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

【摘要】：目的： 1.第一部分：探討平均動脈壓對早期目標導向治療(EGDT)達標末仍有組織灌注異常的患者組織灌注和預后的影響。 2.第二部分：證實感染性休克時存在“血管瀑布”現(xiàn)象,探討擴容和加用去甲腎上腺素對小血管臨界閉合壓(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)學科連續(xù)診治EGDT達標末有組織灌注異常的感染性休克患者126例。EGDT末記為0時,應用去甲腎上腺素提高MAP的方法進一步復蘇6個小時,記為6時。按照感染性6時乳酸是否2mmoL/L分為乳酸正常組和高乳酸組。記錄0時和6時血流動力學資料、乳酸(Lac)、急性生理狀況和慢性健康狀態(tài)(APACHE Ⅱ)評分、6小時內(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)學科診治的感染性休克且休克時間小于6小時的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)學科診治的感染性休克且休克時間小于6小時的62患者。(2)所有患者均經(jīng)右頸內(nèi)靜脈放置中心靜脈導管、經(jīng)左股動脈放置股動脈導管行脈搏指示持續(xù)心排血量(PiCCO)監(jiān)測；(3)待患者完全沒有自主呼吸,且鎮(zhèn)靜深度達到能夠屏氣12s時,調(diào)節(jié)吸氣末平臺壓分別達到5、15、25、35cmH2O,按住吸氣末屏氣鍵,在屏氣開始后7-12s時,讀取心輸出量(CO)、中心靜脈壓(CVP)、平均動脈壓(Pa)；對4個平臺壓下得到的4對心輸出量(CO)和CVP數(shù)值構(gòu)建靜脈回流(VR)曲線。VR曲線在流速為零時壓力軸的截值即為循環(huán)平均充盈壓(Pmsf);對同時得到的4對CO和Pa值進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“血管瀑布”現(xiàn)象。(5)對62例患者行500m1晶體進行擴容,按照上述方法估測Pcc和Pmsf,行血流動力學、皮膚氧分壓監(jiān)測。(6)對62例患者應用去甲腎上腺素逐步上調(diào)Pa65→75→85→95mmHg,每個壓力位點穩(wěn)定30min,待血流動力學平穩(wěn)后,按照上述方法估測Pcc和Pmsf,行血流動力學、皮膚氧分壓監(jiān)測。 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時乳酸和APACHⅡ及血流動力學指標方面的差異均無統(tǒng)計學意義。6時存活組的MAP為86.5±9.8mmHg,高于死亡組的75.2±10.5mmHg,差異有統(tǒng)計學意義。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)計學意義。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)計學意義。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)計學意義。兩組患者其他血流動力學參數(shù)方面的差異均無統(tǒng)計學意義。多因素回歸分析顯示MAP是本組患者28天死亡的獨立危險因素。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)計學意義；兩組患者0時血流動力學指標方面的差異均無統(tǒng)計學意義。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)計學意義。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)計學意義。相關性分析顯示,MAP與6時乳酸高度負相關。兩組患者6時其他血流動力學參數(shù)方面的差異均無統(tǒng)計學意義。按6時血壓分三組,三組在0時血流動力學指標及乳酸的差異無顯著性。MAP在75-85mmHg組乳酸顯著低于MAP75mmHg組,MAP85mmHg與MAP在75-85mmHg乳酸的差異無統(tǒng)計學意義。6時三組患者其他血流動力學指標方面的差異無顯著性。 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動脈阻力(Ra)與全身血管阻力指數(shù)(SVRI)之間呈顯著正相關(P0.0001);③Pcc與外周血管阻力指數(shù)不相關,R=0.27(P=0.032)。(2)①擴容后Pcc由42.9±10.0mmHg變?yōu)?4.8±8.9mmHg,(P=0.188);②擴容后Pcc-Pmsf由21.5±8.6mmHg變?yōu)?0.5±7.9mmHg,(P=0.899);③擴容后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擴容后Pa-Pcc由22.9±10.1mmHg增加到37.2±10.5mmHg,(P0.0001);擴容后Ra降低,Rv無顯著變化,同時SVRI降低到1383.7±643.8dyn.sec.cm-5. m-2,(P0.0001),提示動脈阻力降低,靜脈阻力無顯著變化。⑤擴容后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的整個過程中,需要的NE依次增加,且各壓力位點所用劑量之間均有顯著性差異,(P0.0001)；試驗整個過程中血溫無顯著改變。②Pa由65mmHg增加到75mmHg時：Pmsf和CVP均顯著增加,(P0.05)；但Pmsf-CVP和CO無顯著改變,(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無明顯變化。③Pa由75mmHg增加到85mmHg時：Pmsf-CVP、Pcc-Pmsf、Rv. CO值均無顯著增加,(P0.05); Pmsf-CVP和Rv均大于Pa65mmHg的位點值；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無明顯改變。④Pa由85mmHg增加到95mmHg時：Pmsf, CVP Pmsf-CVP、Rv、CO均顯著增加,與前三個壓力位點值的差異均有統(tǒng)計學意義,(P0.05)。Pcc由45.4±8.8mmHg增加到59.1±14.8mmHg,差異有統(tǒng)計學意義,(P0.05); Pa-Pcc由41.9±8.9mmHg降低為40.6±1.1mmHg,差異無統(tǒng)計學意義,(P0.05); Pcc-Pmsf由17.0±1.8mmHg增加到24.5±4.mmHg,差異有統(tǒng)計學意義,(P0.0001)。該過程中血清乳酸水平?jīng)]有進一步降低,PtcO2/PaO2降低,UO沒有進一步增加,Pv-aCO2沒有進一步降低,(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,進而降低該類患者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,進一步尋找反應最佳灌注壓的方法是臨床中亟待解決的問題。 2.第二部分：(1)感染性休克時Pcc和Pmsf存在壓力梯度,提示存在“血管瀑布”(2)通過擴容增加心輸出量不改變小血管臨界閉合壓；(3)聯(lián)合應用小血管臨界閉合壓和外周血管阻力能夠評估血管收縮藥的血管作用位點；(4)應用血管收縮藥,提高MAP的過程中,臨界閉合壓的突然增大,提示組織灌注可能開始惡化；(5)以平均動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,該灌注壓對應的平均動脈壓范圍75-85mmHg;(6) Pcc可以使最佳灌注壓的選擇實現(xiàn)量化和個體化。
[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.
【學位授予單位】：北京協(xié)和醫(yī)學院
【學位級別】：博士
【學位授予年份】：2013
【分類號】：R459.7

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