Bersten A D, Gnidec A A, Rutledge F S, Sibbald W J
Richard Ivey Critical Care Trauma Centre, University of Western Ontario, London, Canada.
Am Rev Respir Dis. 1990 May;141(5 Pt 1):1198-208. doi: 10.1164/ajrccm/141.5_Pt_1.1198.
Changes in organ blood flow (Q) produced by 20 cm H2O positive end-expiratory pressure (PEEP) were measured before and after the induction of hyperdynamic sepsis in nine unanesthetized sheep. During the baseline nonseptic study, PEEP was associated with a 9% fall in thermodilution-measured systemic Q, although arterial perfusing pressures were unaffected. Concurrently, microsphere-derived Q was maintained to the brain and heart, but fell to liver, spleen, pancreas, kidney, large intestine, and gastrocnemius. Twenty-four to 36 h after cecal ligation and perforation, a pre-PEEP septic study demonstrated an increase in all of the cardiac index (CI) (+43%) and systemic O2 delivery (+54%) when compared with the nonseptic study, whereas whole-body O2 extraction (-30%) was depressed. Although PEEP depressed systemic Q (-17%) during the septic study to a greater extent than during the nonseptic study (p less than 0.02), absolute organ Q fell only to pancreas, liver, and spleen. Relative to the simultaneous fall in the CI, Q to some splanchnic organs was not depressed by PEEP to the same magnitude in the septic as in the nonseptic study. When an infusion of Ringer's lactate (993 +/- 295 ml) subsequently restored systemic Q to pre-PEEP septic levels, individual flows that had been depressed by PEEP were not restored. Furthermore, Q-kidney continued to fall, such that the postfluid Q-kidney (-19%) was significantly less than was demonstrated in the pre-PEEP septic study. We postulate that differences noted in the distribution of organ Q between the nonseptic and hyperdynamic septic studies after the application of PEEP were secondary to the vasculopathy of sepsis and/or an alteration in the function of specific organ microcirculations. However, these data do not address whether the changes in organ Q distribution after a PEEP-mediated depression in systemic Q during sepsis significantly restricted tissue DO2. The inability to acutely reverse the PEEP-mediated changes in organ Q after restoring systemic Q by a fluid infusion also suggests the need to evaluate alternative methods of support to organ Q in acute respiratory failure secondary to sepsis when the addition of PEEP acutely depresses systemic DO2.
在9只未麻醉的绵羊中,测量了20 cm H₂O呼气末正压(PEEP)诱导的高动力性脓毒症前后器官血流(Q)的变化。在基线非脓毒症研究期间,尽管动脉灌注压未受影响,但PEEP使热稀释法测量的全身Q下降了9%。同时,微球衍生的Q在脑和心脏得以维持,但在肝脏、脾脏、胰腺、肾脏、大肠和腓肠肌中下降。在盲肠结扎和穿孔后24至36小时,一项PEEP前的脓毒症研究表明,与非脓毒症研究相比,所有心脏指数(CI)(+43%)和全身氧输送(+54%)均增加,而全身氧摄取(-30%)降低。尽管在脓毒症研究期间PEEP使全身Q降低(-17%)的程度大于非脓毒症研究期间(p<0.02),但绝对器官Q仅在胰腺、肝脏和脾脏中下降。相对于CI同时下降,在脓毒症研究中,与非脓毒症研究相比,PEEP对一些内脏器官Q的降低幅度不同。当输注乳酸林格液(993±295 ml)随后使全身Q恢复到PEEP前的脓毒症水平时,先前被PEEP降低的个体血流并未恢复。此外,肾血流持续下降,使得补液后肾血流(-19%)显著低于PEEP前脓毒症研究中的水平。我们推测,应用PEEP后非脓毒症和高动力性脓毒症研究中器官Q分布的差异继发于脓毒症的血管病变和/或特定器官微循环功能的改变。然而,这些数据并未涉及脓毒症期间PEEP介导的全身Q降低后器官Q分布的变化是否显著限制了组织氧输送。通过补液恢复全身Q后无法急性逆转PEEP介导的器官Q变化也表明,当添加PEEP急性降低全身氧输送时,需要评估脓毒症继发急性呼吸衰竭时支持器官Q的替代方法。