Is the central venous pressure an obsolescent model or a valuable puzzle stone in haemodynamic monitoring?
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.