小剂量尼卡地平对心脏外科围术期心肌缺血/再灌注损伤的保护作用

目的 评价小剂量尼卡地平对心脏外科手术期间心肌缺血/再灌注损伤的保护作用。方法 选择16例心脏瓣膜置换病人,随机分为对照组（C,n=8）和尼卡地平组（N,n=8）;N组在麻醉诱导后泵入小剂量尼卡地平0.5μg·kg-1·min-1,至转机始给予总剂量0.05mg·kg-1。在转机前、主动脉开放后5min、30min、术毕、术后6h、18h,同时采集动脉血（a）及冠状窦血（cs）,测定肿瘤坏死因子（TNF-a）、脂质过氧化物（LPO）的浓度及超氧化物歧化酶（SOD）、心肌同功酶（CK-MB）的活性,并计算心肌TNF-a、LPO的净生成量（TNF-anr,LPOnr）,心肌氧自由基净消耗的SOD量（SODnr）。同时记录除颤次数,脱机指标及转后多巴胺用量。结果 从主动脉开放至术毕,C组病人LPOa和LPOcs浓度较CPB前明显升高（P<0.05）,SODnr也显著增加（P<0.05）;与C组相比,N组LPOnr及SODnr降低（P<0.05）。两组病人在开放主动脉后,TNF-αa均明显增加,且持续至术毕（P<0.05）。N组 TNF-anr仅在开放主动脉后5min有明显增加,而C组病人持续到术毕（P<0.05）。两组CK-MB活性在观察时程内较CPB前均显著上升（P<0.05）,而N组可明显减轻CK-MB释放。两组主动脉开放后的除颤次数,脱机指标无明显差异,但N组停机后的多巴胺用量也显著减少（P<0.05）。结论 小剂量尼卡地平0.05mg     

心脏瓣膜置换术病人体外循环后肺损伤的机制

目的 探讨心脏瓣膜置换术病人心肺转流术(CPB)后肺损伤的机制。方法 选择8例行心脏瓣膜置换术的病人,其中男4例,女4例,全身麻醉后经颈内静脉置入Swan-Ganz导管。分别在CPB前即刻(T0)、腔静脉开放后5 min(T1)、停机时(T2)和术毕(T3)时采集桡动脉(肺静脉)血和混合静脉(肺动脉)血,测定中性粒细胞(PMN)计数、血浆肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)和脂质过氧化物(LPO)浓度,并计算肺动、静脉血各项指标的差值,反映肺内PMN滞留、TNF-α净生成、SOD消耗和LPO净生成;分别测定T0、T2和T3时肺动脉血液动力学指标和肺顺应性,行肺动、静脉血气分析计算肺泡-动脉血氧分压差(PA-aDO2)、肺分流量(QS/QT)和肺氧合指数(paO2/FiO2)。结果 所有病人上、下腔静脉阻断时间及转机时间分别为97±21、(124±27)min。与T0比较,在T3时MPAP升高、肺顺应性显著性降低,T2、T3时PVRI、PA-aDO2和QS/QT显著性升高(P<0.05或0.01),在T1、T2和T3时PMNv、PMNa、TNF-αa、LPOa显著性升高(P<0.05或0.01),在T1、T2时TNF-α和LPOa显著性升高(P<0.01),在T1、T2和T3时SODv、SODa显著性降低(P<0.01)。结论 CPB后肺功能损害与肺外组织生成的氧自由基及炎性反应激活的PMN和TNF-α有关。     

心脏外科围术期应用尼卡地平对心肌能量代谢的影响

目的观察尼卡地平对体外循环(CPB)后心肌能量代谢的影响.方法16例心脏瓣膜外科病人,随机分为对照组(C组,n=8)和尼卡地平组(N组,n=8).N组在麻醉诱导后,开始滴注小剂量尼卡地平(0.5μg@kg-1@min-1)至转机前,给予总剂量为0.5mg@kg-1,不足该剂量者,转机后即刻补足.在转机前即刻、开放主动脉后5min、30min、术毕、术后6h、18h,同时采集动脉血与冠状窦血,测定血乳酸、血糖、血气,由此计算心肌乳酸摄取率(LER)、心肌血糖摄取率(GER)及心肌摄氧指数(MOEI).结果与CPB前相比,C组主动脉开放后GER和LER均明显下降(P＜0.05),至术后6h仍未恢复正常.N组主动脉开放后,GER无明显变化且显著高于C组(P＜0.05);LER显著下降(P＜0.05),但明显高于C组(P＜0.05).两组开放主动脉5min后MOEI明显下降,随后显著恢复(P＞0.05).结论CPB可导致心肌乳酸和葡萄糖代谢受损及恢复延迟,小剂量尼卡地平可明显改善转流后心肌的乳酸与葡萄糖的代谢.     

米力农复合一氧化氮对先天性心脏病患者体外循环后肺动脉高压的影响

目的 评价米力农复合一氧化氮(NO)对先天性心脏病(CHD)患者体外循环(CPB)后肺动脉高压(PH)的影响.方法 先天性左向右分流型心脏病经肺动脉导管确诊为PH患者24例,随机分为3组(n=8):NO组(N组)、米力农组(M组)和米力农复合NO组(NM组).CPB主动脉开放后,N组于CPB结束血液动力学平稳后,吸入20 ppm NO 45 min;M组静脉注射米力农负荷量50 μg/kg,然后持续静脉输注0.5μg/kg-1·min-1至术毕;NM组静脉注射米力农负荷量50 μg/kg,然后持续静脉输注0.5μg/kg-1·min-1至术毕,脱离CPB后,吸入20 ppm NO 30 min.分别于切皮前(T0)、CPB结束血液动力学平稳后、吸入NO15 min、30 min和停止NO吸入后15 min记录血液动力学指标.结果 N组吸入NO时平均肺动脉压(mPAP)和肺血管阻力指数(PVRI)降低(P＜0.05),停止吸入后,均出现不同程度的回升(P＜0.05),平均动脉压(MAP)、体循环阻力指数(SVRI)以及心脏指数(CI)差异无统计学意义(P＞0.05);M组静脉输注米力农期间PVRI下降,CI增加(P＜0.05),mPAP、MAP以及SVRI差异无统计学意义(P＞0.05).NM组给药期间mPAP和PVRI降低,CI增加(P＜0.05),停吸NO前后mPAP、PVRI差异无统计学意义(P＞0.05).结论 CHD合并PH患者CPB后,静脉输注米力农复合吸入NO可降低mPAP和肺循环阻力,增加CI;米力农可预防NO停用后PH反跳.     

尼卡地平对原发性高血压患者围术期胰岛素敏感性的影响

目的观察尼卡地平对原发性高血压(EH)患者围术期胰岛素敏感性的影响。方法择期行肺癌肺叶切除术的EH患者38例随机分为尼卡地平组(N组,20例)和对照组(C组,18例)。N组麻醉诱导后静脉输注尼卡地平1μg·kg-1.min-1至术后1d;C组以相同速率输注等量生理盐水。测定麻醉诱导前即刻(T0)、手术开始后2h(T1)、术后4h(T2)和24h(T3)的血糖(BG)和血浆胰岛素(Ins),计算胰岛素敏感指数(ISI)。结果与T0时比较,C组T2、T3时BG和Ins明显上升,ISI明显降低(P0.05或P0.01),N组T3时BG和Ins明显上升,ISI明显降低(P0.05)。与C组比较,N组T2时BG明显降低(P0.05),T3时Ins明显降低(P0.01),T2和T3时ISI明显升高(P0.05)。结论术中静脉持续输注尼卡地平可增加EH患者术后胰岛素的敏感性,改善术后胰岛素抵抗的程度。     

小剂量氯胺酮对心肺转流后肺损伤的保护作用

目的观察应用小剂量氯胺酮对心肺转流(CPB)后肺损伤的影响。方法30例二尖瓣置换手术病人随机均分为氯胺酮组(K组)和对照组(C组),两组麻醉方法相同。K组于麻醉诱导后和CPB开始前分别缓慢静注氯胺酮1mg/kg;C组静注同等容量的生理盐水。于手术开始前(T0)、CPB停止即刻(T1)、2h(T2)、12h(T3)记录气道峰压(Ppeak)、气道平台压(Pplautue),通过Flow-Directed漂浮导管测定平均肺动脉压(MPAP)、肺毛细血管楔压(PCWP)、心输出量(CO),计算肺血管阻力(PVR),同时抽取动脉血、混合静脉血测动脉血气、血常规、肿瘤坏死因子α(TNF-α)、白细胞介素1(IL-1)、血清可溶性细胞间黏附分子-1(sICAM-1)及中性粒细胞表面CD11b、CD18的表达。结果CPB后两组病人的所测各项指标均明显升高(P<0.05),但K组显著低于C组(P<0.05),CPB后C组中性粒细胞在肺组织中的浸润明显高于K组,CD11b、CD18表达较高的中性粒细胞容易浸润于肺组织中。结论CPB中应用小剂量氯胺酮可以减轻全身性炎症反应和缺血-再灌注损伤导致的肺组织损伤,对肺功能有显著的保护作用。     

尼卡地平、艾司洛尔联合诱导期容量填充对静-吸复合全身麻醉七氟醚用量的影响

目的 观察尼卡地平、艾司洛尔联合诱导期容量填充对静吸复合全身麻醉七氟醚用量的影响.方法 60例择期行脊柱手术的患者.随机均分为四组,诱导期以羟乙基淀粉10 ml/kg快速静滴行容量填充,诱导后插管前1 min时分别静注艾司洛尔1 mg/kg(E组)、尼卡地平20μg/kg(N组)、艾司洛尔1 mg/kg复合尼卡地平20μg/kg(EN组)或生理盐水(C组),于切皮前1 min追加1/2首量药物或生理盐水.记录各组七氟醚用量、清醒、拔管时间及HR、MAP的变化.结果 与C组比较,E组、N组及EN组术中所需七氟醚维持浓度均显著降低(P<0.05),清醒及拔管时间明显缩短(P<0.05).与C组比较.E组HR较慢(P<0.05),但不能完全控制MAP的升高;N组MAP较低(P<0.05);EN组能明显抑制诱导插管及切皮引起的HR、MAP升高(P<0.05).结论 艾司洛尔、尼卡地平联合诱导期容量填充不仅有利于维持血流动力学的平稳,而且能够明显减少静吸复合全身麻醉七氟醚用量、缩短拔管时间.     

尼卡地平与低剂量艾司洛尔联合控制性降压对血液儿茶酚胺、β2-微球蛋白和血乳酸的影响

目的研究尼卡地平与低剂量艾司洛尔联合控制性降压方法的可行性及对血液儿茶酚胺、＆2-微球蛋白(β2-mG)和组织氧代谢的影响.方法择30例择期手术的骨肿瘤病人,随机分为三组对照组(C组,n=10),不实施控制性降压,仅泵入生理盐水;尼卡地平组(N组,n=10),尼卡地平、艾司洛尔联合15组(N+E组,n=10),N组和N+E组尼卡地平起始药物速率为2.5μg@kg-1@min-1,艾司洛尔速率12.5μg@kg-1@min-1(NE=15).降至目标血压后(MAP 60～70mm Hg),调整药物剂量使MAP维持在此范围.分别于降压前、降至目标血压时、降至目标血压后30min、降压停止时以及术毕,采集动脉血分别测定血液儿茶酚胺水平、血清β2-mG含量、血乳酸含量和血红蛋白,同时记录各时间点的HR、MAP、CVP和降压期间的尿量.结果 C组与N组降压期间血去甲肾上腺素(NE)水平明显增加且呈递增趋势(P＜0.05),N+E组病人NE水平虽有升高但保持在低水平(P＞0.05);而其它两组病人则无明显改变.三组病人降压期间β2-mG含量均无明显升高,但降压期间的血乳酸含量升高显著(P＜0.05).结论尼卡地平控制性降压不会造成组织无氧代谢发生及潜在肾损害,其与低剂量艾司洛尔联合(15)可作为一种控制性降压方法,且具有部分抗应激作用,有助于降压期间内脏血流的维护.     

前列腺素E1对急性肺损伤兔微循环灌注的影响

目的 探讨前列腺素E1(PGE1)对急性肺损伤(ALI)兔微循环灌注的影响.方法 健康家兔24只,体重2.6～3.2 kg,随机分为3组:对照组(c组)、ALI组和PGE1 治疗组(PGE组),每组8只.麻醉稳定后15 min(T0),ALI组和PGE组静脉注射油酸0.015 ml/kg制备兔ALI模型,模型制备成功后(T1)PGE组静脉输注PGE1 30 ng·kg-1·min-1,C组和ALI组静脉注射等容量生理盐水,分别于T0、T1及模型制备成功后30 min(T2)、60 min(T3)、90 min(T4)、120 min(T5)和150min(T6)时测定平均动脉压(MAP)、平均肺动脉压(MPAP)、气道峰压(PIP)、动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)及肺、肠系膜微循环的血流量;记录支气管肺泡灌洗液(BALF)中中性粒细胞(PMN)及总细胞计数,计算肺湿/干重比(W/D),行肺组织病理学检查.结果 与C组比较,ALI组和PGE组T1-6时PaO2降低,MPAP及PIP升高,肠系膜微循环血流量降低,BAIF中PMN百分比和肺W/D升高(P＜0.05),ALI组T3-6时肺微循环血流量降低(P＜0.05);与ALI组比较,PGE组T3-6 时PaO2升高,PIP降低,肺微循环血流量增加,T5-6时MPAP降低,T4-6时肠系膜微循环血流量增加,BALF中PMN百分比和肺W/D降低(P＜0.05).ALI组支气管和肺泡腔内可见大量炎性渗出物和红细胞;PGE组肺泡腔内的炎性细胞相对减少,未见红细胞.结论 静脉输注PGE1 30 ng·kg-1·min-1可增加油酸致兔急性肺损伤时肺和肠系,膜微循环血流量,改善肺微循环灌注,减轻肺损伤.     

米力农对心肺转流促炎细胞因子反应及心肌损伤的影响

目的探讨米力农对心肺转流(CPB)诱发的促炎细胞因子反应及心肌损伤的影响。方法24例择期瓣膜替换术病人,随机分成米力农组(M组)和对照组(C组),每组12例。麻醉诱导开始前,M组给予米力农30μg/kg负荷量静注,继以0.5μg·kg-1·min-1持续静脉输注;C组以相同速度输注等量生理盐水。分别于术前(T1)、CPB60min(T2)、CPB结束后2h(T3)、4h(T4)及24h(T5)各时间点测定动脉血中下列各项指标:肿瘤坏死因子α(TNFα)、白细胞介素6(IL6)、白细胞介素8(IL8)、血浆过氧化脂质(LPO)、心肌肌酸激酶同工酶(CKMB)。结果与T1比较,其余各时点两组TNFα、IL6、IL8、LPO、CKMB均明显升高(P<0.05或P<0.01),但M组升高明显低于C组(P<0.05)。结论米力农能有效抑制CPB诱发的促炎细胞因子反应和心肌损伤。     

双心房输注对二尖瓣置换术患者体外循环后肺动脉压的影响

目的 评价双心房输注对二尖瓣置换术患者体外循环后肺动脉压(PAP)的影响.方法 择期行二尖瓣置换术合并肺动脉高压[平均肺动脉压(MPAP)＞50 mm Hg]的患者20例,年龄22～53岁,体重34～57kg,心功能分级Ⅱ或Ⅲ级,随机分为2组(n=10):右心房输注组(R组)和双心房输注组(B组).麻醉诱导后右颈内静脉穿刺置入Swan-Ganz三腔漂浮导管,监测CVP、PAP、肺毛细血管楔压(PCWP)和CO.R组经中心静脉输注前列腺素E130～150 ng·kg-1·min-1和去氧肾上腺素0.2～0.6μg·kg-1·min-1.B组经中心静脉输注前列腺素E130～150 ng·kg·min-1,经左心房输注去氧肾上腺素0.2～0.6μg·kg-1·min-1.分别于给药前5 min(T0)、给药后5 min(T1)、10 min(T2)、30 min(T3)和60 min(T4)时记录MAP、HR、MPAP、PCWP、CVP和CO,计算肺血管阻力指数(PVRI)、体循环血管阻力指数(SVRI)和CI.结果 与T0时比较,R组T1-4时MAP、MPAP、PCWP和PVRI降低,CI升高(P＜0.05),HR、CVP和SVRI差异无统计学意义(P＞0.05),B组T1-4时MAP、CI和SVRI升高,HR、MPAP、PCWP、CVP和PVRI降低(P＜0.05);与R组比较,B组MAP、CI和SVRI升高,HR、MPAP、PCWP、PVRI和CVP降低(P＜0.05).结论 双心房输注可降低二尖瓣置换术患者体外循环后肺动脉压和肺血管阻力.     

门静脉高压犬肝缺血再灌注时肺循环血液动力学及NO/ET和PGI2/TXA2的变化

目的 评价门静脉高压犬肝缺血再灌注时肺循环血液动力学及肺循环一氧化氮(NO)/内皮素(ET)和前列腺素I2(PGI2)/血栓素A2(TXA2)的变化.方法 健康家犬12只,雌雄不拘,体重10～18 kg,随机分为2组(n=6):对照组和模型组.模型组采用部分结扎门静脉的方法 建立犬门静脉高压模型,12周后完全阻断门静脉、肝后下腔静脉30 min,再灌注60 min制备肝缺血再灌注模型.于第2次麻醉后即刻、肝缺血前即刻、缺血5、30 min、再灌注前即刻、再灌注5、10、15、30和60 min(T1-10)时记录心率(HR)、心输出量(CO)、中心静脉压(CVP)、肺动脉楔压(PAWP)和平均肺动脉压(MPAP),计算心脏指数(CI)、肺血管阻力(PVR)和肺血管阻力指数(PVRI),并计算T2-10时CI、CVP、MPAP、PAWP和PVRI相对于T1的变化幅度;于T2、T4和T9时测定肺动脉血浆NO、ET、TXA2和PGI2的浓度,并计算NO/ET和PCI2/TXA2比值.结果 两组肝缺血时CI、CVP、PVRI、PAWP和MPAP均降低,且模型组CI、CVP、PAWP、MPAP降低幅度低于对照组,两组再灌注时CVP、PAWP、MPAP和PVRI均升高,且模型组PAWP和PVRI升高幅度高于对照组(P<0.05或0.01);模型组肝缺血再灌注时肺动脉血浆NO浓度、NO/ET比值和肝缺血时肺动脉血浆TXA2浓度、PGI2/TXA2比值均低于对照组(P<0.01).模型组PVR与肺动脉血浆NO浓度呈负相关(r=-0.567,P<0.05).结论 门静脉高压犬肝缺血再灌注时肺动脉压升高,可能与肺循环NO水平降低、NO与ET失衡有关.     

Management under anesthesia of a patient with renal cell carcinoma extending into the retrohepatic inferior vena cava with the aid of partial cardiopulmonary bypass]

A 70-year-old male with renal cell carcinoma extending into the retrohepatic inferior vena cava was scheduled for radical nephrectomy with vena caval resection under general anesthesia. He had received partial gastrectomy for gastric cancer twelve years before. Computed tomography and inferior vena cavography confirmed that the vena cava was almost completely occluded and that a collateral venous network was well established. It was considered that the surgical approach to the retrohepatic cavals area was technically very difficult, and that there was a high possibility of a pulmonary embolus during the surgical manipulation. To prevent a pulmonary embolus and get good control of the vena cava above the tumor and below the hepatic vein, we decided to use a partial cardiopulmonary bypass (CPB) until the vena cava was clamping above the tumor. Anesthesia was induced with propofol and fentanyl, and maintained with fentanyl and isoflurane-N2O-O2. In the partial CPB blood from the hepatic vein was drained from the inferior vena cava cannula through right atrium, oxygenated by microporus membrane oxygenator, and returned to the left femoral artery. Cannulation to drain the venous circulation entering the vena cava below the tumor was abandoned because the extensive collateral venous network ultimately drains into the superior vena cava. The partial CPB time was 90 min, and the bladder temperature during the CPB was 35-36 degrees C. During the 7.3 hr procedure, the pulmonary embolus did not occur and the total blood loss was 5515 ml. The patient made an uncomplicated recovery and was discharged 30 days after the operation. This newly reported partial-CPB method may be safe and effective for the management under anesthesia of other patients.     

Comparison of nicardipine and isradipine in hypertension following coronary artery bypass graft

OBJECTIVE: Compare the efficacy of isradipine to that of nicardipine for the control of arterial hypertension following coronary artery bypass graft (CABG). STUDY DESIGN: Clinical prospective, randomised study. MATERIAL AND METHODS: 40 patients ASA II or III, mean age 66 +/- 8 years, scheduled for elective CABG were included. If the mean arterial pressure (MAP) was > or = 100 mmHg within the first six post operative hours, the patients were included and randomly attributed to either one of the 2 groups: Gr I (n = 20) received nicardipine, Gr II (n = 20) received isradipine in bolus then in continuous perfusion. HR, MAP, MPAP, CVP, PCWP, CI, SVRI, PVRI and SVI were recorded at: T0 before administration of drugs, T1 = 2 min after the first bolus. T2 when MAP reached 85 +/- 5 mmHg. T3, T4, T5, T6, T7 and T8 at 5, 10, 30, 60, 90 and 120 min after the continuous perfusion. T9 before stopping the perfusion. RESULTS: No significant changes in HR, CVP, PCWP, MPAP or PVRI at any time in both groups. Significant increase in CI at T2 in both groups. Reduction of MAP at T2 was more important (-27%) in Gr I compared to that in Gr II (-22%). This was mainly due to a significant decrease in SVRI. CONCLUSION: Isradipine is effective in the treatment of arterial hypertension following CABG. However there is not any significant beneficial effect of isradipine over nicardipine.     

急性肺损伤时胃黏膜pH值和肺微循环相关性研究

目的 探讨急性肺损伤(acute lung injury,ALI)时胃黏膜pH值(gastric intramucosal pH,pHi)与肺微循环的相关性. 方法 健康家兔24只,体重2.6～3.2 kg,采用随机数字表法分为3组(每组8只):对照组(C组)、模型组(M组)和治疗组(T组).麻醉稳定后30 min (T0),M组和T组制备兔ALI模型,模型制备成功后(T1),T组静脉输注前列腺素E1(prostaglandin E1,PGE1)30 ng·kg-1· min-1.分别于T0、T1及模型成功后30 min(T2)、60 min(T3)、90min(T4)、120min(T5)、150min(T6)、180min(T7),记录平均肺动脉压(mean pulmonary artery pressure,MPAP)、动脉血氧分压(pressure of artery oxygen,PaO2)、气道峰压(peakinspiratory pressure,PIP)及测量肺微循环和pHi.T7时记录支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中中性粒细胞(polymorphonuclear neutrophils,PMN)及总细胞计数,计算肺湿/干重比(wet/dry,W/D).应用线性混合效应模型分析肺微循环和pHi的相关性. 结果 与C组比较,M组与T组T1～T7时PaO2降低,MPAP及PIP升高(P＜0.05);M组和T组BALF中PMN百分比和肺W/D升高(P＜0.05);M组T2～T7时pHi降低,T3～T7肺微循环血流量减少(P＜0.05).与M组比较,T组T3～T7时PaO2升高,T4～T7时PIP降低,T5～T7时MPAP降低(P＜0.05);T组BALF中PMN百分比[(20.341±0.033)比(40.232±0.054)]和肺W/D[(0.191±0.020)比(0.472±0.061)]降低(P＜0.05),T2～T7时pHi升高,T3～T7肺微循环血流量增加(P＜0.05).C组、M组和T组肺微循环的变化与pHi的变化相关(P＜0.05). 结论 随着肺损伤的产生和改善,肺微循环和pHi也发生相应的改变,二者具有相关性,可以通过pHi来预测肺损伤的情况.     

坐位全身麻醉对肺血液动力及肺内分流的影响

目的 观测神经外科手术中坐位全身麻醉对肺血液动力及肺内分流（Ｑｓ／Ｑｔ）的影响。方法 ２８例后颅窝及后颈髓手术病人，采用静脉复合诱导、吸入七氟醚或安氟醚及伍用芬太尼维持麻醉，以Ｓｗａｎ－Ｇａｎｚ导管和动脉、混合静脉缺血气检测方法监测血液动力学和肺内分流状况，参数包括ＣＩ、ＲＡＰ、ＭＰＡＰ、ＰＣＷＰ、ＰＶＲＩ、ｐＨａ、ＰａＣＯ２、ＰａＯ２、ＰａＯ２／ＦｉＯ２及Ｑｓ／Ｑｔ。分别在麻醉前、坐位前、坐位后     

Assessment of pulmonary/systemic blood flow ratio after first-stage palliation for hypoplastic left heart syndrome: development of a new index with the use of doppler echocardiography

OBJECTIVE: Circulatory maldistribution is believed to be a major cause of early death after first-stage palliation for hypoplastic left heart syndrome. Flow reversal in the reconstructed aorta may reflect the pulmonary/systemic blood flow ratio. The purpose of our study was to investigate the utility of arterial PO (2), arterial oxygen saturation, and a newly developed Doppler-derived flow index in predicting the pulmonary/systemic flow ratio after first-stage palliation for hypoplastic left heart syndrome. METHODS: Twenty-four infants who underwent first-stage palliation for hypoplastic left heart syndrome or a variant were studied. Superior vena cava blood samples were drawn to estimate the mixed venous saturation and permit calculation of the pulmonary/systemic blood flow ratio. Fifty-four samples were evaluated within the first 24 hours after surgery. Simultaneous blood draw and Doppler echocardiography were performed with interrogation in the distal aspect of the arch reconstruction. The ratio of the Doppler velocity-time integral of retrograde flow to the velocity-time integral of forward flow was calculated and compared with the pulmonary/systemic blood flow ratio RESULTS: The median mixed venous saturation for the 54 samples was low (38.5%; range, 18%-64%). The median calculated pulmonary/systemic blood flow ratio was 1.4:1 (range, 0.3:1 to 4. 2:1). Pulse pressure, mixed venous saturation, and arterial PO (2) were not statistically significant predictors of the measured pulmonary/systemic blood flow ratio. Although both aortic oxygen saturation (R (2) = 0.84, P <.01) and Doppler flow reversal ratio (R (2) = 0.94, P <.001) were significantly associated with the measured pulmonary/systemic blood flow ratio, the model coefficient of determination was greatest for Doppler flow reversal ratio. CONCLUSION: Measures of arterial oxygen saturation and arterial PO (2) may be misleading in assessing the circulatory status of infants after first-stage palliation for hypoplastic left heart syndrome. Doppler echocardiography, through use of the Doppler flow reversal ratio, provides a more useful measure of pulmonary/systemic blood flow ratio. Low mixed venous saturation after surgery may be due to factors other than pulmonary overcirculation, such as ventricular dysfunction and low cardiac output.     

改良股动、静脉插管体外循环中器官灌注效果的实验研究

目的比较改良股动、静脉插管体外循环(CPB)与常规CPB在相同流量灌注时对脑、肺、肝、肾、肠等重要器官灌注的效果。方法将20条犬(体重10～15kg)随机分为两组,每组10条。胸腔镜组:改良股动、静脉插管后建立CPB,经电视胸腔镜施行手术;常规开胸组:常规建立CPB手术。两组建立CPB后以相同的流量灌注,分别在无名动脉、左颈总动脉、肠系膜上动脉、肾动脉、对侧腘动脉、同侧腘动脉及其所有相伴行的静脉留置套管针,连接测压管道,于麻醉诱导后即刻(T1)、主动脉阻断前(T2)、主动脉阻断15min(T3)、主动脉开放15min(T4)、CPB结束后20min(T5)记录动、静脉压,并在以上时间点抽取相应部位静脉血测定静脉血氧饱和度(SvO2)。结果除了胸腔镜组同侧腘动脉灌注压明显低于常规开胸组(P<0.01)外,两组其余动脉的动脉灌注压比较差异均无统计学意义。主动脉阻断前、主动脉阻断15min、主动脉开放15min,胸腔镜组肾静脉、肠系膜上静脉、对侧腘静脉和同侧腘静脉的静脉压明显高于常规开胸组(P<0.05);胸腔镜组肾静脉、肠系膜上静脉、对侧腘静脉和同侧腘静脉SvO2低于常规开胸组(P<0.05)。结论改良股动、静脉插管与常规CPB相同流量灌注时其动脉灌注压相近,经股动、静脉插管下腔静脉平面以下的静脉压较常规开胸手术略高,因此,对小儿胸腔镜CPB的器官保护提供了理论依据。     

Pulmonary hypertension and leukosequestration after lower torso ischemia.

Ischemia stimulates thromboxane (Tx) synthesis. This study tests the hypothesis that the cardiopulmonary dysfunction that may follow aortic declamping is related to Tx. Anesthetized dogs (N = 15) were subjected to 4 hours of infrarenal aortic cross-clamping. In untreated control animals (N = 7), plasma levels of TxB2 rose from 654 +/- 74 pg/mL to 1238 +/- 585 pg/mL at 5 min (p less than 0.05), and to 3174 +/- 912 pg/mL 3 hours after declamping (p less than 0.05). Mean pulmonary artery pressure (MPAP) rose 5 min after declamping from 13 +/- 2 mmHg to 21 +/- 2 mmHg (p less than 0.05). Cardiac Index (CI) declined during ischemia from 181 +/- 30 mL/kg.min to 128 +/- 16 mL/min.kg (p less than 0.05), and to 80 +/- 8 mL/min.kg after 4 hours of reperfusion (p less than 0.05). Platelet counts declined but platelets labeled with In 111 did not accumulate in the lungs, whereas quantitative counts of polymorphonuclear leukocytes (PMN) in the lungs 4 hours after declamping yielded 213 +/- 33 PMN/25 high power fields (HPF) in dependent areas of the lung and 153 +/- 26 PMN/25 HPF in nondependent areas. The wet/dry weight ratio of the lungs was not elevated, although foci of proteinaceous exudate and PMNs in alveoli were noted. Another group of dogs (N = 8) were pretreated by random choice with the Tx synthase inhibitor OKY-046 2 mg/kg IV every 2 hours, which led to: lower TxB2 levels at baseline 95 +/- 35 pg/mL (p less than 0.05), 5 min after ischemia 140 +/- 93 pg/mL and after 3 hours of reperfusion 122 +/- 36 (p less than 0.05); lower MPAP, 16 +/- 2 mmHg (p less than 0.05); higher CI throughout (p less than 0.05); normal histology and reduced pulmonary PMN sequestration both in dependent 127 +/- 15 PMN/25 HPF and nondependent areas of the lungs 95 +/- 11 PMN/25 HPF (p less than 0.05). In animals undergoing sham ischemia (N = 3), levels of TxB2 and cardiopulmonary function remained unchanged from baseline. There were 150 PMN/25 HPF in dependent and 85 PMN/25 HPF in nondependent lung areas. The results indicate that ischemia-generated Tx mediates a rise in MPAP, a fall in CI, and PMN entrapment in the lungs.     

心脏双瓣置换术麻醉期间血流动力学变化

采用Ｓｗａｎ－Ｇａｎｚ导管及热稀释原理测定心排血量方法，对４９例择期行二尖瓣及主动脉瓣双瓣置换术麻醉期间的血流动力学进行了测定。结果表明：麻醉前心脏指数（ＣＩ）、左心功指数（ＬＶＷＩ）属正常范围，但平均肺动脉压（ＭＰＡＰ）、肺毛细血管嵌压（ＰＣＷＰ）、肺总阻力指数（ＰＴＲＩ）、右心功指数（ＲＶＷＩ）明显异常。诱导后右心前负荷（ＲＡＰ）升高，右心后负荷（ＭＰＡＰ、ＰＣＷＰ）、平均动脉压（ＭＡＰ）、（ＣＩ及左、右心作功降低，显示有心功能可能受抑；气管插管及锯胸骨后血流动力学各项指标均不同程度地回升并超过诱导前，提示心血管功能仍保持对应激的反应能力；主动脉及腔静脉插管时ＣＩ、ＭＡＰ、ＭＰＡＰ、ＰＣＷＰ、ＬＶＷＩ及ＲＶＷＩ均显著降低，显然与此期间近心性、出血及搬动、挤压心脏、严重心律失常等干扰左、右心前后负荷的平衡有关；体外循环后，由于手术纠正了瓣膜病变所致的血流障碍，ＭＰＡＰ、ＰＣＰＰ、ＰＴＲＩ、及 ＲＶＷＩ显著持续下降，而反映肺血管阻力的ＰＶＲＩ无变化；心肺转流（ＣＰＢ）结束后ＭＡＰ、ＳＶＲＩ明显减低，心脏功能也受损，提示此期间应尽早应用心血管活性药并提高患者的血细胞比容。