Venous flow phasicity is not caused by the thoracoabdominal pump, but results from luminal deformation of the inferior vena cava caused by respiratory diaphragmatic movement

BACKGROUND: Phasic variation with respiration is a fundamental feature of venous flow. Dondes (circa 1820) proposed that the flow variation was due to suction by the negative intrathoracic pressure that became more negative with inspiration. Guyton later added an abdominal pump component, suggesting that abdominal pressure increase during inspiration compressed the inferior vena cava (IVC) augmenting flow toward the heart. The thoracoabdominal venous pump is often described as a pull-push mechanism. This review details past relevant work in the literature and includes new data from our institution. The review contradicts the pull-push theory in favor of a different mechanism. METHODS: Duplex venous flow data from the central and major peripheral veins of 20 healthy volunteers and 55 patients undergoing routine echocardiography were analyzed. RESULTS: In healthy volunteers, flow in the tributary veins draining into the superior vena cava is nonphasic and continuous. Flow in the lower limbs and the abdominal IVC is phasic and expiration dominant. There is significant narrowing of the thoracic IVC during inspiration and its flow is expiratory dominant. Images culled from routine echocardiograms in patients also show inspiratory stenosis of the thoracic IVC. Previous work shows that caval intravenous pressures are positive (despite negative pleural pressures) as apparent in routine central venous pressure measurements. It averages +6 mm Hg during inspiration and +13 mm Hg during expiration. Intravascular ultrasound examination of the IVC acquired during venous stenting shows dilatation of upper abdominal IVC by approximately 35% during inspiration. There is no compression of the IVC by the abdominal pump during inspiration. CONCLUSIONS: 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.