title: The effect of dissolved carbon dioxide on cavitation intensity in mechanical heart valves.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Bioengineering, The Pennsylvania State University, University Park, PA 16802, USA.
authors.forename: Luke H
authors.initials: LH
authors.lastname: Herbertson
authors.forename: Keefe B
authors.initials: KB
authors.lastname: Manning
authors.forename: Varun
authors.initials: V
authors.lastname: Reddy
authors.forename: Arnold A
authors.initials: AA
authors.lastname: Fontaine
authors.forename: John M
authors.initials: JM
authors.lastname: Tarbell
authors.forename: Steven
authors.initials: S
authors.lastname: Deutsch
mesh_terms: D002245:Carbon Dioxide / Q000097:blood*; D006350:Heart Valve Prosthesis; D018056:Hemorheology; D008943:Mitral Valve; D008955:Models, Cardiovascular; D008961:Models, Structural; D010313:Partial Pressure; D012995:Solubility
chemical_list: D002245:Carbon Dioxide