Venous Flow Phasicity Is Not Caused by the Thoraco-Abdominal Pump, But Results from Luminal Deformation of the Inferior Vena Cava Caused by Respiratory Diaphragmatic Movement.

Intrapleural pressures are known to be negative and become more negative during inspiration. Nevertheless, thoracic IVC flow is greater during expiration vs inspiration contradicting the pull-push theory. Intravenous pressure in the thoracic IVC is also positive, higher during expiration than inspiration. Flow in superior vena cava tributaries is nonphasic and continuous in our sample of healthy volunteers. Respiratory phasicity appears to be a unique property of flow in the IVC and its tributaries. It is likely caused by flow turbulence and disruption of laminar flow caused by the inspiratory stenosis of thoracic IVC and by the simultaneous dilatation of the abdominal IVC. Both IVC deformations occur as the diaphragm pulls down the intimately attached IVC during inspiration. Both types of conduit deformations are known to cause turbulence, disrupt laminar flow, and reduce flow owing to high resistance. We postulate that this is the underlying cause of respiratory venous flow phasicity, not the pull-push thoracoabdominal pump mechanism. This hypothesis is consistent with currently known flow, pressure, and imaging characteristics of central veins and tributaries.