吸入伊洛前列素对不同类型肺动脉高压患者氧动力学的影响

目的 分析雾化吸入伊洛前列素对动脉型肺动脉高压(PAH)及慢性血栓栓寒性肺动脉高压(CTEPH)患者的氧动力学的急性影响.方法 顺序收集北京朝阳医院2006年6月至2009年1月连续收治的明确诊断为PAH的患者22例及CTEPH患者24例,均行右心导管检查,监测基线状态及吸人伊洛前列素20μg后的即刻血流动力学特征,同步抽取肺动脉及股动脉血行血气分析,计算氧动力学参数.结果 基线状态PAH及CTEPH患者的PaO2分别为(63±10)mm Hg(1 mm Hg=0.133 kPa)及(59 ±10)mm Hg,氧输送指数(DO2I)分别为(458±136)ml·min-1·m-2及(386 ±92)ml·min-1·m-2,氧消耗指数分别为(135±53)ml·min-1·m-2及(131±43)ml·min-1·m-2.吸入伊洛前列素后即刻,2组患者肺内分流率均显著升高(均P<0.01),P4O2显著升高(均P<0.01);动脉血氧含量均显著降低(均P<0.05);混合静脉血氧合指标及氧摄取率无明显变化;DO2I无明显增加,氧消耗指数出现不同程度降低;2组患者各项氧动力学参数变化幅度无差异.基线状态CTEPH患者混合静脉血氧饱和度(SvO2)、静脉血氧含量(CvO2)及DO2I均显著低于PAH患者(均P<0.05).吸药后,CTEPH患者PaO2、SvO2及CvO2均显著低于PAH患者(均P<0.05).结论 PAH及CTEPH患者存在低氧血症及氧动力学异常;雾化吸入伊洛前列素后患者肺内分流增加,氧动力学状态无改善.CTEPH患者的氧动力学状态较PAH患者更差,应用伊洛前列素时需加强氧合功能监测,必要时给予氧疗支持.     

主动脉内球囊反搏在心脏外科围术期的临床应用

目的：探讨主动脉内球囊反搏术（IABP）在心脏外科围术期患者出现低心排血量综合征时应用的有效性及可行性。方法：回顾性分析40例使用IABP的原因及使用12h、24h、48h后平均动脉压（MAP）、心脏指数（CI）、肺动脉嵌压（PAWP）、氧输送指数（DO2I）、氧摄取率（O2ER）等血流动力学指标变化。结果：与IABP前比较,IABP12h、24h、48h后MAP[48h：（56．40±6．51）mmHg比（73．00±3．36）mmHg]、CI[48h：（1．74±0．21）L·min-1·m-2比（2．74±0．21）L·min-1·m-2]、DO2I[48h：（267．36±15．95）ml·min-1·m-2比（429．60±33．19）ml·min-1·m-2]均明显升高,尿量[48h：（25．44±3．88）ml／h比（99．48±9．48）ml／h]明显增加,PAWP[48h：（18．00±1．66）mmHg比（12．60±0．71）mmHg]、O2ER[48h：（44．45±4．00）％比（31．41±1．25）％]均明显下降（P均〈0．01）。40例中死亡7例（19．5％）。结论：主动脉内球囊反搏术可有效改善血流动力学,对于围术期低心排患者的治疗安全且有效。     

去甲肾上腺素与多巴胺治疗感染性休克的比较研究

目的:探讨去甲肾上腺素与多巴胺治疗感染性休克的临床效果。方法:选择我院收治的60例感染性休克患者随机分为去甲肾上腺素组(NE组)和多巴胺组(DA组)。2组均给予有效液体复苏后,DA组由中心静脉泵入多巴胺2μg/(kg·min),NE组泵入去甲肾上腺素0.1μg/(kg·min)。比较2组患者治疗前后血流动力学及微循环灌注指标改善情况,组织氧代谢改善情况。结果:2组治疗前HR、CVP、MAP、尿量血差异无统计学意义(P0.05)。NE组治疗后2、4、6 h HR、CVP、MAP、尿量、血乳酸清除率、中心静脉氧饱和度显著优于DA组(P0.05)。结论:采用多巴胺与去甲肾上腺素治疗感染性休克均可改善微循环及组织氧代谢,但去甲肾上腺素疗效更佳,值得临床推广应用。     

中心静脉压评估感染性休克患者容量反应性的应用

目的 探讨中心静脉压(CVP)评估感染性休克患者容量反应性的作用.方法 对入选的66例感染性休克患者行容量负荷试验,以提高患者CVP 2 mm Hg(1mm Hg=0.133 kPa)为目标,心脏指数(CI)≥300 ml·min-1·m-2为有反应者(有反应组),CI<300 ml·min-1·m-2为无反应者(无反应组).CVP由上腔静脉导管测量,全心舒张末容积指数(CEDVI)、胸腔内血容量指数(ITBVI)、每搏输出量指数(SVI)、CI经肺热稀释法和脉搏指示连续心排血量技术(PiCCO)测量.结果 (1)初始CVP有反应组明显低于无反应组,初始CVP用于诊断容量反应性有意义(P<0.05),其中CVP=11 mill Hg时敏感度为0.884,特异度为0.601.(2)有反应组与无反应组比较,初始ITBVI、GEDVI、CI、收缩压、舒张压、平均动脉压、心率差异无统计学意义.容量负荷试验前后,有反应组与无反应组比较,△ITBVI、△GEDVI、△CI、△SVI差异有统计学意义,△ITBVI、△GEDVI用于诊断容量反应性有意义.(3)CVP≤11 mm Hg者与CVP>11 mm Hg者比较,初始ITBVI、GEDVI差异无统计学意义.容量负荷试验前后,CVP≤11 mm Hg者与CVP>11 mm Hg者比较,△ITBVI、△GEDVI差异有统计学意义.结论 (1)用CVP评估感染性休克患者容量反应性有指导意义,但CVP >11 mm Hg时患者对容量负荷试验有反应的可能性较小;(2)与CVP相比,初始ITBVI、GEDVI评估感染性休克患者容量反应性无明确优势,当CVP无法良好预测容量反应性时△ITBVI、△GEDVI有指导意义.     

呼气末二氧化碳分压的变化对感染性休克机械通气患者容量反应性的预测价值

目的 探讨呼气末二氧化碳分压(PETCO2)在被动抬腿试验中的变化及对感染性休克机械通气患者容量反应性的预测价值.方法 选择行机械通气治疗的感染性休克患者42例.分别在被动抬腿试验、容量负荷试验后采用脉搏指示连续心输出量(PiCCO)监测患者血流动力学变化,呼气末二氧化碳监测装置监测患者PETCO2.以接受者操作特征曲线(ROC曲线)分析被动抬腿试验后PETCO2的变化对容量反应性的预测价值.结果 (1)42例患者中,24例有容量反应性(有反应组),18例无反应(无反应组).有反应组患者被动抬腿试验后心指数(CI)增加(21.4±12.9)％,PETCO2增加(9.6±4.7)％;无反应组CI[(3.2±1.1) L·min-1·m-1]和PETCO2[(33±4) mm Hg(1 mm Hg =0.133 kPa)]较基线值无变化[(3.0±1.0)L· min-1·m-1;(32±4) mm Hg;P值均＞0.05].有反应组患者被动抬腿试验后CI和PETCO2的变化均高于无反应组[(21.4±12.9)％比(6.4±3.5)％,(9.6±4.7)％比(3.0±2.6)％;P值均＜0.05].(2)相关分析:被动抬腿试验后CI的变化与PETCO2的变化呈正相关(r=0.64,P＜0.05).(3)被动抬腿试验后PETCO2的变化预测容量反应性的ROC曲线下面积为0.900±0.056(95％ CI0.775 ～1.000),以5％为临界值,敏感性为88.0％,特异性88.2％.结论 被动抬腿试验后PETCO2的变化可以作为预测感染性休克机械通气患者容量反应性的无创、简便的指标.     

老年肺心病死亡患者的氧动力学变化

目的探讨老年肺心病死亡患者的氧动力学变化。方法选取1980～2000年间入住我院肺心病患者76例,随访5年,期间对死亡43例及存活33例的患者进行各项血流动力学及氧动力学监测对比。对并发消化道出血及感染性休克患者死亡前24～72h行血流动力学及氧动力学监测。结果死亡组及存活组平均肺动脉压(MPAP)分别为(41.3±10.6)mmHg,(28.9±6.5)mmHg(P<0.01);心脏指数(CI)分别为(1.92±0.41)L.min-1.m-2,(2.6±0.48)L.min-1.m-2(P<0.01);死亡组动脉血氧分压(PaO2)为(42.3±4.3)mmHg、氧输送(DO2)与氧耗(VO2)均较存活组明显下降、DO2与VO2呈正相关(r=0.71)。死亡年限愈短,MPAP愈高,CI、DO2、VO2、PaO2愈低。死亡的43例患者临终前39例(90.6%)有复合酸碱平衡紊乱,25例(58.13%)痰菌培养出致病菌57株。41例(95.3%)出现多器官功能障碍综合征(MODS)。12例肺心病感染性休克与消化道出血的临终前24～72h血流动力学及氧动力学变化明显的不同。结论导致肺心病的死亡除严重的低PaO2外,还存在组织氧的释放、摄取和利用障碍。     

中心静脉-动脉二氧化碳分压差/动脉-深静脉氧含量差比值对感染性休克患者复苏后器官功能障碍进展的预测价值

目的探讨中心静脉-动脉二氧化碳分压差(Pv-aCO2)/动脉-深静脉氧含量差(Ca-vO2)比值对感染性休克患者复苏后器官功能障碍进展的预测价值。方法选2018年7月—2019年6月安徽医科大学第一附属医院重症医学科连续收治的完成常规血流动力学复苏且资料完整的感染性休克患者99例,收集患者完成常规复苏时去甲肾上腺素(NE)用量、血乳酸、Pv-aCO2、Pv-aCO2/Ca-vO2比值等资料。根据感染性休克患者完成复苏序贯器官衰竭评分(SOFA)在48h动态变化,将入选患者分为器官功能未恶化者和器官功能恶化者。logistic 多因素回归分析感染性休克患者复苏后器官功能障碍进展的独立危险因素。采用受试者操作特征(ROC)曲线分析Pv-aCO2/Ca-vO2比值对器官功能障碍进展的预测价值。结果 99例感染性休克患者常规复苏完成48 h时, 25例(25.25%)患者器官功能障碍恶化。器官功能障碍未恶化者相比器官功能障碍恶化者,去甲肾上腺素用量[0.61(0.27,1.42)μg·kg-1·min-1 比 0.91(0.47,2.87)μg·kg-1·min-1]、血乳酸[2.93(1.7...     

动态动脉弹性对重症肺炎休克患者扩容后血压变化的预测价值

目的探讨基线动态动脉弹性(Dynamic arterial elasticity,Eadyn)对重症肺炎所致感染性休克患者快速扩容后血压反应的预测价值,同时探索该类患者通过基线Eadyn来调整优化升压治疗的方案可行性。方法选取2018年1月至2019年5月入住佛山市第二人民医院重症监护病房(ICU)的重症肺炎休克患者64例为研究对象,根据快速扩容后患者平均动脉压(Mean arterial pressure,MAP)升高的程度分为MAP有反应组(≥15%)和MAP无反应组(<15%),分析比较两组患者快速扩容前后Eadyn等血流动力学参数有无差异;另外,将Eadyn<0.89分为分为增加去甲肾上腺素(NE增加组),和维持原有NE的使用不变组(NE不变组),快速扩容后予以患者液体复苏,比较两组患者复苏达标率、复苏所用平衡盐溶液量、EVLW、PVPI等预后相关指标。结果MAP有反应组扩容前Eadyn(0.91±0.22)明显高于MAP无反应组(0.70±0.28)(P<0.05);基线Eadyn对重症肺炎休克患者快速扩容后MAP有反应的AUC值高达0.89,其灵敏度90.15%,特异度89.23%,cutoff值为0.84;NE增加组其3 h EGDT达标率明显高于NE不变组(84.21%vs68.42%,P<0.05);NE增加组患者3 h内补液量显著低于NE不变组(1415.4±420.7 mL vs2178.9±399.6 mL,P<0.05);同时,NE增加组其EVLW明显低于NE不变组(7.21±1.68 mL/kg vs10.12±2.33 mL/kg,P<0.05)。结论基线Eadyn可有效预测重症肺炎感染性休克患者快速扩容后的血压改变,另外基线Eadyn值可用于指导对患者单纯快速扩容还是尽早联合应用升压药物之间的治疗分层。     

老年原发性高血压患者红细胞分布宽度与早期肾功能损害的相关性分析

目的探讨老年原发性高血压患者红细胞分布宽度(RDW)与早期肾功能损害的关系。方法入选2014年7~12月首都医科大学宣武医院高血压门诊364例老年原发性高血压患者作为观察组,另连续选取100名同期年龄匹配的体检健康者作为对照组,记录两组年龄、性别、收缩压、舒张压、体质指数(BMI)、空腹血糖(FPG)、三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、尿酸、肌酐、尿素氮、尿蛋白定性及血常规等。采用肾脏病饮食改良(MDRD)简化公式计算估算肾小球滤过率(eGFR),根据eGFR水平将高血压组患者分为两组:eGFR下降组(eGFR<90 ml·min-1·1.73 m-2)102例与e GFR正常组(eGFR≥90 ml·min-1·1.73 m-2)262例。并比较RDW、eGFR、BMI和生化指标等参数在各组间的变化差异,分析RDW与eGFR的相关性。结果 (1)与对照组比较,高血压组患者BMI[(25.84±2.95)kg/m2比(23.79±3.12)kg/m2]、TG[(1.96±1.34)mmol/L比(1.58±0.69)mmol/L]、血尿酸[(325.37±88.97)mmol/L比(296.63±80.11)mmol/L]和RDW(13.05%±0.87%比12.59%±0.61%)水平升高,HDL-C[(1.43±0.38)mmol/L比(1.61±0.33)mmol/L]和e GFR[(104.63±28.47)ml·min-1·1.73 m-2比(124.49±25.96)ml·min-1·1.73 m-2]水平下降,差异均有统计学意义(均为P<0.05);(2)在高血压患者中,与e GFR正常组比较,e GFR下降组的年龄[(62.6±9.3)岁比(59.9±8.8)岁]、BMI[(26.99±3.05)kg/m2比(25.39±2.78)kg/m2]、收缩压[(163.44±15.18)mm Hg比(154.42±12.27)mm Hg]、高血压病程[(12.4±3.7)年比(9.8±3.6)年]、血尿酸[(358.84±97.93)mmol/L比(312.34±81.79)mmol/L]、肌酐[(87.56±21.16)μmol/L比(58.60±11.01)μmol/L]、尿蛋白阳性率(46.10%比21.00%)及RDW(13.45%±0.94%比12.90%±0.79%)均升高,而eGFR[(73.85±12.32)ml·min-1·1.73 m-2比(116.61±23.54)ml·min-1·1.73 m-2]下降,差异均有统计学意义(均为P<0.05);经Pearson相关分析显示,高血压组患者RDW与eGFR水平呈负相关(r=-0.237,P=0.000);(3)Logistic多元回归分析显示,RDW是eGFR的危险因素(OR=1.485,P=0.015)。结论老年原发性高血压患者的RDW与eGFR呈负相关,RDW可作为评估老年原发性高血压患者早期肾功能损害的预测因素。     

阿拉明或多巴胺对感染性休克患者血流动力学血乳酸及预后的影响

目的比较感染性休克患者起始应用阿拉明或多巴胺对血流动力学、血乳酸及病死率的影响。方法选择2008年9月至2010年8月广东省人民医院88例感染性休克患者起始应用阿拉明升压治疗37例、多巴胺51例,观察血流动力学、血乳酸、病死率。结果阿拉明组治疗后6 h心率增快[(119.2±12.2)次/min对(136.5±18.3)次/min,P<0.01],平均动脉压(MAP)升高[(36.6±11.0)mmHg对(65.8±17.1)mmHg,P<0.01];多巴胺组治疗后6 h心率增快[(112.2±12.3)次/min对(131.3±16.8)次/min,P<0.01],MAP升高[(39.1±10.9)mmHg对(70.5±17.4)mmHg,P<0.01]。阿拉明组治疗后6 h与治疗前血乳酸差值大于多巴胺组[(-1.07±0.77)mmol/L对(-0.66±0.42)mmol/L,P<0.01];乳酸清除率差异亦有统计学意义[(20.5±14.7)%对(14.4±10.4)%,P<0.05]。结论阿拉明和多巴胺均能有效维持感染性休克患者血流动力学稳定,阿拉明较多巴胺更有效清除血乳酸。     

艾司洛尔对瑞芬太尼诱导气管插管时血流动力学的影响

目的研究艾司洛尔在抑制瑞芬太尼联合丙泊酚诱导气管插管时心血管反应的临床效果与安全性。方法美国麻醉医师协会(ASA)分级Ⅰ级的100例患者按随机数法均分为对照组和艾司洛尔组。两组患者均采用瑞芬太尼、丙泊酚及罗库溴铵诱导,插管前1 min给予药物,对照组给予生理盐水10 ml静脉注射,艾司洛尔组给予0.5 mg/kg艾司洛尔稀释于生理盐水10 ml中静脉注射。监测并比较麻醉诱导前(T0)、气管插管前(T1)、插管后1 min(T2)、2 min(T3)和3 min(T4)时的平均动脉压(MAP)和心率(HR)。结果 T1时,艾司洛尔组和对照组的MAP[(76±13)mm Hg,(75±12)mm Hg]及HR[(65±9)次/min,(64±8)次/min]较T0时的MAP[(87±12)mm Hg,(86±12)mm Hg]及HR[(75±12)次/min,(74±12)次/min]明显下降(P<0.01),下降程度组间比较差异无统计学意义(P>0.05)。T2、T3和T4时,对照组的MAP[(103±23)mm Hg,(106±21)mm Hg,(89±19)mm Hg]和HR[(85±7)次/min,(83±8)次/min,(79±9)次/min]较T1时MAP[(75±12)mmHg]和HR[(64±8)次/min]明显升高(P<0.05),而艾司洛尔组的MAP和HR在插管后升高不明显[插管后MAP:(89±15)mm Hg,(86±14)mm Hg,(74±12)mm Hg,HR:(66±13)次/min,(74±12)次/min,(72±5)次/min;插管前MAP:(76±13)mm Hg,HR(65±9)次/min,P<0.01]。艾司洛尔组有8例患者在插管后HR下降到60次/min以下,最低为53次/min。结论艾司洛尔能有效抑制气管插管时的心血管反应,0.5 mg/kg艾司洛尔与瑞芬太尼合用是安全的。     

Effect of dopamine vs norepinephrine on hemodynamics in septic shock. Emphasis on right ventricular performance

The effects of continuously infused dopamine and norepinephrine on hemodynamics, oxygen metabolism, and right ventricular (RV) performance were studied by crossover design in ten patients with septic shock who needed treatment with vasoactive drugs after fluid replacement. Standard hemodynamic measurements were obtained and RV performance assessed before and 1 h after the start of the infusion. All but one patient had pulmonary hypertension, and in seven the RV ejection fraction (RVEF) was lower than 50 percent at baseline. Drugs were titrated to a systolic arterial blood pressure of mean 106 +/- 18 mm Hg for dopamine and 116 +/- 20 mm Hg for norepinephrine (NS). Dopamine infusion increased the cardiac index (CI) 16 percent (p less than 0.02), but heart rate and systemic and pulmonary vascular resistances were unchanged. With norepinephrine CI was unchanged, a heart rate decreased 7 percent (p less than 0.05), and systemic and pulmonary vascular resistance increased 35 and 26 percent, respectively (p less than 0.05). With both drugs, RV volumes and RVEF remained unchanged, and systemic oxygen consumption increased equally (by 19 percent for dopamine and 22 percent for norepinephrine, p less than 0.05); systemic oxygen delivery rose by 17 percent during dopamine infusion and was unchanged during norepinephrine infusion. Norepinephrine increased oxygen extraction vs dopamine (p less than 0.05). There were no differences in urinary output. Norepinephrine may improve the RV oxygen supply/demand ratio, but this potentially beneficial effect on RV ejection fraction may be offset by a concomitant increase in pulmonary vascular resistance and RV afterload. Norepinephrine may not adversely affect the peripheral circulation. In short-term treatment of volume-resuscitated, severe septic shock complicated by pulmonary hypertension and impaired RV performance, norepinephrine may be at least as effective as dopamine.     

Effects of dobutamine on gastric mucosal perfusion and hepatic metabolism in patients with septic shock

We prospectively evaluated the effects of dobutamine on gastric mucosal perfusion and hepatocytic clearance in patients with septic shock. After resuscitation with volume expansion and norepinephrine (12 patients) as needed, 14 hemodynamically stable patients (median age: 60 yr, median SAPS II score: 47) were given an infusion of 7.5 microg/kg/min dobutamine for 1 h. Gastric mucosal perfusion and hepatocytic clearance were assessed with tonometry and indocyanine green (ICG) elimination, respectively. All measurements were made before dobutamine infusion, after 1 h of dobutamine infusion, and 1 h after the infusion ended. Cardiac output (thermodilution technique) increased with dobutamine from a baseline median level of 4.0 L/min/m(2) (range: 1.7 to 7.4 L/min/m(2)) to 5.0 L/min/m(2) (range: 3.5 to 8.9 L/min/m(2)) (p = 0.004) and returned to baseline levels after dobutamine infusion ended. The gastric-arterial PCO(2) difference decreased from a baseline median level of 13 mm Hg (range: 5 to 54 mm Hg) to 7 mm Hg (range: 5 to 48 mm Hg) (p = 0.005). ICG elimination was low in all patients at baseline (median plasma disappearance rate: 12.2%; range: 7.6 to 16.2%) and did not change significantly during or after dobutamine infusion. In summary, dobutamine increases gastric mucosal perfusion but does not alter hepatocytic clearance in patients with septic shock. The absence of a beneficial effect of dobutamine on hepatocytic clearance may be related to profound alterations in hepatocellular metabolism during septic shock.     

The effects of dobutamine on cardiac sympathetic activity in patients with congestive heart failure

OBJECTIVES: The goal of this work was to study the effects of short-term infusion of dobutamine on efferent cardiac sympathetic activity. BACKGROUND: Increased efferent cardiac sympathetic activity is associated with poor outcomes in the setting of congestive heart failure (CHF). Dobutamine is commonly used in the therapy of decompensated CHF. Dobutamine, through its effects on excitatory beta-receptors, may increase cardiac sympathetic activity. METHODS: Seven patients with normal left ventricular (LV) function and 13 patients with CHF were studied. A radiotracer technique was used to measure cardiac norepinephrine spillover (CANESP) before and during an intravenous infusion of dobutamine titrated to increase the rate of rise in LV peak positive pressure (+dP/dt) by 40%. RESULTS: Systemic arterial pulse pressure increased significantly in response to dobutamine in the normal LV function group (74 +/- 3 mm Hg to 85 +/- 3 mm Hg, p = 0.005) but remained unchanged in the CHF group. Dobutamine caused a significant decrease in LV end-diastolic pressure in the CHF group (14 +/- 2 mm Hg to 11 +/- 2 mm Hg, p = 0.02), an effect not observed in the normal LV group. In the normal LV function group, CANESP did not change in response to dobutamine (75 +/- 22 pmol/min vs. 72 +/- 22 pmol/min, p = NS). In contrast, dobutamine infusion was associated with a significant reduction in CANESP in patients with CHF (199 +/- 43 pmol/min to 128 +/- 30 pmol/min, p < 0.0009). CONCLUSIONS: Dobutamine infusion caused a significant sympatholytic response in patients with CHF. This sympathetic withdrawal response is probably related to reduction of LV filling pressures and/or activation of ventricular mechanoreceptors with dobutamine infusion.     

乳酸清除率监测在老年感染性休克液体复苏中的价值

目的:观察老年感染性休克患者早期目标指导治疗(EGDT)过程中乳酸清除率的变化与复苏达标指标间的关系,探讨其对液体复苏疗效评价的价值。方法:50例符合感染性休克诊断标准的老年患者入选进行EGDT。分析达标组和未达标组患者复苏前后平均动脉压(MAP)、右房压(RAP)、混合静脉血氧饱和度(SvO2)、和急性生理和慢性健康评分(APACHEII)的变化,测定血乳酸浓度,计算乳酸清除率,并与上述指标作相关分析。结果:感染性休克进行EGDT,达标率70%;达标患者中RAP(14.38±1.04)与未达标组(13.08±1.08)比较差异有显著性意义(P<0.05);乳酸清除率(%)与未达标组比较差异有显著性意义(25.20±14.03,8.51±19.24,P<0.05);SvO2(%)在两组间比较有显著性差异(73.62±2.33,64.34±4.29,P<0.05)。达标患者乳酸清除率与复苏后SvO2呈显著相关性(r=0.50,P<0.05)。结论:应用动脉血乳酸清除率监测全身组织灌注和氧代谢变化,对评价复苏疗效更有意义,应作为感染性休克患者EGDT液体复苏中的达标指标之一加以重视。     

Low-dose vasopressin in the treatment of septic shock in sheep

After induction of cecal perforation, 20 anesthetized sheep were randomized to be treated, when arterial blood pressure fell below 75 mm Hg, with vasopressin (fixed dose of 0.02 U/minute), norepinephrine (0.5-5 microg/kg/minute titrated to maintain mean arterial pressure between 75 and 85 mm Hg), vasopressin + norepinephrine (vasopressin at fixed dose 0.01 U/minute plus norepinephrine titrated as for norepinephrine only group), or no vasopressor (Ringer's lactate [control]). Mean arterial pressure was well maintained in all treatment groups. Superior mesenteric arterial blood flow was significantly lower in the vasopressin + norepinephrine group than in the vasopressin group. Vasopressin alone or combined with norepinephrine limited the increase in blood lactate concentration and ileal PCO2-gap compared with control and norepinephrine groups. Urine output was higher in the vasopressin group than in control and norepinephrine groups. Survival time was longer in the vasopressin (30 +/- 6 hours) and vasopressin + norepinephrine (30 +/- 3 hours) groups than in the norepinephrine group (20 +/- 1 hours, p < 0.05) and in all treatment groups than in the control group (17 +/- 2 hours, p < 0.05). Tissue injury was less severe in the vasopressin and vasopressin + norepinephrine groups than in the others. In this clinically relevant model of septic shock due to peritonitis, vasopressin administration (alone or with norepinephrine) can prolong survival.     

Characterization of a hyperdynamic murine model of resuscitated sepsis using echocardiography.

A small animal model of sepsis that reproduces the vasodilation, hypotension, increased cardiac output, and response to treatment seen in patients with septic shock would be useful for studies of pathophysiology and treatment, but no current models replicate all of these features. Mice were made septic by cecal ligation and puncture and resuscitated with fluids and antibiotics every 6 h. Blood pressure was measured in anesthetized mice with manometric catheters, and echocardiography was performed in these animals every 6 h. Survival in treated septic mice was improved compared with untreated mice (44% versus 0%, p < 0.01). In control mice, heart rate (HR, 420 +/- 31 beats/min), mean arterial pressure (Pa, 100 +/- 8 mm Hg), stroke volume (SV, 26 +/- 4 microl), and cardiac output (12.5 +/- 6.6 ml/min) were unchanged over 48 h. In septic mice Pa was significantly decreased (102 +/- 14 to 65 +/- 19 mm Hg, p < 0.02), starting at 12 h. HR and cardiac output increased significantly (HR, 407 +/- 70 to 524 +/- 76 beats/min, cardiac output, 11.6 +/- 2.0 to 17.1 +/- 1.5 ml/min, p < 0.01). SV (24 +/- 5 microl) remained constant. This fluid-resuscitated, antibiotic-treated model replicates the mortality, hypotension, and hyperdynamic state seen in clinical sepsis. Precise determination of serial hemodynamics in this model may be useful to elucidate pathophysiologic mechanisms and to evaluate new therapies for septic shock.     

Effects of inhibition of basal nitric oxide synthesis on carotid-femoral pulse wave velocity and augmentation index in humans

Aortic stiffness, as measured by carotid-femoral pulse wave velocity (PWV), is a powerful, independent predictor of vascular risk. PWV in muscular arteries is influenced by basal nitric oxide (NO) release. It is not known whether NO also influences carotid-femoral PWV. We examined the effects of an NO synthase inhibitor, NG-monomethyl-l-arginine (L-NMMA), on carotid-femoral PWV and aortic augmentation index (AIx, an indirect measure of arterial stiffness). To control for effects of L-NMMA on distending pressure, we used doses of norepinephrine and dobutamine that caused similar changes in mean arterial blood pressure (MAP). Healthy men (32 to 48 years old, n=8) were studied on 4 occasions and received, in random order, vehicle, L-NMMA (3 mg x kg(-1) by intravenous bolus followed by 3 mg x kg(-1) x h(-1)), norepinephrine (50 ng x kg(-1) x min(-1)), and dobutamine (2.5 to 10 microg x kg(-1) x min(-1)), each for 30 minutes. PWV and AIx were measured by carotid-femoral PWV and radial tonometry, respectively. L-NMMA and norepinephrine increased MAP by 7.8+/-1.7 and 9.7+/-2.1 mm Hg, respectively (each P<0.05 vs vehicle) and increased PWV by 0.7+/-0.2 and 1.0+/-0.3 m x s(-1) (each P<0.01 vs vehicle). Dobutamine, at doses that produced a similar increase in MAP (9.6+/-2.9 mm Hg), increased PWV by 0.8+/-0.2 m x s(-1) (P<0.01 vs vehicle). Changes in PWV caused by the 3 pressor agents were closely correlated with changes in MAP (R>0.99, P<0.0001). L-NMMA and norepinephrine increased AIx, but dobutamine decreased AIx (P<0.01 vs norepinephrine and L-NMMA). Effects of inhibition of basal NO release on carotid-femoral PWV can be explained by the change in MAP that this causes rather than any specific effect of NO inhibition within the aorta.     

Systemic and coronary effects of intravenous milrinone and dobutamine in congestive heart failure

The effects of dobutamine and intravenous milrinone on systemic hemodynamics, coronary blood flow and myocardial metabolism were studied in 11 patients with severe congestive heart failure. Although milrinone and dobutamine similarly increased cardiac index from 1.9 +/- 0.4 to 2.5 +/- 0.4 liters/min per m2 (p less than 0.001) and from 1.9 +/- 0.4 to 2.8 +/- 0.8 liters/min per m2 (p less than 0.001), respectively, milrinone decreased left ventricular end-diastolic pressure to a greater extent than dobutamine, that is, from 26 +/- 6 to 12 +/- 8 mm Hg (p less than 0.001) versus 26 +/- 8 to 20 +/- 8 mm Hg (p less than 0.001). In contrast to dobutamine, milrinone significantly reduced mean systemic arterial and right atrial pressures. Dobutamine increased the first derivative of left ventricular pressure (dP/dt) from 1,013 +/- 309 to 1,360 +/- 538 mm Hg/s (p less than 0.01) but milrinone did not. Similarly, blood flow and myocardial oxygen consumption were increased by dobutamine from 152 +/- 87 to 187 +/- 118 ml/min (p less than 0.05) and from 17.7 +/- 10.9 to 21.5 +/- 14.9 ml O2/min (p less than 0.05), respectively, but were unchanged by milrinone. Both drugs significantly decreased coronary vascular resistance and myocardial oxygen extraction but did not change myocardial lactate extraction. Thus, dobutamine and milrinone produce similar improvement in cardiac index. However, dobutamine increases myocardial oxygen consumption, whereas milrinone does not. This difference can probably be explained by the substantial vasodilating properties of milrinone.     

增强型体外反搏治疗对老年射血分数保留心力衰竭患者的疗效

目的:探讨增强型体外反搏(EECP)治疗老年左心室射血分数保留的心力衰竭(HFpEF)患者的作用和血流动力学效应。方法:回顾性分析2018年1月至2019年12月在山东大学齐鲁医院体外反搏中心登记治疗的66例老年HFpEF患者的临床资料。主要观察指标为6 min步行距离试验,次要指标为明尼苏达心力衰竭生活质量调查表(M...