单肺通气时氧化应激反应的研究进展

单肺通气广泛应用于心胸外科手术中.但单/双肺通气模式的转变能诱发明显的氧化应激反应,可进一步损伤肺和心脏等重要器官.卤族类麻醉药能够减少肺缺血再灌注时氧自由基的产生,静脉麻醉药丙泊酚的抗氧化特性也已得到证实,因此均具有一定的抗氧化损伤作用.本文综合分析了单肺通气时氧化应激反应及麻醉药物时其影响的研究进展,以期减少术后并发症的发生.     

静脉输注高氧液对单肺通气期间低氧血症的治疗作用

目的:探讨静脉输注高氧液对家猪OLV时肺内分流与氧合的影响.方法:30头健康家猪(25～35 kg)建立OLV模型后,随机分为2组,每组15头,即高氧液组(H组)和对照组(C组),H组动物在单肺通气后经右静内静脉以15 mL·kg-1·h-1的速度恒速输入高氧液,C组动物则以相同的方式和速度输入等量的乳酸林格氏液.分别于双肺通气时、单肺通气30 min、单肺通气60 min时抽取动脉血和混合静脉血做血气分析,并计算肺内分流率(Qs/Qt％),同时记录血流动力学指标.结果:与双肺通气时相比,单肺通气时两组PaO2,SaO2,PvO2和SvO2均显著降低,而Qs/Qt％明显升高(P＜0.01).单肺通气30 min以及60 min后,H组的PaO2,SaO2,PvO2和SvO2等指标均显著高于C组(P＜0.05),而对于肺内分流率(Qs/Qt％),两组间比较差异无统计学意义.结论:静脉输注高氧液虽然对肺内分流影响不大,却能够明显改善氧合,治疗单肺通气引起的低氧血症.     

慢性高山病低氧通气反应降低与肺功能缺损

对１４例慢性高山病（ＣＭＳ）患者的低氧肺泡通气不足的发病机理和肺功能作了研究。与对照组比较,ＣＭＳ组的ＰＥＴＣＯ２高,ＶＴ低,低氧通气反应（ＨＶＲ）Ａ值低;吸入高浓度Ｏ２后,ＣＭＳ已降低的ＨＶＲ。ＣＭＳ的ＦＥＶ１／ＶＣ比值降低并加重动脉低氧血症。结果表明：周围性ＨＶＲ降低和中枢性低氧通气抑制是引起高原低氧肺泡通气不足的因素。而肺泡通气不足与阻塞性肺疾病是导致ＣＭＳ发生的主要原因。     

容量与压力控制通气模式对胸科手术单肺通气肺内分流及氧合的影响

目的:为观察术前肺功能正常的开胸手术病人在单肺通气(OLV)期间,定压控制通气模式(PCV)和定容控制通气模式(VCV)对气道压力、肺内分流及氧合的影响.方法:选择40例术前肺功能正常进行开胸手术的病人,随机分为A、B两组.A组:单肺通气采用VCV模式30 min后转换为PCV模式.B组:单肺通气采用PCV模式30 min后转换为VCV模式.在麻醉前(TI)、单肺通气前(T2),容量控制通气(压力控制通气)30min(T3)、转换为压力控制通气(容量控制通气)30min(T4)四个时间段测气道压力和采动脉及混合静脉血行血气分析及计算肺内分流.结果:发现;无论VCV还是PCV在单肺通气期间动脉血氧分压(PaO2)无统计学意义(P=0.534),两组间的肺内分流量(Qs/Qt)比较差异无显著性(p>0.05),PCV气道压力比VCV低((P<0.01).结论:肺功能正常的患者在OLV期间,PCV模式与VCV模式比较并不能提高氧合作用,但PCV模式气道压力低,有利于减少气道损伤.     

离子通道在肺动脉的分布及在低氧肺血管收缩反应中的作用

低氧性肺血管收缩反应（HPV）是指在急性低氧时,肺泡氧分压降到某一临界值,肺血管发生的快速、可逆的收缩反应,以纠正肺泡通气／灌流的不匹配。HPV的发生与肺动脉平滑肌细胞上K^＋、Ca^2＋、Cl^-通道的状态密切相关,而这些通道在不同部位的肺动脉上分布存在差异,因此不同部位的肺动脉在低氧中所表现的收缩反应程度也不同,本综述将对上述通道在肺动脉上的分布特点及其在HPV中的作用做一总结。     

单肺通气时两种通气模式对PetCO2与PaCO2相关性的影响

目的：探讨胸科开胸手术单肺通气定容通气模式下和定压通气模式下PetC02（呼气末二氧化碳分压）与PaCO2（动脉二氧化碳分压）的相关性。方法：选择40例择期左侧开胸手术单肺通气成年患者,ASAI～II级,随机分为A组（n=20）采用VCV（容量控制通气）模式通气、B组（n=20）采用PCV（压力控制通气）模式通气。比较两组各时段的PaCO2和PetCO2的差异及相关性。结果：经统计学分析,除第一时间点,两组同一时间点的PetC02比较及PaCO2比较差异均有统计学意义（P〈O．05）,A组PetC02四个时间点比较及PaCO2四个时间点比较差异均有有统计学意义（P〈0．001）,B组除PetCO2第三与第四个时间点比较差异无统计学意义外,余PetCO2各时间点相比较及PaCO2各时间点相比较差异均有统计学意义（P〈0．05）。单肺通气定压通气模式下PetCO2与PaCO2在各个时间点的相关系数均大于定容通气模式时。无论是定容还是定压通气模式,单肺通气时间越长,其PetCO2与PaCOz的相关系数也越小。结论：1．同双肺通气相比,单肺通气时定压通气模式下PaCO2及PetCO2的改变小于定容通气模式时。2．单肺通气时,定压通气模式下PetCO2与PaCO2的相关性好于定容通气模式时。3．在这两种通气模式下PetCO2与PaCO2的相关性与单肺通气的时间成反比。     

石河子大学医学院第一附属医院

目的：探讨胸科开胸手术单肺通气定容通气模式下和定压通气模式下PetCO2（呼气末二氧化碳分压）与PaCO2（动脉二氧化 碳分压）的相关性。方法：选择40 例择期左侧开胸手术单肺通气成年患者,ASAⅠ～Ⅱ级,随机分为A组（n=20）采用VCV（容量 控制通气）模式通气、B组（n=20）采用PCV（压力控制通气）模式通气。比较两组各时段的PaCO2和PetCO2的差异及相关性。结 果：经统计学分析,除第一时间点,两组同一时间点的PetCO2比较及PaCO2比较差异均有统计学意义(P＜0.05),A 组PetCO2四个 时间点比较及PaCO2四个时间点比较差异均有有统计学意义(P＜0.001),B组除PetCO2第三与第四个时间点比较差异无统计学 意义外,余PetCO2各时间点相比较及PaCO2各时间点相比较差异均有统计学意义(P<0.05)。单肺通气定压通气模式下PetCO2与 PaCO2在各个时间点的相关系数均大于定容通气模式时。无论是定容还是定压通气模式,单肺通气时间越长,其PetCO2与PaCO2 的相关系数也越小。结论：1.同双肺通气相比,单肺通气时定压通气模式下PaCO2及PetCO2的改变小于定容通气模式时。2.单肺 通气时,定压通气模式下PetCO2与PaCO2的相关性好于定容通气模式时。3.在这两种通气模式下PetCO2与PaCO2的相关性与单 肺通气的时间成反比。     

三种兔单肺通气模型的比较

目的采用三种方法建立兔单肺通气模型并比较其效果。方法日本大耳白兔30只,随机分为3组(即A、B、C组)各10个,分别采用自制双腔气管导管法、左主支气管结扎法和插管过深法。呼吸机通气参数为:FiO21.0,RR 40/min,VT 10 mL/kg。单肺通气2 h后恢复双肺通气。记录各组单肺通气实施的一次成功率、总成功率、从气管切开开始到单肺通气实施所需要的时间、动物失血量。实验结束后开胸测量兔气管、左主支气管、右主支气管的长度和内径。结果各组进入实验的动物数分别为10、6、8只。与B、C组比较,A组一次成功率和总成功率高,所需时间明显较少(P<0.01),且出血量明显少于B组(P<0.01)。结论采用自制双腔气管导管能迅速有效的建立单肺通气模型,是用于研究与单肺通气相关病理生理机制的理想模型。     

糖尿病合并侵袭性肺真菌感染的危险因素及预后分析

目的:分析糖尿病合并侵袭性肺真菌感染(IPFI)的危险因素及预后。方法:选取我院收治的糖尿病合并IPFI患者51例作为观察组,选取同期收治的糖尿病未合并IPFI患者49例作为对照组,对两组资料进行回顾性分析,通过多因素Logistic回归分析侵袭性肺真菌感染的危险因素。结果:白蛋白、血红蛋白、住院时间、广谱抗生素使用时间、体内保留导管、有创机械通气、长期糖皮质激素使用均是侵袭肺真菌感染的危险因素,有统计学意义(P0.05)。对单因素相关分析结果进行筛选,选择P0.05者,进行多因素Logistic回归分析,根据向后剔除法筛选变量,结果显示,低蛋白血症、贫血、长期使用广谱抗生素、有创机械通气均是侵袭性肺部真菌感染的独立危险因素,有统计学意义(P0.05)。结论:糖尿病合并侵袭性肺真菌感染的危险因素较多,预后较差,因此需要有针对性的预防工作和适宜的处理方法。     

呼末二氧化碳监测在ERCP麻醉中预防麻醉期间低氧血症应用效果

摘要 目的：探讨呼末二氧化碳监测在内镜下经胰胆管造影（ERCP）麻醉中预防麻醉期间低氧血症应用效果。方法：选择2022年1月-2023年6月本院-行ERCP治疗的300例患者,用随机数表法分为试验组（n=150）和对照组（n=150）。对照组给予行常规心电图、血压和血氧饱和度监测,试验组在对照组基础上行呼末二氧化碳监测。比较两组一般资料、低氧血症、呼吸暂停、面罩加压给氧及改变头部姿势发生情况。结果：两组一般资料进行比较,无统计学差异（P>0.05）;试验组低氧血症、呼吸暂停、面罩加压给氧均显著低于对照组,改变头部姿势发生率显著高于对照组,两组比较有统计学意义（P<0.05）。结论：ERCP麻醉患者中使用呼末二氧化碳监测可实时指导对患者进行辅助呼吸处理,降低ERCP 麻醉期间低氧血症的发生率和面罩加压给氧率。     

Pulmonary embolization causes hypoxemia by redistributing regional blood flow without changing ventilation

To explore mechanisms of hypoxemia after acutepulmonary embolism, we measured regional pulmonary blood flow andalveolar ventilation before and after embolization with 780-µm beadsin five anesthetized, mechanically ventilated pigs. Regionalventilation and perfusion were determined in~2.0-cm³ lung volumes by using1-µm-diameter aerosolized and 15-µm-diameter injected fluorescentmicrospheres. Hypoxemia after embolization resulted from increasedperfusion to regions with low ventilation-to-perfusion ratios.Embolization caused an increase in perfusion heterogeneity and a fallin the correlation between ventilation and perfusion. Correlationbetween regional ventilation pre- and postembolization was greater thancorrelation between regional perfusion pre- and postembolization. Themajority of regional ventilation-to-perfusion ratio heterogeneity wasattributable to changes in regional perfusion. Regional perfusionredistribution without compensatory changes in regional ventilation isresponsible for hypoxemia after pulmonary vascular embolization in pigs.

     

Hypoxemia, atelectasis, and the elevation of arterial pressure and heart rate in paralyzed artificially ventilated rat.

Rats prepared while anesthetized with halothane, ether or pentobarbital, subsequently paralyzed with curare, and maintained with or without anesthetic, by artificial ventilation with room air are hypoxemic in association with elevated arterial pressures and heart rates. The hypoxemia can occur with normal Pa_CO2, is associated with a marked increase in the alveolar-arterial P_O2 difference, and is not reversed by hyperventilation or hyperinflation. The lungs, visualized directly through a thoracotomy during ing artificial ventilation, are segmentally collapsed and at postmortem demonstrate focal and diffuse signs of atelectasis. Hypoxemia and an elevation of the alveolar-arterial P_O2 difference occur within 20 minutes after the onset of anesthesia, prior to paralysis. We conclude that anesthetized rats develop atelectasis soon after the onset of anesthesia. The atelectasis, and resultant hypoxemia persist during subsequent paralysis despite an adequate minute volume and absence of anesthesia. Despite atelectasis, blood gases, arterial pressures and heart rates may be maintained near normal values by ventilation of paralyzed rats with 50% O₂ and 50% N₂.     

Noninvasive Measurement of Carbon Dioxide during One-Lung Ventilation with Low Tidal Volume for Two Hours: End-Tidal versus Transcutaneous Techniques

BackgroundThere may be significant difference between measurement of end-tidal carbon dioxide partial pressure (PetCO₂) and arterial carbon dioxide partial pressure (PaCO₂) during one-lung ventilation with low tidal volume for thoracic surgeries. Transcutaneous carbon dioxide partial pressure (PtcCO₂) monitoring can be used continuously to evaluate PaCO₂ in a noninvasive fashion. In this study, we compared the accuracy between PetCO₂ and PtcCO₂ in predicting PaCO₂ during prolonged one-lung ventilation with low tidal volume for thoracic surgeries.MethodsEighteen adult patients who underwent thoracic surgeries with one-lung ventilation longer than two hours were included in this study. Their PetCO₂, PtcCO₂, and PaCO₂ values were collected at five time points before and during one-lung ventilation. Agreement among measures was evaluated by Bland-Altman analysis.ResultsNinety sample sets were obtained. The bias and precision when PtcCO₂ and PaCO₂ were compared were 4.1 ± 6.5 mmHg during two-lung ventilation and 2.9 ± 6.1 mmHg during one-lung ventilation. Those when PetCO₂ and PaCO₂ were compared were -11.8 ± 6.4 mmHg during two-lung ventilation and -11.8 ± 4.9 mmHg during one-lung ventilation. The differences between PtcCO₂ and PaCO₂ were significantly lower than those between PetCO₂ and PaCO₂ at all five time-points (p < 0.05).ConclusionsPtcCO₂ monitoring was more accurate for predicting PaCO₂ levels during prolonged one-lung ventilation with low tidal volume for patients undergoing thoracic surgeries.     

NT-pro-BNP during hypoglycemia and hypoxemia in normal subjects: impact of renin-angiotensin system activity.

Brain-derived natriuretic peptide (BNP) is a cardioprotective peptide released, together with the inactive NH(2)-terminal part of its prohormone (NT-pro-BNP), in response to different kinds of myocardial stress. Hypoglycemia and hypoxemia are conditions that threaten cellular function and hence potentially stimulate BNP release. BNP interacts with the renin-angiotensin system (RAS). The aim of this study was, therefore, to explore if basal RAS activity has an impact on NT-pro-BNP concentrations during myocardial stress induced by hypoglycemia and hypoxemia. From a cohort of 303 healthy young men, 10 subjects with high-RAS activity and 10 subjects with low-RAS activity (age 26 +/- 1 yr; mean +/- SE) were studied in a single-blinded, randomized, counterbalanced, crossover study on three occasions separated by at least 3 wk: 1) hypoglycemia (mean nadir plasma glucose 2.7 +/- 0.5 mmol/l), 2) hypoxemia (mean nadir Po(2) 5.8 +/- 0.5 kPa), and 3) normoglycemic normoxia (control). NT-pro-BNP was measured at baseline, during the stimuli, and in the recovery phase. Hypoxemia was associated with a 9% increase in NT-pro-BNP from 2.2 +/- 1.5 pmol/l at baseline to 2.4 +/- 1.5 pmol/l during hypoxemia (P < 0.001). Hypoglycemia did not affect the NT-pro-BNP level. RAS activity had no impact on NT-pro-BNP levels during hypoglycemia and hypoxemia. Hypoxemia, but not hypoglycemia, stimulates NT-pro-BNP. This indicates that cardiac defense mechanisms against hypoglycemia, if any, are probably different from those against hypoxemia. Basal RAS activity had no impact on NT-pro-BNP levels.     

Canine renal vascular response to bilateral carotid occlusion during hypoxia

Chloralose-urethane anesthetized dogs were utilized to determine if hypoxemic potentiation of the baroreceptor-mediated increase in renal sympathetic nerve activity (RSNA) results in sufficient renal vascular vasoconstriction to reduce renal blood flow (RBF) during bilateral carotid occlusion (BCO). Additionally, hypercapnia and mechanical ventilation were randomly combined with hypoxemia during BCO to determine if further augmentation of renal vasoconstriction could be accomplished. BCO resulted in a similar increase in blood pressure (renal perfusion pressure) in all periods. RBF was not reduced significantly by BCO during any period even though renal vascular resistance was significantly increased by BCO during each period. When hypoxemia was combined with hypercapnia and mechanical ventilation simultaneously, there was a greater percentage increase in renal resistance with BCO. During BCO, when renal perfusion pressure was returned to control values by suprarenal aortic constriction, RBF remained unchanged and renal resistance decreased to control values. These results indicate that the BCO-induced increase in RSNA is relatively moderate and, even when potentiated by hypoxemia, hypercapnia, and mechanical ventilation, is not sufficient to reduce RBF in the presence of an increase in blood pressure and renal autoregulation.     

Closed loop control of oxgenation and ventilation

Closed loop control of oxygenation and ventilation during mechanical ventilatory support is essential for remote medical care in an austere environment. Closed loop control allows for expert systems to provide the current standard of care in the absence of on-site expertise. Ventilation may be controlled by simple systems incorporating patient height or by advanced systems incorporating measurements of end-tidal carbon dioxide (ETCO2) and pulmonary impedance. Oxygenation may be controlled by adjustments of inspired oxygen concentrations (FIO2) and positive end-expiratory pressure (PEEP) using pulse oximetry (SpO2) as the input. Control of oxygenation can prevent hypoxemia and has the potential to reduce oxygen requirements. A double closed loop system of oxygenation control including control of FIO2 via SpO2 and control of oxygen generation by a portable oxygen generator (POG) based on FIO2 and minute ventilation (VE) promises safety and efficiency. Remote control of ventilation and oxygenation is possible using existing technology.     

Level of ventilation influences the cardiovascular response to hypoxemia in lambs

Newborn animals of a number of species display a brisk increase in ventilation followed by a gradual drop toward or below baseline within minutes of exposure to acute hypoxemia. Heart rate and cardiac output (a determinant of systemic oxygen transport along with the arterial oxygen content) appear to follow a similar pattern, but whether or not the cardiovascular response is influenced by the respiratory response is unknown. We therefore carried out experiments in which the level of ventilation was controlled during normoxemia and hypoxemia to test the hypothesis that the level of ventilation influences the cardiovascular response to acute hypoxemia. Six lambs ranging in age from 17 to 22 days were anesthetized, tracheostomized, and instrumented for measurement of cardiovascular variables. A recovery period of at least 3 days was allowed before the study when each lamb was artificially ventilated with a mixture of 70% nitrous oxide and 30% oxygen in nitrogen. A control respiratory frequency (f) of 30 breaths per min was set and a control tidal volume (VT) was chosen to achieve normocapnia. Cardiovascular measurements were made during normoxemia and hypoxemia (FIO2 0.10) 5 min after f or VT was changed to simulate a decrease, no change, or an increase in ventilation. During normoxemia, the level of ventilation had little effect on the measured cardiovascular variables. At control levels of ventilation, hypoxemia caused an increase in cardiac output that was due solely to an increase in stroke volume as heart rate decreased; blood pressure was unchanged. Increasing ventilation during hypoxemia did not augment cardiac output or alter blood pressure as compared with that observed at control levels of ventilation. Decreasing ventilation during hypoxemia, however, decreased cardiac output due to a profound bradycardia; blood pressure increased significantly. Our data provide evidence that the level of ventilation significantly influences the cardiovascular response to hypoxemia in young lambs.     

Effect of hypoxemia on the renin-angiotensin-aldosterone system in humans

Hypoxemia was induced in five subjects older than 40 (group 1) and five younger than 35 yr (group 2) on normal and low-salt diets by having the subjects breathe hypoxic gas. The fractional inspired O2 of the hypoxic gas was regulated so that group 1 hemoglobin saturations fell to 90% for 1 h. Group 2 subjects had desaturation to 90% for 1 h followed by desaturation to 80% for a 2nd h. Plasma renin activity (PRA), angiotensin-converting enzyme activity (ACE), and plasma cortisol levels did not change during hypoxemia. Plasma aldosterone levels fell in both groups during the 1st h of hypoxemia. Decreases were greatest during salt restriction and were significant (P less than 0.01) for the combined groups. Plasma aldosterone levels plateaued during the 2nd h of more severe hypoxemia in group 2. Hepatic blood flow, measured by indocyanine green clearance, and the adrenal response to exogenous adrenocorticotropic hormone, measured by changes in plasma cortisol and aldosterone, were not changed by hypoxemia in group 2 subjects. These results indicate that plasma aldosterone falls during hypoxemia despite unchanged PRA, ACE, hepatic blood flow, and adrenal function.     

Pre-existing diseases of patients increase susceptibility to hypoxemia during gastrointestinal endoscopy

Hypoxemia is the most common adverse event that happened during gastrointestinal endoscopy. To estimate risk of hypoxemia prior to endoscopy, American Society of Anesthesiology (ASA) classification scores were used as a major predictive factor. But the accuracy of ASA scores for predicting hypoxemia incidence was doubted here, considering that the classification system ignores much information about general health status and fitness of patient that may contribute to hypoxemia. In this retrospective review of clinical data collected prospectively, the data on 4904 procedures were analyzed. The Pearson's chi-square test or the Fisher exact test was employed to analyze variance of categorical factors. Continuous variables were statistically evaluated using t-tests or Analysis of variance (ANOVA). As a result, only 245 (5.0%) of the enrolled 4904 patients were found to present hypoxemia during endoscopy. Multivariable logistic regressions revealed that independent risk factors for hypoxemia include high BMI (BMI 30 versus 20, Odd ratio: 1.52, 95% CI: 1.13-2.05; P?=?0.0098), hypertension (Odd ratio: 2.28, 95% CI: 1.44-3.60; P?=?0.0004), diabetes (Odd ratio: 2.37, 95% CI: 1.30-4.34; P?=?0.005), gastrointestinal diseases (Odd ratio: 1.77, 95% CI: 1.21-2.60; P?=?0.0033), heart diseases (Odd ratio: 1.97, 95% CI: 1.06-3.68; P?=?0.0325) and the procedures that combined esophagogastroduodenoscopy (EGD) and colonoscopy (Odd ratio: 4.84, 95% CI: 1.61-15.51; P?=?0.0292; EGD as reference). It is noteworthy that ASA classification scores were not included as an independent predictive factor, and susceptibility of youth to hypoxemia during endoscopy was as high as old subjects. In conclusion, some certain pre-existing diseases of patients were newly identified as independent risk factors for hypoxemia during GI endoscopy. High ASA scores are a confounding predictive factor of pre-existing diseases. We thus recommend that youth (≤18 yrs), obese patients and those patients with hypertension, diabetes, heart diseases, or GI diseases should be monitored closely during sedation endoscopy.