Jul 292017

Jon-Emile S. Kenny MD [@heart_lung]

Please read part 1 and view the vodcast on IVC collapse prior to reading below; this post seeks to explain the interesting findings of Juhl-Olsen & colleagues [1] as well as provide a physiological rationale to Dr. Marik’s comments on my vodcast; there is a new explanatory animation at the conclusion of this post.

PEEP & Venous Return

While initially postulated decades ago and then demonstrated by Fessler and colleagues, the venous return curve is changed significantly by the application of PEEP [2-4].  Firstly, and interestingly, PEEP increases the mean systemic filling pressure – the pressure head for venous return to the right heart [5].  The mechanisms are probably due to both increased adrenergic tone and redistribution of venous blood from the thorax to lower capacitance venous beds [3, 6-8].  Nevertheless, this effect of PEEP is expected to drive more venous blood to the right heart and engorge the IVC at end-expiration.  Further, volume status alters venous return in that diminished blood volume increases the resistance to venous return and a high venous blood volume blunts the resistance to venous return [9, 10].  In summary, increased venous blood volume and the application of PEEP is expected to augment the pressure head for venous return.

PEEP & Intra-thoracic Pressure

PEEP is also expected to raise intra-thoracic, or pleural pressure.  At end-expiration, PEEP acts upon the compliance of the lung and chest wall together to [i.e. the respiratory system] to increase thoracic volume.  How much of the PEEP is felt by the pleural space depends upon the relative compliances of the lungs and chest wall individually.  In health, the compliance of the lungs and chest wall are roughly similar such that 50% of the applied PEEP is used to ‘lift’ the lungs and the other 50% is used to ‘lift’ the chest wall.  Accordingly, 50% of the PEEP ends up as pleural pressure, stenting open the thoracic wall [3, 11]; clearly, in diseases of the lungs and chest wall, these values will vary.  The rise in ITP increases the right atrial pressure and favours dilation of the IVC.  On the Guyton diagram, the increase in ITP moves the x-intercept of the cardiac function curve rightwards.

PEEP & Intra-abdominal Pressure

Yet, if PEEP is expected to increase the pressure head for venous return, as well as raise the ITP how does its application increase IVC collapsibility?  It is important to appreciate that the aforementioned physiology relates only to end-expiration.  Of equal importance is how PEEP changes inspiratory physiology.  As seen on the venous return curve, PEEP lowers the maximal venous return as represented by the plateau of this curve.  This leveling of flow represents the generation of a Starling Resistor [10]; when the pressure within a distensible tube falls below its ambient pressure, the tube transiently collapses and then immediately reopens as the upstream pressure [mean systemic filling pressure] rises above the collapsing pressure.  This happens rapidly and cyclically and the result is not cessation of flow, but maximal flow.  The mechanism of IVC collapse/Starling Resistor physiology in response to increased intra-abdominal pressure is likely complicated and dependent upon hepatic contact pressure as well as relative blood volume in the splanchnic and non-splanchnic circulations [12].

Thus, when the patient inspires, and intra-thoracic pressure falls, the cardiac function curve drags leftwards and is more likely to fall into Starling Resistor physiology.

PEEP & Cardiac Function

To simplify this analysis, only the effect on right ventricular function [RV] will be analyzed.  As described above, while PEEP increases the ambient cardiac pressure, the provision of pressure to the airways also alters RV function.  PEEP above 10-15 cm H2O begins to afterload the RV and even diminish its contractility because of increased lung volume [13, 14]; in other words, the RV enlarges in size due to increased outflow impedance.  If we assume that a supine, healthy person has a left atrial pressure of ~ 5 mmHg [7 cm H2O] or less, then a pulmonary distending pressure [trans-pulmonary pressure] greater than 7 cm H2O is expected to collapse the pulmonary veins, generate West Zone II physiology and afterload the right heart in all areas of the lung anterior to the supine left atrium.  Indeed, if 50% of PEEP – in healthy individuals – is added to the pleural pressure [Ppl], then 15 cmH2O of PEEP applied at the mouth will generate an end-expiratory trans-pulmonary pressure [PEEP – Ppl] or 15 cmH2O – 7.5 cm H2O = 7.5 cmH2O.  Thus, all of the lung anterior to the left atrium would be West Zone II – an afterloaded state for the RV.

The effect of high RV afterload is to bend the cardiac function curve downwards [lower its slope or impair its function].  When this individual inspires, the cardiac function curve will shift leftwards as ITP falls, but because of the RV’s impaired ability to eject blood into the lung, IVC collapse will be less likely.

Clarifying the Findings

Returning to the notable findings of Juhl-Olsen described in Part 1 [1], the provision of higher PEEP in the horizontal position is expected to increase the collapsibility of the IVC during inspiration because of diminished maximal venous return, to the contrary, PEEP above 15 cmH2O is expected to afterload the RV and attenuate IVC collapse.

In the volume loaded volunteers in Trendelenberg, the lung will be entirely in West Zone III, so the RV afterload effects of high PEEP will diminish.  Therefore, the effects of reduced maximal venous return will dominate and higher PEEP facilitates inspiratory IVC collapse.

The aforementioned illustrates the complexity of inspiratory IVC collapse in healthy volunteers.  Without considering all factors affecting IVC collapse, study of heterogeneous and physiologically complicated patients will continue to yield conflicting results [15-19] and more debate will ensue.

Have we not learned from the central venous pressure and pulmonary artery occlusion pressure?  If we insist that simplified surrogates of intricate, intertwined physiologies be employed in patient management, then disappointment and danger await.

Please check out other posts in this series,



  1. Juhl-Olsen, P., C.A. Frederiksen, and E. Sloth, Ultrasound assessment of inferior vena cava collapsibility is not a valid measure of preload changes during triggered positive pressure ventilation: a controlled cross-over study. Ultraschall Med, 2012. 33(2): p. 152-9.
  2. Fessler, H.E., et al., Effects of positive end-expiratory pressure on the canine venous return curve. Am Rev Respir Dis, 1992. 146(1): p. 4-10.
  3. Fessler, H.E., Effects of CPAP on venous return. J Sleep Res, 1995. 4(S1): p. 44-49.
  4. Fessler, H.E., Heart-lung interactions: applications in the critically ill. Eur Respir J, 1997. 10(1): p. 226-37.
  5. van den Berg, P.C., J.R. Jansen, and M.R. Pinsky, Effect of positive pressure on venous return in volume-loaded cardiac surgical patients. J Appl Physiol (1985), 2002. 92(3): p. 1223-31.
  6. Peters, J., et al., Regional blood volume distribution during positive and negative airway pressure breathing in supine humans. J Appl Physiol (1985), 1993. 75(4): p. 1740-7.
  7. Gelman, S., Venous function and central venous pressure: a physiologic story. Anesthesiology, 2008. 108(4): p. 735-48.
  8. Luecke, T. and P. Pelosi, Clinical review: Positive end-expiratory pressure and cardiac output. Crit Care, 2005. 9(6): p. 607-21.
  9. Takata, M., R.A. Wise, and J.L. Robotham, Effects of abdominal pressure on venous return: abdominal vascular zone conditions. J Appl Physiol (1985), 1990. 69(6): p. 1961-72.
  10. Robotham, J.L. and M. Takata, Mechanical abdomino/heart/lung interaction. J Sleep Res, 1995. 4(S1): p. 50-52.
  11. Gattinoni, L., et al., Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients. Crit Care, 2004. 8(5): p. 350-5.
  12. Takata, M. and J.L. Robotham, Effects of inspiratory diaphragmatic descent on inferior vena caval venous return. J Appl Physiol (1985), 1992. 72(2): p. 597-607.
  13. Biondi, J.W., et al., The effect of incremental positive end-expiratory pressure on right ventricular hemodynamics and ejection fraction. Anesth Analg, 1988. 67(2): p. 144-51.
  14. Cassidy, S., et al., Cardiovascular effects of positive-pressure ventilation in normal subjects. J Appl Physiol, 1979. 47(2): p. 453-461.
  15. Corl, K., A.M. Napoli, and F. Gardiner, Bedside sonographic measurement of the inferior vena cava caval index is a poor predictor of fluid responsiveness in emergency department patients. Emerg Med Australas, 2012. 24(5): p. 534-9.
  16. Corl, K.A., et al., Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. Journal of Critical Care, 2017. 41: p. 130-137.
  17. Bodson, L. and A. Vieillard-Baron, Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness? Let the physiology reply. Crit Care, 2012. 16(6): p. 181.
  18. Muller, L., et al., Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Crit Care, 2012. 16(5): p. R188.
  19. Airapetian, N., et al., Does inferior vena cava respiratory variability predict fluid responsiveness in spontaneously breathing patients? Critical Care, 2015. 19(1): p. 400.



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ICU Physiology in 1000 Words: IVC Collapse, Revisited – Part 2