In a recent issue of the European Journal of Anaesthesiology, Marx et al.1 present the guideline ‘Intravascular volume therapy in adults’ by the Association of the Scientific Medical Societies in Germany. Among other parameters, the authors evaluate the role of the central venous pressure in diagnosis of hypovolaemia and volume therapy. In brief, central venous pressure measurement is prohibited to diagnose a volume deficit [recommendation 1 to 3, grade of recommendation A (GoR A)] and flow based and/or dynamic preload variables should be favoured over the evaluation of the central venous pressure during volume therapy (recommendation 7b-2, GoR A).1 Indeed, many original studies, meta-analyses and authors have frequently questioned the role of this parameter in the context of fluid therapy, pointing out the poor relationship between central venous pressure and volume state, and opening a sometimes emotional debate.
Over the last few decades, there have been controversial discussions about adequate monitoring strategies and the types of fluids to be used. Especially in the critically ill population, it might be necessary to rapidly escalate administration of intravenous fluids but – with regard to haemodynamic monitoring – to avoid harm through fluid overload. Although physicians are confronted with the dilemma of a missing gold standard to evaluate intravascular volume state, guidelines aim to support the clinical decision process by summarising the current body of evidence. However, although they are a useful and valuable tool in the management of specific medical topics, guidelines can also suffer from certain methodological limitations.2 In some cases, recommendations in medical guidelines led to the implementation of initiatives, which retrospectively lacked any outcome benefits or even caused harm.3
The authors of the German guidelines state that ‘the measurement of central venous pressure has only minimal predictive power in determining the status of intravascular volume’.1 But can a vascular pressure value be considered as a direct surrogate of intravascular volume? More than a century ago, Earnest Starling published his findings about the relationship of cardiac output and the pressure in the right atrium using canine heart–lung preparation techniques.4 Starling and other researchers not only demonstrated how the heart interacts with the blood returning from circulation. Through experimental manipulation of the cardiac performance, it could be shown that central venous pressure both determines and results from cardiac output.4 A further important contribution to the understanding of cardiovascular physiology was made by Arthur Guyton by taking into consideration the determinants of venous return. Guyton integrated a venous return function into Starling's curve and thus generated a circulatory model, in which the venous return depends on the gradient between the pressure in the vasculature (mean systemic filling pressure) and the right atrium. The mean systemic filling pressure itself results from the interaction between the wall of the vessel and the blood within the vascular lumen.5 Accordingly, the interplay of three major components affects the cardiovascular performance: first, cardiac efficiency; second, the volume inside the blood vessel and third, vascular compliance. The central venous pressure is inevitably interwoven in this interaction and with Guyton's model, it becomes clear that alterations of cardiac and venous return function can result in both high or low central venous pressure values without any changes in blood volume.6 Given that, we agree that ‘isolated’ central venous pressure measurements should not be used to determine intravascular volume state.
However, although the central venous pressure ‘per se’ does not directly reflect volume status, it can be used as a safety parameter in volume therapy, when continuously measured. As the central venous pressure expresses the interaction of cardiac function and venous return, conditions in which central venous pressure is elevated should induce vigilance to avoid venous congestion with consequences on perfusion, microcirculation and the function of affected upstream organs, like the kidneys. Conversely, a hypovolaemic state must be taken into consideration when a low central venous pressure is combined with a low cardiac output (or an appropriate surrogate).6 During surgery, rapid changes in volume state because of blood loss without changes in the patient's position are almost certainly accompanied by a fall of the central venous pressure. Thus, in our opinion, it is not justified to replace this parameter by other (expensive) monitoring devices or to completely abstain from central venous pressure measurement as haemodynamic surveillance option.
In their invited commentary, ‘The quest for holy volume therapy’, Robertis and colleagues2 accentuate the peculiarity of critically ill patients (i.e. alterations in the integrity of the vascular barrier), which necessitates an individual approach to optimal hemodynamic monitoring. Is central venous pressure measurement an obsolescent model? Today, 15 years after the first early goal-directed therapy study in patients with sepsis and septic shock resulting in the inclusion of central venous pressure measurement in the Surviving Sepsis Campaign guidelines,7,8 the value of this parameter in the perioperative setting and the ICU appears to be fairly unsettled. In three recently published randomised controlled early goal-directed therapy trials (Australasian Resuscitation In Sepsis Evaluation, Protocolised Management in Sepsis, Protocolized Care for Early Septic Shock), central venous pressure measurement proved to be neither harmful nor beneficial in the subset of septic patients. On the other hand, central venous pressure measurement is still valuable in other settings, such as management of patients during and after cardiovascular surgery or as a component in bleeding control during liver surgery.
Adequate fluid management is a pivotal component of peri-interventional and postoperative care to prevent adverse events and poor outcomes. It requires consideration of patient's individual comorbidities and factors influencing the performance of the cardiovascular system. As many patients have a central venous line inserted, measurement of central venous pressure represents an easily accessible, safe, cost-effective and feasible monitoring option with regard to elementary measurement principles (i.e. referencing and timing of measurement during the cardiac cycle). Interpretation of central venous pressure values necessitates a fundamental understanding about the interplay between heart, vessels and the intravascular volume. Furthermore, central venous pressure values should always be interpreted in view of clinical signs (i.e. cold extremities), laboratory parameters (i.e. lactate, base excess) and, if at hand, other monitoring devices reflecting volume state. Although the German guidelines do not forbid central venous pressure measurement ‘in general’.1 The above mentioned recommendations in conjunction with a general lack of consensus among clinicians should not mislead to stop central venous pressure measurement as a valuable puzzle stone in haemodynamic monitoring.8
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1. Marx G, Schindler AW, Mosch C, et al. Intravascular volume therapy in adults: guidelines from the association of the scientific medical societies in Germany. Eur J Anaesthesiol
2. De Robertis E, Afshari A, Longrois D. The quest for the holy volume therapy. Eur J Anaesthesiol
3. Prielipp RC, Coursin DB. All that glitters is not a golden recommendation. Anesth Analg
4. Berlin DA, Bakker J. Starling curves and central venous pressure. Crit Care
5. Berlin DA, Bakker J. Understanding venous return. Intensive Care Med
6. Magder S. Understanding central venous pressure: not a preload index? Curr Opin Crit Care
7. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Med
2017; [Epub ahead of print].
8. Dellinger RP, Schorr CA, Levy MM. A users’ guide to the 2016 surviving sepsis guidelines. Intensive Care Med
2017; [Epub ahead of print].