The driving
force for blood to move across any cardiac valve is the presence
of a slight pressure difference normally found between the chambers
(or chamber and great vessel) on either side of the valve. For example,
systolic pressure builds within the left ventricle until it reaches
a point where it exceeds the pressure in the aorta. The aortic valve
is suddenly thrown open and blood is ejected into the aorta. In
normal individuals, there is a very slight (1-2 mmHg) pressure difference
between the left ventricle and aorta that helps drive the blood
across the aortic valve.
 |
| Fig.3.11 |
Normal aortic valve blood flow is laminar (Fig. 3.11) and most of
the red cells in the aortic root during systole are moving at approximately
the same speed. Graphically, this translates into a narrow band
of dark grey on the pulsed wave (PW) Doppler spectral recording
(Fig. 3 11, arrow). Normal peak systolic velocity of blood flow
across the aortic valve rarely exceeds 1.5 m/s.
 |
| Fig.3.12 |
When the aortic valve is diseased, the leaflets become thickened
and progressively lose their mobility. Eventually, the valve itself
becomes narrowed to the point where it begins to obstruct flow,
and aortic stenosis is created. In the presence of aortic stenosis,
systolic pressure in the ventricle must rise high enough to force
the blood across the obstruction into the aorta. Thus, a pressure
drop, or pressure gradient, is generated (Fig. 3.12). Severe degrees
of aortic stenosis may result in aortic valve gradients that exceed
100 mmHg in systole. As discussed in Unit 1, the presence of such
an obstruction results in both turbulent flow and increased velocity,
two characteristics readily detected by Doppler echocardiography.
Because of the large gradient, the pressures within the left ventricle
rise significantly and left ventricular hypertrophy results.
 |
| Fig.3.13 |
Doppler detection and evaluation of the presence or absence of aortic
stenosis is based on recording turbulence and increased flow velocity
in the ascending aorta. In Figure 3.13 these characteristics are
shown in a continuous wave (CW) spectral velocity recording of aortic
systolic flow obtained from the apical window. Turbulent flow is
represented by broadening of the velocity spectrum. There is also
an increase in peak aortic velocity to 4 m/s. The Doppler audio
in this case had a harsh, higher pitched quality during systole
that was easily distinguished from the sound of laminar flow.
 |
| Fig.3.14 |
Similarly, the presence of these characteristics in the pulmonary
artery during systole would indicate the presence of obstruction
to right ventricular ejection. Figure 3.14 demonstrates a CW Doppler
spectral recording from the left parasternal window in a patient
with mild pulmonic stenosis and insufficiency. Turbulent diastolic
and systolic flows are noted with a slight increase in the peak
systolic velocity to 1.4 m/s (normal <1 m/s).
 |
| Fig.3.15 |
The PW Doppler examination shown in Figure 3.15 is from the same
patient as Figure 3.1 and demonstrates the ability of PW to localize
the level of the obstruction. With the cursor positioned on the
ventricular side of the pulmonic valve (Fig. 3.15, A), the turbulent
diastolic spectral recording of pulmonic insufficiency is noted,
while systolic flow is undisturbed (laminar) with a peak systolic
velocity of about 1 m/s. When the sample volume is positioned distal
to the diseased pulmonic valve (Fig. 3.15, B) the systolic flow
becomes turbulent and the peak systolic velocity is elevated. The
spectral recording of pulmonic insufficiency is lost because the
sample volume is located distal to this lesion.
While PW Doppler is very useful for the localization of such obstructive
lesions, it has limited value in establishing the severity of obstruction
because most significant valvular obstructions result in velocities
above 1.5 m/s. As emphasized previously, velocities above 1.5 m/s
will usually cause aliasing of the PW recording. This prevents the
faithful recording of peak velocities necessary for the calculation
of valve gradients.