第三軍醫(yī)大學學報99017第三軍醫(yī)大學學報舊J萬數(shù)據(jù)資源系統(tǒng) ACTA ACADEMIAE MEDICINAE數(shù)化期刊WANFANG DATA (CHINAINFO)MILITARIS TERTIAEDIGITIZED PERIODICAL1999年第21卷第5期Vo.21No.51999危重病人的氧動力學改變郭振輝鄒霞英毛寶齡提要目的:研究肺心病失代償期和膿毒癥患者入院早期(6~48h的血液動力學和氧動力學改變。方法∶采用漂浮導管檢査術(shù),測定肺動脈壓(PAP)、右心室壓(RP)、肺楔壓(PCWP)、中心靜脈壓(CVP)、外周動脈壓(AP)、心排量(CO)和動脈血、混合靜脈血行血氣分析并同步測定混合靜脈血LA。結(jié)果:肺心病失代償期患者G1組)∶肺動脈平均壓(mPAP)和肺循環(huán)阻力(PVR均顯著升高,氧供(DO2)顯著降低,上述改變以入院2h為甚;膿毒癥組(G2組):心指數(shù)(C〕顯著增加,體循環(huán)阻力顯著降低,DO2和氧消耗(VO以)大致正常,但乳酸水平顯著升高。結(jié)論:G1組患者以肺循環(huán)高阻力和氧供不足為特征;而G2組患者以高排低阻,高代謝及氧利用障礙為特點關(guān)鍵詞肺心病;膿毒癥;血液動力學;氧動力學中圖法分類號R85215R5415:R63Changes of oxydynamics in critical casesGuo Zhenhui, Zou Xiaying, Mao Baoling(Department of Respiratory Diseases, XinqiaoHospital, Third Military Medical University, Chongqing, 400037)abstract Objective: To investigate the changes of hemodynamics and oxydynamicsin critical patients with decompensable cor pulmonale or sepsis. Methods: PAP, RVPPCWP, CVP, AP, CO and la were measured using swan-Ganz catheterization meanwhileblood-gas analysis of arterial blood and mixed venous blood was conducted Results: Inpatients with decompensable cor pulmonale(group 1), pulmonary arterial mean pressure andpulmonary vascular resistance index were significantly increased but oxygen deliverymarkedly decreased. In patients with sepsis(group 2), cardiac output index was remarkablyincreased while systemic vascular resistance index markedly decreased. Though dO, andoxygen consumption were relatively normal, the lactic acid was sig中國煤化工Conclusion: Patients in group I show a high pulmonary vascular relHHCNMHGcientoxygen delivery and those in group 2 have a high cardiac output with low systemic vascularresistance, high metabolism and obstacle of oxygen usagefile ///E yak/dsiydxxb/dsyy99/ds 9905/990517 htm(1/53)2010-3-22 17: 48: 31第三軍醫(yī)大學學報99017Key words hemodynamics; oxydynamics; cor pulmonale; sepsis通過氧動力監(jiān)測氧供(DO2)、氧消耗(O2、氧攝取率(O2ER)和乳酸(LA),以觀察呼吸,循環(huán)綜合功能和組織代謝狀況是目前危重醫(yī)學研究的重要課題[1。機體嚴重損傷可產(chǎn)生全身炎癥反應綜合征(SIRS)而致多臟器功能障礙綜合征(MODS)[2]。由感染所致的SRS表現(xiàn)為膿毒癥( Sepsis),它是引起MoDS的最常見病因,而急性肺損傷(ALI是MODS的首發(fā)表現(xiàn)[3]。肺心病失代償期以呼吸衰竭和右心功能不全為特征,它與膿毒癥及其所致的ALI是呼吸系常見的危重病癥。它們均存在著呼吸、循環(huán)功能和組織代謝障礙,但各自的病理生理改變存在明顯差異。本研究擬通過一組肺心病失代償期和膿毒癥危重病人早期的血液動力學和氧動力學改變,探討其病理生理改變的差異及其臨床意義。對象和方法1.1研究對象共17例病人,其急性生理和慢性健康狀況評分( APACH-Ⅱ)積分[4]均≥12分,肺心病失代償期病人10例,男9例,女1例,年齡(08)歲,均符合1977年全國肺心病專業(yè)會議制定的診斷標準;另冽例為膿毒癥病人,男5例,女2例,年齡(61±3)歲,均符合SIRS診斷標準[2],全部患者有一次或一次以上血培養(yǎng)細菌或真菌陽性,或有明確的感染灶?；颊呷胫匕Y監(jiān)護病房(ICU),6h內(nèi)經(jīng)右頸內(nèi)靜脈穿刺,在床旁監(jiān)護儀(西門子Sirecust-961)監(jiān)測下,插入帶外鞘管的Swan-Gan導管以測定肺動脈壓(PAP)、右心室壓(RP)、肺楔壓(PCWP)、中心靜脈壓(CVP),上述各參數(shù)均于呼吸末測定,連續(xù)3個呼吸周期,取其均值;熱稀釋法測心排量(CO),取3次均值(每次數(shù)值誤差<5%);外周血壓(MAP采用上肢無創(chuàng)袖帶測壓( Severo-732)。輸入測定數(shù)據(jù)由監(jiān)護儀自動計算出血液動力學參數(shù)數(shù)值;氧動力學參數(shù)數(shù)值由下列公式算出[5]DO2139×Hg×SaO2XCO(Hg:血紅素、Sa02:動脈血氧飽和度);O2-1.39× Gbx STO2XC0(SvO2:混合靜脈血氧飽和度)測定壓力參數(shù)的同時,取外周動脈血和混合靜脈血行血氣分析( Radiometer abl4并同步測定混合靜脈血LA。入院時62448h測定血液動力學和氧動力學參數(shù)。1.2統(tǒng)計學方法計量資料采用檢驗2結(jié)果不同時間監(jiān)測的氧動力學結(jié)果見表1。G1肺心病失代償患者組,各期DO入VO2大致正常,與入院4相比,2址1D.顯著降低而LA顯著升高,6Y牛國爆化王G2膿毒癥患者組,各期DO2VO2和OzER大致正常,但LA均較正常顯著升高,與入院48hfle∥/Eyqk/ dsiydxxb/dy99/dy990590517hm(第2/5頁)2010322174831第三軍醫(yī)大學學報99017相比,6h的DO2和LA均顯著升高而OzER顯著降低,與G1組比較,G2組各期LA均顯著高于G1組。表1肺心病組與膿毒癥組氧動力學比較(x±$Tab 1 Comparison of oxydynamic changes in patients with cor pumonale and sepsis(+ s)TimeDOVOO2ER LAGroup(h)l(/min m2)(ml/min- m2)(%)(mmol/L)661472179221619074(=10)24568±138*1784132+10200.8486501331894330±91.70.567215184±7527.644±1.36G2(n724598±195177428±y34+1448567±107181±1232102612G1: Cor pumonale: G2: Sepsis; * P005, *k: P0.01 vs48 h group; 4: p<0.05,4:P0.01 VSG1不同時間監(jiān)測的血液動力學結(jié)果見表2G1組患者,6、24h和48h的mPAP和肺血管阻力指數(shù)(PVR均顯著高于正常。與入院后48h相比,624h的mPAP和外周血管阻力指數(shù)(SVRI)顯著升高而24h的心排指數(shù)(C顯著降低;G2組患者,各期mPAP和PVR均正常,而sVRI偏低,以6h為著;與G2組相比,G1組病人各期mPAP、PVR均數(shù)顯著升高;G2較之G1組,SVRI顯著降低而CI顯著升高。表2肺心病組與膿毒癥組血液動力學比較(x±STab 2 Comparison of hemodynamic changes in patients with cor pumonale and sepsis+ sTIME mPAPPVRISVRICIGroup(h)(kPa)(dyne. S/cm5 mz)/(dyne.S/cm5 m2)(L/min m2)649±18*610±34120374736±05G1(n=10)2451±19697±4371987±35534±0.9648451.7472751682±3173908624±094231±17441453±575*44+134G2242084220140(7165V凵中國煤化工CNMHG「4823071912185+394x104fle∥/Evqk/ dsjydxxb/dsy99dy9905990517hm(第3/5頁)2010322174831第三軍醫(yī)大學學報99017G1: Cor pumonale: G2: Sepsis; * P005, *k: P0.01 vs48 h group; 4: P<0.05,AP<0.01 VS G13討論本組肺心病失代償期,mPAP和PνRI顯著升高,存在著肺動脈高壓(PAH),這與我們既往的研究結(jié)果相類似[6]。在其動態(tài)早期監(jiān)測中,PAH以入院24h為最顯著,隨著病程的延長和臨床干預,PAH逐步改善。本組病人均存在低氧血癥和/或高碳酸血癥因紅細胞增多和心排量增加,DO2尚可維持正常;同時,通過攝氧率增加,組織利用氧增加[],使νO2和LA保持正常。本組有3例病人因嚴重低氧(DO2均≤450mmnm致∨O2顯著降低和LA顯著升高;∨O2對DO2呈現(xiàn)了病理性依賴[1],經(jīng)積極干預而改善。本組病人PAH、DO2和LA改變均以24h為最顯著,提示病人入院24h內(nèi)病情明顯進展,經(jīng)臨床干預24h后病情趨于好轉(zhuǎn)。膿毒癥病人,存在著高排低阻的血液動力學改變,本組病人以入院初期的改變尤為顯著。有報道,膿毒癥時,誘導型一氧化氮合成酶(iNOS激活,一氧化氮(NO)合成增加導致以血管擴張為主要表現(xiàn)的血管功能紊亂[7。由于血管阻力的降低和應激反應,因而在膿毒癥早期出現(xiàn)了高排低阻的血液動力學改變。本組患者,其早期的DO2VO2和O2ER雖維持正常,但LA顯著升高,尤以入院初期為甚,表明組織高代謝致氧供的相對不足和氧攝取障礙。膿毒癥時,灸癥效應細胞和單核細胞、中性粒細胞分泌大量炎癥介質(zhì),而某些炎癥介質(zhì),尤其是腫瘤壞死因子(TNF可介導組織的高代謝[2],同時,TNF-α等炎癥細胞因子可直接損傷毛細血管內(nèi)皮細胞[8]致微血管通透性增加,組織水腫;微血栓形成,血流重新分布,從而導致氧攝取障礙。對于高氧耗型組織缺氧且氧攝取障礙,維持正常的DO’顯然是不夠的[5]。本組病人經(jīng)臨床干預后LA雖呈下降趨勢,但始終高于正常(正常血LA<2 mmol/L),且DO2呈下降趨勢,表明氧供不足和氧攝取障礙仍未根本改善。綜上所述,肺心病失代償病人存在著PAH,部分病人DO2絕對不足致∨O2下降;膿毒癥病人存在高排低阻、氧供相對不足和氧利用障礙。兩組枏比較,肺心病失代償期組以肺循環(huán)高阻力而膿毒癥組以體循環(huán)低阻力為特征,膿毒癥組因高代謝而使氧需高于肺心病組,LA變化也更敏感,故肺心病失代償病人應改善肺循環(huán)高阻力以降低PAH并增加氧供為重,而膿毒癥患者則以糾正高排低阻,改善氧供和組織氧利用為要作者簡介∶郭振輝,男,36歲,主治醫(yī)師,博士研究生作者單位:郭振輝毛寶齡第三軍醫(yī)大學附屬新橋醫(yī)院呼吸內(nèi)科研究所重慶400037中國煤化工鄒霞英廣州軍區(qū)總醫(yī)院呼吸內(nèi)科廣州,510010CNMHG參考文獻file ///E yak/dsiydxxb/dsyy99/ds 9905/990517 htm(4/53)2010-3-22 17: 48: 31第三軍醫(yī)大學學報99017I Koch S M. 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World J Surg, 1996,20(4): 4068 Edwards m.heniford b t miller f n.tnf mediates disseminated ininflammation in the genesis of multiple organ edema.J Surg res, 1993, 54(1): 140(編輯張大春(收稿:1998-11-30;修回:19990426中國煤化工CNMHGfle∥/Eqk/dydb/dy99d990590517hm(第5/5頁)2010322174831