Herbertson Luke H, Manning Keefe B, Reddy Varun, Fontaine Arnold A, Tarbell John M, Deutsch Steven
Department of Bioengineering, The Pennsylvania State University, University Park, PA 16802, USA.
J Heart Valve Dis. 2005 Nov;14(6):835-42.
Mechanical heart valves (MHVs) are known to induce cavitation during closure and rebound. Cavitation may lead to blood element damage and stable bubble formation, with the latter introducing emboli into the cranial circulation and increasing the risk of stroke. Previous research has suggested that CO2 is the primary blood gas involved in stable bubble growth, due to its high solubility compared to that of oxygen or nitrogen. The primary objective of this study is to determine the role that CO2 plays in MHV-induced cavitation bubble formation.
Degassed water (5 ppm) was supplemented with CO2 at partial pressures of 0, 40 and 100 mmHg. Cavitation was visualized using high-speed videography for 29 mm Björk-Shiley Monostrut and Medtronic Hall MHVs in the mitral position. Experimental parameters (heart rate, systolic duration, and left ventricular pressure) were adjusted to provide dp/dt values of 500, 2,500 and 4,500 mmHg/s. High-frequency pressure fluctuations of cavitation bubble collapse were detected using a hydrophone.
Root-mean square (RMS) values were calculated to quantify the cavitation intensity for both MHVs at the three loading conditions. The images of cavitation bubble formation and collapse were correlated to their respective RMS values. This study revealed no statistical difference between the cavitation intensities produced by either of the MHVs for the range of CO2-supplemented degassed water tested. For example, at the most physiologic loading condition of 2,500 mmHg/s, the RMS values for the Björk-Shiley Monostrut valve in degassed water containing 0 and 100 mmHg CO2 were 32.7 +/- 3.5 and 34.3 +/- 6.1 mmHg, respectively.
The results of this in-vitro study show that, despite affecting stable bubble growth, the presence and quantity of dissolved CO2 does not affect the intensity of the cavitation events occurring during impact of the valve occluder with its housing. Therefore, the role of CO2 is limited to stable bubble development.
已知机械心脏瓣膜(MHV)在关闭和回弹过程中会引发空化现象。空化可能导致血液成分受损并形成稳定气泡,后者会将栓子带入颅内循环并增加中风风险。先前的研究表明,由于二氧化碳与氧气或氮气相比具有较高的溶解度,因此它是参与稳定气泡生长的主要血液气体。本研究的主要目的是确定二氧化碳在MHV诱导的空化气泡形成中所起的作用。
向脱气水(5 ppm)中补充分压为0、40和100 mmHg的二氧化碳。使用高速摄像技术观察二尖瓣位置的29 mm Björk-Shiley Monostrut和Medtronic Hall MHV的空化现象。调整实验参数(心率、收缩期时长和左心室压力)以提供500、2500和4500 mmHg/s的dp/dt值。使用水听器检测空化气泡坍塌时的高频压力波动。
计算均方根(RMS)值以量化两种MHV在三种加载条件下的空化强度。空化气泡形成和坍塌的图像与其各自的RMS值相关。本研究表明,在所测试的补充二氧化碳的脱气水范围内,两种MHV产生的空化强度之间没有统计学差异。例如,在最接近生理状态的2500 mmHg/s加载条件下,含0和100 mmHg二氧化碳的脱气水中Björk-Shiley Monostrut瓣膜的RMS值分别为32.7±3.5和34.3±6.1 mmHg。
这项体外研究的结果表明,尽管溶解的二氧化碳会影响稳定气泡的生长,但其存在和数量并不影响瓣膜封堵器与其外壳碰撞期间发生空化事件的强度。因此二氧化碳的作用仅限于稳定气泡的形成。