Quantitative Doppler

Christopher J. Gallagher, Christina Matadial and Jadelis Giquel

Here I think they’re driving at pulsed-wave Doppler versus continuous-wave Doppler. (It’s tough going through this and wondering “What are they thinking?”) To review, then, pulsed-wave Doppler takes a specific look at a specific velocity at a specific place. The pulse wave (PW) transducer is used as both a receiver and transmitter of ultrasound waves. A complete cycle of transmission waiting and receiving is called the pulse repetition frequency (PRF). The greater the depth of interrogation of the pulsed ultrasound beam the longer the waiting period. Therefore, the deeper the interrogation, the lower the PRF, and the lower the maximal velocity that can be measured. Pulsed-wave ultrasound is used to provide data for Doppler sonograms and color flow images.

Continuous-wave Doppler, in contrast, takes velocity measurements along the entire length of the beam, allowing you to measure high velocities, but not allowing you to know exactly where that measurement is made (also known as “range ambiguity”). In this modality, ultrasound is continually transmitted by one crystal and continually received by another.

Another thing they might be driving at here is PISA, the proximal iso velocity surface area.

This, too, is gone over ad nauseum in Chapter 3, but here goes. As blood flow converges toward a tight spot (Analogy? Think of a broad river coming to a narrow gorge), the flow will speed up. At a certain concentric area, the flow should all be at the same speed as the “chaos” of a broad river becomes the “organized tightness” of a narrow channel. This area will, when measured by color flow Doppler, hit the Nyquist limit and will start aliasing. Red flow will become blue, for example, in a semicircle. You can measure the area of this by the equation

This will come in handy as you do volume measurements and try to assess valve areas. At the risk of sounding like a broken record, go to the hemodynamic section to see these ideas put into action. (And into the kind of thing that would appear on an exam.)

This gets into the realm of the material in Chapter 3, the volume equations you use to measure valve areas, cardiac outputs, stroke volumes, and the like. The sample problems in that chapter illustrate better than this explanation, but here goes.

The main volume you will lug around through the heart is best thought of as a cylinder of blood. You will make various area measurements (area is 0.785 × diameter squared) and “length” measurements (the TVI, or time-velocity integral, which you get by outlining the flow through an area, and then the echo machine computer spits out a TVI, the integrated area under the flow curve).

A million times, you will make these measurements and apply them to get valve areas. Yeah, verily, I say unto you, do all the problems in the hemodynamics section and you will see what all of this means.

The gradient, or change in pressure, across a valve is measured by the Bernoulli equation:

The real Bernoulli equation is understood only by “brilliant French physicists at the turn of the 18th century”. You know, when all this stuff was figured out. Here are a few examples of Bernoulli’s equation in action:

Example 1: The velocity across a stenotic mitral valve is 4 meters/second. What is the gradient?

Note that the velocity has to be in meters/second to get a pressure in mmHg. Ask Bernoulli if you want to know why.

Example 2: The velocity going back across a regurgitant valve is 2 meters/second. What is the gradient?

So how does all this cool stuff translate into valve areas? Look no further than the continuity equation (which was mentioned at least 4 million times during the meeting). The continuity equation says this:

No more, no less. A cylinder of blood that you calculate passing through one valve will (if no VSD or ASD or regurgitant flow “diverts” it) pass through another valve. In equation-ese:

Characteristically, you will have the area at one place and a velocity (which you can then outline, get a TVI, and thus have a “length”) at the same place. Then you get a velocity (which you again outline and thus get a “length” by the same TVI gig) at an unknown valve, and solve for that valve area by cross multiplying and dividing.

A typical example involves the LVOT (where you can figure the area and get a TVI) and the aorta (where you can get a TVI but don’t know the area):

The unknown in this equation is the area of the aortic valve.

You can flip it, turn it, bake it, braise it, blacken it, serve it with tartar sauce or salsa—the continuity equation is always a variant of this theme. Even in the “spooky” realm of PISA, you are still just doing the same thing, using the continuity equation:

The unknown is the area of the other valve. You cross multiply and divide and there you have it. Note that in PISAville, you don’t use the TVI; rather, you use a velocity. All is well, though, because you use a velocity on the other side of the equation, too, so the units cancel out. But you’re still working the continuity idea.

Figuring this stuff (again, see examples in Chapter 3) requires the Bernoulli equation and one commonsense principle. In the problem you’ll wrestle with, you’ll be given a valve with a velocity across the valve. Use the Bernoulli equation to figure what the pressure gradient is across that valve. So far so good.

Now, use your common sense and figure this out: Where is the high-pressure end of this gradient, and where is the low-pressure end? Recall that this will be specific to the cardiac cycle. So, for example, if you have mitral regurgitation, then during systole, you will have high pressure in the left ventricle, a gradient across the mitral valve as the blood flows backward into the atrium, and a low “leftover” pressure in the left atrium:

If you have, say, mitral stenosis, then during diastole, the high-pressure area will be the left atrium, the pressure gradient will be “pressure lost” crossing the mitral valve as blood struggles to get into the left ventricle, and the “leftover” pressure will be the left ventricular pressure. (Assuming no aortic regurgitation muddies the waters.)

As long as you think of:

then you can figure any of these “what’s the pressure in chamber or vessel X?” questions.

Tissue Doppler looks at movement of the cardiac walls themselves, rather than the blood racing around in the chambers. Tissue moves about 10% as fast as blood, but our magical machines can tease out tissue movement from blood movement. What will they think of next?

In systole, as seen on tissue Doppler, the heart tissue moves away from the transducer. The first movement, S1, is isovolumic contraction. The second movement, S2, is systolic shortening velocity.

In diastole, there are also two velocities. Both are toward the transducer. The first diastolic movement, E velocity, corresponds to the rapid filling of the ventricle in early diastole. The second diastolic velocity, A velocity, corresponds to the atrial contraction.

Myocardial velocity is not the be-all, end-all of cardiac imaging, because it can get goofed up by “tethering” and translational movement.

During the meeting they showed some tissue Doppler, but not too much. Just know that it exists and know what S1, S2, E velocity, and A velocity are.

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