缺氧的原因及治疗──低氧血症与组织缺氧

低氧血症是指血液中含氧不足 ,主要表现为血氧分压与血氧饱和度下降 ,低氧血症是呼吸科常见危重症之一 ,也是呼吸衰竭的重要临床表现之一。组织缺氧与低氧血症是不同的二个概念 ,适当的 Ｐａ(Ｏ2 )只是组织器官进行正常氧合的条件之一 ,组织缺氧的严重程度有时也不能从Ｐａ(Ｏ2 )上得到良好的反映。呼吸支持治疗的最终目的是改善组织器官的氧合 ,对呼吸科医生来讲 ,一定要了解低氧血症与组织缺氧的关系 ,在适当提高血氧分压的同时兼顾重要脏器的氧合功能。1　正常组织器官氧合的必要条件组织器官氧供给是否充分取决于以下多种因素。①适当的…     

低氧血症与组织缺氧时细胞的损伤及其机制

氧为生命活动所必需。低氧血症是指各种原因所致的动脉血氧分压(partialpressureofarterialbloodoxygen ,PaO2 )低于同龄人的正常下限,PaO2的正常范围的计算公式为1 3.3～0 .0 4×年龄±0 .6 7kPa(即1 0 0 - 0 .3×年龄±5mmHg)。临床上常根据PaO2 的高低将低氧血症分为轻度[PaO2 高于8.0kPa (6 0mmHg ) ]、中度[PaO2 在5 .3～8.0kPa(6 0mmHg ) ]和重度[PaO2 低于5 .3kPa(4 0mmHg) ]。组织缺氧(tissuehypoxia)与低氧血症是两个相关但并不等同的概念,它是指组织细胞得不到充足的氧,或不能充分利用氧,导致组织细胞的代谢、功能,甚至形…     

低氧血症与氧疗

急性低氧血症急性低氧血症与引起低氧血症(hypoxe-mia,HXA)的原发病或伴随的障碍如 CO_2潴留在临床表现上很难区别,脑功能也比其他生命重要脏器先受到 HXA 损害。肺泡氧分压(P_AO_2)接近55mmHg 时,可有近期记忆改变,动脉氧分压(PaO_2)接近30mmHg 时,可能发生意识丧失。显然,有循环机能异常的人,即使 HXA     

低氧血症

低氧血症和水电解质失衡、酸碱紊乱同样常见。本文仅就低氧血症的病理生理、临床表现、实验室检查和治疗等问题作一阐述。     

低氧血症与血清肌钙蛋白

目的评价低氧血症患者血清TnT水平变化的临床意义。方法选取本院急诊住院的50例患者。患者血气分析示均有低氧血症存在，以往无冠心病史，本次入院时EKG排除心梗及心绞痛存在。结果TnT均有不同程度的升高，随着病情控制，TnT值恢复至正常。病情加重者，TnT回落减慢，或始终异常。结论TnT对临床病情的发展及预后有预测价值。     

低氧血症的原因与鉴别

缺氧是指任何原因所致的机体组织细胞得不到充足的氧供 ,或组织细胞不能很好地利用氧进行代谢活动的病理过程。根据缺氧的原因和血氧的变化可将缺氧分为低氧血症性缺氧、血液性缺氧、循环性缺氧和组织缺氧 4大类 ,其中低氧血症性缺氧是最常见的临床类型。低氧血症是指各种原因所致的动脉血氧分压[Ｐａ(Ｏ2 ) ]低于同龄人的正常下限。Ｐａ(Ｏ2 )正常范围为13 3- 0 0 4×年龄± 0 6 7ｋＰａ (10 0 - 0 3×年龄±5ｍｍＨｇ)。临床上常根据Ｐａ(Ｏ2 )高低将低氧血症分为轻度Ｐａ(Ｏ2 )正常下限～ 8 0ｋＰａ(6 0ｍｍＨｇ)、中度 8 0ｋＰａ >Ｐ…     

中性粒细胞凋亡与低氧血症

中性粒细胞是机体最主要的炎性反应细胞,其数量、功能和生命期限影响着炎性反应的发生、发展和转归。中性粒细胞主要通过凋亡被单核巨噬细胞识别、吞噬,不释放其细胞内毒性内容物,从而限制中性粒细胞介导的组织损伤、并促进炎性反应消散。如果中性粒细胞生存力延长,周围细胞或组织将会被破坏。中性粒细胞凋亡(neutrophil apoptosis,NA)由胞内死亡/存活信号路径的复杂网络介导并受一系列的细胞外刺激如     

急性肺栓塞低氧血症机制的初步探讨

目的：探讨急性肺栓塞通气灌注比例（Ｖ／Ｑ）失调、肺内分流、弥散损伤及右向左心内分流在低氧血症中各自所起的作用。方法：８例确诊为急性肺栓塞的患者，卧位休息１０分钟，行血流动力学检查，同时取动脉及混合静脉血，作血气分析；计算肺内分流及Ｖ／Ｑ。结果：患者出现症状３天内Ｘ线胸片无异常，３天后患者有局限性肺不张或小灶性浸润。血流动力学显示肺动脉平均压中、重度升高［平均５．１±１．１ｋＰａ（３８±８ｍｍＨｇ）］，肺血管阻力上升（平均７８．６±３２．８ｋＰａｓ／Ｌ），心脏指数降低［平均２．６±０．５Ｌ／（ｍｉｎｍ２）］。所有患者都有低氧血症［平均动脉氧分压７．１±０．９ｋＰａ（５３±７ｍｍＨｇ）］和低碳酸血症。肺泡动脉氧差增宽，分流量增加，死腔量升高。结论：急性肺栓塞的低氧血症主要原因为Ｖ／Ｑ失调，同时发生的心功能抑制也进一步促进了低氧血症，而肺内分流只在有肺膨胀不全或肺容积丧失时才起作用。     

Hypoxemia in acute pulmonary embolism

Most patients with severe, acute pulmonary embolism (PE) have arterial hypoxemia. To further define the respective roles of ventilation to perfusion (VA/Q) mismatch and intrapulmonary shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean PaO2, 67 +/- 11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVA/QT 16.6 +/- 5.1 percent) was present in all patients. The relative contributions of VA/Q mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study. Although all patients had some degree of VA/Q mismatch, the two patients studied early (ie, less than 48 hours following acute PE) had normal chest x-ray film findings and no significant shunt; VA/Q mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 +/- 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute PE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.     

Hypoxemia and elevated tachykinins in rat monocrotaline pneumotoxicity

This study was performed to test whether monocrotaline (MCT)-induced early airway dysfunction and gas exchange abnormalities result in arterial hypoxemia. Thirty young male Sprague-Dawley rats were divided into four groups: control, MCT1, MCT2, and MCT3. Each of the control animals was injected (subcutaneously) with saline; each of the MCT rats was injected with MCT (60 mg/kg, subcutaneously). The rats were tested 1 (MCT1), 2 (MCT2), or 3 (MCT3) weeks after MCT injection. Two days before each animal was tested, it was anesthetized with sodium pentobarbital, and its carotid artery was chronically cannulated. Blood was sampled from the arterial catheter of the conscious rat, and blood gases and pH were measured. Pulmonary arterial pressure (Ppa) was determined in the anesthetized, open chest animal. Heart weight was measured and a weight ratio obtained of right ventricle (RV) to left ventricle plus septum (LV+S). The amount of lung substance P and airway neutral endopeptidase (NEP) activity were also measured. MCT significantly decreased arterial oxygen tension (Pao2) and increased the RV/(LV+S) weight ratio 2 and 3 weeks after administration, whereas it did not significantly increase Ppa until 3 weeks after injection. MCT significantly increased lung substance P levels and decreased airway NEP activities 1–3 weeks after administration. These data suggest that tachykinins cause hypoxemia and RV hypertrophy: then hypoxia may augment the development of pulmonary hypertension. Offprint requests to: Yih-Loong Lai