经鼻高流量氧疗联用呼吸兴奋剂在AECOPD无创正压通气中的意义

目的分析经鼻高流量氧疗联用呼吸兴奋剂在慢性阻塞性肺疾病急性加重(AECOPD)无创正压通气中的意义。 方法选择2018年3月至2021年4月我院收治的AECOPD患者78例，随机分为观察组41例与对照组37例。对照组给予无创正压通气联合呼吸兴奋剂治疗。观察组在对照组的基础上给予经鼻高流量氧疗。对比治疗前、治疗后24 h两组PaCO₂、PaO₂水平、改良呼吸困难指数(mMRC)、TNF-α以及IL-1β水平。 结果观察组总有效率(95.12%)比对照组(75.68%)高(P<0.05)；两组治疗前的PaCO₂、PaO₂水平、血清TNF-α、IL-1β水平比较无显著性差异(P>0.05)；两组治疗后24 h的PaCO₂水平、血清TNF-α、IL-1β水平均降低(P<0.05)；两组治疗后24 h的PaO₂水平均升高(P<0.05)；治疗前，两组mMRC评分比较P>0.05；治疗后24 h，两组mMRC评分降低(P<0.05)。 结论经鼻高流量氧疗联用呼吸兴奋剂在AECOPD患者无创正压通气治疗中疗效显著，改善患者的血气指标与呼吸困难程度，减轻机体炎症因子水平。     

经鼻高流量湿化氧疗对老年AECOPD合并Ⅱ型呼吸衰竭患者肺动脉压、ET-1及NLR的影响

目的探讨经鼻高流量湿化氧疗治疗老年慢性阻塞性肺疾病急性加重期(AECOPD)合并Ⅱ型呼吸衰竭患者临床疗效及对肺动脉压力、内皮素(ET)-1及中性粒细胞/淋巴细胞(NLR)的影响。方法老年AECOPD合并Ⅱ型呼吸衰竭患者82例按照随机数表法分为观察组和对照组,每组各41例。患者均给予常规治疗,对照组在此基础上给予常规氧疗,观察组在此基础上给予经鼻高流量湿化氧疗。分析两组治疗前后心率、呼吸频率、肺动脉压(PAP)、pH值、动脉血二氧化碳分压(PaCO_2)、动脉血氧分压(PaO_2)、血氧饱和度(SaO_2)、血浆氨基末端脑钠肽前体(NT-proBNP)、ET-1、NLR、白细胞介素(IL)-6及肿瘤坏死因子(TNF)-α水平变化。比较两组临床疗效、28 d病死率及治疗期间不良反应。结果治疗前,两组心率、呼吸频率、PAP、pH值、PaCO_2、PaO_2、SaO_2、血浆NT-proBNP、ET-1、NLR、IL-6及TNF-α水平比较无统计学差异(P0.05)。治疗后,两组心率、呼吸频率、PAP、PaCO_2、NT-proBNP、ET-1、NLR、IL-6及TNF-α水平较治疗前均有所下降,且观察组水平显著低于对照组(P0.05);两组PaO_2、SaO_2水平较治疗前均有所上升,且观察组PaO_2水平显著高于对照组(P0.05);两组pH值较治疗前无统计学差异(P0.05)。治疗后观察组总有效率(97.6%)明显高于对照组(80.5%,χ~2=4.493,P=0.034);观察组28 d病死率(2.4%)与对照组(7.3%)无统计学差异(χ~2=0.263,P=0.608)。结论经鼻高流量湿化氧疗可显著缓解老年AECOPD合并Ⅱ型呼吸衰竭患者临床症状、改善氧合状况、降低肺动脉血压,并降低患者NT-proBNP、ET-1及NLR水平,改善炎性反应,疗效确切。     

经鼻高流量氧疗辅助治疗慢性阻塞性肺疾病急性加重期合并Ⅱ型呼吸衰竭临床观察

目的 探讨经鼻高流量氧疗辅助治疗慢性阻塞性肺疾病急性加重期(AECOPD)合并Ⅱ型呼吸衰竭患者的临床效果。方法 选择AECOPD合并Ⅱ型呼吸衰竭患者80例,根据通气治疗方式不同分为观察组和对照组各40例。两组均采取抗感染、化痰、解痉、扩张支气管以及黏液溶解、维持酸碱和电解质平衡等常规治疗。在常规治疗基础上,对照组予呼吸机常规无创正压通气治疗,观察组予湿化氧疗仪经鼻高流量氧疗,两组均连续治疗7 d。治疗前、治疗24 h和治疗7 d,采用血气分析仪检测血液pH、PaO₂、PaCO₂,采用心电监护仪检测心率(HR)、呼吸频率(RR)和平均动脉压(MAP)。治疗前和治疗7 d,采用全自动血细胞分析仪检测中性粒细胞与淋巴细胞比值(NLR),采用半定量固相免疫法检测血清降钙素原(PCT),采用酶联免疫法检测血清肿瘤坏死因子α(TNF-α)。治疗7 d,采用Kolcaba根据舒适分类结构编制的舒适状况量表(GCQ)评分评估治疗舒适度,评估临床疗效和不良事件情况。结果 两组治疗前血液pH、PaO₂、PaCO₂、HR...     

无创通气治疗慢性阻塞性肺疾病急性加重期合并Ⅱ型呼吸衰竭临床分析

目的评价双水平气道正压(BiPAP)无创机械通气治疗慢性阻塞性肺疾病急性加重期(AECOPD)合并Ⅱ型呼吸衰竭患者的临床疗效及其安全性。 方法回顾我院呼吸内科2015年1月至2018年6月住院治疗的378例AECOPD合并Ⅱ型呼吸衰竭患者的临床资料，根据治疗方式分为观察组198例和对照组180例。对照组采用常规治疗，观察组在对照组治疗基础上接受经口鼻面罩BiPAP无创机械通气。记录治疗前、治疗2 h、治疗后24 h的血气分析指标、临床缓解情况以及不良反应发生情况，并比较组间差异。 结果治疗2 h后，观察组患者pH、氧合指数(PaO₂/FiO₂)、动脉血氧分压(PaO₂)、乳酸水平改善显著(P<0.05)，对照组无显著改善(P>0.05)。治疗24 h后，两组患者pH、PaO₂/FiO₂、PaO₂、乳酸水平均显著改善，且观察组患者比对照组患者改善更显著(P<0.05)。两组患者治疗后3 d临床缓解率无显著差异(χ²＝1.042，P＝0.307)，治疗后5 d、7 d观察组患者临床缓解率均明显高于对照组(P<0.05)。两组患者胃胀气、口咽溃疡、口腔真菌发生率均无显著差异(P>0.05)，观察组肺性脑病发生率(3.03% vs. 10.0%，P＝0.006)及气管插管率(7.57% vs. 11.11%，P＝0.033)均明显低于对照组；无创通气合理使用可有效降低患者的平均住院日和医疗费用。 结论经口鼻面罩BiPAP无创机械通气是治疗AECOPD合并Ⅱ型呼吸衰竭的一种有效安全的治疗手段。     

高流量氧疗对慢性阻塞性肺疾病伴Ⅱ型呼吸衰竭的疗效分析

目的 探讨经鼻高流量氧疗(high-flow nasal cannula oxygen therapy, HFNC)应用于慢性阻塞性肺疾病急性发作(acute exacerbation of chronic obstructive pulmonary disease, AECOPD)伴轻中度Ⅱ型呼吸衰竭患者的疗效。方法 通过回顾性评价2019年1月1日-2022年6月30日期间南京医科大学第一附属医院及南京市高淳人民医院156例AECOPD伴轻中度Ⅱ型呼吸衰竭患者使用不同呼吸支持方式的临床疗效。研究纳入HFNC患者94例,无创辅助通气(non-invasive ventilation, NIV)患者62例。观察两组患者治疗前、治疗后第1天及第7天临床症状、血气分析,比较HFNC及NIV的疗效、并发症发生率,并探讨HFNC应用时机。结果 HFNC组与NIV组治疗后第1天及第7天时pH、PaCO₂、氧合指数(PaO₂/FiO₂,P/F)较治疗前明显改善(P<0.05);组间比较,上述各项指标改善率无统计学差异(P>...     

主动呼吸循环技术对胸部创伤患者肺功能康复的影响

目的分析主动呼吸循环技术对胸部创伤患者肺功能康复的影响。 方法选择2018年1月到2020年9月在我院治疗的70例胸部创伤患者,随机分为观察组36例、对照组34例。对照组给予常规康复训练治疗,观察组给予主动呼吸循环技术治疗。比较两组拔管时间、住院时间、1秒用力呼气容积(FVE₁)、用力肺活量(FVC)及呼气峰流速(PEF)、呼吸频率、最大通气量及时间通气量、SpO₂、PaO₂及并发症发生情况。 结果观察组拔管时间、住院时间均显著低于对照组(P<0.05);与干预前比较,观察组和对照组FVE₁、FVC及PEF检验结果比较无显著差异;干预后,观察组和对照组FVE₁、FVC及PEF均随着时间的推移而升高,观察组高于对照组(P<0.05);与干预前比较,两组呼吸频率、最大通气量及时间通气量检验结果比较无显著差异;干预后,两组呼吸频率均随着时间的推移而升降低,观察组低于对照组,最大通气量及时间通气量均随着时间的推移而升高,观察组高于对照组(P<0.05);与干预前比较,观察组和对照组SpO₂、PaO₂检验结果比较无显著差异;干预后,观察组和对照组SpO₂、PaO₂均随着时间的推移而升高,且观察组高于对照组,差异有统计学意义(P<0.05);治疗后,观察组并发症发生情况显著低于对照组(P<0.05)。 结论在胸部创伤患者中应用主动呼吸循环技术效果显著,可有效改善患者肺功能康复。     

肺表面活性物质联合NCPAP对新生儿呼吸衰竭血清ET-1及CC16的影响

目的探讨肺表面活性物质联合鼻塞式正压通气(NCPAP)对新生儿呼吸衰竭血清ET-1及CC16的影响。 方法选取2017年1月至2018年11月来院就诊患新生儿呼吸衰竭患儿共114例,采用随机数表分组随机分为观察组60例和对照组54例。两组患儿入组后均予对症治疗,对照组患儿予NCPAP,观察组患儿在此基础上加予肺表面活性物质治疗,均连续治疗3 d。比较两组总有效率、治疗前后的血清内皮素-1(ET-1)、Clara细胞蛋白-16(CC16)、血氧分压(PaO₂)、动脉血二氧化碳分压(PaCO₂)、动脉血氧饱和度(SaO₂)以及不良反应发生率。 结果观察组总有效率81.67%(49/60),高于对照组64.81%(35/54),差异有统计学意义(P<0.05)。治疗后,两组患儿血清ET-1、CC16水平均明显降低,且观察组低于对照组(P<0.05)。治疗后两组患儿PaO₂、SaO₂均明显上升、PaCO₂明显下降(P<0.05)。观察组治疗后的PaO₂、SaO₂高于对照组,PaCO₂低于对照组,差异有统计学意义(P<0.05)。观察组和对照组不良反应发生率分别为8.33%(5/60)、9.26%(5/54),差异无统计学意义(P>0.05)。 结论新生儿呼吸衰竭采用肺表面活性物质联合NCPAP治疗效果更好,能有效降低血清ET-1及CC16水平。     

双水平无创正压通气对急诊Ⅱ型呼吸衰竭并心衰患者NT-proBNP及hs-CRP的影响

目的探讨双水平无创正压通气(BiPAP)对急诊Ⅱ型呼吸衰竭合并心衰患者NT-proBNP及hs-CRP的影响。 方法选择2019年3月至2019年9月于我院急诊科治疗的Ⅱ型呼衰合并心衰患者61例,按照随机数字表法将所有患者分为对照组31例及实验组30例。两组患者入院后均给予Ⅱ型呼衰合并心衰常规治疗,对照组在此基础上给予面罩吸氧治疗,而实验组则给予BiPAP治疗。分别比较患者治疗前(T₁)及治疗后24 h(T₂)、48 h(T₃)时一般资料、动脉血气分析及心功能相关指标、血浆NT-proBNP及hs-CRP以及治疗过程中转为有创通气治疗人数之间的差异。并对患者进行12个月的随访,比较两组患者间死亡风险的差异。 结果两组患者一般资料比较无显著差异(P>0.05);实验组患者治疗总有效率与对照组相比较显著较高(χ²＝6.318,P<0.05);实验组患者治疗后T₂及T₃时HR及BR与对照组比较显著较低,SpO₂则显著较高(P<0.05)。实验组患者T₂及T₃时PCO₂与对照组比较显著较低,pH、PaO₂、LVEF及SV则显著较高(P<0.05)。实验组T₂及T₃时时NT-proBNP及hs-CRP值与对照组比较显著较低(P<0.05)。两组患者治疗过程中转为有创机械呼吸人数比较无显著差异(χ²＝2.074,P＝0.149)。Log rank分析结果显示实验组的死亡风险较对照组显著较低(Log rank χ²＝4.563,P＝0.034)。 结论BiPAP能有效改善Ⅱ型呼吸衰竭并心衰患者呼吸功能及心功能情况,有效治疗上述疾病的同时还能改善患者1年内病死率。     

镇静疗法在慢性阻塞性肺疾病急性加重期合并呼吸衰竭患者无创通气治疗中的应用观察

目的 观察镇静疗法在慢性阻塞性肺疾病急性加重期(AECOPD)合并呼吸衰竭患者无创通气(NIV)治疗中的应用效果。方法 将84例AECOPD合并呼吸衰竭患者随机分为观察组(42例,其中Ⅱ型呼衰患者26例,记为A组)和对照组(42例,其中Ⅱ型呼衰患者26例,记为B组),两组均行NIV治疗,观察组在此基础上给予泵注镇静药物咪达唑仑治疗,镇静药应用时间为2 h,期间比较观察组和对照组的治疗有效率、不良反应情况及治疗前后氧合指数(PaO₂/FiO₂)、血二氧化碳分压(PCO₂)、平均动脉压(MAP),另比较A组和B组治疗前后PCO₂、呼吸频率(RR)。结果与对照组比较,观察组治疗有效率高,人机对抗、面部受压发生率低(P均<0.05);与同组治疗前比较,观察组和对照组治疗后PaO₂/FiO₂增加,观察组治疗后PCO₂减小(P均<0.05);与对照组比较,观察组治疗后PCO₂减小(P<0.05)。与同组治疗...     

改良动态ROX指数对急性呼吸衰竭患者HFNC治疗失败的预测价值

目的 分析改良动态ROX指数对急性呼吸衰竭患者高流量鼻导管(HFNC)治疗失败的预测价值。方法 选取2021年3月至2023年3月的急性呼吸衰竭患者102例,HFNC成功66例,失败36例,改良ROX指数为PaO₂/FIO₂与RR×HR的比值×100,动态指数定义为HFNC前与HFNC 2 h指数的差值,分析不同指数对HFNC失败的预测效能及相关因素。结果 HFNC失败组年龄、APACHE II评分高于HFNC成功组。HFNC 2 h时,HFNC成功组HR、RR和FiO₂低于HFNC失败组,SpO₂、PaO₂、PaCO₂、SpO₂/FIO₂和PaO₂/FIO₂高于HFNC失败组。HFNC成功组HFNC持续时间、HFNC 2 h ROX,动态ROX,HFNC 2 h改良ROX和改良动态ROX指数均高于HFNC失败组。动态ROX、HFNC 2 h改良ROX和改良动态ROX的...     

Scaling respiratory pattern and respiratory 'drive'

We tested three predictions regarding the relationship between body size and respiratory 'drive' and timing in mammals. Mechanical considerations had led to the prediction that TE/TTOT and probably TI/TTOT would be interspecific constants. In eleven species of mammals, ranging in size from 0.033 kg to 520 kg, TE/TTOT during awake quiet breathing was an interspecific constant with a value of 0.65 (+/- 0.004); TI/TTOT was 0.345 (+/- 0.004). Given that VT is directly proportional to BW1.0 (Stahl, 1967), if TE and TI are directly proportional to BW0.28 (Bennett and Tenney, 1982), and if VT/TI is an index of respiratory 'drive', then 'drive' should be directly proportional to BW0.72, following the same proportionality with body size as does basal metabolic rate (VO2). Data for the same eleven species gave the relationship VT/TI BW0.74. Testing further the notion that 'drive', on a weight specific basis, is proportional to BW-0.26, we studied the response, % delta VI, in eleven species to approximately 12% inspired O2. This 'output' of the system in response to a hypoxic stimulus was found to scale with BW-0.27. The question whether this reflects a higher set 'gain' of the respiratory controller of smaller animals and/or some feature of the innervation, or intrinsic properties of the respiratory muscles that varies with body size is discussed.     

Acute respiratory distress syndrome caused by respiratory syncytial virus

Acute respiratory distress syndrome (ARDS) complicating severe respiratory syncytial virus (RSV) infection has been described in only a few infants. In contrast to the low mortality rates usually associated with RSV infections (<5%), mortality rates in the range of 40–70% have been reported in pediatric patients with ARDS. However, studies on patients with ARDS are usually lumped with respect to causation, and the disease course of RSV-induced ARDS has not been previously studied. We examined the pulmonary function abnormalities of 37 infants with RSV-induced respiratory failure who were admitted to our pediatric intensive care unit for assisted ventilation. Measurements included respiratory mechanics, maximum expiratory flow-volume curves, and lung volumes. These allowed the calculation of a Murray lung injury score (modified for pediatric use) in which radiographic findings, ventilator settings, lung compliance, and blood gas results were considered. We identified ten infants with severe restrictive lung disease who fulfilled the clinical criteria for classification as ARDS. All had lung injury scores above 2.5, compatible with a diagnosis of ARDS. Twenty-seven infants had obstructive patterns of lung function consistent with a clinical diagnosis of RSV bronchiolitis. The patients with RSV-induced ARDS were significantly younger, and had a longer time on assisted ventilation (P < 0.05) and a higher proportion of predisposing illnesses (P < 0.05, odds ratio = 6.67, two-tailed Fisher's exact test) when compared with the patients who had obstructive disease. Only one patient (who had immunodeficiency) died, and all others were successfully managed on conventional mechanical ventilation. We conclude that RSV-induced respiratory failure represents a relatively benign cause of ARDS in pediatric patients. Our observations support the notion of differentiating ARDS with respect to causation, especially when novel and experimental therapy is considered and mortality rates are analyzed. Pediatr. Pulmonol. 1997; 23:176–183 © 1997 Wiley-Liss, Inc.     

Total respiratory pressure-volume curves in the adult respiratory distress syndrome

To assess the value of measuring compliance in the adult respiratory distress syndrome, sequential pressure-volume curves were obtained in 19 patients with this syndrome. Analysis of the pressure-volume curves allowed separation of the patients into the following four groups: (1) group 1 (n = 6), normal compliance measured during deflation, little hysteresis, and no inflection in the ascending limb of the pressure-volume tracing; (2) group 2 (n = 8), normal compliance during deflation, increased hysteresis, and presence of an inflection; (3) group 3 (n = 10), decreased compliance during deflation, marked hysteresis, and presence of an inflection; and (4) group 4 (n = 10), reduced compliance during deflation, no increased hysteresis, and no inflection. These patterns were correlated with the stage of the adult respiratory distress syndrome and to the pattern of the chest x-ray film. Group 2 corresponds to the initial stage of the syndrome and to pure alveolar opacities on the chest x-ray film. Group 3 is seen later in the course of the syndrome and corresponds to mixed alveolar and interstitial opacities. Group 4 corresponds to patients with end-stage adult respiratory distress syndrome (two weeks) and a predominant interstitial pattern on the chest x-ray film. Group 1 corresponds to a nearly normal chest x-ray film and to recovery.     

老年慢性呼吸衰竭的氧疗与呼吸锻炼

对老年慢性呼吸衰竭的氧疗和呼吸锻炼就四方面的问题阐述如下。1　呼吸衰竭的概念　　呼吸衰竭 (简称呼衰 )可分两个类型 :Ⅰ型是休息状态下呼吸空气时 ,患者存在低氧血症 (ＰａＯ2 <8ｋＰａ)和正常或低ＰａＣＯ2 (<6ｋＰａ) ,此可称为弥散功能障碍型呼衰 ;Ⅱ型呼衰为低ＰａＯ2 和高ＰａＣＯ2 (>6 6 7ｋＰａ) ,也可称之为通气功能障碍型呼衰 ;Ⅰ型到后期多转变为Ⅱ型。至于急性呼衰和慢性呼衰的区别在于前者是指由于某种原因在短期内引起的呼吸功能失代偿 ,例如脑炎、脑外伤、电击、溺水、药物中毒、吸入毒性气体等 ,最典型的代表就是成人…     

Parental childhood respiratory illness and respiratory illness in their infants

Parental histories of childhood respiratory trouble (CRT) were examined as risk factors for lower respiratory tract illnesses in healthy infants enrolled in the Children's Respiratory Study, Tucson, Arizona. A parental history of childhood respiratory trouble before age 16 was a risk factor for infantile lower respiratory tract illnesses (LRIs). Early age of onset of the parental CRT and those illnesses described as asthma or bronchiolitis showed the greatest risk: odds ratio = 2.8, P < 0.05. After controlling for known and suspected confounders, a parental history of CRT described as asthma or bronchiolitis with onset before age 3 was associated with wheezing LRls in their children, with an odds ratio of 2.6, P < 0.05. A parental history of CRT described as bronchitis/croup was associated with nonwheezing LRls in their children: odds ratio = 2.2, P < 0.05. These findings suggest a familial component to childhood respiratory trouble which may have a hereditary basis. Pediatr Pulmonol. 1993; 16:275–280. © 1993 Wiley-Liss, Inc.