AbstractBackground 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 intra-thoracic 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 augmenting flow towards the heart. The thoraco-abdominal ‘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. Subjects and methods Duplex venous flow data in central and major peripheral veins of 20 healthy volunteers and 55 patients undergoing routine echocardiography were analyzed. Results Healthy Volunteer data: Flow in the tributary veins draining into the superior vena cava (SVC) is non-phasic 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. Patient data: Images culled from routine echocardiograms also show inspiratory stenosis of the thoracic IVC. Previous work: Caval intravenous pressures are positive (despite negative pleural pressures) as apparent in routine CVP measurements. It averages +6 mm Hg during inspiration and +13 mm Hg during expiration. IVUS examination of IVC acquired during venous stenting shows dilatation of upper abdominal IVC by ≈35% during inspiration. There is no compression of the IVC by the "abdominal pump" during inspiration. Conclusion Intra-pleural 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 SVC tributaries is non-phasic and continuous in our sample of healthy volunteers. Respiratory phasicity appears to be a unique property of flow in IVC and 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 due to high resistance. We postulate that this is the underlying cause of respiratory venous flow phasicity, not the pull-push thoraco-abdominal pump mechanism. This hypothesis is consistent with currently known flow, pressure and imaging characteristics of central veins and tributaries.
Raju et al. (Sun,) studied this question.