This guideteachesthe basicfundamentals of cavitationto providethe reader with an understanding of what causescavitation,when it occurs,and the potentialproblems cavitation can causeto a valve and pipingsystem. The documentprovidesguidelines for understanding howto reducethe cavitationand/or selectcontrolvalves for a cavitating system. The guide providesa methodfor predictingthe cavitationintensityof control valves, and how the effect of cavitationon a systemwill vary with valve type, valve function,valve size, operatingpressure,durationof operationand details of the piping installation. The guide defines six cavitation,limits identifyingcavitationintensities ranging from inception to the maximum intensity possible. The intensity of the cavitationat each limit is described,includinga brief discussionof how each level of cavitationinfluencesthe valve and system. Examplesare includedto demonstratehowto apply the method, includingmaking both size and pressurescale effects corrections. Methods of controlling cavitation are discussed providing information on various techniqueswhichcan be used to designa newsystemor modifyan existingone so it can operate at a desiredlevelof cavitation.
Diminished poststenotic pressure and flow accompanied experimental application of multiple subcritical arterial stenoses in series. Effects of additional stenoses, causing equivalent constrictions, were cumulative in a nonlinear fashion. Seven-hundred-twenty measurements were performed using 10 cm ileofemoral canine arterial segments in vitro and in vivo with pulsatile and nonpulsatile blood flow. Pressures and flow volumes utilized for testing were within normal physiologic ranges. Data analysis included correlations of experimental observations with predictions generated from a theoretic hydraulic model. Kinetic energy losses with multiple subcritical stenoses were associated with decreased pressure and flow. Poststenotic pressure decreased as much as 51% in some experiments. Diminutions in flow paralleled pressure changes. Measured pressure changes were nonlinear and followed mathematic predictions of appreciable but lesser effects of added stenoses. Hemodynamic alterations of magnitudes documented in this study assume clinical importance. The assumption that a solitary critical stenosis must exist before significant hemodynamic changes occur is no longer tenable.
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