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获得性免疫缺陷综合征和卡氏肺孢子虫肺炎患者的呼吸衰竭

Respiratory failure in patients with acquired immunodeficiency syndrome and Pneumocystis carinii pneumonia.

作者信息

Maxfield R A, Sorkin I B, Fazzini E P, Rapoport D M, Stenson W M, Goldring R M

出版信息

Crit Care Med. 1986 May;14(5):443-9. doi: 10.1097/00003246-198605000-00001.

DOI:10.1097/00003246-198605000-00001
PMID:3516574
Abstract

Seven patients with acquired immunodeficiency syndrome (AIDS) and Pneumocystis carinii pneumonia were studied to define the pathophysiology of their respiratory failure. The patients had fever, cough, dyspnea, hypoxemia, and diffuse infiltrates on chest x-ray. Biopsies revealed a spectrum of alveolar filling, interstitial edema and infiltration, and fibrosis. The patients were studied on mechanical ventilation to assess the effect of positive end-expiratory pressure (PEEP) and supplemental oxygen on shunt fraction. Mean anatomic shunt (measured on 100% oxygen) was 34 +/- 8%, which increased significantly (p less than .001) to 43 +/- 9% when the FIO2 was decreased to 40% to 60% (physiologic shunt), indicating ventilation/perfusion (V/Q) imbalance or impaired diffusion. Increasing PEEP by 9 +/- 2 cm H2O reduced the anatomic shunt to 30 +/- 7% (p less than .01) and the physiologic shunt to 37 +/- 7% (p less than .02). There was a similar decrease in anatomic and physiologic shunts in five studies, a greater decrease in physiologic shunt in four, and a greater decrease in anatomic shunt in two. Evidence of alveolar recruitment with PEEP, measured by an increase in static thoracic compliance, was found in only one study. There was no correlation between the effect of PEEP on compliance and its effect on shunt. The data suggest that in patients with AIDS and P. carinii pneumonia, PEEP can decrease shunt by reducing the anatomic shunt, improving V/Q imbalance, and converting areas of anatomic shunt to areas of low V/Q. P. carinii pneumonia in patients with AIDS can produce a clinical and pathophysiologic pattern similar to that described in the adult respiratory distress syndrome.

摘要

对7例获得性免疫缺陷综合征(AIDS)合并卡氏肺孢子虫肺炎患者进行研究,以明确其呼吸衰竭的病理生理机制。这些患者有发热、咳嗽、呼吸困难、低氧血症,胸部X线显示弥漫性浸润。活检显示肺泡填充、间质水肿和浸润以及纤维化的一系列表现。对患者进行机械通气研究,以评估呼气末正压(PEEP)和补充氧气对分流分数的影响。平均解剖分流(在吸入100%氧气时测量)为34±8%,当FIO2降至40%至60%(生理分流)时,显著增加(p<0.001)至43±9%,表明通气/灌注(V/Q)失衡或弥散受损。将PEEP增加9±2 cm H2O可使解剖分流降至30±7%(p<0.01),生理分流降至37±7%(p<0.02)。在五项研究中解剖分流和生理分流有类似程度的降低,四项研究中生理分流降低幅度更大,两项研究中解剖分流降低幅度更大。仅在一项研究中发现通过静态胸廓顺应性增加来衡量的PEEP使肺泡复张的证据。PEEP对顺应性的影响与其对分流的影响之间无相关性。数据表明,在AIDS合并卡氏肺孢子虫肺炎患者中,PEEP可通过减少解剖分流、改善V/Q失衡以及将解剖分流区域转变为低V/Q区域来降低分流。AIDS患者的卡氏肺孢子虫肺炎可产生与成人呼吸窘迫综合征中描述的类似的临床和病理生理模式。

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A sequential ultrastructural study of rat lungs infected with Pneumocystis carinii to investigate the appearances of the organism, its relationships and its effects on pneumocytes.
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Int J Exp Pathol. 1990 Dec;71(6):895-904.
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