Change of Pulmonary Artery Hemodynamics and Pulmonary Vascular Resistance in Experimental Pulmonary Embolism.
10.4046/trd.1995.42.6.913
- Author:
Hee Soon CHUNG
1
;
Jae Ho LEE
;
Cheol Ho KIM
Author Information
1. Department of Internal Medicine, Seoul City Boramae Hospital, Korea.
- Publication Type:Original Article
- Keywords:
Pulmonary embolism;
Pulmonary vascular resistance;
Effective outflow pressure of the pulmonary vasculature;
Incremental pulmory vascular resistance
- MeSH:
Animals;
Arteries;
Cardiac Output;
Dogs;
Fistula;
Hemodynamics*;
Pulmonary Artery*;
Pulmonary Embolism*;
Vascular Resistance*;
Vasoconstriction
- From:Tuberculosis and Respiratory Diseases
1995;42(6):913-922
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: When we define the pressure of pulmonary vasculature in which a recruitment of blood flow occurs as P1 and the proportion of change in pulmonary artery to that in cardiac output as IR and then we compare PI and IR with pulmonary vascular resistance, we would find some problems in pulmonary vascular resistance. In other words, it is the theory that, IR should be increased mainly in pulmonary embolism in which decreases the cross sectional area of pulmonary vasculature. But there are many contradictory reports resulted from various researches and the fact is known widely that any difference exists between PVR and PI, IR. For this reason, the purpose of this study is to observe how PI and IR change at the time of the outbreak and during treatment of the pulmonary embolism, and to find out the meaning of these new indicators and the difference from the pulmonary vascular resistance used generally when we subdivide the pulmonary vascular resistance into PI and IR. METHOD: After making AV fistula in experimental dog, we controlled cardiac output at the intervals of 15 minute in case of three kinds(all AV fistula are obstructed, only one of fistula is open and all of fistula is open), and after evoking massive pulmonary embolism with radioactive autologous blood clots, we measured the mean pulmonary artery pressure, and calculated PI and IR. We observed the pattern of change in PI and IR, without giving the control group any specific treatment and with injecting intravenously rtPA in the Group 1 and Group 2 at the dose of lmg per kg, for 15 minutes fot the former and 3 hours for the latter. RESULT: 1) Pulmonary vascular resistance showed a change similar to that of pulmonry artery pressure and in all three group, PVR increased significantly, but group 1 and group 2 showed tendency that PVR keeps on decreasing after treatment, and the rate of decrease in group 1 is more rapid than group 2 significantly. 2) Both intersection(PI) and degree(IR) are proved statistically significant, in view of the straight line relationship between cardiac output and pulmonary artery pressure, calculated by minimal regression method. 3) PI changed similarly to pulmonary vascular resistance, while in the IR which is theoretically more similar to PVR, there was no significant difference or change after rtPA infusion. CONCLUSION: In the pulmonary embolism, Both change in IR which means real resistance of pulmonary vasculature and PI which was developed due to secondary vasoconstriction by pulmonary embolism are reflected same time.
