VISCERAL, HEMATOLOGIC AND BACTERIOLOGICAL CHANGES AND NEUROLOGIC OUTCOME AFTER CARDIAC-ARREST IN DOGS - THE VISCERAL POSTRESUSCITATION SYNDROME

被引:61
作者
CERCHIARI, EL [1 ]
SAFAR, P [1 ]
KLEIN, E [1 ]
DIVEN, W [1 ]
机构
[1] UNIV PITTSBURGH,INT RESUSCITAT RES CTR,DEPT ANESTHESIOL,3434 5TH AVE,PITTSBURGH,PA 15260
关键词
CARDIOPULMONARY RESUSCITATION; CEREBRAL RESUSCITATION; COAGULATION; HEPATIC FAILURE; RENAL FAILURE; SEPTICEMIA;
D O I
10.1016/0300-9572(93)90090-D
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
We studied the post-resuscitation syndrome in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (less-than-or-equal-to 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We reported previously, in the same dogs, no difference in resuscitability, mortality, or neurologic outcome between the three insult groups. There was no pulmonary dysfunction, but postarrest cardiovascular failure, of greater severity in the 12.5 min arrest group. This report concerns renal, hematologic, hepatic and bacteriologic changes. Renal function recovered within 1 h after arrest, without permanent dysfunction. Clotting derangements at 1-24 h postarrest reflect transient disseminated intravascular coagulation with hypocoagulability, more severe after longer arrests, which resolved by 24 h after arrest. Hepatic dysfunction was transient but more severe in the animals that did not recover consciousness and correlated with neurologic dysfunction, but not with brain histologic damage. Bacteremia was present in all animals postarrest. We conclude that in the previously healthy organism after cardiac arrest of 7.5-12.5 min no flow, visceral and hematologic changes, although transient, can retard neurologic recovery.
引用
收藏
页码:119 / 136
页数:18
相关论文
共 40 条
[31]  
Snedecor, Cochran, Statistical methods, (1973)
[32]  
Shoemaker, Shock states: pathophysiology, monitoring, outcome prediction and therapy, Textbook of critical care, pp. 977-993, (1989)
[33]  
Fath, Cyz, Konstantinides, Alden, Ascher, Bianco, Foyer, Cerra, Alterations in amino acid clearance during ischemia predict hepatocellular ATP changes, Surgery, 98, pp. 396-404, (1985)
[34]  
Siegel, The physiologic and metabolic basis for critical care of the seriously ill septic patient, Critical care: state of the art, 7, pp. 63-91, (1986)
[35]  
Rosen, Yoshimura, Hodgman, Fischer, Plasma amino acid patterns in hepatic encephalopathy of differing etiology, Gastroenterology, 72, pp. 483-487, (1977)
[36]  
Deitch, Potential role of gut failure and bacterial translocation as promoters and potentiators of the multiple organ failure syndrome, Multiple organ failure, pp. 297-325, (1989)
[37]  
Carter, Essentials of veterinary bacteriology and micology, (1982)
[38]  
Adams, Feustel, Donnelly, Dutton, Hypoxia, hyperammonemia and cerebrospinal fluid metabolites, Adv Shock Res, 1, pp. 209-220, (1979)
[39]  
Fischer, Rosen, Ebeid, James, Keane, Soeters, The effect of normalization of plasma amino acids on hepatic encephalopathy in man, Surgery, 80, pp. 77-91, (1976)
[40]  
Cerra, Border, McMenamy, Siegel, Multiple systems organ failure, Pathophysiology of shock, anoxia and ischemia, pp. 254-270, (1982)