Experimental And Clinical Study Of Right Ventricular Pressure Overload

Part IEXPERIMENTAL STUDY ON MECHANISM OFBIVENTRICULAR FUNCTION CHANGE WHILE ACUTERIGHT VENTRICULAR PRESSURE OVERLOAD DUE TOACUTE PULMONARY EMBOLISMBackground: The right ventricular pressure overload is a pathophysiological progression which involved in many heart diseases with pulmonary hypertension including congenital heart diseases, rheumatic valvular heart diseases, chronic obstructive pulmonary diseases, acute and chronic pulmonary embolism, cardiomyopathies and end-stage left heart failure, etc. The right ventricular pressure overload usually companied with the right heart failure cardiac output has been increasingly recognized clinically. Acute pulmonary embolism (APE) is a clinical syndrome in which the embolus from systemic veins have obstructed the pulmonary arteries and pulmonary vascular bed and increase right ventricular pressure load. APE is one of the typical cardiovascular disease with right ventricular pressure overload.Objectives: With Doppler echocardiography, cardiac catheterization and hemodynamic monitoring system based on virtual instruments (LabVIEW software), The purposes of the present study are that (1) to establish the experimental dog model with moderate right ventricular pressure overload (moderate APE), to evaluate the mechanism about hemodynamic changes of left and right ventricles, and the methodology in the objective assessment of moderate APE; (2) to establish the experimental dog model with severe right ventricular pressure overload (severe APE), to evaluate the deteriorated hemodynamic mechanism and prognostic evuluation in severe APE; (3) to screen out the practical and reliable indexes about the objective assessment of left and right ventricular systolic and diastolic function in the acute right ventricular pressure overload (moderate and severe APE); (4) to approach the clinical applicative value of the hemodynamic monitoring system based on virtual instruments (LabVIEW software) in the evaluation of left and right ventricular function; (5) to assess the clinical value of echocardiography (including tissue Doppler image ) in the evaluation of cardiovascular hemodynamics after the acute right ventricular pressure overload.Methods: The present study consisted of seven anesthetized mongrel dogs that were divided into the control group, group with moderate right ventricular pressure overload (group with moderate APE) and group with severe right ventricular pressure overload (group with severe APE) by G50 injection through right cardiac catheterization according to the various phase and different pressure load during the experiment. The hemodynamic indexes were measured respectively by the simultaneous echocardiography, cardiac catheterization and hemodynamic monitoring system based on virtual instruments in three groups, including as follow: RV> PA^ EDV-RV> ESV-RV> EF-RV^ EF-LV> PER-RV> PFR-RV> LV, EDV-LV> ESV-LV> PER-LV> PFR-LV^ CO> K-RV^ t-RV, K-LV* t -LV> RVSP^ RVEDP , PASP > PADP , dp/dtmax-RV , -dp/dtmax-RV , dp/dtmax-LV > -dp/dtmax-LV; Va-S, Va-D, Va-Aand Va-D/Va-Aofa> b> c> d, e, f. The charts of the left and right ventricular pressure-volume relationship have been respectively drawed in the different overload situations.Result: One dog died of unexpected anaesthetization, the rest 6 dogs had accorded with the experimental demand, and had been killed within 120-360 min after the experiment.(1) The measurement results in group with moderate APE: comparing with control group, the diameter of the right ventricular and pulmonary artery were dilated, RV(18.17±1.32mm vs 13.86± 1.46mm), PA(15.83±1.17mm vs 11.43±1.51mm), EDV-RV(10.38±2.49ml vs 6.00±4.23ml), ESV-RV(5.73± 1.70ml vs 3.38±2.64ml), p<0.05-0.01; right ventricular systolic function increased, EF-RV(0.53±0.09 vs 0.46±0.11), p<0.05; right ventricular diastolic function decreased, PFR-RV(4.35 ±1.86EDV/s vs 5.5O±3.13 EDV/s),K-RV(0.21±0.09 vs 0.13±0.06), t.RV(43.8± 13.4ms vs 31.7±11.2ms), p<0.05-0.01; The pressure of right heart system increased, RVSP(66.7±18.4 mmHg vs 16.0±9.8mmHg), RVEDP(11.53 ±0.43 mmHg vs 3.57±O.18mmHg), PASP(66.5±11.6mmHg vs 18.29±4.77mmHg), PADP (37.8±21.7 mmHg vs 14.49±5.53mmHg), (p<0.05-0.01); The pressure-volume relationship of right ventricle tended to right-upward shift, the area of chart increased, the shape chart of transformed form triangle to rectangle; The mild parallel leftward shift, the area of chart decreased mildly and no change of chart shape could be seen in the pressure-volume relationship of left ventricle.(2) The measurement results in group with severe APE: comparing with group with moderate APE, the dilatation of the right ventricle and pulmonary artery increased, RV(21.94±0.16mm vs 18.17±1.32mm,p<0.01)> EDV-RV(15.18±3.21ml vs 10.38±2.49ml,p<0.01); the diameter and volume of left ventricule decreased, LV(20.46±2.87mm vs 25.67±3.50mm),EDV-LV(13.87±7.07ml vs 17.22±9.72ml), ESV-LV(7.99±2.92ml vs 8.82±2.75ml),p<0.05~0.01; the left and right ventricular systolic function decreased, EF-RV(0.53±0.09 vs 0.46±0.11), p<0.05; EF-RV(0.37 ±0.14 vs 0.53±0.09), EF-LV(0.42±0.18 vs 0.50±0.11), PER-RV(2.25±0.55EDV/s vs 6.03±0.87EDV/s),PFR-RV(3.65±1.53EDV/s vs 4.35±1.86EDV/s), PER-LV (2.68± 1.32 EDV/s vs 6.95±0.73EDV/s), PFR-LV(3.86±3.15EDV/s vs 5.05±2.95 EDV/s), t -LV(46.7± 16.4ms vs 32.2±11.7ms),K-LV(0.26±0.11 vs 0.19±0.06), x -RV (52.4±15.3 ms vs 43.8±13.4ms),K-RV(0.32±0.09 vs 0.21±0.09), p<0.05~0.01. The...