双肺移植围手术期一氧化氮吸入治疗——附5例报告

目的:探索一氧化氮吸入疗法在双肺移植围手术期的临床应用。方法:5例序贯式双肺移植病例围手术期予一氧化氮吸入治疗(iNO),其中男性4例,女性1例,年龄37-56岁;一氧化氮(NO)吸入与监测装置采用Siements Servo 300A (Siemins-Elema AB,Sweden)呼吸机,或Aeronox(Pulmonox,Canada)NO吸入与监测仪。在麻醉开始后开始iNO,开始剂量20 ppm,待供体肺吻合完成并开始开放血液循环时将剂量增至40-60 ppm。结果:5例均顺利渡过围手术期。术后机械通气时间为36-79 h,平均48．8±6．3 h。iNO治疗时间为86-160 h,平均102．6±12．2 h。术后48 h病人肺动脉压达到高峰,氧合(PaO2／FiO2)降低,并随着综合治疗逐步好转。iNO治疗过程中与治疗结束后病人与工作人员未发现可疑的不良反应。结论:本组病人在iNO中未发生意外事件,iNO治疗有效,在术后早期未发生明显低氧血症或肺动脉高压。     

复杂先天性心脏病伴肺动脉高压患儿围手术期的呼吸道护理

目的 总结复杂危重先天性心脏病伴肺动脉高压患儿行体外循环术围手术期呼吸道管理的护理经验.方法 回顾分析2012年7月至2013年2月1 10例复杂危重先天性心脏病伴肺动脉高压行体外循环手术患儿的临床资料,总结围手术期呼吸道管理的护理经验.室间隔缺损、房间隔缺损93例,完全性房室通道6例,主动脉缩窄3例,完全性肺静脉异位引流4例,右室双出口3例,永存左上腔静脉1例,均伴肺动脉高压,肺动脉收缩压≥55 mm Hg;年龄1～12个月,平均(5.6±6.2)个月;体质量3.6～12.5 kg.术后均使用呼吸机辅助呼吸,呼吸机使用时间(36.5±10.6)h.术后均使用一氧化氮气体吸入.术前详细评估,术后重点观察预防呼吸机相关性肺炎的发生,控制肺动脉压力.结果 110例患儿监护室停留时间为(3.2±24)d,均未发生呼吸机相关性肺炎及肺动脉高压危象.平均住院时间19.4 d,均顺利出院.结论 复杂先天性心脏病伴肺动脉高压的患儿做好围手术期呼吸道的管理能有效改善患儿的呼吸功能,减少ICU停留时间.危重患儿特别是伴有肺动脉高压患儿围手术期降低肺动脉压力,术后积极预防呼吸机相关性肺炎是患儿快速恢复呼吸功能的关键.     

一氧化氮吸入治疗体外循环术后危重症合并ARDS效果观察及护理

应用一氧化氮(NO)吸入治疗体外循环心脏外科术后危重症合并急性呼吸窘迫综合征(ARDS)患者44例,于吸入治疗后的1 h、4 h、8 h抽取动脉血行血气分析检查,记录动脉血氧分压(PaO2)、动脉血氧饱和度(SaO2)变化;并根据术后血气分析、胸部X线片,以及患者的临床表现、末梢血氧饱和度(SpO2)监测等,观察NO吸入的效果,为体外循环心脏外科术后危重症患者护理总结经验及方法 .结果本组吸入NO后1 h、4 h、8 h 的PaO2 、SaO2明显升高(P<0.01), 8例患者因合并严重的多脏器衰竭死亡,36例患者在停用NO后病情稳定、预后良好、未发现明显出血及其他不良反应.认为NO吸入治疗体外循环心脏外科术后危重症合并ARDS患者,可提高手术成功率.     

一氧化氮吸入治疗婴幼儿先天性心脏病合并肺动脉高压的术后护理

目的:探讨一氧化氮(NO)吸入治疗婴幼儿先天性心脏病(先心病)合并肺动脉高压(PH)术后的护理方法及效果。方法:回顾性分析我科2010年2月～2011年2月期间的先心病合并中重度PH患儿20例的临床资料,均术后予以NO吸入治疗,总结其治疗效果和护理方法。结果:吸入后患儿肺动脉压力(PAP)和动脉血氧分压(PaO2)明显优于治疗前。心率和有创动脉压与治疗前比较无差异。20例患儿无明显发绀,凝血酶原时间正常,均治愈出院,无死亡病例。结论:NO吸入是治疗肺动脉高压的有效方法,有利于减少术后肺高压危象的发生,但在吸入治疗时需加强监测,提高护理质量,防治不良反应发生。     

一氧化氮对创伤后ARDS患者血流动力学和氧合功能的影响

目的研究一氧化氮(NO)对严重创伤后ARDS患者血流动力学和肺氧合功能的影响。方法选择20例严重创伤后并发ARDS的患者，在呼吸机支持治疗下吸入0．003％的NO，于吸入NO前、吸入NO后第1、2、3天和停止吸入后30min内测定平均动脉压(MAP)、中心静脉压(CVP)、肺动脉平均压(MPAP)、肺毛细血管嵌压(PCWP)、心排指数(CI)并计算出肺动脉阻力(PVRI)、体循环阻力(SVRI)、氧合指数(PaO2／FiO2)、氧输送(DO2I)、氧消耗(VO2I)及肺内分流率(Qs／Qt)。结果吸入NO后的3d内MPAP、PVRI、Qs/Qt明显降低，PaO2／FiO2、DO2明显升高，停止吸入后的30min内MPAP明显回升并超过吸NO前的水平，PaO2、DO2呈下降趋势但仍高于吸入NO前的水平。吸入NO期间MAP、HR、CI、SVRI、VO2I无显著变化。结论吸入NO可明显降低严重创伤后ARDS患者的肺动脉压和提高氧合指数。     

右室Tei指数对伴肺动脉高压房间隔缺损患者右心室功能的研究

目的 (1)运用组织多普勒测量右心室Tei指数评价伴肺动脉高压的房间隔缺损(atrial septal defect,ASD)患者右心室功能;(2)通过右心室Tei指数研究房间隔缺损患者成功施行修补术后右心室功能的改善情况.方法 伴有不同程度肺动脉高压的房间隔缺损患者28例,正常人33例.运用组织多普勒方法计算右室Tei指数.通过三尖瓣反流估测房间隔缺损患者的肺动脉压力.结果 (1)伴有肺动脉高压的房间隔缺损患者右心室Tei指数明显大于正常对照组.(2)房间隔缺损患者修补术后1周右心室Tei指数及肺动脉压力较术前明显减小.结论 (1)伴肺动脉高压的房间隔缺损患者存在不同程度的右室功能降低.(2)房间隔缺损患者成功施行修补术后肺动脉压力明显降低,右心室功能明显改善.(3)由组织多普勒测得的右室Tei指数简便、易行、准确性高,能较全面准确地评价右心综合功能情况.     

急性肺栓塞性肺高压局部溶栓和全身溶栓的比较

目的研究经导管肺动脉局部溶栓与外周静脉全身溶栓在急性肺栓塞性肺动脉高压治疗中的作用。方法20只小猪自体血栓注入建立急性肺栓塞性肺动脉高压模型。随机分成两组:经导管肺动脉局部溶栓(A组10只),外周静脉全身溶栓(B组10只)。溶栓前、溶栓后2h测肺动脉压,肺动脉收缩压(PASP),心率(HR),心输出量(CI),血气分析(PaO2、PaCO2、pH),纤溶酶_抗纤溶酶复合物(PAP),DD二聚体(DD),一氧化氮(NO)。结果两组肺动脉压、CI、PaO2、PaCO2、PAP、DD、NO均较治疗前有显著变化(P<0.05),A组的肺动脉压、PaO2、PaCO2、PAP的变化较全身溶栓组B组的变化更显著(P<0.05)。结论肺栓塞治疗中局部溶栓的疗效优于全身溶栓。     

一氧化氮吸入治疗体外循环术后危重症合并ARDS效果观察及护理

应用一氧化氮（NO）吸入治疗体外循环心脏外科术后危重症合并急性呼吸窘迫综合征（ARDS）患者44例,于吸入治疗后的1 h、4 h、8 h抽取动脉血行血气分析检查,记录动脉血氧分压（PaO2）、动脉血氧饱和度（SaO2）变化;并根据术后血气分析、胸部X线片,以及患者的临床表现、末梢血氧饱和度（SpO2）监测等,观察NO吸入的效果,为体外循环心脏外科术后危重症患者护理总结经验及方法。结果本组吸入NO后1 h、4 h、8 h的PaO2、SaO2明显升高（P〈0.01）,8例患者因合并严重的多脏器衰竭死亡,36例患者在停用NO后病情稳定、预后良好、未发现明显出血及其他不良反应。认为NO吸入治疗体外循环心脏外科术后危重症合并ARDS患者,可提高手术成功率。     

局部溶栓加抗凝对急性肺栓塞性肺高压的疗效观察

目的　研究经导管肺动脉局部溶栓加抗凝治疗在急性肺栓塞性肺动脉高压的作用。方法　2 0只小猪自体血栓注入建立急性肺栓塞性肺动脉高压模型。随机分2组,经导管肺动脉局部溶栓加抗凝(A组10只)、局部溶栓不加抗凝(B组10只)。溶栓前、溶栓后2h测肺动脉收缩压(SPAP)、股动脉收缩血压(SABP)、心率(HR)、心输出量(CI)、血气分析(PaO2 、PaCO2 、pH)、纤溶酶 抗纤溶酶复合物(PAP)、DD二聚体(DD)、一氧化氮(NO)。结果　两组SPAP、CI、PaO2 、PaCO2 、PAP、DD、NO均较治疗前有显著变化(P <0 0 5 ) ,A组的SPAP、PAP的变化较B组的变化更显著(P <0 .0 5 )。结论　肺栓塞治疗中,局部溶栓加抗凝的疗效优于单纯局部溶栓。     

小潮气量容量控制反比通气改善急诊重度吸入性肺炎合并ARDS患者早期氧合功能的临床分析

目的:探讨呼吸机小潮气量容量控制反比通气(LTVC-IRV)改善急诊重度吸入性肺炎并发急性呼吸窘迫综合征(ARDS)患者早期氧合功能的临床效果及其可能的作用机制.方法:回顾性分析20例重度吸入性肺炎并发ARDS患者的临床资料及治疗护理措施,统计对比分析LTVC-IRV治疗前后股动脉血气指标﹑平均气道压(mAP)及右上肢袖带平均动脉压(MAP)的变化.结果:LTVC-IRV治疗1 h及4 h后与治疗前(CMV治疗1 h)相比:①PaO2/FiO2比值在1 h后与治疗前比较差异无统计学意义(P＞0.05),但4 h后较治疗前显著增加(P＜0.01);②1 h及4 h后较治疗前的PAP显著降低,mAP逐渐显著增加,比较差异均有统计学意义(P＜0.01);③1 h及4 h后的MAP与治疗前比较差异无统计学意义(P＞0.05).结论:LTVC-IRV治疗重度吸入性肺炎合并ARDS时,早期降低PAP及增加mAP,数小时后可明显改善患者肺氧合功能而对血流动力学无明显影响.     

单肺移植治疗伴有肺动脉高压的终末期肺病

目的观察单肺移植治疗对伴有肺动脉高压的终末期肺病患者的疗效。方法2002年9月—2005年11月我院22例单肺移植患者,其中肺气肿10例、肺纤维化10例、矽肺1例、肺淋巴管平滑肌瘤病1例。受体肺移植术前评估肺动脉压均显示有不同程度的升高。手术方式:左肺移植10例,右肺移植12例。术前常规心脏超声监测肺动脉收缩压,并通过动脉血气分析计算氧合指数(PaO2/FiO2)。结果术后1周用Swan-Ganz导管测定患者平均肺动脉收缩压,较术前有明显下降,从(50.00±13.00)mmHg(1mmHg=0.133kPa)降至(39.50±7.36)mmHg(P<0.05);PaO2/FiO2明显改善,从(241.26±79.54)mmHg升到(348.23±99.31)mmHg(P<0.05)。结论单肺移植是治疗伴肺动脉高压终末期肺病的有效和可选方法。     

Concurrent administration of amrinone with nitric oxide most improves PaO2/FiO2 in acute respiratory and cardiac failure.

A 55-year-old man developed acute respiratory failure, pulmonary hypertension and left heart failure due to acute myocardial infarction. Nitric oxide (NO) inhalation improved arterial oxygenation, decreased pulmonary arterial pressure and increased cardiac output (CO), but combined use of dobutamine with NO produced increases in pulmonary arterial pressure and pulmonary capillary wedge pressure (PCWP). In this patient, amrinone decreased pulmonary arterial pressure and PCWP, and increased PaO2/FiO2 effectively while increasing CO. Combined use of inhaled NO and intravenous amrinone may have beneficial effects for a patient with acute respiratory and cardiac failure.     

高频振荡通气结合低浓度一氧化氮吸入对急性缺氧大鼠肺动脉高压的作用

目的：观察高频振荡通气（ＨＦＯ）联合低浓度一氧化氮（ＮＯ）吸入对急性缺氧大鼠肺动脉高压的治疗作用。方法：在ＨＦＯ下,经气管插管给大鼠１２％氧３０分钟制成急性缺氧肺动脉高压模型,行肺泡再充气,吸入低浓度ＮＯ（１０、５、２ｍｍｏｌ／Ｌ）对模型动物进行治疗,测定血流动力参数和血气值。结果：２～１０ｍｍｏｌ／Ｌ ＮＯ吸入均可逆转急性缺氧大鼠肺动脉压（ＰＡＰ）,收缩压（ｓＰＡＰ）从４．４４～４．５３ｋＰａ（     

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study

BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (QVA/QT), and a dose-dependent increase in PaO2/FiO2 (P 相似文献   

西地那非治疗婴幼儿先天性心脏病术后肺动脉高压

[目的]观察西地那非对婴幼儿先天性心脏病(简称先心病)手术后严重肺动脉高压的疗效.[方法]总结本院2009年1月至2010年6月应用西地那非治疗婴幼儿室间隔缺损合并重度肺动脉高压共33例.本组术毕停体外循环后置管测定肺动脉压力仍超过体动脉压力(桡动脉置管测定外周动脉压)50%以上,术后1d给予鼻饲西地那非,初始剂量0....     

吸入低浓度一氧化氮在猪急性肺栓塞中的作用

目的 探讨低浓度一氧化氮(NO)吸入在实验猪肺栓塞中的作用机制及治疗意义.方法 15只健康幼猪分成两组,分别建立肺栓塞模型.对照组8只,不做任何处理;NO组7只,模型建立后,持续吸入10×10-6的NO.每组于栓塞前30 min,栓寨后0 min,30 min,60min,120 min 5个时间点分别测定生理死腔(VDphy)、肺泡死腔(VDalv)、肺内分流(Qs/Qt)、平均肺动脉压(PAP)、血压(SBP)、心率(HR)、心输出量(CO)、动脉血pH值(pH)、动脉血二氧化碳分压(PaCO2)、动脉血氧分压(PaO2).结果 研究发现两组动物Vdphy[NO组栓寒前(64.1±18.0),栓塞后(109.1±30.0),(107.6±26.8),(97.1±24.1);对照组栓塞前(51.1±10.8),栓寨后(129.2±22.1),(116.9±32.5),(103.9±22.8)],VDalv[NO组栓塞前(8.8±4.3),栓寨后(64.3±26.9),(54.0±25.9),(45.7±22.4);对照组栓塞前(10.9±3.6),栓塞后(97.9±21.5),(80.7±25.3),(70.9±22.5)],Qs/Qt[NO组栓寨前(1.76±0.6),栓塞后(2.90±0.8),(3.1±0.6),(2.9±0.8);对照组栓塞前(1.05±1.5),栓塞后(3.4±0.7),(3.4±0.9),(3.5±0.8)],PAP[NO组栓塞前(16.6±3.4),栓塞后(31.7±3.1),(18.7±3.6),(18.0±3.4),(16.6±3.6);对照组栓塞前(15.8±2.6),栓塞后(35.4±3.3),(25.0±2.2),(25.0±3.5),(24.8±2.8)]栓塞后较栓塞前明显增大(P<0.01).PaO2栓塞后较栓塞前明显减小(P<0.05和P<0.01).HR、SBP、CO、pH、PaCO2栓塞前后差异无统计学意义(P>0.05).NO组PAP和VDalv较对照组明显减小(P<0.05和P<0.01),而PaCO2和PaO2较对照组明显增大(P<0.05).其余指标两组动物各时间点之间差异无统计学意义.结论 肺栓塞发生后,低浓度NO吸入可以降低肺动脉压,使肺泡死腔减小,氧分压增大,但不会发生血液动力学恶化.     

Continuous inhalation of nitric oxide protects against development of pulmonary hypertension in chronically hypoxic rats.

Exposure to hypoxia and subsequent development of pulmonary hypertension is associated with an impairment of the nitric oxide (NO) mediated response to endothelium-dependent vasodilators. Inhaled NO may reach resistive pulmonary vessels through an abluminal route. The aim of this study was to investigate if continuous inhalation of NO would attenuate the development of pulmonary hypertension in rats exposed to chronic hypoxia. In conscious rats previously exposed to 10% O2 for 3 wk, short-term inhalation of NO caused a dose-dependent decrease in pulmonary artery pressure (PAP) from 44 +/- 1 to 32 +/- 1 mmHg at 40 ppm with no changes in systemic arterial pressure, cardiac output, or heart rate. In normoxic rats, acute NO inhalation did not cause changes in PAP. In rats simultaneously exposed to 10% O2 and 10 ppm NO during 2 wk, right ventricular hypertrophy was less severe (P < 0.01), and the degree of muscularization of pulmonary vessels at both alveolar duct and alveolar wall levels was lower (P < 0.01) than in rats exposed to hypoxia alone. Tolerance to the pulmonary vasodilator effect of NO did not develop after prolonged inhalation. Brief discontinuation of NO after 2 wk of hypoxia plus NO caused a rapid increase in PAP. These data demonstrate that prolonged inhalation of low concentrations of NO induces sustained pulmonary vasodilation and reduces pulmonary vascular remodeling in response to chronic hypoxia.     

Efficiency of inhaled nitric oxide as rescue therapy during severe ARDS: Survival and factors associated with the first response

PURPOSE: The purpose of this study was to determine if the response to inhaled nitric oxide (NO) as salvage therapy is an independent factor for survival in adult respiratory distress syndrome (ARDS) patients and to identify the factors that predict the response to inhaled NO during ARDS. MATERIALS AND METHODS: This was a multicenter, 2-year retrospective, clinical study in five university surgical or medical intensive care units, including all consecutive patients with ARDS in whom inhaled NO was tried. Clinical data (medical history, diagnoses), general severity scores (SAPS II, OSF), biological data, radiological and hemodynamic data at admission, at the beginning of the ARDS, and under treatment with inhaled NO were recorded. The NO response was defined as the variation of PaO2/Fio2 ratio before initiation and after 30 minutes of NO inhalation (VarPaO2/FiO2). RESULTS: Ninety-three patients aged 49 +/- 18 years were studied. Mean SAPS II was 45 +/- 16. Before the beginning of inhaled NO, PaO2/Fio2 ratio was 95 +/- 53 mm Hg and lung injury score 2.7 + 0.3. VarPao2/Fio2 when NO was started (11 +/- 4 ppm) was 26 +/- 44.5 mm Hg (median 17 mm Hg). Intensive care unit mortality was 74%. None of the parameters studied were predictors of response to inhaled NO, although there was a tendency for the youngest patients with the more severe hypoxemia to have a better response. Response to first inhaled NO test (VarPaO2/FiO2) was univariately associated with survival (Survivors: 45 +/- 44 mm Hg vs. Nonsurvivors: 20 +/- 43 mm Hg, P = .01), but this difference disappeared after adjusting for other prognostic factors (P = .16) selected by multivariate analysis. Finally, inhaled NO was continued for more than 1 day for 75 patients, and definitively stopped for 18 patients. Intensive care unit mortality (73% vs. 78%) was not different between these groups (P = .25, Log-rank test). CONCLUSIONS: We conclude that (1) efficacy of inhaled NO in improving oxygenation was moderate and difficult to predict, (2) response to first NO inhalation was not associated with prognosis, and (3) treatment of the most severe ARDS patients with inhaled NO did not influenced their intensive care unit survival.     

一氧化氮和尿激酶在猪急性肺栓塞中的作用

目的 探讨联合低浓度一氧化氮(NO)吸入和尿激酶在实验猪肺栓塞中的作用机制及治疗意义.方法 12只健康幼猪分成两组,分别建立肺栓塞模型.尿激酶组6只,模型建立后静脉给予2万U/(kg·h)共2 h;联合组6只,模型建立后静脉给予2万U/(kg·h)的同时持续2 h吸入10 ppmNO,两组均观察180min.每组于栓塞前30 min,栓塞后0 min,30 min,60 min,120 min,180 min共6个时间点分别测定生理死腔(Vophy)、肺泡死腔(Vdalv)、肺内分流(Qs/Qt)、平均肺动脉压(PAP)、血压(SBP)、心率(HR)、心输出量(CO)、动脉血pH值、动脉血二氧化碳分压(PaCO2)、动脉血氧分压(PaO2).数据分析采用单因数方差分析(SNK-q检验),以P<0.05为差异具有统计学意义.结果 与栓塞前比较,两组栓塞后VDphv,Vdalv,Qs/Qt,PAP明显增大(P<0.01),但PAP于栓塞后随着时间推移在逐渐减小.PaO2栓寨后较栓塞前明显减小(P<0.05和P<0.01).HR、SBP、CO、pH、PaCO2栓塞前后相比,差异无统计学意义(P>0.05).栓塞后联合组PAP较尿激酶组明显减小(P<0.05和P<0.01),其余指标两组动物各时间点之间差异无统计学意义.结论 肺栓塞发生后,尿激酶溶栓基础上联合低浓度NO吸入可以快速降低肺动脉压,但不会发生血液动力学和气体交换的恶化,NO反跳也不会出现.     

Improving paediatric and newborn life support training by the use of modified manikins allowing airway occlusion

OBJECTIVE: To assess the management of patients with blunt traumatic pulmonary contusion admitted to our hospital. To identify the role of early blood gas analysis, non-invasive ventilation and to assess the validity of the current Advanced Trauma Life Support manual statement that "Patients with significant hypoxia, i.e. PaO(2)<65 mm Hg or 8.6 kPa on room air, SaO(2)<90%, should be intubated and ventilated within the first hour after injury". SETTING: A 24 bed Intensive Care Unit in a major Trauma Centre situated in South Western Sydney, Australia. METHODS: Retrospective review of adults with blunt traumatic pulmonary contusion identified from the trauma registry. RESULTS: A total of 75 patients with an age range of 16-81 years were identified over a 2-year period. Arterial blood gas measurement was available for 32 patients during the immediate resuscitative period (<1 h from admission). All patients received supplemental oxygen and a PaO(2)/FiO(2) ratio was calculated. Seven patients had significant pulmonary contusion, indicated by an initial PaO(2)/FiO(2) ratio of <300, and were treated successfully with non-invasive ventilatory support. A further five patients without arterial blood gas (ABG) analysis on admission but with PaO(2)/FiO(2) ratio of <300 in the ICU were also managed with non-invasive ventilatory support. Multi-modal analgesia was commonly used. CONCLUSIONS: All major trauma patients admitted to our hospital received supplemental oxygen. Interpretation of ABG breathing room air was not used as an indicator for intubation. Most decisions to intubate early were based on clinical need. Patients with significant pulmonary contusion required intubation for reasons other than respiratory failure. Patients with significant pulmonary contusion were managed safely with non-invasive ventilatory support. Further investigation will determine the role of non-invasive ventilatory support in the management of these patients.