本文選題：感染性休克 + 平均動(dòng)脈壓　； 參考：《北京協(xié)和醫(yī)學(xué)院》2013年博士論文

【摘要】：目的： 1.第一部分：探討平均動(dòng)脈壓對(duì)早期目標(biāo)導(dǎo)向治療(EGDT)達(dá)標(biāo)末仍有組織灌注異常的患者組織灌注和預(yù)后的影響。 2.第二部分：證實(shí)感染性休克時(shí)存在“血管瀑布”現(xiàn)象,探討擴(kuò)容和加用去甲腎上腺素對(duì)小血管臨界閉合壓(Pcc)和循環(huán)平均充盈壓(Pmsf)的影響及其臨床意義。 方法： 1.第一部分：回顧性分析2012年1月-2012年12月北京協(xié)和醫(yī)院重癥醫(yī)學(xué)科連續(xù)診治EGDT達(dá)標(biāo)末有組織灌注異常的感染性休克患者126例。EGDT末記為0時(shí),應(yīng)用去甲腎上腺素提高M(jìn)AP的方法進(jìn)一步復(fù)蘇6個(gè)小時(shí),記為6時(shí)。按照感染性6時(shí)乳酸是否2mmoL/L分為乳酸正常組和高乳酸組。記錄0時(shí)和6時(shí)血流動(dòng)力學(xué)資料、乳酸(Lac)、急性生理狀況和慢性健康狀態(tài)(APACHE Ⅱ)評(píng)分、6小時(shí)內(nèi)去甲腎上腺素平均用量(NE)和休克診斷后第28d生存狀況。 2.第二部分：(1)前瞻性觀察2012年7月1日-2012年8月1日北京協(xié)和醫(yī)院重癥醫(yī)學(xué)科診治的感染性休克且休克時(shí)間小于6小時(shí)的20例患者。前瞻性觀察2012年7月1日-2013年2月1日北京協(xié)和醫(yī)院重癥醫(yī)學(xué)科診治的感染性休克且休克時(shí)間小于6小時(shí)的62患者。(2)所有患者均經(jīng)右頸內(nèi)靜脈放置中心靜脈導(dǎo)管、經(jīng)左股動(dòng)脈放置股動(dòng)脈導(dǎo)管行脈搏指示持續(xù)心排血量(PiCCO)監(jiān)測(cè)；(3)待患者完全沒(méi)有自主呼吸,且鎮(zhèn)靜深度達(dá)到能夠屏氣12s時(shí),調(diào)節(jié)吸氣末平臺(tái)壓分別達(dá)到5、15、25、35cmH2O,按住吸氣末屏氣鍵,在屏氣開(kāi)始后7-12s時(shí),讀取心輸出量(CO)、中心靜脈壓(CVP)、平均動(dòng)脈壓(Pa)；對(duì)4個(gè)平臺(tái)壓下得到的4對(duì)心輸出量(CO)和CVP數(shù)值構(gòu)建靜脈回流(VR)曲線。VR曲線在流速為零時(shí)壓力軸的截值即為循環(huán)平均充盈壓(Pmsf);對(duì)同時(shí)得到的4對(duì)CO和Pa值進(jìn)行線性回歸曲分析構(gòu)建心室輸出(VO)曲線。心室輸出曲線在流速為零時(shí)壓力軸的截值為小血管臨界閉合壓(Pcc)。(4)根據(jù)Pcc和Pmsf的差值,確定感染性休克患者中有無(wú)“血管瀑布”現(xiàn)象。(5)對(duì)62例患者行500m1晶體進(jìn)行擴(kuò)容,按照上述方法估測(cè)Pcc和Pmsf,行血流動(dòng)力學(xué)、皮膚氧分壓監(jiān)測(cè)。(6)對(duì)62例患者應(yīng)用去甲腎上腺素逐步上調(diào)Pa65→75→85→95mmHg,每個(gè)壓力位點(diǎn)穩(wěn)定30min,待血流動(dòng)力學(xué)平穩(wěn)后,按照上述方法估測(cè)Pcc和Pmsf,行血流動(dòng)力學(xué)、皮膚氧分壓監(jiān)測(cè)。 結(jié)果： 1.第一部分：126例患者28d天死亡率為46.03%。兩組患者0時(shí)乳酸和APACHⅡ及血流動(dòng)力學(xué)指標(biāo)方面的差異均無(wú)統(tǒng)計(jì)學(xué)意義。6時(shí)存活組的MAP為86.5±9.8mmHg,高于死亡組的75.2±10.5mmHg,差異有統(tǒng)計(jì)學(xué)意義。存活組NE為0.72(0.43,1.6) ug/kg/min顯著高于死亡組0.48(0.45,1.4) ug/kg/min,差異有統(tǒng)計(jì)學(xué)意義。存活組UO顯著高于死亡組(1.8±1.lml/kg/hr vs.1.38±1.2ml/kg/hr),差異有統(tǒng)計(jì)學(xué)意義。存活組Lac顯著低于死亡組(5.3±3.8mmol/L vs.2.1±1.7mmol/L),差異有統(tǒng)計(jì)學(xué)意義。兩組患者其他血流動(dòng)力學(xué)參數(shù)方面的差異均無(wú)統(tǒng)計(jì)學(xué)意義。多因素回歸分析顯示MAP是本組患者28天死亡的獨(dú)立危險(xiǎn)因素。乳酸正常組患者28d死亡率為29%,乳酸增高組患者28d死亡率為62.5%,差異有統(tǒng)計(jì)學(xué)意義；兩組患者0時(shí)血流動(dòng)力學(xué)指標(biāo)方面的差異均無(wú)統(tǒng)計(jì)學(xué)意義。乳酸正常組的MAP為85.6±10.3mmHg,死亡組為77.2±10.7mmHg,差異有統(tǒng)計(jì)學(xué)意義。乳酸正常組UO顯著高于乳酸增高組(1.8±1.2ug/kg/min vs.1.3±0.9ug/kg/min),差異有統(tǒng)計(jì)學(xué)意義。相關(guān)性分析顯示,MAP與6時(shí)乳酸高度負(fù)相關(guān)。兩組患者6時(shí)其他血流動(dòng)力學(xué)參數(shù)方面的差異均無(wú)統(tǒng)計(jì)學(xué)意義。按6時(shí)血壓分三組,三組在0時(shí)血流動(dòng)力學(xué)指標(biāo)及乳酸的差異無(wú)顯著性。MAP在75-85mmHg組乳酸顯著低于MAP75mmHg組,MAP85mmHg與MAP在75-85mmHg乳酸的差異無(wú)統(tǒng)計(jì)學(xué)意義。6時(shí)三組患者其他血流動(dòng)力學(xué)指標(biāo)方面的差異無(wú)顯著性。 2.第二部分：(1)①感染性休克中Pcc和Pmsf分別為49.59±13.6mmHg和28.31±6.3mmHg,(P0.0001)。Pcc-Pmsf為21.27±11.1mmHg,提示感染性休克中存在“血管瀑布”；②動(dòng)脈阻力(Ra)與全身血管阻力指數(shù)(SVRI)之間呈顯著正相關(guān)(P0.0001);③Pcc與外周血管阻力指數(shù)不相關(guān),R=0.27(P=0.032)。(2)①擴(kuò)容后Pcc由42.9±10.0mmHg變?yōu)?4.8±8.9mmHg,(P=0.188);②擴(kuò)容后Pcc-Pmsf由21.5±8.6mmHg變?yōu)?0.5±7.9mmHg,(P=0.899);③擴(kuò)容后Pmsf-CVP由增加12.2±6.1mmHg增加到14.5±7.0mmHg,(P=0.002); CO由6.0±1.9L.min-1增加到,(P0.0001);④擴(kuò)容后Pa-Pcc由22.9±10.1mmHg增加到37.2±10.5mmHg,(P0.0001);擴(kuò)容后Ra降低,Rv無(wú)顯著變化,同時(shí)SVRI降低到1383.7±643.8dyn.sec.cm-5. m-2,(P0.0001),提示動(dòng)脈阻力降低,靜脈阻力無(wú)顯著變化。⑤擴(kuò)容后ScvO2由75.9±9.3%增加到81.6±4.2%,(P0.05)。(3)①在Pa由65mmHg升高到95mmHg的整個(gè)過(guò)程中,需要的NE依次增加,且各壓力位點(diǎn)所用劑量之間均有顯著性差異,(P0.0001)；試驗(yàn)整個(gè)過(guò)程中血溫?zé)o顯著改變。②Pa由65mmHg增加到75mmHg時(shí)：Pmsf和CVP均顯著增加,(P0.05)；但Pmsf-CVP和CO無(wú)顯著改變,(P0.05); Pcc由42.8±10.0變?yōu)?4.5±8.8mmHg,(P0.05); Pa-Pcc由22.8±10.1mmHg增加到32.6±9.1mmHg,(P0.0001)。Ra、Rs顯著增加,Rv無(wú)明顯改變；皮膚氧合指數(shù)(PtcO2/PaO2)和尿量(UO)增加,(P0.05); Lac和Pv-aCO2顯著降低,(P0.05); ScvO2堿剩余(BE)、PH無(wú)明顯變化。③Pa由75mmHg增加到85mmHg時(shí)：Pmsf-CVP、Pcc-Pmsf、Rv. CO值均無(wú)顯著增加,(P0.05); Pmsf-CVP和Rv均大于Pa65mmHg的位點(diǎn)值；Pcc由44.5±8.8mmHg變?yōu)?5.4±8.8mmHg,(P0.05); Pa-Pcc由22.8±10.1mmHg增加到41.9±8.9mmHg,(P0.0001); SVRI和Ra增加。PtcO2/PaO2、UO增加；Lac降低(P0.05),ScvO2、 Pv-aCO2、BE、PH無(wú)明顯改變。④Pa由85mmHg增加到95mmHg時(shí)：Pmsf, CVP Pmsf-CVP、Rv、CO均顯著增加,與前三個(gè)壓力位點(diǎn)值的差異均有統(tǒng)計(jì)學(xué)意義,(P0.05)。Pcc由45.4±8.8mmHg增加到59.1±14.8mmHg,差異有統(tǒng)計(jì)學(xué)意義,(P0.05); Pa-Pcc由41.9±8.9mmHg降低為40.6±1.1mmHg,差異無(wú)統(tǒng)計(jì)學(xué)意義,(P0.05); Pcc-Pmsf由17.0±1.8mmHg增加到24.5±4.mmHg,差異有統(tǒng)計(jì)學(xué)意義,(P0.0001)。該過(guò)程中血清乳酸水平?jīng)]有進(jìn)一步降低,PtcO2/PaO2降低,UO沒(méi)有進(jìn)一步增加,Pv-aCO2沒(méi)有進(jìn)一步降低,(P0.05)。 結(jié)論： 1.第一部分：(1)EGDT末有組織灌注異常的感染性休克患者死亡率很高；(2)一定程度提高血壓能夠降低血清乳酸水平,進(jìn)而降低該類(lèi)患者28d的死亡率；(3)目前尋找灌注壓的方法改善組織灌注的效果并不理想,進(jìn)一步尋找反應(yīng)最佳灌注壓的方法是臨床中亟待解決的問(wèn)題。 2.第二部分：(1)感染性休克時(shí)Pcc和Pmsf存在壓力梯度,提示存在“血管瀑布”(2)通過(guò)擴(kuò)容增加心輸出量不改變小血管臨界閉合壓；(3)聯(lián)合應(yīng)用小血管臨界閉合壓和外周血管阻力能夠評(píng)估血管收縮藥的血管作用位點(diǎn)；(4)應(yīng)用血管收縮藥,提高M(jìn)AP的過(guò)程中,臨界閉合壓的突然增大,提示組織灌注可能開(kāi)始惡化；(5)以平均動(dòng)脈壓與小血管臨界閉合壓最大差值作為灌注壓能夠最有效的改善組織灌注,該灌注壓對(duì)應(yīng)的平均動(dòng)脈壓范圍75-85mmHg;(6) Pcc可以使最佳灌注壓的選擇實(shí)現(xiàn)量化和個(gè)體化。
[Abstract]:Objective:
1. part I: To investigate the effect of mean arterial pressure on tissue perfusion and prognosis in patients with early stage target directed therapy (EGDT) with abnormal perfusion at the end of standard.
2. the second part: to confirm the phenomenon of "vascular waterfall" in septic shock, and to explore the effect and clinical significance of dilatation and addition of norepinephrine on the critical closed pressure (Pcc) and circulating mean filling pressure (Pmsf) of small vessels.
Method:
1.. Part one: retrospective analysis of 126 cases of septic shock in the Department of severe medicine of Peking Union Medical College Hospital in December -2012 January 2012. The end of.EGDT was recorded at the end of EGDT, and the end of.EGDT was recorded as 0. The method of using norepinephrine to improve MAP was further resuscitation for 6 hours. It was recorded at 6 when the infection was 6 of 2mmoL. /L was divided into normal lactate group and high lactic acid group. The hemodynamic data at 0 and 6 hours, lactic acid (Lac), acute physiological status and chronic health state (APACHE II) score, average dosage of norepinephrine within 6 hours (NE) and 28d survival after shock diagnosis were recorded.
2. second parts: (1) prospective observation of 20 patients with septic shock and shock time less than 6 hours in the Department of severe medicine, Peking Union Medical College Hospital, August 1st -2012 July 1, 2012. A prospective observation of septic shock and less than 6 hours of shock time in the Department of intensive medicine in February 1st July 1, 2012 62 patients. (2) all the patients placed the central venous catheter in the right internal jugular vein and placed the femoral artery catheterization through the left femoral artery for continuous cardiac output (PiCCO) monitoring. (3) when the patients were completely free of breathing, and the sedative depth reached the ability to hold the breath of 12s, the pressure of the terminal platform was reached to 5,15,25,35cmH2O, respectively. At the end of the breath holding key, the heart output (CO), central venous pressure (CVP) and mean arterial pressure (Pa) are read at the beginning of the breath holding 7-12s; the 4 pairs of cardiac output (CO) and the CVP value of the 4 platforms are constructed to construct the VR curve.VR curve at zero velocity when the velocity is zero, and the 4 pairs of CO are obtained at the same time. The ventricular output (VO) curve was constructed by linear regression analysis with the Pa value. The cut-off value of the pressure axis of the ventricular output curve at zero velocity was small critical closed pressure (Pcc). (4) according to the difference between Pcc and Pmsf, there was no "vascular waterfall" in the patients with septic shock. (5) 62 patients were treated with 500m1 crystal expansion, according to the above Methods Pcc and Pmsf were estimated, and the hemodynamics and oxygen partial pressure of skin were monitored. (6) 62 patients with norepinephrine were gradually up-regulated by norepinephrine, and each pressure loci was stable 30min. After the hemodynamics were stable, Pcc and Pmsf were estimated according to the above methods, and the hemodynamics and oxygen partial pressure were monitored.
Result:
1. first part: the mortality of 126 patients with 28d days was 46.03%. two, and there was no significant difference in lactate, APACH II and hemodynamic indexes at 0. The MAP of the survival group was 86.5 + 9.8mmHg when.6, higher than the 75.2 + 10.5mmHg in the death group, the difference was statistically significant. NE in the survival group was 0.72 (0.43,1.6) ug/kg/min significantly higher than death. Group 0.48 (0.45,1.4) ug/kg/min, the difference was statistically significant. The survival group UO was significantly higher than that of the death group (1.8 + 1.lml/kg/hr vs.1.38 + 1.2ml/kg/hr), the difference was statistically significant. The survival group Lac was significantly lower than the death group (5.3 + 3.8mmol/L vs.2.1 + 1.7mmol/L), the difference was statistically significant. The difference of other hemodynamic parameters in the two groups of patients There was no statistical significance. Multivariate regression analysis showed that MAP was an independent risk factor for 28 days of death in this group. The mortality of 28d in the normal lactate group was 29%, and the mortality of 28d in the higher lactate group was 62.5%, the difference was statistically significant. There was no statistically significant difference in the hemodynamic index in the two groups at 0. The MAP was 85.6 + 10.3mmHg, and the death group was 77.2 + 10.7mmHg, and the difference was statistically significant. The UO in the normal lactate group was significantly higher than that of the higher lactate group (1.8 + 1.2ug/kg/min vs.1.3 + 0.9ug/kg/min). The difference was statistically significant. The correlation analysis showed that MAP and 6 were negatively correlated with lactic acid. The difference of other hemodynamic parameters in the two group was 6. There was no statistical significance. There was no significant difference in the hemodynamic index and lactic acid between the three groups at 6 hours and the three groups at 6. The lactic acid in the group 75-85mmHg was significantly lower than that in the group MAP75mmHg, and there was no significant difference between the MAP85mmHg and MAP in the difference of other blood flow mechanics indexes in the three groups of patients with 75-85mmHg lactate difference.6.
2. second parts: (1) (1) (1) Pcc and Pmsf in septic shock were 49.59 + 13.6mmHg and 28.31 + 6.3mmHg respectively, and (P0.0001).Pcc-Pmsf was 21.27 + 11.1mmHg, suggesting that there was a "vascular waterfall" in septic shock; (2) there was a significant positive correlation between arterial resistance (Ra) and systemic vascular resistance index (SVRI); (3) Pcc and peripheral vascular resistance index (P0.0001) Number is unrelated, R=0.27 (P=0.032). (2) (2) (1) after dilatation, Pcc changes from 42.9 + 10.0mmHg to 44.8 + 8.9mmHg, (P=0.188); and after expansion, Pcc-Pmsf changes from 21.5 + 8.6mmHg to 20.5 + 7.9mmHg, (P=0.899); thirdly, Pmsf-CVP increases 12.2 + 6.1mmHg to 14.5 +. .9 + 10.1mmHg increased to 37.2 + 10.5mmHg, (P0.0001), Ra decreased, Rv had no significant change, and SVRI decreased to 1383.7 + 643.8dyn.sec.cm-5. m-2, (P0.0001), suggesting that arterial resistance decreased and venous resistance had no significant change. (5) ScvO2 increased from 75.9 + 9.3% to 81.6 + 4.2%, (P0.05). (3) During the process, the required NE increased in turn, and there was a significant difference between the dosage of the stress loci (P0.0001), and there was no significant change in the blood temperature in the whole process. (2) when Pa increased from 65mmHg to 75mmHg, Pmsf and CVP increased significantly (P0.05), but Pmsf-CVP and CO did not change significantly (P0.05); Pcc changed from 42.8 + 10 to 44.5 +. (05): Pa-Pcc increased from 22.8 + 10.1mmHg to 32.6 + 9.1mmHg, (P0.0001).Ra, Rs significantly increased, Rv had no obvious changes, the skin oxygenation index (PtcO2/PaO2) and urine volume (UO) increased, (P0.05), Lac and Pv-aCO2 significantly decreased. Significantly increased, (P0.05); both Pmsf-CVP and Rv were greater than the locus of Pa65mmHg; Pcc changed from 44.5 + 8.8mmHg to 45.4 + 8.8mmHg, (P0.05); Pa-Pcc increased from 22.8 + 10.1mmHg to 41.9 + 8.9mmHg. MSF, CVP Pmsf-CVP, Rv, CO were all significantly increased, and the differences in the values of the first three pressure loci were statistically significant. (P0.05).Pcc increased from 45.4 + 8.8mmHg to 59.1 + 14.8mmHg, and the difference was statistically significant, (P0.05); Pa-Pcc was reduced to 40.6 + from 41.9 + 8.9mmHg, and the difference was increased from 17 + to 24.5. The difference was statistically significant (P0.0001), (P0.0001). The level of serum lactic acid was not further reduced, PtcO2/PaO2 decreased, UO did not further increase, and Pv-aCO2 did not further decrease, (P0.05).
Conclusion:
1. first part: (1) the death rate of patients with septic shock with abnormal tissue perfusion at the end of EGDT is very high; (2) a certain degree of blood pressure can reduce the level of serum lactic acid, and then reduce the mortality of 28d in this type of patient; (3) the effect of perfusion pressure seeking to improve tissue perfusion is not ideal at present, and the best perfusion pressure is further sought. The method is an urgent problem to be solved in the clinic.
2. second parts: (1) there is a pressure gradient in Pcc and Pmsf during septic shock, suggesting that there is a "vascular waterfall" (2) not changing the critical closed pressure of the small vessels by enlarging the volume of the heart, and (3) the critical closed pressure of the small vessels and the resistance of the peripheral vessels can be used to evaluate the vascular site of the vasoconstrictor; (4) the application of vasoconstriction. During the process of improving MAP, the sudden increase of critical closure pressure suggests that tissue perfusion may begin to deteriorate; (5) the maximum difference between the mean arterial pressure and the critical close pressure of the small vessels can be the most effective improvement of tissue perfusion, and the mean arterial pressure range corresponding to the perfusion pressure is 75-85mmHg; (6) Pcc can make the best perfusion pressure selected. Choose to quantify and individualized.
【學(xué)位授予單位】：北京協(xié)和醫(yī)學(xué)院
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2013
【分類(lèi)號(hào)】：R459.7

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1 紀(jì)木火;左西蒙旦聯(lián)合精氨酸加壓素對(duì)豬膿毒血癥引起急性肺損傷的保護(hù)作用[D];南京大學(xué);2012年

2 蔣金華;比較限制性和開(kāi)放性輸液對(duì)老年結(jié)直腸癌手術(shù)患者預(yù)后及炎癥反應(yīng)的影響[D];蘇州大學(xué);2013年

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