Central venous pressure (CVP) monitoring is widely used in critically ill patients, but its role is often criticized. It has been said that CVP indicates neither blood volume nor fluid responsiveness. However, these arguments ignore the true importance of CVP. CVP provides a constant indication of the balance between venous blood return and cardiac processing capacity. We believe that the emphasis on liquid responsiveness obscures the clinical importance of CVP surveillance.
Measured and normal values
The pressure measured with a liquid-filled system is relative to a reference level. In cardiovascular physiology, this level is the midpoint of the right atrium, approximately 5 cm below the sternal angle. CVP in an upright posture is usually sub-atmospheric. Even at the peak of exercise, CVP only rises to about 4mmHg, and is in a similar range when lying on your back. The heart is surrounded by pleural pressure (Ppl), while the body is at atmospheric pressure. When CVP is used to assess preload and heart function, it is important to note the difference between CVP relative to atmospheric pressure and Ppl. This is called transmembrane pressure (CVPtm). Here, we focus on the downstream pressure that determines venous return, i.e., CVP relative to the atmosphere, and emphasize its important role in organ function and outcomes.
The effect of high CVP values
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Reduced survival in critically ill patients with elevated CVP has been well described. A re-analysis of the VASST trial found that patients with a CVP of <8 mmHg during shock had a 35% lower mortality rate than those with a CVP > 8 mmHg. Similarly, critically ill patients with longer CVP> 10 mmHg have a poorer prognosis. However, these studies only show an association, not that elevated CVP leads to increased mortality. To get closer to this, it would be helpful to study the relationship between high CVP and organ dysfunction.
kidney
Elevated CVP values are associated with an increased risk of acute kidney injury (AKI) in critically ill patients. In isolated animal kidneys, elevated venous pressure reduces urine output and urine output stops at CVP > 25 mmHg. The proposed mechanism is that increased interstitial pressure within the encapsulated kidneys creates renal tamponade. In patients with cardiovascular disease, CVP>6 mmHg is associated with worsening renal function and decreased survival. Acute elevation of CVP has proven to be more important than chronic elevation. A retrospective study of critically ill patients found that for every 1 cmH2O increase in CVP over 7 cmH2O on admission, the risk of AKI increased by 2%. Similarly, early CVP > 14 mmHg after cardiac surgery is an important factor in determining AKI. Ostermann showed that a decrease in mean perfusion pressure (MPP) was associated with progression from AKI phases I to III; CVP is a component of MPP and has an independent effect on the progression of AKI, while mean arterial pressure does not. While these studies remain relevant, the gradual decline in function as CVP rises supports a causal relationship.
liver
Elevated CVP is associated with liver damage and failure. Sherlock demonstrated in patients with heart failure that elevated bilirubin was associated with elevated CVP but not cardiac output. In animal studies, an increase in CVP directly increased portal pressure and decreased portal and hepatic artery blood flow, suggesting that there is a mechanistic process.
How can elevated CVP itself cause organ damage?
Causality can also be supported by identifying a credible mechanism of harm for elevated CVP. This boils down to simple biophysics. Liquid filtration in microcirculation is determined by the force that drives the fluid out of the blood vessel (hydrostatic pressure) and the force that retains the fluid (intravascular osmotic pressure). Assuming no change in venous resistance, any increase in CVP directly increases capillary hydrostatic pressure (Figure 1). To make matters worse, albumin is a major determinant of intravascular pressure, but is often reduced in critically ill patients. Therefore, CVP >10 mmHg is likely to overload the filtration balance in the capillaries and produce tissue edema. Inflammatory conditions, such as sepsis or trauma, increase the permeability of capillaries and exacerbate this phenomenon. The filtrate that enters the interstitial space from the capillaries is drained back into the central vein through the lymphatic system. The lymphatic system is also hindered by elevated CVP. The effects of elevated CVP may be much greater in encased organs, where the increased volume of parenchyma suppresses blood flow and collapses the catheters, sinuses, and veins.
Figure 1 Effects of increased intrathoracic pressure (PPL). CVP central venous pressure, Ppl intrathoracic pressure, CVPtm transmural central pressure, or right ventricular preload (CVP–Ppl). The heart pumps resistance vessels and capillaries (shown as thin lines) through the arterial system. The pressure in the capillaries on the arterial side is about 25 mmHg and on the venous side is 20 mmHg. When Ppl increases from 0 mmHg (left) to 6 mmHg (right), the same CVPtm is likely to occur only if the same amount is increased from 4 to 10 mmHg. The capillary pressure on the arterial side is 31 mmHg. Other physiological adaptations were not considered
Changes in Ppl due to mechanical ventilation
CVP values that are important for venous return are relative to atmospheric values, not CVPtm. A fundamental role of the right heart is to bring CVP as close to zero as possible. In spontaneous breathing, Ppl descends on inhalation, while on passive mechanical ventilation, Ppl rises on inspiration. In addition, positive end-expiratory pressure (PEEP) is applied, always making the PPL positive. Therefore, in order to maintain the front load (i.e., the same CVPtm), a higher CVP is required (Figure 1). The body physiologically counteracts the effects of a decrease in CVPtm by retaining sodium and water. The corresponding increase in CVP is transmitted to the portal vein, causing jaundice and liver swelling. Therefore, positive pressure ventilation always creates a conflict between the higher CVP required to maintain the preload (CVPtm) and the prevention of organ congestion and injury. Although a decrease in CVPtm can be addressed by increasing cardiac contraction, lowering right ventricular afterload, or increasing heart rate, there is little way to reduce tissue congestion other than lowering venous pressure.
In one animal study, fluid accumulation was directly related to mechanical ventilation and was further increased by increasing PEEP. Positive fluid balance in mechanically ventilated patients is also associated with mortality. In patients with acute respiratory distress syndrome (ARDS), survivors have a much smaller daily fluid balance than non-survivors. PEEP requires high systemic venous pressure to maintain cardiac output. Therefore, if CVP starts high, the organizational consequences are worse and may hinder weaning.
Key information
CVP is usually low; Higher than normal CVP values proportionally increase the risk of systemic tissue edema. The increase in CVP comes at a cost, and costs and benefits must be balanced. When CVP is elevated, strategies to maintain low tidal volume and airway pressure and/or use inotropes should be considered, particularly in the setting of increased capillary permeability. The emphasis on liquid reactivity masks awareness of the potential hazards posed by high CVP. CVP and its change over time are important safety parameters that need to be monitored.
来源：The forgotten relevance of central venous pressure monitoring
Intensive Care Med
https://doi.org/10.1007/s00134-023-07101-z
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