CVP is not the MVP, but should still be on the team
Ethan Sanford MD, Shawn Jackson MD PhD, Justin L. Lockman MD MSEd
Intensive, high frequency, physiologic monitoring is the core of our specialty. Despite this fact, which monitors to use and how to use the data they generate to inform clinical decisions is often unclear. Like making a political statement during a holiday family gathering, we assume that today’s PAAD will stir up some (welcome) discussion about what we know, what we don’t know, and how to interpret the data.
Original Article
Pesenti A, Slobod D, Magder S. The forgotten relevance of central venous pressure monitoring. Intensive Care Med. Jul 2023;49(7):868-870. doi:10.1007/s00134-023-07101-z. Epub 2023 Jun 9. PMID: 37294343.
The forgotten relevance of central venous pressure monitoring1 is a modern review of an old monitoring modality, namely central venous pressure. The authors acknowledge the revolt against CVP monitoring as it does not intrinsically indicate blood volume or that a patient will have a blood pressure response to fluid resuscitation. As an aside, the simple use of “fluid responsiveness” as an outcome may not ideally serve the patient, either. Simply because a fluid bolus increases blood pressure does not mean it is the best treatment for hypotension; we are wise to also consider other treatments including anesthetic titration, vasoactive medications, blood product administration, or perhaps even watchful waiting (if we deem oxygen and other substrate delivery adequate). In other words, fluid responsiveness should not mandate fluid resuscitation. Today’s PAAD points out that monitoring CVP and identifying CVP elevation may help us avoid over-resuscitation and the morbidity associated with it.
First of all, let’s state the obvious: CVP values can be affected by the site of placement, positioning of the catheter, patient positioning, positive vs. negative pressure ventilation, and flow dynamics of the venous system. Certainly, a femoral venous catheter ending in the iliac vein will provide a different pressure and waveform reading than an internal jugular catheter which terminates in the right atrium – at least in an upright patient. Today’s PAAD focuses on CVP measured at the right atrium. Rather than looking at fluid responsiveness, the authors focus on mortality and organ specific outcomes. In critically-ill adults, elevated CVP (greater than 8 to 10) has been associated with increased death2, 3. Kidney injury has also been associated with elevated CVP in cardiac surgery, critical illness, and heart failure4, 5.
Why might elevated CVP cause harm? We have previously discussed the current state (and deficiencies) of arterial blood pressure monitoring without sufficient appreciation of microvascular perfusion pressures (You did an Allen test, didn’t you!? Rethinking pre-procedural assessment for arterial line placement, 11/4/2024,
https://ronlitman.substack.com/p/you-did-an-allen-test-didnt-you-rethinking,). Elevated central venous pressure increases the hydrostatic pressure leading to net loss of fluid to the extravascular spaces (third-spacing). This is compounded in critically-ill patients who frequently have hypoalbuminemia and increased capillary permeability due to systemic inflammatory response syndrome. This lost “third-spaced” fluid should then be drained back into central veins by the lymphatic system, but this system is also dysfunctional in the setting of elevated CVP.
Finally, the authors review the impact of positive pressure ventilation on both CVP and cardiac output. Preload to the right atrium is maintained by the pressure difference between the right atrium and the intrathoracic pressure. This is termed the transmural pressure and is determined by the formula: CVP – intrathoracic pressure. During spontaneous ventilation, a low CVP is well tolerated due to negative intrathoracic pressure. The intrathoracic pressure becomes positive during controlled (invasive or non-invasive) ventilation. In this circumstance, higher CVP may be required to maintain preload and correlated cardiac output. This can be achieved with a fluid bolus or with an increase in venous resistance using vasopressors. Alternatively, cardiac output may be maintained with increased inotropy, increased chronotropy, decreased RV afterload, or any combination of the above.
What is the right thing to do? We don’t know, but we suspect it may vary based on the clinical situation and the patient condition. However, today’s PAAD points out that our frequent instinct to give fluid boluses in the operating room may increase CVP and negatively impact perfusion pressures. A problem for anesthesiologists is that negative outcomes associated with over-resuscitation may not be obvious during our time with the patient. We are biased towards interventions which improve the numbers during a relatively short amount of time, but sometimes underestimate how our management affects the patient’s total hospital/perioperative course.
Assessing and managing changes in oxygen delivery demands consideration of all aspects of cardiopulmonary and microvascular systems. Frequently and for good reason, anesthesiologists and critical care physicians demand high quality (RCT) data that a monitor changes a major clinical outcome prior to implementation of a new monitor. We remind our readers that in the OR, such a demand for high level data would result in simply monitoring temperature and pulse; all other monitoring modalities fail to meet these requirements. As such, we believe (as the authors conclude) that CVP may offer extra information to guide optimal decisions on how to address disturbances in certain clinical situations, and we think CVP has suffered a premature death because of the lack of “signal” in attempted studies. We do not need an RCT to know we are better off with end-tidal CO2 monitoring. We believe the same about CVP monitoring. The value of this information must be weighed against the risk of the monitoring modality (i.e., central venous line placement), but let’s not pretend there is no benefit at all to CVP. This is where the art still supersedes the science.
Do you use CVP monitoring routinely in major surgery? What is your threshold for incorporating non-standardized monitors? Send your thoughts to Myron at myasterster@gmail.com and he will include in a Friday Reader Response.
1. Pesenti A, Slobod D, Magder S. The forgotten relevance of central venous pressure monitoring. Intensive Care Med. Jul 2023;49(7):868-870. doi:10.1007/s00134-023-07101-z
2. Li DK, Wang XT, Liu DW. Association between elevated central venous pressure and outcomes in critically ill patients. Ann Intensive Care. Aug 9 2017;7(1):83. doi:10.1186/s13613-017-0306-1
3. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. Feb 2011;39(2):259-65. doi:10.1097/CCM.0b013e3181feeb15
4. Damman K, van Deursen VM, Navis G, Voors AA, van Veldhuisen DJ, Hillege HL. Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease. J Am Coll Cardiol. Feb 17 2009;53(7):582-588. doi:10.1016/j.jacc.2008.08.080
5. Legrand M, Dupuis C, Simon C, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care. Nov 29 2013;17(6):R278. doi:10.1186/cc13133