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 P MS and CVP. An increase in CVP can result in decrease of CO when it is not associated with concomitant P MS 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

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