffer responses which is a somewhat symbiotic system so in other words you increase the portal flow the Atlantic artery responds by dropping its by dropping its flow so this is a lot more complicated

than just simply stealing if you have too much flow going into the liver you basically will get a response by slowing down there by recorder II the Japanese we're talking about about about this the Germans were talking about stealing and

it's actually both okay and it could be a bit of both it could be it could be a combination of both and we still haven't figured that out so let me give you another layer of complexity to this in actuality this is a closed circuit it is

a balance on the arterial side of the house between the resistive index of the spleen and the resistive index of the liver if the liver the spleen is very large in stealing blood and the liver is diseased then blood will flow

preferentially to the spleen and that's a splenic steal phenomenon okay but it's two things at the same time things that would actually increase the resistance in the spleen in the liver and decrease the resistance of the Saline will tilt

it towards the spleen so it's a balance on two things on the arterial side of the house on the portal or venous side

the expiration. And this range should show a, S, v and D waves when they are patent. There may be change in the amplitude with the phase of the respiration. This is a waveform which is obtained with free breathing in the IVC. It shows a reflection in the amplitude, which is combination of respiratory as well as cardiac phasicity. But when you acquire with the free breathing, there are clearly a, S, v

and D waves seen in these major veins. Hepatic veins are probably the best to see these a, S, v and D waves because they are closest to the heart, but the exception is in neonatal hepatic veins. In the neonates you my not see this reflection because of the different

compliance of the [UNKNOWN] Parenchyma, and they may be a monophasic wave in the hepatic veins of the neonate, and it still concern normal. Hepatic artery shows a typical monophasic low resistance waveform. The resistive index in the hepatic artery increases with age and

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