Mechanical ventilation and acute renal failure

被引:161
作者
Kuiper, JW [1 ]
Groeneveld, ABJ
Slutsky, AS
Plötz, FB
机构
[1] Vrije Univ Amsterdam Med Ctr, Dept Pediat Intens Care, Amsterdam, Netherlands
[2] Univ Toronto, St Michaels Hosp, Div Resp Med, Interdept Div Crit Care, Toronto, ON M5B 1W8, Canada
[3] Univ Toronto, Dept Med, Toronto, ON M5B 1W8, Canada
关键词
acute renal failure; mechanical ventilation; multiple system organ failure; apoptosis; acute respiratory distress syndrome; sepsis;
D O I
10.1097/01.CCM.0000165808.30416.EF
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objective. To review the current literature on possible mechanisms by which mechanical ventilation may initiate or aggravate acute renal failure. Data Source: A Medline database and references from identified articles were used to perform a literature search relating to mechanical ventilation and acute renal failure. Data Synthesis. Acute renal failure may be initiated or aggravated by mechanical ventilation through three different mechanisms. First, strategies such as permissive hypercapnia or permissive hypoxemia may compromise renal blood flow. Second, through effects on cardiac output, mechanical ventilation affects systemic and renal hemodynamics. Third, mechanical ventilation may cause biotrauma - a pulmonary inflammatory reaction that may generate systemic release of inflammatory mediators. The harmful effects of mechanical ventilation may become more significant when a comorbidity is present. In these situations, it is more difficult to maintain normal gas exchange, and moderate arterial hypoxemia and hypercapnia are often accepted. Renal blood flow is compromised due to a decreased cardiac output as a consequence of high intrathoracic pressures. Furthermore, the effects of biotrauma are not limited to the lungs but may lead to a systemic inflammatory reaction. Conclusions: The development of acute renal failure during mechanical ventilation likely represents a multifactorial process that may become more important in the presence of comorbidities. Development of optimal interventional strategies requires an understanding of physiologic principles and greater insight into the precise molecular and cellular mechanisms that may also play a role.
引用
收藏
页码:1408 / 1415
页数:8
相关论文
共 142 条
[31]   From ventilator-induced lung injury to multiple organ dysfunction? [J].
Dreyfuss, D ;
Saumon, G .
INTENSIVE CARE MEDICINE, 1998, 24 (02) :102-104
[32]   THE EFFECTS OF CONTINUOUS PRESSURE BREATHING ON KIDNEY FUNCTION [J].
DRURY, DR ;
HENRY, JP ;
GOODMAN, J .
JOURNAL OF CLINICAL INVESTIGATION, 1947, 26 (05) :945-951
[33]  
EPSTEIN FH, 1994, ANN NY ACAD SCI, V718, P72
[34]   Diagnosis and treatment of acute tubular necrosis [J].
Esson, ML ;
Schrier, RW .
ANNALS OF INTERNAL MEDICINE, 2002, 137 (09) :744-752
[35]   ABNORMALITIES OF SODIUM AND H2O HANDLING IN CHRONIC OBSTRUCTIVE LUNG-DISEASE [J].
FARBER, MO ;
ROBERTS, LR ;
WEINBERGER, MH ;
ROBERTSON, GL ;
FINEBERG, NS ;
MANFREDI, F .
ARCHIVES OF INTERNAL MEDICINE, 1982, 142 (07) :1326-1330
[36]   INTERACTIONS BETWEEN HEMODYNAMIC AND HORMONAL MODIFICATIONS DURING PEEP-INDUCED ANTIDIURESIS AND ANTINATRIURESIS [J].
FARGE, D ;
DELACOUSSAYE, JE ;
BELOUCIF, S ;
FRATACCI, MD ;
PAYEN, DM .
CHEST, 1995, 107 (04) :1095-1100
[37]   ROLE OF SINOAORTIC BARORECEPTORS IN INITIATING THE RENAL RESPONSE TO CONTINUOUS POSITIVE-PRESSURE VENTILATION IN THE DOG [J].
FEWELL, JE ;
BOND, GC .
ANESTHESIOLOGY, 1980, 52 (05) :408-413
[38]  
FEWELL JE, 1979, P SOC EXP BIOL MED, V161, P574
[39]   CONTINUOUS POSITIVE-PRESSURE VENTILATION DECREASES RIGHT AND LEFT-VENTRICULAR END-DIASTOLIC VOLUMES IN THE DOG [J].
FEWELL, JE ;
ABENDSCHEIN, DR ;
CARLSON, CJ ;
MURRAY, JF ;
RAPAPORT, E .
CIRCULATION RESEARCH, 1980, 46 (01) :125-132
[40]   KIDNEY FUNCTION IN COR PULMONALE - PARTICULAR CONSIDERATION OF CHANGES IN RENAL HEMODYNAMICS AND SODIUM EXCRETION DURING VARIATION IN LEVEL OF OXYGENATION [J].
FISHMAN, AP ;
MAXWELL, MH ;
CROWDER, CH ;
MORALES, P .
CIRCULATION, 1951, 3 (05) :703-721