Congestive kidney failure in cardiac surgery: the relationship between central venous pressure and acute kidney injury

被引:78
|
作者
Gambardella, Ivancarmine [1 ]
Gaudino, Mario [1 ]
Ronco, Claudio [2 ]
Lau, Christopher [1 ]
Ivascu, Natalia [1 ]
Girardi, Leonard N. [1 ]
机构
[1] New York Weill Cornell Med Ctr, Dept Cardiothorac Surg, 525 East 68th St,Box 110, New York, NY 10021 USA
[2] Int Renal Res Inst IRRIV, San Bortolo Hosp Viale Rodolfi, Dept Nephrol Dialysis & Transplantat, Vicenza, Italy
关键词
Acute kidney failure; Cardiac surgery; Central venous pressure; Congestive kidney failure; DECOMPENSATED HEART-FAILURE; VENTILATED SEPTIC PATIENTS; VENA-CAVA DIAMETER; RENAL-FUNCTION; FLUID RESPONSIVENESS; MORTALITY; THERAPY; NOREPINEPHRINE; HEMODYNAMICS; REABSORPTION;
D O I
10.1093/icvts/ivw229
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute kidney injury (AKI) in cardiac surgery has traditionally been linked to reduced arterial perfusion. There is ongoing evidence that central venous pressure (CVP) has a pivotal role in precipitating acute renal dysfunction in cardiac medical and surgical settings. We can regard this AKI driven by systemic venous hypertension as 'kidney congestive failure'. In the cardiac surgery population as a whole, when the CVP value reaches the threshold of 14 mmHg in postoperative period, the risk of AKI increases 2-fold with an odds ratio (OR) of 1.99, 95% confidence interval (95% CI) of 1.16-3.40. In cardiac surgery subsets where venous hypertension is a hallmark feature, the incidence of AKI is higher (tricuspid disease 30%, carcinoid valve disease 22%). Even in the non-chronically congested coronary artery bypass population, CVP measured 6 h postoperatively showed significant association to renal failure: risk-adjusted OR for AKI was 5.5 (95% CI 1.93-15.5; P = 0.001) with every 5 mmHg rise in CVP for patients with CVP < 9 mmHg; for CVP increments of 5 mmHg above the threshold of 9 mmHg, the risk-adjusted OR for AKI was 1.3 (95% CI 1.01-1.65; P = 0.045). This and other clinical evidence are discussed along with the underlying pathophysiological mechanisms, involving the supremacy of volume receptors in regulating the autonomic output in hypervolaemia, and the regional effect of venous congestion on the nephron. The effect of CVP on renal function was found to be modulated by ventricular function class, aetiology and acuity of venous congestion. Evidence suggests that acute increases of CVP should be actively treated to avoid a deterioration of the renal function, particularly in patients with poor ventricular fraction. Besides, the practice of treating right heart failure with fluid loading should be avoided in favour of other ways to optimize haemodynamics in this setting, because of the detrimental effects on the kidney function.
引用
收藏
页码:800 / 805
页数:6
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