Flow & Stroke Volumes in Valve Disease & Shunts

Audio transcript:

I’d like to talk about several methods for estimating blood flow and describe the effect of valvular heart disease and congenital heart disease on ventricular stroke volumes and flow. First, let me start out by saying that I believe every cardiac MRI exam should include a measurement of Qp &Qs.

The reasons for this are #1. You need to know the Qp and Qs to be able to quantify a shunt, and even if you’re not imaging a patient with known congenital heart disease, sometimes these patients arrive unannounced, especially patients. For instance, with partial anomalous pulmonary venous return. Secondly, valvular disease is much more common than intracardiac shunts, and if you want to be able to confidently quantify regurgitant valve disease, you’re going to need flow measure. Aortic flow measurements for aortic and mitral regurgitation and pulmonic flow measurements for pulmonic and tricuspid regurgitation. And finally, even in patients who don’t have any regurgitant valve disease or any shunts, it’s helpful to have flow data because it can help determine the accuracy of your ventricular segmentation on your cine images, which is what we all use to quantify ventricular stroke volumes and ejection fraction.

So, here’s a schematic of the normal circulatory system. You can see that the heart is really best thought of as two pumps in series. The right ventricle, which pumps deoxygenated blood into the main pulmonary artery and out to the lungs and the left ventricle which pumps oxygenated blood into the aorta to supply the systemic circulation. And because these two pumps are in series, if there is no valve disease and no shunt the right ventricular stroke volume has to equal the pulmonary artery blood flow, which has to equal the left ventricular stroke volume, which has to equal the systemic blood flow.

Now I’d like to talk for a minute about estimating pulmonary blood flow, typically pulmonary artery blood flow is made with a phase contrast image perpendicular to the main pulmonary artery. However, there are sometimes problems with this measurement, for instance. Some patients will have turbulent flow in the main pulmonary artery due to pulmonic stenosis. Others may have an artifact such as metal wires in the sternum, or in a stent in the main pulmonary artery, which can obscure some of the signal within the pulmonary artery. These kinds of abnormalities can lead to an underestimation of the blood flow in the pulmonary circulation. Furthermore, some patients with certain congenital heart disease may not even have a pulmonary artery. And finally, there are some technical issues that one needs to consider. Sometimes the technologist may not do a good job at getting truly perpendicular to the main pulmonary artery. When the phase contrast images are acquired and there are other errors as well, such as errors in the baseline which depends on interpolation, typically from stationary tissues. In any case, because of these limitations, sometimes it’s helpful to have another method for estimating pulmonary blood flow. One can, for instance, measure pulmonary blood flow by summing the blood flow in the right main pulmonary artery and the left main pulmonary artery. And that’s because the main pulmonary artery doesn’t have any other branches.

Now, there are several methods for estimating systemic blood flow. The most common method is again making a phase contrast image perpendicular to flow, but in this case perpendicular to flow in the mid ascending aorta. Again, there are certain issues that can crop up with these types of images, for instance, you can have turbulent flow, but in this case, it might be due to aortic stenosis or an aortic aneurysm. You could have again an artifact due to sternal wires obscuring part of the ascending aorta, and that could cause you to underestimate systemic blood flow. And as in the last case, there are technical issues as well with regard to the scan plane being perpendicular to the aorta or an error in the baseline.

And so in these cases, it’s sometimes helpful to look at the blood flow in the superior vena cava and in the proximal descending aorta. Now it’s fortunate that if you make an image perpendicular to the mid ascending aorta, you’ll frequently be very close to perpendicular to the superior vena cava and the proximal descending aorta so you can get all three of these flow measurements in one acquisition, which is very iffy. Now you might say, well, why does the sum of the superior vena cava and the proximal descending aorta equal the blood flow in the mid ascending aorta? And the answer is, it’s a good estimate because the superior vena cava collects the blood from the arms and the head and the proximal descending aorta essentially has all the blood flow except, but which goes to the arms and to the head. And because these two values are approximately equal, this winds up being a good estimate, often of systemic blood.

Now I’d like to talk about another method for estimating systemic blood flow. You could make the measurement instead of in the mid ascending aorta and the proximal ascending aorta. That sometimes gets away from the problem with sternal wires, but you can have turbulent blood flow not only from aortic stenosis, but now from left ventricular outflow tract obstruction as well. So, it also has potential disadvantages. Another place you could make the measurement is in the left ventricular outflow tract. That will get rid of turbulent flow due to aortic stenosis, but you’ll still have the problem with LVOT obstruction. And then there are some other methods as well. For instance, one could measure the blood flow at the superior vena cava and the inferior vena cava and some of those, and that is a good estimate of systemic blood flow. It has everything except the venous return to the heart from the coronary sinus.

And also you could have this hybrid method where you use the SVC and the distal descending aorta that approximates systemic flow.

Now I’d like to talk for a moment about how the relationship is between stroke volumes and flow. As I said earlier in this talk, typically in the normal patient you’ll find the values for the RV stroke volume, the LV stroke volume, the Qp and the Qs to all be equal, and when that’s the case, you can feel pretty good, usually about your flow values as well as about your ventricular segmentation.

Now in a patient with isolated aortic regurgitation. What happens is the LV stroke volume is increased. It’s increased because the left ventricle needs to pump out more flow than it would normally because some of that blood flow is going to leak back from the aorta into the left ventricle. So, in order to maintain the same systemic flow, the same forward flow out the aorta, you will need to have a larger left ventricular stroke volume. Now the right ventricular stroke volume and the Qp will be unchanged. So, in patients with aortic regurgitation, because there’s no shunt, the Qp will equal the Qs, and that’s correct. The RV stroke volume will equal both of those and the LV stroke volume will be increased and the amount it will be increased will be by the amount of aortic regurgitation. And so, when we measure aortic regurgitation directly, we can measure it typically one of two ways one might be at the proximal ascending aorta near the sinotubular junction. We’ll measure the flow there and integrate the area under the curve in diastole. That reversal of flow, which is just above the aortic valve, is a good estimate of the severity of aortic regurgitation. Alternatively, if you don’t have this measurement, you could go further up at the level of the mid ascending aorta. The further away you get from the aortic valve, though, you’ll start to underestimate the amount of aortic regurgitation, but typically at the level of the mid aorta, you’ll still have a good estimate as to how bad the aortic regurgitation is. And of course, if you want, you can also if you trust your traces, your LV stroke volume and your RV stroke volume values from your short axis segmentations, then that value that you get from the reversal of flow and diastole should equal the difference between the LV and the RV stroke volumes.

Now what about mitral regurgitation? With mitral regurgitation, the physiology is similar. The left ventricular stroke volume is elevated compared to the RV stroke volume. And the RV stroke volume will still equal the Qp and the Qs, and that’s because the LV has to pump a bigger stroke volume to maintain the same forward flow because some of that LV stroke volume is going to be going into the left atrium, and so if one wants to quantify mitral regurgitation. You could, for instance, take the LV stroke volume from your short axis cine segmentation, and you could subtract the Qs, the systemic flow, and again because there’s no shunt. The Qp will equal the Qs, so alternatively you could take your LV stroke volume and subtract your pulmonary artery flow and so you’ll have two independent measures, at least insofar as the flow goes to be able to quantify the severity of mitral regurgitation.

Now, what about the patient that has both? They have both mitral and aortic regurgitation. How can you assess that? Well, in that case the left ventricle is enlarged due to the mitral regurgitation and due to the aortic regurgitation. But still the RV stroke volume, the Qp and the Qs will all be equal. So, in this particular case, one way of measuring it would be to measure the flow and the ascending aorta just distal to the valve measure the reversal flow and the proximal ascending aorta and that will equal the amount of aortic regurgitation. And then to calculate the mitral regurgitation one will take the LV stroke volume, which is this big square. Here you’ll subtract the amount of blood that is coming into the aorta. The cues from here and you’ll subtract the amount of aortic regurgitation that you got from your flow measurements, and that residual will give you the severity of the mitral regurgitation. Now again, because the Qp and the Qs are equal, because there’s no shunt, you could either subtract the Qs and the aortic regurgitation or the Qp and the aortic regurgitation from the LV stroke volume.

Now, how about some simple congenital heart disease? How about an atrial septal defect with a left to right shunt? Well, in that case what happens is you’ve got blood traveling directly from the left atrium to the right atrium. And so, as a result, what happens is there will be an increase in the RV stroke volume. And of course, because the RV stroke volume will be increased, the pulmonic flow will also be increased by the same amount, and so in this particular case, if you want to quantify the shunt, you could just take the Qp, which will be increased divided by the Qs.  In this particular case Both the RV stroke volume and the Qp are increased by the amount of blood that is passing through the ASD.

Now, what happens if you have a patient with mitral regurgitation and an atrial septal defect? So you’ve got left to right shunt from the ASD, but now you’ve added mitral regurgitation. Well, now we have the same situation that we had before, but the LV stroke volume is now increased, just like it was originally with the mitral regurgitation. And so, when we want to quantify the mitral regurgitation, we will look at the LV stroke volume, which is increased and subtract the cues. And we’ll be able to do that. But we will not be able to do the LV stroke volume minus the Qp like we could with just mitral regurgitation. And the reason, of course, is because the Qp has been elevated due to the shunt. So, we still have a way of quantifying the mitral regurgitation in these patients just by comparing the LV stroke volume to the systemic flow.

Now, how about a patent ductus arteriosus with a left to right shunt. So, as you recall, the patent ductus arteriosus happens usually in the distal arch or proximal descending aorta, where there is a connection between the aorta and the main pulmonary artery, and so you typically have increased pulmonary artery blood flow because blood is traveling from the aorta directly into the pulmonary artery and its branches. But the interesting thing is, you need to remember that when we use cardiac MRI measure pulmonary and systemic blood flow, we typically make those measurements much more proximally. So here you can see the proximal main pulmonary artery. This is where we typically make our pulmonary flow measurement and approximately sending aorta is. Typically, where people make the systemic flow measurement, and so if you think about the pathophysiology and where we make our measure. The pulmonary flow measurement is not going to capture the increase in flow due to the PDA. The PDA inserts distally compared to where we make our pulmonary artery measurement. However, the blood that goes into the pulmonary arteries from the aorta will return to the heart via the pulmonary veins go into the left atrium and the left ventricle and then out the aorta so the aortic flow will be increase.

It’s almost paradoxical, but when we measure it this way, your MRI scans will show the LV stroke volume and the queues are increased. In these patients with the PDA and the RV stroke volume and the Qp are not changed and so therefore when we report a shunt with a patient with a PDA, you need to be careful because typically if you were to take this particular case and take the Qp divided by the Qs, you’d wind up with a shunt of less than one, which is not really descriptive of what’s happening, and in fact in these patients what we would do is we would invert the ratio and report the Qp/Qs as the Qs divided by the Qp and that will give us a ratio of greater than one, which will be truly reflective of the increased pulmonary artery, blood flow distal to the main pulmonary artery.

Now, how about somebody who has mitral regurgitation and a patent ductus arteriosus? Well, this is similar to before. Now, the LV stroke volume is increased, not just due to the PDA, but also due to the mitral regurgitation. So, if one wants to quantify the mitral regurgitation, one needs to subtract the Qs from the LV stroke volume. It will not work to subtract the QP from the LV stroke volume because the LV stroke volume is increased both due to the shunt and due to the mitral regurgitation and the QP is not increased due to either.

Now, how about a patient with a restrictive VSD who has a left to right shunt? Well, in this case, the restrictive VSD will result in an increase in the LV stroke volume because the LV will need to pump blood out the aorta as well as into the right ventricle. And that blood that is going into the right ventricle is going to go out into the pulmonic circulation. So, the Qp is going to be increased. And what we see here is an important point that the sum total of the RV stroke volume and the LV stroke volume has to equal the sum total of the QP and the QS. But in this case, and it appears somewhat paradoxical. What happens is the LV stroke volume will equal the pulmonary blood flow. And the RV stroke volume will equal the systemic blood flow.

Now what if we have a patient with mitral regurgitation and a restrictive VSD? While in this case the LV stroke volume is increased due to both the mitral regurgitation and the VSD, the pulmonic blood flow is increased just due to the VSD, and so to calculate the regurgitant volume, one needs to subtract the Qp from the LV stroke volume. It won’t work to subtract the Qs from the LV stroke volume because the Qs doesn’t take into account the shunt.

Finally, there are other shunts as well. This is an example of what you could expect from a fistula from the right coronary artery, for instance to the right atrium. What happens here is you’ve got blood flow going from the aorta into the coronary artery and then directly into the right atrium that will serve to increase the LV stroke volume because the LV stroke volume has to go up to supply the extra blood to the shunt. The RV stroke volume is going to go up because that’s the blood comes from the right atrium and goes into the right ventricle, and then it gets injected into the pulmonary artery. So, in this particular lesion, what one will see is increased stroke volumes of both ventricles and pulmonic flow, but not systemic flow.

So, to conclude, flow quantification should be an integral part of every cardiac MRI examination because it can be used to quantify shunts and regurgitant valvular disease, and it only takes a minute or so to acquire the data, even in patients without valve disease or shunt.

Flow quantification can help assess the accuracy of ventricular stroke volumes and ejection fractions that are obtained from segmented cine functional images. I can’t emphasize this point enough. If we rely on the quantitative data from our functional images to report ejection fractions, then this is a good way of ensuring the integrity of the data to be able to compare the values that we get from the functional images with regard to the stroke volume to the flows that we’re getting even in patients without valve disease or shunts.

As you may recall from earlier in the talk, there are several independent methods that are available for quantifying Qp and Qs, because in some cases due to artifacts and turbulent flow, the flow values may not be accurate, so there are other methods that one can use to confirm that.

Getting the correct values and then finally understanding the patient’s pathophysiology and the location of the flow measurements is essential for accurate diagnosis, especially in patients with more than one abnormality. Thank you very much.

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