Source: Hatle L, Angelsen B. Doppler Ultrasound in Cardiology, 2d ed. Philadelphia: Lea & Febiger; 1985.
Doppler Assessment of Diastolic Function in recent years, there has been a great deal of interest in using mitral inflow velocity patterns to evaluate LV diastolic properties.6474-74a Transmitral filling velocities reflect the pressure gradient between the LA and LV during diastole65 Fig. 13-34). In early diastole, pressure in the LV normally falls below that in the LA, producing an increase in velocity due to rapid transmitral inflow (E wave). Flow decelerates as the pressures equilibrate in middiastole. in late diastole, LA contraction restores a small gradient, causing transmitral flow to accelerate to a second peak (A wave) that is of less magnitude than the E wave. In individuals in whom early LV relaxation is impaired, the transmitral pressure gradient is blunted, resulting in a decrease in both the velocity of early filling and rate of E-wave deceleration66-68-70 Fig. 13-38).
Conversely, in patients with marked increases of LA pressure and LV stiffness, early diastolic filling velocities are high, deceleration is rapid, and late filling following atrial contraction is markedly reduced. This is the so-called restrictive pattern of LV filling Fig. 13-39). Accordingly, an E-wave velocity that is substantially less than the A-wave velocity and is accompanied by a prolonged deceleration time represents evidence of impaired early diastolic relaxation by Doppler, while an increased E-wave velocity and decreased A-wave velocity (E/A ratio greater than 2.5 or 3 to 1) accompanied by a diminished deceleration time (less than 100 ms) is indicative of a noncompliant LV with markedly elevated lef atrial pressures.69-70-73-73a Although a restrictive pattern can be seen with restrictive cardiomyopathy or advanced LV dysfunction of any cause, it also occurs in pericardial disease.75 Of significance, a restrictive pattern of LV filling has been associated with an increased mortality rate in patients with advanced congestive heart failure,76 and persistence of this pattern despite changes in loading condition is an additional poor prognostic sign.76a>76b
These abnormal mitral inflow patterns can be clinically useful and, when they are markedly distorted, are generally reliable in identifying and characterizing diastolic dysfunction. A number of variables other than diastolic function, however, are capable of influencing transmitral filling velocities. it has been shown that transmitral Doppler filling dynamics are affected by the age of the patient,7778 changes in heart rate,7980 respiration,8! and even the position of the Doppler sample volume within the mitral valve orifice.82-84 Of greatest significance, transmitral inflow is very sensitive to loading conditions, and reductions in LV preload induced by nitroglycerin and/or lower-body negative pressure can induce a striking decrease in early transmitral filling velocities independent of changes in diastolic properties.8586 The influence of LV loading upon transmitral filling is most striking when an increase in LA pressure due to cardiac dysfunction restores early diastolic filling velocities and obscures impaired relaxation, thus inducing "pseudonormalization."68 Therefore, as Doppler transmitral filling dynamics have many limitations in assessing diastolic function, particular filling patterns should not be interpreted as "pathognomonic" findings of diastolic dysfunction but rather as a component of a complete clinical and echocardiographic evaluation.
Recently, attention has focused upon ancillary Doppler techniques to evaluate LV diastolic dysfunction and LA pressure. An impaired systolic filling wave and increased A-wave flow reversal in the velocity recordings from pulmonary veins in the setting of a relatively normal transmitral pattern of diastolic filling suggests elevated LV filling pressures and may be useful in distinguishing normal from pseudonormal mitral inflow pattern (Fig. 13-36). In addition, an increased amplitude of the pulmonary vein A-wave reversal in comparison with the forward transmitral A-wave velocity, especially in regard to duration, has been found to be of value in detecting elevated LV filling pressures by Doppler.87,88 Tissue Doppler recordings also yield early diastolic and late atrial velocity signals which are altered in a similar fashion to transmitral filling in the setting of diastolic dysfunction.53^ Tissue Doppler recordings are less influenced by LV loading, and may be of value in distinguishing pseudonormalization.53^ The rate of propagation of the transmitral LV filling stream into the LV may also be utilized to detect impaired diastolic function as well as constrictive pericarditis.53^
Doppler Assessment of Systolic Function and Cardiac Output
Although measurements of LV volumes and ejection fraction can be obtained by 2D echocardiography, Doppler interrogation provides a unique and complementary noninvasive assessment of systolic function. Thus, LV systolic dysfunction often results in decreased aortic velocity and acceleration time.89-91 As discussed below, in the presence of mitral regurgitation (MR), the acceleration of the MR jet can provide information regarding contractile function.92
One of the most important applications of Doppler is in the calculation of the stroke volume.93 The theory involved is relatively simple. The volume of flow through any orifice or tube can be calculated as the product of the cross-sectional area through which flow occurs and the velocity of that flow (Fig. 13-40). Measures of anatomic cross-sectional area can be derived from echocardiographic images, while velocity can be determined by Doppler. As the annulus of the aortic valve is nearly circular, its cross-sectional area can be estimated from a measurement of diameter, as p(diameter/2)2. The pulsed-wave Doppler envelope also can be recorded at the same level. The mean flow velocity through the orifice is calculated by integrating velocity over time. (that is, by measuring the area under the Doppler curve). This velocity-time integral, often called the stroke distance, is then multiplied by the cross-sectional area at the level of the Doppler interrogation to obtain the stroke volume.93-96 The product of the stroke volume and heart rate then yields cardiac output.
Figure 13-40: Calculation of stroke volume. Multiplying the cross-sectional area (CSA) of the blood column in the ascending aorta by the distance the column moves during a single cardiac contraction yields the stroke volume (SV). The velocity-time integral (VTI), expressed in units of length, represents the "stroke distance." (Modified from Pearlman AS. Technique of Doppler and color flow Doppler in the evaluation of cardiac disorders and function. In: Schlant RC, Alexander RW, eds. The Heart, Arteries, and Veins, 8th ed. New York: McGraw-Hill; 1994:2229, with permission.)
Calculation of stroke volume by the Doppler method involves a number of assumptions. The orifice must be circular and constant in size, and the flow velocity must be uniform throughout the cross-sectional area. In addition, the angle between flow and the interrogating beam must be less than 20 degrees. Despite the uncertainty of these assumptions, Doppler-derived measurements of cardiac output and stroke volume have been shown to correspond well with thermodilution, Fick, and the angiographic calculations, though the correlation is not perfect.93-99
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