婴幼儿室间隔缺损合并肺动脉高压的麻醉处理

目的探讨婴幼儿先天性心脏病室间隔缺损合并肺动脉高压行室缺修补术的麻醉处理要点。方法室间隔缺损伴肺动脉高压的婴幼儿86例,均在静吸复合全麻、低温体外循环下行室缺修补术。全组持续监测有创血压(ABP)、CVP、ECG、SpO2、体温、尿量、电解质、血气,术中加测右房压(RVP)、平均肺动脉压(PAP)。结果本组体外循环时间27min～114min,主动脉阻断时间15min～87min,74例自动复跳;12例电击除颤后复跳;除1例外,肺动脉压力均较术前下降;术后并发低心排综合征12例;术后出现心律失常2例;无1例出现肺动脉高压危象。结论麻醉前做好充分准备,提高患儿耐受能力;麻醉诱导平顺,配合术者尽快建立体外循环;麻醉深度适宜,维持血流动力学平稳,是保证肺动脉压不进一步增高的重要因素;合理应用血管活性药物,防治肺动脉高压危象鸦积极防范及处理术后并发症,可使患儿安全度过手术期。     

肺动脉灌注低温Perfadex液在法乐四联症根治术中对肺功能的保护作用

目的 探讨体外循环中肺动脉灌注低温Perfadex液对婴幼儿法乐四联症的肺功能保护作用.方法 将24例法乐四联症患儿分为对照组(12例)和肺动脉灌注组(12例),均在体外循环下行法乐四联症根治手术.肺动脉灌注组体外循环期间于心脏阻断后向肺动脉灌注低温Perfadex液,对照组不灌注.分别于转流前,转流结束,手术结束,术后6h及术后24 h测定两组白介素6(IL-6),白介素8(IL-8),白介素10(IL-10)以及血浆脂质过氧化物丙二醛(MDA)水平;计算氧合指数( PaO2 /FiO2)和肺静态顺应性(TV/Ppause).结果两组体外循环后IL-6,IL-8,IL-10及MDA水平均升高[转流结束灌注组IL-6(367.1±32.6)pg/ml,IL-8(376.6±40.4)pg/ml,IL-10(265.4±42.1)pg/ml;对照组IL-6(392.7±41.5)pg/ml,IL-8(477.2±39.7)pg/ml,IL-10(197.8±42.6)pg/ml],手术结束时达峰值[灌注组IL-6 (369.6±37.8) pg/ml,IL-8(536.7±31.7)pg/ml,IL-10(511.5±44.0)pg/ml;对照组IL-6(480.3±46.3) pg/ml,IL-8(585.5±47.8)pg/ml,IL-10(390.8±34.3)pg/ml],以后逐渐下降,术后24 h仍高于术前;肺动脉灌注组在转流结束,手术结束及术后6h的IL-6,IL-8及MDA上升幅度低于对照组[术后6h灌注组IL-6(266.5±31.1)pg/ml,IL-8 (373±32.4)pg/ml,MDA(12.2±4.6)nmol/ml;对照组IL-6(311.8±42.2)pg/ml,IL-8 (477.6±47.7)pg/ml,MDA(19.2 ±5.5) nmol/ml,P＜0.01],各时点IL-10上升幅度高于对照组(P＜0.01);肺动脉灌注组手术结束、术后6h及24 h氧合指数[(367.2±32.0)mmHg,(359.1±39.8)mmHg,(401.1±54.8)mmHg]高于对照组[(316.6±48.5)mmHg,(289.5±42.8)mmHg,(346.6±68.0)mmHg,P＜0.05或0.01];两组肺静态顺应性[手术结束灌注组(3.53±0.57) ml/cmH2O,对照组(3.02±0.63) ml/cmH2O]较术前灌注组[(5.21±0.61 )ml/cmH2O,对照组(4.96±0.82)ml/cmH2 O]明显降低,肺动脉灌注组变化程度[手术结束(3.53±0.57) ml/cmH2O,术后6 h(3.11±0.8)ml/cmH2O,术后24 h (3.95±0.61) ml/cmH2 O]明显低于对照组[手术结束(3.02±0.63) ml/cmH2O,术后6 h(2.71±0.56) ml/cmH2O,术后24 h(3.26±0.54)ml/crnH2O,P＜0.05].结论肺动脉灌注低温Pefadex液能明显减轻婴幼儿法乐四联症术后肺损伤.     

婴幼儿室间隔缺损合并肺动脉高压的外科治疗

目的 总结婴幼儿大型室间隔缺损（Ventricular Septal Defects,VSD）合并肺动脉高压的外科治疗经验.方法 2008年10月至2009年5月共收治婴幼儿大型VSD 98例,男56例,女42例,年龄4～24个月,体重5.1～15.3 kg;均为单发,其中合并房间隔缺损（Atrial Septal Defect,ASD）26例,合并三尖瓣关闭不全（Tricuspid Insufficiency,TI）18例,动脉导管未闭（Patent Ductus Arteriosus,PDA）12例.患儿均在全麻低温体外循环下实施一期矫治术.结果 治愈95例,死亡3例,术后并发症16例,其中低心排出量综合征6例,肺不张4例,肺炎3例,心律紊乱2例,气胸1例,术后早期复查彩超,除5例有少量残余分流外,其余患儿心功能及瓣膜关闭均正常,患儿均痊愈出院.结论 低体重、低年龄的大型室间隔缺损应尽早手术根治;术中尽量减轻体外循环损伤,保护脏器功能;术后加强呼吸道管理、预防低心排出量综合征和肺动脉高压危象是降低死亡率的关键.     

室间隔缺损合并肺动脉高压肺血管床功能状态评估指标的研究

目的探讨室间隔缺损合并肺动脉高压肺血管床功能状态的评估指标。方法对室间隔缺损合并重度肺动脉高压的患儿，于心导管术中应用酚妥拉明，将轻度全肺循环阻力（ＴＰＲ）增加的２７例与重度全肺循环阻力增加的１２例患儿的试验结果进行比较。结果两组患儿的单一肺动脉压降幅（Ｐｐ降幅）分别为２．３ｋＰａ（１７ｍｍＨｇ，１ｋＰａ＝７．５ｍｍＨｇ）和２．２ｋＰａ，Ｐ＞０．０５，差异无显著意义；而肺动脉压降幅（Ｐｐ降幅）／体循环压降幅（Ｐｓ降幅）的比值，试验前后肺动脉血氧饱和度变化值这二项指标的差异有非常显著意义（Ｐ＜０．０１）。Ｐｐ降幅／Ｐｓ降幅比值与全肺循环阻力的相关性良好［ｒ＝－０．８９９），Ｙ（ＴＰＲ）＝２６６８－１８９２Ｘ（Ｐｐ降幅／Ｐｓ降幅）］。结论用酚妥拉明作扩血管降压试验时，单一的肺动脉压降幅不能完全反映肺血管床的功能状态；而Ｐｐ降幅／Ｐｓ降幅比值，试验前后肺动脉血氧饱和度变化值这二项指标对室间隔缺损合并肺动脉高压患儿的肺血管床功能状态的评估，对手术适应证的选择具有一定指导意义。     

婴幼儿室间隔缺损合并肺动脉高压的外科治疗

目的 报道婴幼儿先天性室间隔缺损(VSD)伴肺动脉高压的手术修补结果及体会。方法 1998年1月-2002年12月，对86例VSD伴肺高压的婴幼儿采用中深低温体外循环行手术治疗。术中术后加强心肌保护和呼吸道管理。结果 治愈出院83例，死亡3例，死亡率为3．49％(3／86)，均为肺高压临床4级病例。术后主要并发症为肺部感染、肺高压危象、低心排综合征。出院病人随访6月～5年，无死亡病例，心功能(NYHA)一级62例，二级18例，三级3例。结论 婴幼儿VSD合并肺动脉高压者，应积极早期手术。围术期的心肌保护和呼吸道管理是手术成败的关键。     

婴儿室间隔缺损合并肺动脉高压急诊和亚急诊心脏手术的麻醉处理

目的 总结急诊和亚急诊手术治疗婴儿室间隔缺损(VSD)伴肺动脉高压(PH)的麻醉处理要点。方法 2002年10月～2004．年6月,采用急诊和亚急诊手术治疗61例VSD PH的婴儿,其中男48例,女13例,年龄27天～1岁。体重3．0～8kg。分析术中术后麻醉处理中,注意事项及并发症的防治。结果 主动脉开放后55例自动复跳,6例除颤后复跳,5例出现术后并发症,5例有残余小VSD,58例痊愈出院。结论 术中良好的呼吸管理,保持血流动力学的稳定,术中术后重视肺动脉高压危象的防治,可使VSD PH婴儿安全渡过手术期。     

肺动脉压监测在幼婴室间隔缺损并中、重度肺高压修补术中的意义探讨

目的 探讨幼婴先天性心脏病间隔缺损（ＶＳＤ）合并肺动脉高压手术前,后肺动脉压力（ＰＡＰ）改变与预后的关系。方法 １９９４年１月－１９９８年１２月我科施行幼婴ＶＳＤ并中,重度肺动脉高压心内直视手术７０例,对比缺损修补前,后ＰＡＰ改变,持续监测其中３５例术后ＰＡＰ变化。结果 术前未作心志管检查者,术中测ＰＡＰ可初步判断其肺高压程度。     

深低温体外循环方法对婴儿肺功能及肺表面活性物质的影响

目的 研究比较深低温停循环(DHCA)和深低温低流量(DHLF)对先心病婴儿肺功能及肺表面活性物质(PS)活性水平的影响。方法 20例室间隔缺损伴肺动脉高压婴儿,根据行心肺转流(CPB)方法的不同,随机平均分为DHCA组和DHLF组。分别测定两组CPB前,CPB后5min,CPB后2h的肺静态顺应性、肺气道阻力、呼吸指数及饱和卵磷脂/总磷脂(SatPC/APL)和饱和卵磷脂/总蛋白(SatPC/TP)值。结果 CPB后5min和CPB后2h,两组的肺静态顺应性都较CPB前明显降低(P均<0.01);肺气道阻力和呼吸指数都明显升高(P均<0.01)。CPB后2hDHLF组肺静态顺应性下降的幅度和呼吸指数增加的幅度都明显大于DHCA组(P均<0.01)。CPB后5min和CPB后2h,二组的SatPC/TPL和SatPC/TP都较CPB前明显降低(P均<0.01)。CPB后5min,DHLF组Sat-PC/TPL下降的幅度明显大于DHCA组(P<0.05);CPB后2h,DHLF组SatPC/TPL和SatPC/TP下降的幅度都明显大于DHCA组(P均<0.01)。DHLF组术后ICU滞留时间明显高于DHCA组(P<0.05)。结论 DHCA和DHLF都能明显引起先心病婴儿肺功能受损及PS活性水平的下降,但DHLF较DHCA对肺的损伤更为严重。     

静脉-动脉方向持续超滤对婴幼儿体外循环手术肺保护的研究

目的研究在婴幼儿体外循环心内直视手术中应用静脉-动脉方向持续超滤对排除炎症介质,浓缩血液,防止和减轻体外循环后怖损伤的效果。方法将50例先天性心脏病患儿随机分成对照组和实验组,对照组作常规体外循环,不应用超滤。实验组在体外循环中应朋静脉-动脉方向持续超滤,观察患儿血浆中炎症介质浓度、红细胞压积（HCT）、白蛋白浓度和肺功能指标。结果实验组体外循环后白介素IL-6、TNF血浆浓度明显低于对照组,红细胞压积（HCT）和血白蛋白浓度明显高于对照组,实验组肺功能损害减轻。结论体外循环中采用静脉-动脉方向持续超滤,可有效地排除部分炎症介质,浓缩血液,缩短手术时间,减轻肺水肿和肺损伤。     

先天性心脏病合并肺动脉高压的药物治疗进展

先天性心脏病合并肺动脉高压(PAH)是儿科最常见的心血管疾病之一.传统治疗药物包括α1、α2-受体阻滞剂、钙通道阻滞剂、腺苷和镁离子等,目前治疗上已从单纯的对症降压治疗转向逆转肺血管重构治疗,临床上出现了前列环素、内皮素受体拮抗剂、磷酸二酯酶抑制剂、一氧化氮及其供体等治疗药物.近年来,PAH治疗又出现了以下三大研究热点:钾通道开放剂、5-羟色胺载体抑制剂和羟甲基戊二酰辅酶A还原酶抑制剂,但尚处于动物实验阶段,需进一步研究以得出正确的结论,提高PAH的治疗水平.     

硝普钠对乳猪体外循环中肺损伤的保护作用

目的 探讨硝普钠预处理对乳猪体外循环(CPB)中的肺保护作用.方法 20只幼猪,数字随机分为实验组(A组)及对照组(B组).A组CPB前30min股静脉滴入硝普钠(20μg·kg-1·min-1)至实验结束,B组滴入生理盐水.CPB前(T1)、主动脉开放(T2)、CPB后5 min(T3)、20 min(T4)、40 min(T5)、60 min(T6)时点测定气道峰压(Ppk).T1、T3、T6时点行动脉血气分析、血浆TNF-a、IL-6、IL-8、IL-10检测及肺动脉、左心房血中性粒细胞检测.实验结束后,切取3块肺组织行肺湿干比(W/D)测定、光镜及电镜组织形态学观察.结果 中性粒细胞滞留率T6[A组(0.48±0.21),B组(0.77±0.29)]、血清炎症因子水平:TNF-α浓度T3[A组(45.20±14.00)pg/ml,B组(71.19±11.65)pg/ml]、IL-6浓度T3[A组(33.38±9.72)pg/ml,B组(46.09±12.12)pg/ml]、IL-8浓度T3及T6[A组(27.84±11.96)pg/ml、(24.94±1 4.24)pg/ml,B组(56.73±14.78)pg/ml、(40.99±7.94)pg/ml]和IL-10浓度T3[A组(37.88±7.79)pg/ml,B组(27.62±11.53)pg/ml]、氧合指数(OI)T3[A组(463.05±40.50)%,B组(382.62±80.01)%]及动脉-肺泡氧分压比率(Pao2/PAo2)T3及T6[A组(0.75±0.10)、(0.76±0.07),B组(0.56±0.12)、(0.60±0.07)]、气道峰压(Ppk)T3[A组(16.57±1.51)mmHg,B组(23.00±2.00mmHg]以及肺湿干比(W/D)[A组(0.21±0.03),B组(0.27±0.04)].A组与B组相比,差异均有统计学意义.光镜、电镜检查显示A组肺损伤明显减轻.结论 CPB期间,硝普钠预处理能抑制炎症因子上调,减轻急性炎症反应,改善肺功能.

Abstract：

Objective To investigate the protective effects of sodium nitroprusside on lung injury induced by cardiopulmonary bypass (CPB). Methods Twenty piglets were randomly divided into group A (n = 10) and group B (n = 10). The piglets of the group A were administered with sodium nithe end of the experiment. The piglets of group B were continuously injected with saline. Peak pressure (Ppk) of the airway was measured before CPB (T1), at the time releasing aortic cross-clamp,and 5 min (T3), 20 min (T4), 40 min (T5), 60 min (T6) after CPB. The blood gases, neutrophils count and TNF-α, IL-8, IL-6 and IL-10 levels were measured at T1, T3, and T6. Lung tissue was collected to measure the wet to dry weight ratio (W/D). The morphologic changes of the lung were also studied. Results At T3, TNF-α, IL-6, and IL-8 levels, Ppk and W/D ratios of group A were significantly lower than those of group B 33.38 ± 9. 71 pg/ml vs 46. 09 ± 12. 12 pg/ml, 27. 84 ±11. 96 pg/ml vs 40. 99 ± 7. 94 pg/ml, 16. 57 ± 1.51 mmHg vs 23. 00 ± 2. 00 mmHg, 0. 21 ± 0. 03 vs 0. 27 ± 0. 04,respectively). At T3, IL-10, oxygenation index, and alveolar-arterial oxygen ratio of group A were significantly higher than those of group B (37. 88 ± 7. 79 pg/ml vs 27. 62 ± 11. 53 pg/ml, 463. 05 ±40. 50% vs 382. 62 ± 80. 01 %, 0. 75 ± 0. 10 vs 0. 56 ± 0. 12). At T6, the neutrophil sequestration,IL8 level, and alveolar-arterial oxygen ratio of group A were significantly higher than those of group B (0. 48 ± 0. 21 vs 0. 77 ± 0. 29, 24. 94 ± 14. 24 pg/ml vs 40. 99 ± 7. 94 pg/ml, 0. 76 ± 0. 07 vs 0. 60 ±0. 07). Lung morphology study also showed group A had less injury. Conclusions Sodium nitroprusside protects lung from injury by suppressing inflammation on piglets with cardiopulmonary bypass.     

Nitric oxide and prostacyclin lower suprasystemic pulmonary hypertension after cardiopulmonary bypass

In a 3-week-old male newborn persistent suprasystemic pulmonary hypertension developed after surgical valvulotomy for a critical aortic valve stenosis. Because of a residual transvalvular pressure gradient of 35 mm Hg and postoperative left as well as right ventricular dysfunction, treatment with inhaled nitric oxide (NO) and intravenously infused prostacyclin (PGI₂) was attempted. Low-dose inhaled NO and low dose PGI₂ corrected severe pulmonary hypertension and led to an increase in cardiac output. Treatment with NO but not PGI₂ was accompanied by a rise in PaO₂ and systemic blood pressure. Interruption of NO administration led to a rapid increase in pulmonary arterial pressure to suprasystemic levels. With continued i.v. PGI₂ and decreasing concentrations of NO, severe pulmonary hypertension resolved after a few days suggesting that a transient endothelial dysfunction was partially responsible for pulmonary vasoconstriction. NO inhalation appears to be an effective new tool in the treatment of severe pulmonary hypertension following cardiac surgery.     

Residual pulmonary hypertension in children after treatment with inhaled nitric oxide: a follow-up study regarding cardiopulmonary and neurological symptoms

Inhaled nitric oxide is a potent vasodilator in acute severe pulmonary hypertension and is increasingly used as rescue treatment in intensive care algorithms aiming at reducing severe hypoxaemia in neonates and children. Although the immediate effects may seem impressive, longterm outcome regarding residual pulmonary hypertension and other sequelae has been studied in only a very few patients. The aim of the present study was to evaluate residual pulmonary hypertension, cardiopulmonary or neurological symptoms in children after treatment with inhaled nitric oxide in severely hypoxaemic and/or pulmonary hypertensive mechanically ventilated children. The study was performed in four paediatric intensive care units in university hospitals in Sweden, Norway and Australia. Patients who had received inhaled nitric oxide as part of their intensive care treatment for severe hypoxaemia and/or pulmonary hypertension, and in whom 6 mo had elapsed since treatment, were included for evaluation. Thus 36 paediatric or neonatal patients were examined for circulatory, respiratory or neurological disorders with clinical examination, echocardiography, chest X-ray and a capillary blood sample. Four patients with congenital heart disease had residual pulmonary hypertension. Nine patients were receiving bronchodilators. Sixteen patients had minor (n = 15) or moderate (n = 1) changes on a chest X-ray. One patient had a possible delay in psychomotor development. Conclusions: In spite of the severity of their primary illness, we found that the overwhelming majority of the surviving children were asymptomatic and doing well. The few residual circulatory and respiratory symptoms could be related to the initial condition.     

水通道蛋白-1,-5与新生鼠高氧肺损伤肺水肿的关系研究

目的：水通道蛋白(aquaporin,AQP)是新近发现的一组与水通透性有关的细胞膜转运蛋白,该文旨在探讨高氧损伤状态下,肺组织内AQP1,AQP5的动态变化规律及其在肺水肿中的作用。方法：新生鼠200只,依据吸氧浓度(F iO2)分组:实验组1(F iO2=0.8)、实验组2(F iO2=0.6)、实验组3(F iO2=0.4)、空气对照组(F iO2=0.21)。每组分别于实验后1,3,5,7,14 d行AQP1、AQP5W estern印迹检测,同时检测肺湿/干重比值(wet/dry we ight ratio,W/D),BALF中蛋白含量。结果：高氧各组肺W/D比值、BALF中蛋白含量与空气组相比均显著增加,并随吸氧浓度、暴露时间的增加而增加。实验组AQP1第3天表达开始降低,第5天,第7天明显降低(P<0.05),第14天有所恢复。实验组AQP5表达低于对照组,第1,3天呈稍高表达,以后随日龄增加逐渐降低(P<0.05)。总趋势上AQP1,AQP5的表达在实验组3、实验组2、实验组1依次降低。结论：AQP1,AQP5在高氧肺损伤时表达降低,并与肺水肿的严重程度相关。     

先天性心脏病肺动脉高压肺组织超微结构的改变及临床意义

目的　探讨先心病肺动脉高压 (PH)患儿肺组织超微结构的改变及其临床意义。方法　 2 1例先心病患儿为 1997年 11月～ 1999年 2月间住院行心血管手术者 ,全组平均肺动脉压为 (5 8± 2 1)mmHg ,肺血管阻力 (760± 2 0 6)dyn·s·cm-5。除 4例动脉导管未闭 (PDA)行导管结扎外 ,其余患儿均在体外循环下行心内直视手术 ,于开胸后立即取肺组织在电镜下观察肺组织超微结构的变化。结果　 2 1例PH患儿肺组织均有不同程度的纤维化 ,且在毛细血管两侧不对称 ,主要集中于非气血交换侧 ,以胶原纤维增生最显著 ,弹力纤维增生次之。肺泡Ⅱ型细胞显著增多 ,其胞质内可见大量的线粒体、粗面内质网 ,板层小体增多并可见其内容物丢失。肺泡Ⅰ型细胞基膜显著增厚 ,肺小动脉平滑肌细胞增生 ,毛细血管基膜增厚。结论　重症先心病PH患儿肺组织超微结构发生明显改变 ,结合临床 ,提示对于先心病患儿宜尽早手术纠治 ,以从根本上消除形成PH的条件。     

肺动脉平滑肌细胞钙含量与先心病肺动脉高压的关联性研究

目的探讨肺动脉平滑肌细胞钙含量与肺动脉高压(Pulmonary Hypertension,PH)的关系。方法采用流式细胞术分别检测先天性心脏病合并(PH组)或未合并(非PH组)PH患儿的肺动脉平滑肌钙离子含量。结果PH组中肺动脉平滑肌细胞钙含量较非PH组高,差异有显著统计学意义(3.044±0.732vs1.079±0.409,P<0.01)。结论肺动脉平滑肌细胞中钙含量与PH的发生有关联,检测其平滑肌细胞中钙离子含量可为临床分型提供依据。     

Pulmonary arterial changes in patients with ventricular septal defects and severe pulmonary hypertension

Summary In 25 patients, aged eight months to 31 years, with ventricular septal defect (VSD; isolated in 15, the others with atrial septal defect, PDA, coarctation or patent ductus arteriosus + coarctation), each with severe pulmonary artery hypertension (pulmonary artery systolic pressure [Ppa] at least 75% of systemic and an elevated pulmonary vascular resistance), we related morphologic and morphometric data from open-lung biopsy to hemodynamic measurements obtained at cardiac catheterization during the same hospital admission. Of the hemodynamic features measured, only the ratios of pulmonary-to-systemic flow and pulmonary-to-systemic resistance correlated significantly with structure. Neither pulmonary artery pressure (Ppa) nor pulmonary vascular resistance correlated significantly with any structural feature studied. The increased external diameter of respiratory bronchiolar arteries in those with the more advanced Heath-Edwards grades reflects dilatation and suggests that it is in the small arteries of the distal arterial bed that the changes of pulmonary hypertension are most significant. Neither age nor body weight correlated significantly with the degree of structural or hemodynamic abnormality. In the ten patients who underwent VSD closure, Ppa was measured postoperatively. The Heath-Edwards grade (no more than one grade-III lesion) and arterial density (at least one-half that normal for age) were the best correlates of the difference between preoperative Ppa and Ppa immediately after corrective surgery. The presurgical catheterization data, including pulmonary resistance and the resistance ratio, did not correlate significantly with change in Ppa following VSD closure. Lung biopsy is an important diagnostic aid because it helps in predicting the early response in postoperative Ppa in patients with VSD and elevated pulmonary vascular resistance.