Ventricle left, pressure curves

For determination of LVP, a Millar micro tip catheter (type PC 350) is inserted via the left common carotid artery into the left ventricle. LVEDP is measured on a high-sensitivity scale. From the pressure curve, dP/dtmax is differentiated and heart rate is counted. The LVP-signal also triggers a cardiotachometer. 

FIGURE 17.11 Isovolumic pressure curves computed from the model for canine left ventricles at three different heart rates. As heart rate increases, the time course of the activation function f(t) narrows and pressure increases via increased model parameter c. Results compare favorably to experimental measurements [56]. 

Left Ventricle (LV) A simple inverted U curve is drawn that has its baseline between 0 and 5 mmHg and its peak at 120 mmHg. During diastole, its pressure must be less than that of the CVP to enable forward flow. It only increases above CVP during systole. The curve between points A and B demonstrates why the initial contraction is isovolumic. The LV pressure is greater than CVP so the mitral valve must be closed, but it is less than aortic pressure so the aortic valve must also be closed. The same is true of the curve between points C and D with regards to IVR. 

FIGURE 8.5 Ventricular and root aortic pressures (solid curves, left ordinate) and ventricular outflow (dashed curve, right ordinate) computed using the model of Equation 8.8 for a normal canine left ventricle pumping into a normal arterial circulation. The topmost solid curve corresponds to a clamped aorta (isovolumic). This ventricle has initial volume of 45 ml and pumps out 30 ml, for an ejection fraction of 66%, about normal. 

Figure 13. Left. Comparison of predicted pressure-volume curves for the normal ventricle and ventricles with fibrous aneurysms. Right. Variation of the parameter a with aneurysm size. For aneurysms encompassing less than 20% of wall volume, the curves are linear. (Reproduced from Janz and Waldron Predicted effect of chronic apical aneurysms on the passive stiffness of the human left ventricle, Circ Res 42 255,1978 with permission of the American Heart Association.)...

Figure 1. Schematic explanation of coupling the left ventricular contraction with the systemic arterial tree. In the middle left panels, left ventricular contraction is represented by its end-systolic pressure-volume relationship. Given a particular end diastolic volume (EDV), this relationship can be converted into ventricular end-systolic pressure P s) stroke volume (5Vj relationship, which is shown by the rectilinear curve coursing from the lower left to upper right corner in the graph at the bottom. In the right middle panel, the aortic input impedance property is represented by a rectilinear arterial end-systolic pressure fF, )-stroke volume SV) relationship curve (Eq. (5)). See the text for the explanation of this representation. This arterial Pes-SV relationship is transcribed in the bottom panel in superposition with the ventricular Pe -SV relationship. The intersection of the two Pes-SV relationship curves indicates the end-systolic pressure and stroke volume which should result from coupling a left ventricle with the given EDV and the slope parameter with a systemic arterial tree with the slope parameter...

FIGURE 17.15 The ejection effect incorporated in the ventricle model (left) with the uncorrected ventricular pressure and outflow curves for the same conditions at right for comparison. Ventricular outflow is normalized by 1/5 to use the same numeric scale as for ventricular pressure. 

Matsubara H, Takaki M, Yasuhara S, Araki J, and Suga H. Logistic time constant of isovolumic relaxation pressure-time curve in the canine left ventricle. Better alternative to exponential time constant. Circulation 1995 92 2318-26. 

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