Cardio renal syndrome is the result of many hemodynamic, physiological, hormonal, biochemical or structural interactions. The interactions are bidirectional: acute or chronic cardiac failure may induce acute or chronic renal failure. The renal blood flow is kept constant for mean arterial pressure (MAP) between 70 and 130 mmHg. This self-regulation is made possible by two mechanisms. The first is myogenic by the contraction/relaxation of the afferent vessels in reaction to pressure, and the second is the tubule-glomerular feedback, which also regulates the diameter of the afferent arteriole as a function of NaCl concentration in the filtration liquid arriving at the macula densa.[3,4] The sodium concentration is a function of the quantity of blood, which arrives in the afferent arteriole and the glomerulus.[3,4] In pathological situations such as septic shock, the MAP is reduced below 65 mmHg. The collapse of MAP spectacularly reduces the afterload with a cardiac output capable of increasing due to sepsis to values ranging from 10 to 15 L/min. At the same time, fall in MAP decreases renal blood flow following the loss of self-regulation leading to renal failure and so-called “kidney shock”.
Previous animal studies have shown that an isolated elevation in central venous pressure (CVP) can impair renal function.[6,7] Mullens et al. studied the impact of CVP measured by a Swan-Ganz catheter on the worsening of renal function (WRF) in patients with advanced decompensated heart failure. Patients who developed WRF had a higher central venous pressure on admission (CVP, 18 ± 7 vs. 12 ± 6 mmHg, P < 0.001) and after intensive medical therapy (11 ± 8 vs. 8 ± 5 mmHg, P = 0.04). The development of WRF occurred less frequently in patients who achieved a CVP < 8 mmHg (P = 0.01).
In the context of septic shock, Legrand et al. studied 137 cases of septic shock and distinguished two populations: patients developing acute kidney injury (AKI) and those without kidney injury or improving their renal function (no-AKI). In this series, there was no significant difference in MAP pressure, cardiac output and central venous oxygen saturation (ScVO2) between AKI and no-AKI. In contrast, the CVP was higher in the AKI group (11 [8.5–13]) than in the no-AKI group (8.5 [7–11.1], P = 0.0032). The CVP value was associated with a risk of developing new or persistent AKI even after adjustment for fluid balance (OR = 1.22 (1.08–1.39), for an increase of 1 mmHg; P = 0.002). A linear relationship between CVP and the risk of new or persistent AKI was observed. This article suggests a role for venous congestion in the onset of AKI and challenges the paradigm that high CVP reduces the onset of AKI.
Venous return to the heart and disturb microcirculatory blood flow might be reduced by a high CVP causing tissue congestion and organ failure. CVP is a bedside measure and has long been used to assess preload and response to fluid loading. However, measurement of CVP is not reliable to assess patient’s hemodynamic status. An excessive fluid administration may increase CVP and enddiastolic pressure without increasing enddiastolic or stroke volume. But in a cohort of 4,761 critically ill patients with admission CVP measurements, each increase of 1 cm
H2O CVP was associated with a 2% increase in the adjusted risk of AKI (95% CI, 1.00–1.03; P = 0.02). In this same study, pulmonary edema was not associated with a risk of developing AKI.
In conclusion, the main aim of CVP monitoring should be to ensure a CVP below renal venous pressure (RVP). An increase in CVP induces an increase in RVP that reduces glomerular filtration inducing a feedback in the macula densa with vasodilatation of the afferent arteriole and renin secretion. This increase in “renal afterload” will ultimately lead to a decrease in glomerular filtration and an increase in cardiac afterload via renin and will worsen the cardiorenal syndrome.
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