In Defense of the Central Venous Pressure

Jon-Emile S. Kenny M.D.

In the waning days of my fellowship I received a hemoptysis consult in the cardiac care unit. Sifting through CT scans, I overheard two house-officers giving sign-out for the evening. When reviewing the clinical data, one of the residents referred to the central venous pressure [CVP] as a ‘random number generator.’ I spied them, gave a stern look and recalled being on morning rounds as a sleep-deprived intern; I was mercilessly grilled on the nuances of the central venous pressure and its measurement. I paused and thought: is this what we’re teaching housestaff? That this measurement is random? The Venetian Marionette Years ago, while strolling the promenade along Venice Beach, I saw a young street performer. He was a puppeteer, with an oddly dressed marionette; from the corner of my eye it appeared that his control over his puppet was poor. The marionette haphazardly bobbed up and down, extremities akimbo in utter randomness. On close inspection, however, the puppeteer was actually quite good, with fine control. Focused traction of each string created nuanced movements, even in the face of a waxing and waning ocean breeze. The CVP is a physiological marionette - its value being pulled in different directions by multiple biological strings. On first blush, it may seem random, especially with waxing and waning intra-thoracic pressure, but the informed intensivist must make sense of this dance. Strings Attached The stressed venous volume, venous compliance and the resistance to venous flow are three such physiological strings and collectively known as venous return. Importantly, these variables have multiple determinants each of which can be altered in various ways following a plethora of ICU interventions [1, 2]. Together the stressed venous volume and venous compliance form the mean circulatory filling pressure which is the pressure head for venous return to the right heart [3-5]. The stressed venous volume may be increased directly with volume infusion or indirectly with alpha-agonists. Alpha-agonists cause venoconstriction which recruits unstressed venous volume into stressed venous volume [6, 7]. In either case, augmenting mean circulatory filling pressure favors increased venous return to the right heart and a higher central venous pressure. Pure alpha receptor agonism, however, also increases the resistance to venous return which retards blood flow to towards the thorax while beta-2 agonism lowers this resistance and ‘opens the flood gates’ for the right heart as it were [1]. Importantly, the opposite is also true – venodilation, volume loss, sympatholysis [e.g. relief of hypoxemia, sedation] tend to lower the pressure head for venous return and consequently lower CVP. But the strings of venous return are only half of the story because cardiac contractility, afterload, heart rate, rhythm and valve function are another group of strings serving to pull the CVP up or down. Collectively this group of strings is known as cardiac function. Intuitively, any intervention that improves cardiac function will favor ejection of blood from the thorax and lower CVP while any state that impairs cardiac function will encourage retention of blood within the central compartment and raise CVP. While Arthur Guyton described in great detail the determinants of venous return, perhaps his greatest contribution was a graphical analysis that superimposed both the venous return function and cardiac function onto a single graph [3, 8]. Thus the Guyton Diagram teaches us that interpretation of the CVP requires knowledge of both a patient’s cardiac pump function [e.g. from a full bedside echocardiogram] and venous return function [i.e. from a clinical exam] – just as interpretation of a patient’s pH requires knowledge of both the PaCO2 and venous bicarbonate [9]. The Importance of the CVP Am I arguing that a static CVP value should be used to predict a patient’s volume status, or volume responsiveness? Absolutely not [10-12]. However, there is tremendous meaning in the CVP as the starting point for a basic lesson in hemodynamics. The CVP is the fulcrum of cardiovascular physiology at the bedside; understanding the genesis of the CVP lays the foundation for interpretation of hemodynamic intervention in the ICU as well as interpretation of bedside echocardiography. There is no magic to IVC collapse and distention, they follow the same biophysical principles as the CVP. Ultrasound of the IVC is a visual method to qualitatively track dynamic changes of the central venous pressure relative to the intra-abdominal pressure. When the CVP falls below intra-abdominal pressure, the IVC will tend to collapse and when the CVP rises above the intra-abdominal pressure the IVC will tend to distend, both as a function of IVC compliance [13]. Further, in a number of recent, elegant studies, Maas and colleagues have used instantaneous CVP and cardiac output monitoring to construct venous return curves at the bedside [14-16]. This has, once again, confirmed Guyton’s early work, but also given us a potentially objective measure of ‘volume status’ by extrapolating the venous return curve to the x-intercept [i.e. determination of the mean systemic filling pressure] [15]. Additionally, this work has confirmed that the vasoactive agents used in the ICU [e.g. norepinephrine] may exert more of their hemodynamic effect via alteration of venous return [17-20]. So the next time you infuse volume into a patient, but also change the ventilator settings, increase the FiO2, sedate the patient and alter the dose or composition of a vasoactive substance, realize that each of these interventions will pull the strings of both venous return and cardiac function. At first blush, the effect upon the CVP may be seemingly aimless, but like the skilled Venetian puppeteer jigging his marionette within the ebb and flow of an ocean breeze, the dance of the CVP is anything but random. Read more from Jon-Emile Kenny on his website at Heart-Lung.org. References:

Gelman, S., Venous function and central venous pressure: a physiologic story. Anesthesiology, 2008. 108(4): p. 735-48.
Rothe, C.F., Physiology of venous return. An unappreciated boost to the heart. Arch Intern Med, 1986. 146(5): p. 977-82.
Magder, S., Bench-to-bedside review: An approach to hemodynamic monitoring - Guyton at the bedside. Crit Care, 2012. 16(5): p. 236.
Feihl, F. and A.F. Broccard, Interactions between respiration and systemic hemodynamics. Part I: basic concepts. Intensive Care Med, 2009. 35(1): p. 45-54.
Broccard, A.F., Cardiopulmonary interactions and volume status assessment. J Clin Monit Comput, 2012. 26(5): p. 383-91.
Jacobsohn, E., R. Chorn, and M. OConnor, The role of the vasculature in regulating venous return and cardiac output: historical and graphical approach. Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie, 1997. 44(8): p. 849-867.
Funk, D.J., E. Jacobsohn, and A. Kumar, The role of venous return in critical illness and shock-part I: physiology. Crit Care Med, 2013. 41(1): p. 255-62.
Guyton, A.C., Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev, 1955. 35(1): p. 123-9.
Magder, S., How to use central venous pressure measurements. Current Opinion in Critical Care, 2005. 11(3): p. 264-270.
Marik, P.E. and R. Cavallazzi, Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Crit Care Med, 2013. 41(7): p. 1774-81.
Shippy, C.R., P.L. Appel, and W.C. Shoemaker, Reliability of clinical monitoring to assess blood volume in critically ill patients. Crit Care Med, 1984. 12(2): p. 107-12.
Kumar, A., et al., Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med, 2004. 32(3): p. 691-9.
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.
Maas, J.J., et al., Assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients. Crit Care Med, 2009. 37(3): p. 912-8.
Jansen, J.R., J.J. Maas, and M.R. Pinsky, Bedside assessment of mean systemic filling pressure. Curr Opin Crit Care, 2010. 16(3): p. 231-6.
Maas, J.J., et al., Determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit. Anesth Analg, 2012. 114(4): p. 803-10.
Maas, J.J., et al., Cardiac output response to norepinephrine in postoperative cardiac surgery patients: interpretation with venous return and cardiac function curves. Crit Care Med, 2013. 41(1): p. 143-50.
Persichini, R., et al., Effects of norepinephrine on mean systemic pressure and venous return in human septic shock. Crit Care Med, 2012. 40(12): p. 3146-53.
Rastegarpanah, M. and S. Magder, Role of neurosympathetic pathways in the vascular response to sepsis. J Crit Care, 1998. 13: p. 169-176.
Datta, P. and S. Magder, Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia. Am J Respir Crit Care Med, 1999. 160(6): p. 1987-93

ICU Physiology in 1000 Words: In Defense of…

Comments on this post are for paid subscribers