Sep 012014
 

ICU Physiology in 1,000 Words 
"The Hemodynamics of Prone"
by Jon-Emile S. Kenny MD

A physiological maelstrom has recently swirled about the hemodynamic effects of the prone position in severe ARDS [1-5]; but how exactly does this maneuver alter the cardiovascular system?  A good approach to this problem is a Guytonian one whereby we consider the consequences of the prone position firstly on venous return and secondly on cardiac function.

Prone Positioning Effects on Venous Return

The upstream, or driving pressure for venous return is the mean systemic filling pressure [MSFP].  The MSFP is directly related to the stressed venous volume and indirectly related to the compliance of the venous tree.  The MSFP is the x-intercept of the venous return curve [i.e. the pressure within the vascular system when blood flow is ceased] [6-9].  If the stressed venous blood volume is increased [e.g. volume infusion, passive leg raise] or venous compliance decreases, the x-intercept [and therefore the entire venous return curve] shifts rightwards and this tends to augment venous return.  However, the slope of the venous return curve is also important as it depicts the resistance to venous return [10].  Increased resistance to venous return results in a down-left shift of the venous return curve without a change in the x-intercept; intuitively, increased resistance to venous return tends to diminish venous return.

The presumed mechanism by which the prone position alters venous return is via abdominal pressurization.  Increased intra-abdominal pressure has two competing effects upon venous return.  Firstly, it facilitates venous return by increasing the MSFP [11], illustrated as a rightwards shift of the venous return x-intercept [12].  Secondly, it may impair venous return by increasing the resistance to venous return.  However, the degree to which it increases the resistance to venous return is greatly influenced by the patient’s underlying volume status [11, 13].  Simply, when the abdominal venous beds are ‘full’ [e.g. like West Zone III in the lungs], pressurization of the abdomen does not retard venous return to the same degree as a venous tree that is relatively ‘empty’ [e.g. like West Zone I in the lungs] [14].  In summary, because prone position tends to increase intra-abdominal pressure [1], this will shift the venous return curve rightwards which favors venous return, but will have variable effects upon the resistance to venous return depending on the patient’s underlying volume status.  The point at which the systemic venous return curve intersects the cardiac function curve defines the steady state cardiac output, such that increased MSFP without an increased resistance to venous return raises cardiac output as long as the operating point lies upon the ascending portion of the cardiac function curve as described below.

Prone Positioning Effects on Cardiac Function

Prone positioning has complex and conflicting effects upon right ventricular load.  Because prone positioning reduces the compliance of the chest wall [15], the passive patient receiving mechanical ventilation will experience a relatively large increase in intra-thoracic pressure for a given tidal volume [16, 17].  Assuming that the intra-thoracic pressure is transmitted integrally to the pericardial space [18], the increased intra-thoracic pressure shifts the cardiac function curve rightwards relative to the systemic venous return curve [19]; to the extent that the cardiac function curve shifts rightwards relative to the right-shift of the MSFP, as elaborated above, there will be reduced cardiac output.  Conversely, and less intuitively, the increase in intra-thoracic pressure will also reduce right ventricular afterload.  The reason is that right ventricular afterload is determined by the distending pressure of the lung [i.e. the trans-pulmonary pressure] which is the pressure within the alveolar compartment less the pressure within the pleural compartment.  Consequently, reduced chest wall compliance raises the pleural [or intra-thoracic] pressure relative to the alveolar pressure and this unloads right ventricular ejection [20-22].  Additionally, prone positioning recruits compressed dorsal lung [23] which lowers pulmonary vascular resistance [24], and improves oxygenation which releases hypoxemic vasoconstriction in the pulmonary bed [25].  Right ventricular afterload reduction is illustrated by an increase in the slope of the cardiac function curve [i.e. an up and to the left shift].

This conflicting physiology is summarized in an excellent review by Jardin and Vieillard-Baron [26].  In their summary, they reconcile conflicting data pertaining to the effect of PEEP on right ventricular volume in ARDS, and they do so within the framework of Gattinoni’s distinction pulmonary and extra-pulmonary ARDS [27].  Briefly, pulmonary ARDS is a consequence of direct pulmonary insult and leads to a profound reduction in pulmonary compliance, whereas, extra-pulmonary ARDS arises in the context of systemic unrest and results in severely diminished chest wall compliance.  In the former, less of the alveolar pressure is transmitted to the pleural space [28-30], therefore, trans-pulmonary pressure rises and right ventricular afterload is heightened.  This physiology favors enlargement of right ventricular volume and diminished cardiac output.  In contradistinction, extra-pulmonary ARDS is typified by raised pleural pressure relative to alveolar pressure such that trans-pulmonary pressure and right ventricular afterload are diminished; this favors diminution of right ventricular volume and improved cardiac output.

Hemodynamic Effects of Prone Positioning: Conclusions

Placing a patient in the prone position has important implications for both venous return and right ventricular function.  While an increase in intra-abdominal pressure tends to raise the pressure head for venous return, improved venous return will only be realized in the absence of a contemporaneous rise in the resistance to venous return.  Therefore, careful consideration should be paid to a patient’s volume status prior to initiating prone positioning.  Additionally, the degree to which ventilator-applied airway pressure partitions into the alveolar space relative to the pleural space will determine to what extent the intra-thoracic milieu favors diminished right ventricular preload, afterload or some combination thereof.  It follows that careful consideration should be given to underlying cardiac function as well as the relative contributions of the pulmonary and chest wall compliances to the overall compliance of the respiratory system.  Integration of these multiple, co-varying physiological elements may explain conflicting hemodynamics both in ARDS and other mechanically-ventilated patient populations.

Read more from Jon-Emile Kenny on his website at Heart-Lung.org.

References:

1.                  Jozwiak, M., et al., Beneficial hemodynamic effects of prone positioning in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med, 2013. 188(12): p. 1428-33.

2.                  Magder, S., Is all on the level? Hemodynamics during supine versus prone ventilation. Am J Respir Crit Care Med, 2013. 188(12): p. 1390-1.

3.                  Albert, R.K. and R.D. Hubmayr, The hemodynamic effects of prone positioning in patients with acute respiratory distress syndrome remain to be defined. Am J Respir Crit Care Med, 2014. 189(12): p. 1567.

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9.                  Guyton, A.C., D. Polizo, and G.G. Armstrong, Mean circulatory filling pressure measured immediately after cessation of heart pumping. Am J Physiol, 1954. 179(2): p. 261-7.

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11.                  Robotham, J.L. and M. Takata, Mechanical abdomino/heart/lung interaction. J Sleep Res, 1995. 4(S1): p. 50-52.

12.                  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.

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15.                  Pelosi, P., et al., Effects of the prone position on respiratory mechanics and gas exchange during acute lung injury. Am J Respir Crit Care Med, 1998. 157(2): p. 387-93.

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18.                  Morgan, B.C., W.G. Guntheroth, and D.H. Dillard, Relationship of Pericardial to Pleural Pressure during Quiet Respiration and Cardiac Tamponade. Circ Res, 1965. 16: p. 493-8.

19.                  Marini, J.J., B.H. Culver, and J. Butler, Effect of positive end-expiratory pressure on canine ventricular function curves. J Appl Physiol Respir Environ Exerc Physiol, 1981. 51(6): p. 1367-74.

20.                  Vieillard-Baron, A., et al., Cyclic changes in right ventricular output impedance during mechanical ventilation. J Appl Physiol (1985), 1999. 87(5): p. 1644-50.

21.                  Jardin, F., et al., Relation between transpulmonary pressure and right ventricular isovolumetric pressure change during respiratory support. Cathet Cardiovasc Diagn, 1989. 16(4): p. 215-20.

22.                  Jardin, F., et al., Reevaluation of hemodynamic consequences of positive pressure ventilation: emphasis on cyclic right ventricular afterloading by mechanical lung inflation. Anesthesiology, 1990. 72(6): p. 966-70.

23.                  Gattinoni, L., et al., Body position changes redistribute lung computed-tomographic density in patients with acute respiratory failure. Anesthesiology, 1991. 74(1): p. 15-23.

24.                  Whittenberger, J.L., et al., Influence of state of inflation of the lung on pulmonary vascular resistance. J Appl Physiol, 1960. 15: p. 878-82.

25.                  Orchard, C.H., R. Sanchez de Leon, and M.K. Sykes, The relationship between hypoxic pulmonary vasoconstriction and arterial oxygen tension in the intact dog. J Physiol, 1983. 338: p. 61-74.

26.                  Jardin, F. and A. Vieillard-Baron, Right ventricular function and positive pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings. Intensive Care Med, 2003. 29(9): p. 1426-34.

27.                  Gattinoni, L., et al., Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med, 1998. 158(1): p. 3-11.

28.                  O'Quin, R.J., et al., Transmission of airway pressure to pleural space during lung edema and chest wall restriction. J Appl Physiol (1985), 1985. 59(4): p. 1171-7.

29.                  Jardin, F., et al., Influence of lung and chest wall compliances on transmission of airway pressure to the pleural space in critically ill patients. Chest, 1985. 88(5): p. 653-8.

30.                  Venus, B., L.E. Cohen, and R.A. Smith, Hemodynamics and intrathoracic pressure transmission during controlled mechanical ventilation and positive end-expiratory pressure in normal and low compliant lungs. Crit Care Med, 1988. 16(7): p. 686-90.

 

 

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ICU Physiology in 1000 Words: The Hemodynamics of Prone