Fifty shades of central venous pressure in the cardiorenal syndrome

Sebastien Redant 1 , Patrick M. Honoré MD, PhD, FCCM 1  and David De Bels 1
  • 1 Department of Intensive Care, Brugmann University Hospital, Université Libre de Bruxelles (ULB), Brussels, Belgium
Sebastien Redant
  • Department of Intensive Care, Brugmann University Hospital, Université Libre de Bruxelles (ULB), Brussels, Belgium
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, Professor Patrick M. Honoré
  • Corresponding author
  • Department of Intensive Care, Brugmann University Hospital, Université Libre de Bruxelles (ULB), Brussels, Belgium
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and David De Bels
  • Department of Intensive Care, Brugmann University Hospital, Université Libre de Bruxelles (ULB), Brussels, Belgium
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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.[1] The renal blood flow is kept constant for mean arterial pressure (MAP) between 70 and 130 mmHg.[2] 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.[5] 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).[8]

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.[9]

Venous return to the heart and disturb microcirculatory blood flow might be reduced by a high CVP causing tissue congestion and organ failure.[10] 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.[11] An excessive fluid administration may increase CVP and enddiastolic pressure without increasing enddiastolic or stroke volume.[10] 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.[12]

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.[4] 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.

Conflict of Interest

Conflict of Interests: The authors declare to have no competing interests.

References

  • 1

    Naranjo M, Lerma EV, Rangaswami J. Cardio-Renal Syndrome: A double edged sword. Dis Mon 2017; 63: 92–100.

  • 2

    Burke M, Pabbidi MR, Farley J, Roman RJ. Molecular Mechanisms of Renal Blood Flow Autoregulation. Curr Vasc Pharmacol 2014; 12: 845–58.

  • 3

    Navar LG, Inscho EW, Majid SA, Imig JD, Harrison-Bernard LM, Mitchell KD. Paracrine regulation of the renal microcirculation. Physiol Rev 1996;76: 425–36.

  • 4

    Schnermann J, Briggs JP. Tubuloglomerular feedback mechanistic insights from gene-manipulated mice. Kidney Int 2008;74: 418–26.

  • 5

    Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369:1726–34.

  • 6

    Firth JF, Raine AE, Ledingham JG. Raised venous pressure: a direct cause of renal sodium retention in oedema? Lancet 1988; 1: 1033–5.

  • 7

    Winton FR. The influence of venous pressure on the isolated mammalian kidney. J Physiol 1931; 72: 49–61.

  • 8

    Mullens W, Abrahams Z, Francis G, Sokos G, Taylor D, Starling R, et al. Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure. J Am Coll Cardiol 2009; 53: 589–96.

  • 9

    Legrand M, Dupuis C, Simon C, Gayat E, Mateo J, Lukaszewicz AC, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care 2013; 17: R278.

  • 10

    Chen X, Wang X, Honore PM, Spapen HD, Liu D. Renal failure in critically ill patients, beware of applying (central venous) pressure on the kidney. Ann Intensive Care 2018; 8: 91.

  • 11

    Ho KM. Pitfalls in haemodynamic monitoring in the postoperative and critical care setting. Anaesth Intensive Care 2016; 44: 14–9.

  • 12

    Chen KP, Cavender S, Lee J, Feng M, Mark RG, Celi LA, et al. Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness. Clin J Am Soc Nephrol 2016;11: 602–8.

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  • 1

    Naranjo M, Lerma EV, Rangaswami J. Cardio-Renal Syndrome: A double edged sword. Dis Mon 2017; 63: 92–100.

  • 2

    Burke M, Pabbidi MR, Farley J, Roman RJ. Molecular Mechanisms of Renal Blood Flow Autoregulation. Curr Vasc Pharmacol 2014; 12: 845–58.

  • 3

    Navar LG, Inscho EW, Majid SA, Imig JD, Harrison-Bernard LM, Mitchell KD. Paracrine regulation of the renal microcirculation. Physiol Rev 1996;76: 425–36.

  • 4

    Schnermann J, Briggs JP. Tubuloglomerular feedback mechanistic insights from gene-manipulated mice. Kidney Int 2008;74: 418–26.

  • 5

    Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369:1726–34.

  • 6

    Firth JF, Raine AE, Ledingham JG. Raised venous pressure: a direct cause of renal sodium retention in oedema? Lancet 1988; 1: 1033–5.

  • 7

    Winton FR. The influence of venous pressure on the isolated mammalian kidney. J Physiol 1931; 72: 49–61.

  • 8

    Mullens W, Abrahams Z, Francis G, Sokos G, Taylor D, Starling R, et al. Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure. J Am Coll Cardiol 2009; 53: 589–96.

  • 9

    Legrand M, Dupuis C, Simon C, Gayat E, Mateo J, Lukaszewicz AC, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care 2013; 17: R278.

  • 10

    Chen X, Wang X, Honore PM, Spapen HD, Liu D. Renal failure in critically ill patients, beware of applying (central venous) pressure on the kidney. Ann Intensive Care 2018; 8: 91.

  • 11

    Ho KM. Pitfalls in haemodynamic monitoring in the postoperative and critical care setting. Anaesth Intensive Care 2016; 44: 14–9.

  • 12

    Chen KP, Cavender S, Lee J, Feng M, Mark RG, Celi LA, et al. Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness. Clin J Am Soc Nephrol 2016;11: 602–8.

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