Fluid Therapy: Double-Edged Sword during Critical Care?

Table 2

The risks of increased central venous pressure.

Consequence	Comment
Decreased venous return and cardiac index	CVP is not a reliable characteristic of preload and, when exceeding 8 mmHg, can be an independent predictor of the mortality [31]. The normal CVP value is close to 0. According to Guyton model, both venous return and cardiac output are determined by difference between and CVP. An increase in CVP can result in decrease of CO when it is not associated with concomitant augmentation
Acute kidney injury	Increased CVP is associated with increased renal (subcapsular) (interstitial) pressure resulting in decreased renal blood flow, GFR, and derangement in lymph drainage. CVP is a sole hemodynamic parameter that can independently predict the risk of AKI starting from the values above 4 mmHg! In CVP above 15 mmHg, the risk of sepsis-induced AKI exceeds 80%
Splanchnic congestion/and microcirculatory changes [32]	The microcirculation should be recognized as a low pressure part of circulation due to abrupt decrease in blood pressure on the level of resistive arterioles. Therefore, the critical changes in microcirculation have been demonstrated in CVP > 12 mmHg. Any increase in downstream pressure (CVP) results in microcirculation distress

: mean (systemic) filling pressure, CVP: central venous pressure, and CO: cardiac output.