The central venous pressure, and ‘a plea for some common-sense’

Editor, Nearly 10 years ago, anaesthesiologist Simon Gelman mindfully acknowledged that 'The main reason for lack of correlation between values of CVP and blood volume is that the body does everything possible to maintain homeostasis'.1 Then, asserted that: 'The correlation between CPV and circulating blood volume has never been found simply because it does not exist'.1 It is my purpose – within the restrictions of the format of a letter – to highlight some features surrounding the analysis of the central venous pressure (PCV) in the context of the subject of clinical haemodynamics, and the several issues raised by Siegler et al. in their article,2 which may help to provide a coherent framework to analyse this curiously controversial haemodynamic variable. What is the PCV? And how does it arise as a Variable? What does it mean? Whenever this haemodynamic variable is analysed and revisited in the biomedical literature, the inquiry about its 'usage' in clinical practice has always prevailed, and, therefore, the approach through meta-analyses, systematic reviews and clinical trials. In order to address the first group of questions, I have found a different approach to the PCV more appropriate based on the underlying physics and physiology, properly designated as 'longitudinal' and 'transversal' approaches. The former analyses the PCV primarily in relation to the systemic flow (cardiac output, QC),3 and the latter focuses in vascular capacitance and its intrinsic role in determining ventricular preload and cardiac performance4; both viewpoints are complementary, and fully explain the meaning of the PCV. Let us briefly explain what this approach is about. Blood pressure (P) in a vascular segment represents the ratio of the blood volume accumulated in time and vascular compliance (C), which in turn represents the time integral of the difference between the flow entering and leaving the vascular compartment (Q1−Q2). Altogether, it forms the flow-pressure-volume-relationship within a compliant chamber, where This way, we get the unitary phenomenon by which blood pressures arises, and it is applicable to any vascular segment including the one we call the 'central vascular compartment', roughly, the intrathoracic low-pressure subdivision of the cardiovascular system. But, it is important to clarify that the limits of the central vascular compartment are more physiological than anatomical; shortly, the PCV is the product of the functional interaction between the heart and vasculature – as emphasised by Siegler et al.2 – directly influenced by other surrounding forces1 (hydrostatic, intrapleural and intra-abdominal pressures). In particular, flow entering the central vascular compartment (or, 'venous return', QV) accumulates at a rate equal to (QV−QC), which time integral yields a volume, called 'venous excess' by Reddi and Carpenter3: And being P = V/C, and solving for pressure, the PCV is Turning to the role of vascular capacitance ('transversal approach'), the PCV is the result of the interaction between the lumped venous system and the right heart in terms of pressure-volume relations, phenomenon called 'veno-ventricular coupling' by Tyberg.4 Thus, in conclusion, both perspectives intersect emphasising the first the dependence of the PCV on the flow, and the second on the venous capacitance. This summary of the physiological background is crucial for any further analysis and understanding of the PCV in the clinical scenario, just because it unequivocally shows its origin and meaning, in terms of the energetics: 'a residual portion of the energy supplied by the left ventricle, which supplies the work done in expansion of the right ventricle during diastole'.5 The problem of the classical models Traditionally, the physiology of the PCV is analysed following interpretations of the classical models of modern cardiovascular physiology that are often misleading.3 As Siegler et al.2 mentioned, Guyton's and Starling's classical models share the PCV as an active 'effector' in the circulation, which is reasonable as both physiologists artificially manipulated the PCV in their respective experiments (although, not directly; Starling: adjustments of the height of an artificial blood reservoir and its outflow resistance,3 and, Guyton: adjustment of the height of a Starling resistor, which throttled the output of an artificial pump6). Moreover, they both share the PCV in a 'divergent' fashion: in Guyton's view, right atrial pressure (and, by extension, the PCV) is a 'back-pressure' opposing steady flow, whereas in Starling's experimental set-up, PCV increases cardiac output via the Frank– Starling mechanism. The bottom line of this dichotomic role is that in a flow-driven circuit such as the peripheral circulation, vascular pressures – including the PCV – are always the dependent variable, which connected to the cardiac subsystem forms a closed-loop negative feedback regulator of the cardiovascular circuit. If the approach pioneered by Guyton (i.e. the overlay of venous return curves and cardiac output curves in the same coordinate system) is innovative in any way, it is that it shows graphically the negative feedback interaction between the cardiac and vascular subdivisions of the system – a convenient way to visualise consequences of changes in cardiac function or of properties of the systemic circulation for equilibrium Q and PCV6 – but not venous return driven by the gradient between mean systemic filling pressure and right atrial pressure,7 as suggested by Siegler et al.2 Blood volume and the PCV Third, the central issue discussed in the debate is the use of the PCV to assess volume status to guide fluid therapy and haemodynamic management. From the definitions given above, it is certain that PCV and total blood volume are different things (if, by 'volume status' is meant the patient's volaemia). Then, there is another major problem with the classical models in this respect: the dismissal of blood volume as an effective haemodynamic variable. To Guytonians, it is the 'stressed fraction' of the volaemia – manifested in the 'mean systemic filling pressure' – that is haemodynamically 'active' or 'effective'1 (which also brings up the issue of the physical legitimacy of this conception); meanwhile, the assessment and prediction of the 'fluid responsiveness' (based on Starling's ventricular function curve) and the preload-dependence of the ventricles – manifested in the stroke volume variation through the so-called 'dynamic parameters', like the ΔPCV – is what determines the patient's volume therapy ('responder' versus 'nonresponder'), ignoring the fact that the vasculature buffers acute fluid loading and haemorrhage by adjusting its capacitance.4 So, the rationale of the dynamic parameters focuses in the real relationship between ventricular preload and stroke volume, but through an isolated interpretation of Starling's curve – isolated in the sense that it ignores the fundamental principle that the 'position' in the curve depends on the distribution blood volume – something completely opposite to the veno-ventricular coupling. However, the approach of a 'flow-based' haemodynamic management,8 and in relation to PCV measurement – distinctly pertaining to the domain of functional haemodynamics – seems to represent a 'step in the right direction' (at least, theoretically), as cardiac output is not considered an absolute isolated variable, but in terms of its effectiveness. Finally, it is important to remember that blood volume is not a fixed homogeneous fluid. Knowledge of the blood volume enables the practitioner to obtain related parameters such as normalised haematocrit,9 that is to truly analyse this variable. What is even more curious, PCV becomes valuable when total blood volume is known, as it indicates how it is distributed. After all, what is haemodynamic management if not optimising cardiac output and maintaining blood volume homeostasis? Acknowledgements relating to this article Assistance with the letter: the author extends thanks to Enrique Carcar, MD, Rosario, Argentina, for bringing the article to my attention, and being open to interchange opinions in everyday practice; and to George L. Brengelmann, PhD, Department of Physiology and Biophysics, University of Washington, whose fascinating insights into the complex dynamics of the human circulatory system and uncountable and invaluable teachings made me value more cardiovascular physiology in clinical practice. Financial support and sponsorship: none. Conflicts of interest: none.