Gambardella Ivancarmine, Gaudino Mario, Ronco Claudio, Lau Christopher, Ivascu Natalia, Girardi Leonard N
Department of Cardiothoracic Surgery, New York Weill Cornell Medical Center, New York, NY, USA
Department of Cardiothoracic Surgery, New York Weill Cornell Medical Center, New York, NY, USA.
Interact Cardiovasc Thorac Surg. 2016 Nov;23(5):800-805. doi: 10.1093/icvts/ivw229. Epub 2016 Jul 15.
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.
心脏手术中的急性肾损伤（AKI）传统上一直与动脉灌注减少有关。目前有证据表明，中心静脉压（CVP）在心脏内科和外科环境中引发急性肾功能障碍方面起着关键作用。我们可以将这种由系统性静脉高压驱动的AKI视为“肾性充血性衰竭”。在整个心脏手术人群中，术后当CVP值达到14 mmHg阈值时，AKI风险增加2倍，优势比（OR）为1.99，95%置信区间（95%CI）为1.16 - 3.40。在以静脉高压为标志性特征的心脏手术亚组中，AKI的发生率更高（三尖瓣疾病为30%，类癌瓣膜病为22%）。即使在非慢性充血的冠状动脉搭桥人群中，术后6小时测量的CVP与肾衰竭也显示出显著关联：对于CVP<9 mmHg的患者，CVP每升高5 mmHg，AKI的风险调整后OR为5.5（95%CI 1.93 - 15.5；P = 0.001）；对于CVP高于9 mmHg阈值每增加5 mmHg，AKI的风险调整后OR为1.3（95%CI 1.01 - 1.65；P = 0.045）。本文将讨论这一情况及其他临床证据，以及潜在的病理生理机制，包括容量感受器在高血容量时调节自主神经输出方面的主导作用，以及静脉充血对肾单位的局部影响。研究发现CVP对肾功能的影响受心室功能分级、静脉充血的病因和严重程度的调节。有证据表明，应积极治疗CVP的急性升高以避免肾功能恶化，特别是在心室射血分数较差的患者中。此外，由于对肾功能有不利影响，应避免通过液体负荷治疗右心衰竭的做法，而应采用其他方法来优化这种情况下的血流动力学。
