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TELECONFRENCES
2004
The Changing Left Ventricle

2003
Aortic Valve Disease: New Dimensions in Evaluation and Management

2002
Heart Failure: Echo's Role in and Emerging Health Crisis

2001
Chest Pain in Children & Adults: The Role of Echo

2000
Mitral Regurgitation: New Concept

1998
The Falling Left Ventricle: Diastolic & Systolic Function

1997
Changing the Outcome of Coronary Artery Disease
ECHO GRAND ROUNDS
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Echocardiography
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VIDEO ARCHIVES

Chest Pain in Children and Adults

Mitral Regurgitation: New Concepts

Diastolic and Systolic Function

Changing the Outcome of CAD

BROADCAST SUPPLEMENTS
2000 MV
2001 Chest Pain
2002 Heart Failure



Estimation of the Severity of Valvular Stenosis
Effect of Stenosis on Blood Flow

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.

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