Interrupted Circulation: The ‘Stasis’ Hypothesis and the Significance of Venous Valves

Abstract

The notion that ‘blood stasis’ is a causal or contributory factor in DVT is shown to be problematic: it has Galenic connotations. ‘Stasis’ in the literal English sense (absolute cessation of movement) entails local or organismic death; it has been shown experimentally to be anti-coagulatory and therefore antithrombogenic. The use of ‘stasis’ to denote ‘retarded flow’ or ‘interrupted flow’ is confusing not only for semantic and historical reasons, but also because it focuses attention on mean blood velocity in veins rather than on the pulsatility of blood movement. We contend that the (temporary) cessation of pulsatility in venous blood movement is instrumental in DVT. Since the aetiological hypothesis developed in this book focuses on the venous circulation and particularly on the venous valve pockets (VVP), we survey the history of the discovery of venous valves and the establishment of their function by Harvey, and explore the evolution of the ‘stasis’ concept against this background. We argue that sustained non-pulsatile (streamline) blood flow in veins results in hypoxaemia in the VVP, and that this initiates a potentially thrombogenic sequence of events.