I am not arguing that a static CVP value should be used to predict a patient’s volume status, or volume responsiveness? Absolutely not. 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.
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. 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. 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. ure 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. 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. 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.
Arthur Guyton described in great detail the determinants of venous return, by a 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](Fig 1)
Guyton’s graphical analysis of the interaction of venous return and cardiac function makes it clear that a single value of CVP cannot predict blood volume or cardiac status. For example, low CVP is the norm in healthy individuals. In the resting upright posture, CVP usually is less than atmospheric pressure because of the negative pressure in the thorax at functional residual capacity and optimal cardiac function. On the contrary, a low CVP can be seem in someone with loss of volume and low cardiac output and normal or even impaired cardiac function. (Fig 2)
Guyton provided a comprehensive analysis of the interaction of cardiac function and the venous return function. He showed that the cardiac output and CVP values are determined by the intersection of these two functions. Knowledge of these processes can help guide clinicians in their resuscitative strategies for treatment of hemodynamic instability. Guyton’s concepts help one understand the limits of the cardiovascular system and thus what is physiologically possible.
Ref:
1. ICU Physiology in 1000 Words: In Defense of the Central Venous Pressure. Pulm CCM.
2. Magder S. Bench-to-bedside review: An approach to hemodynamic monitoring–Guyton at the bedside. Crit Care. 2012 Oct 29;16(5):236. doi: 10.1186/cc11395. PMID: 23106914; PMCID: PMC3682240.
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