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The aim of this session is to explain the theory underlying the quantitative and semiquantitative methods used in TEE. Most quantitative methods use algebra, geometry and physics. The information obtained by TEE should always be interpreted on the basis of clinical profile of the patient.
WHY?
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Hemodynamic instability encompasses hypotension, low/high cardiac output, and abnormal filling pressures. Evaluation of hemodynamic instability include Hemodynamic parameters. Preload and fluid responsiveness. LV afterload. Ventricular function. Valvular function. LVOT obstruction Cardiac Tamponade.
BASIC CONCEPTS
Blood is a fluid capable of flowing form one place to another by a force. Pressure is force acting on an unit area. Pressure and flow are integrally related because fluid flows down a pressure gradient. Neither flow nor pressure can be measured directly from TEE, but velocity of blood can be estimated by Doppler echocardiography.
Dimensions of cardiac structures can be evaluated from 2D TEE. From the above information, volumes and flows can be derived.
JETS
As blood flowing down a pressure gradient approaches a narrow orifice, it speeds up. This produces a characteristic appearance proximal and distal to the orifice. Proximal to the orifice, depending on its size, the pressure gradient and PISA may be visible on color Doppler. The dimensions of PISA can be used to assess the size of valvular orifice.
The narrowest point of flow occurs just distal to the orifice and is called vena contracta. The width of VC can be used to grade the severity of regurgitant lesions. Distal to the VC, a jet is formed. Here the blood velocity decreases, but its volume increases in accordance with the principle of momentum.
The area of a jet, on color Doppler is usually assumed to be proportional to its volume. Therefore jet area may be an index of lesion severity. But it has to noted that jets are usually 3D and their cross section varies from plane to plane. Free jets are those that flow into the center of a large chamber (eg: LA)
Confined jets are limited by the boundaries of the chamber (eg: AS or eccentric MR) and are thus modified by the Coanda effect. Dual jet interaction tends to attenuate the size of jets if they are in the opposite direction and accentuate the size if in the same direction.
V=s/t
Flow Q, will be the product of velocity and the cylinders cross sectional area (CSA)
Q = V x CSA
Due to the difficulty in obtaining a CSA of cardiac structures, certain shapes have been attributed to particular structures.
STRUCTURE LVOT PISA MV ANNULUS AV ASSUMED SHAPE CIRCLE HEMISPHERE ELLIPSE/CIRCLE EQUILATERAL TRIANGLE FORMULA FOR AREA r2 2r2 r1r2 0.433 s2
The assumption that flow is laminar with a flat profile is reasonable in LVOT and across the normal cardiac valves. It may not be true for ascending aorta due to its curvature producing a parabolic flow, making it unfavorable for measuring SV. CSA changes as blood progresses through the heart and great vessels leading to a change in velocity to maintain constant flow.
Blood flow is pulsatile, which is represented by velocity-time curves on Doppler displays. Hence mean velocities have to used i.e velocities obtained over one pulse period have to be employed. s = V mean / t This distance is the area under the velocity time curve and is called Velocity Time Integral (VTI).
In the absence of valvular regurgitation, the total volume passing through a structure during systole or diastole is the stroke volume (SV ).
Q max = CSA x V max Q mean = CSA x V mean SV = Q mean x t = CSA x V mean x t SV = CSA x VTI
The dimensions of MV change throughout diastole and TR is found in 90% of individuals, so SV estimation is unreliable from MV and TV. In the absence of regurgitation, cardiac output (CO) CO = SV x Heart rate Cardiac index (CI) = CO / BSA. CO estimation by using PW across LVOT, CW across AV and PW across MV have shown correlation with PAC derived CO.
Eg : The diameter of LVOT from ME AV LAX is approx 2.4 cm. The VTI across LVOT measures20 cm from TG/Deep TG LAX views by PW Doppler and HR = 70 beats/min. CSA LVOT =r2 = 4.5 cm2
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Adjacent structures during the same phase of cardiac cycle ( AV and LVOT ) Non adjacent structures on the same side of the height during different phases of cardiac cycle ( MV in diastole and AV in systole) Structures on opposite side of the heart (PA and MV)
The ratio of the maximum velocity in LVOT and that of the AV is called Doppler Velocity Index. It has been used as an index of severity of AS. A ratio less than 0.25 suggests severe stenosis. This can be extrapolated to the PV and RVOT, but obtaining the views are cumbersome, and pulmonary stenosis is rare in adults.
Non adjacent structures on the same side of the height during different phases of cardiac cycle
At steady state, the same amount of blood must enter a given cardiac chamber as leaves it. Thus LV inflow in diastole must be equal to outflow in systole. Assuming no shunts or regurgitation
This method can be employed to calculate the MV orifice area, but for assessing the AV area the former method is preferable. Multiple measurements have to be made to reduce errors in the measurement. If both the valves are incompetent, mitral inflow and AR in diastole must equal the MR and aortic outflow in systole rendering the equation meaningless.
But, if one valve is incompetent then an equation applies in which EROA can be employed to calculate the orifice area. This equation reflects that SV ejected from LV must now contain not just the blood entering LV through MV in diastole but also the blood entering through the AR or MR.
In MR,
CSA MV x VTI MV (diastole) = CSA LVOT x VTI LVOT + ERO MV x VTI MR (systole)
In AR,
The regurgtitant volume (V reg) in isolated MR or AR is the difference between mitral inflow and aortic outflow V reg jet = SV reg valve SV normal valve This is typically used to assess MR/AR, but not TR/PR. The regurgtitant fraction (RF) can be calcuated by RF = V reg jet / SV reg valve
As blood flow converges towards a narrow orifice, it accelerates. Imagine a series of hemispheres of radius r, centered on the orifice. The velocity at all points on the surface of any one of these hemispheres will be constant. Each of these surfaces is called PISA. PISA becomes evident with CFD at every point where the velocity exceeds Nyquist Limit.
When PISA assumes a contour of a hemisphere, then CSA PISA = 2r2 If the Nyquist limit produces a flat PISA, then the area will be over-estimated and if a tall PISA is produced, then area is underestimated. The morphology of the valve also alters the PISA. In MR the base of PISA will be flat due to closure of the valve during PISA formation.
In MS, the base will be cone shaped, as the valve is partially open. So in MS, an angle of correction () will be required where is the angle between the two leaflets. CSA PISA = 2r2 x /180
CSA valve x V max-valve = CSA PISA x NL CSA valve = (CSA PISA x NL) / Vmax-valve
P1-P2 = QR
If R=0, then P1=P2, which is true for widely open heart valves. So pressures in LV and aorta are the same during systole, and that in LA and LV in diastole, in the absence of stenosis.
Bernoulli equation
This is based on the principle of conservation of energy. For a given volume, the work done by pressure in moving an incompressible fluid from one point to another along a rigid pipe is related to gain in KE, the change in PE and the work done overcoming viscous resistance. If P1, V1 and P2, V2 are proximal and distal pressures and velocities respectively then,
P1- P2 = x 4 (V22-V12)
The density of blood is taken as 1, so for maximum velocities, the equation is reduced to
P1- P2 = 4 (V22-V12)
If the proximal velocity is small comparatively then we can simplify it to P1- P2 (P) = 4V2
This does not apply to normal valves (R=0) and to stenotic valves (friction loss is significant). In severe anemia, reduced blood viscosity results in over-estimation of pressure gradients, making this equation meaningless. It becomes unreliable in PHV and valvular stenosis where continuity equation is preferable to calculate the orifice area as CO affects the gradient across MS/AS.
LAP from MR jet and LVSP P LV-LA = 4 (V MR )2 P LA = P LVS + P LV-LA LAP from ASD jet and RAP P LA-RA = 4 (V ASD )2 P LA = P RA + P LA-RA LVEDP from AR jet and ADP P aorta-LV = 4 (V AR )2 LVEDP = P aorta diastolic P aorta-LV
Using pressure acceleration and deceleration to estimate systolic function and PAP and valve area
Pressure acceleration and systolic function If MR is present, the rate at which its flow increases during IVCT provides an estimate of LV systolic function. A reduction in this rate reflects reduction in function
dP/dt = 32 mm Hg/ t
where t is the time taken for the flow velocity to increase from 1 to 3 m/s. Normally values are more than 1200, values below 800 reflect severe LV dysfunction.
Pressure acceleration and PAP The pulmonary acceleration time is the time to peak velocity of systolic ejection in RVOT. This is an inverse function of mPAP. Values less than 80-100 msec indicate PAP >20mm Hg.
Pressure deceleration and pressure half time During diastole, the rate of decrease in PG between the LA and LV or between aorta and LV is a function of severity of lesion. The time from maximum to zero velocity on the velocity-time curve is called deceleration time (DT). In AR, as the lesion becomes more severe and EROA increases, DT decreases. The opposite occurs in MS.
However, deceleration of PG is preferable over DT as it is less dependant on flow. PG deceleration is quantified as time in ms for gradient to fall from P to P/2, called half time. As pressure is related to the square of velocity, the velocity associated with P/2 is obtained by multiplying P with 0.7 i.e (P x 2/2). The pressure half time is therefore defined as time between V max and 0.7 V max.
ME 4C ME 4C
Pressure gradients
TV MV AV PV
CONCLUSION
Multiple views recommended for all measurements. For a dimension the average has to be taken. 3-5 cardiac cycles needed (more in AF). Precise orientation of the Doppler beam with the desired structure is necessary.