郭 華,戴 敏
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長(zhǎng)期氧療對(duì)改善慢性阻塞性肺疾病患者右心功能的療效觀察
郭 華1*,戴 敏2
(無(wú)錫市人民醫(yī)院:1老年病科,2心功能科,無(wú)錫 214000)
評(píng)價(jià)長(zhǎng)期氧療對(duì)改善慢性阻塞性肺疾病(COPD)患者右心功能的療效。選擇2011年10月至2012年3月無(wú)錫市人民醫(yī)院門(mén)診或住院檢查二維心臟超聲未見(jiàn)異常、肺功能Ⅰ級(jí)的COPD患者40例,其中男性22例、女性18例,每日夜間連續(xù)吸氧10h,氧流量為2L/min,觀察1年。并于氧療前1d、氧療后3個(gè)月、6個(gè)月、1年,同時(shí)進(jìn)行心臟超聲及肺功能檢測(cè)。比較氧療前后右心功能、肺功能各項(xiàng)指標(biāo)的變化。應(yīng)用心臟超聲斑點(diǎn)追蹤技術(shù)測(cè)得右室游離壁基底段應(yīng)變(Sbasfw)、右室游離壁基底段應(yīng)變率(SRbasfw)、右室游離壁中間段應(yīng)變(Smidfw)及右室游離壁中間段應(yīng)變率(SRmidfw)于氧療后3個(gè)月比氧療前1d升高,且差異有統(tǒng)計(jì)學(xué)意義(<0.05);隨著氧療持續(xù)時(shí)間的延長(zhǎng),Sbasfw,SRbasfw,Smidfw及SRmidfw升高更加顯著(<0.01);右心室縱向縮短率(Tm%)于氧療后3個(gè)月即有升高,且與氧療前比較,差異有統(tǒng)計(jì)學(xué)意義(<0.05),隨著氧療持續(xù)時(shí)間的延長(zhǎng)繼續(xù)升高(<0.01);右室游離壁三尖瓣環(huán)收縮期峰值位移(T1),室間隔三尖瓣環(huán)收縮期峰值位移(T2),三尖瓣環(huán)連線中點(diǎn)收縮期峰值位移(Tm)在氧療后6個(gè)月出現(xiàn)升高,與氧療前比較,差異有統(tǒng)計(jì)學(xué)意義(<0.05),并隨氧療持續(xù)升高。1s用力呼氣容積(FEV1)、FEV1占預(yù)計(jì)值百分比氧療后1年比氧療前升高,且差異有統(tǒng)計(jì)學(xué)意義(<0.05)。長(zhǎng)期氧療可明顯改善COPD患者的右心收縮功能,且對(duì)右心功能的改善早于肺功能。
斑點(diǎn)追蹤;氧療;肺疾病,慢性阻塞性;右心功能
慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一種破壞性的肺部疾病,以不完全可逆氣流受限為特征,病程呈慢性進(jìn)行性發(fā)展。COPD除了影響呼吸系統(tǒng),還能導(dǎo)致全身炎癥反應(yīng),最終導(dǎo)致呼吸衰竭和肺源性心臟病,甚至右心衰竭,引起死亡[1]。大規(guī)模臨床試驗(yàn)結(jié)果表明,長(zhǎng)期氧療可以改善COPD患者的肺功能,改善預(yù)后和病死率,且越早治療,預(yù)后越好。但氧療對(duì)右心功能的影響未見(jiàn)報(bào)道,本研究將應(yīng)用斑點(diǎn)追蹤技術(shù)評(píng)價(jià)氧療對(duì)改善COPD患者右心功能的療效。
選擇2011年10月至2012年3月無(wú)錫市人民醫(yī)院門(mén)診或住院檢查二維心臟超聲未見(jiàn)異常、肺功能Ⅰ級(jí)的COPD患者40例,其中男性22例、女性18例,所有患者均能堅(jiān)持每日低流量吸氧(2L/min)10h 1年以上。
COPD診斷標(biāo)準(zhǔn):進(jìn)行性加重的氣急史,肺功能提示殘氣量(residual volume,RV)/肺總量(total lung capacity,TLC)增加,1s用力呼氣容積(forced expiratory volume in one second,F(xiàn)EV1)/用力肺活量(forced vital capacity,F(xiàn)VC)減低,分鐘最大通氣量(maximal breathing capacity,MBC)降低,經(jīng)支氣管擴(kuò)張劑治療,肺功能無(wú)明顯改善。
排除標(biāo)準(zhǔn):(1)COPD急性加重期的患者;(2)嚴(yán)重肝腎功能不全的患者;(3)惡性腫瘤患者;(4)糖尿病患者;(5)藥物治療仍未得到控制的心律失?;颊?;(6)結(jié)締組織疾病患者;(7)冠心病及高血壓患者;(8)內(nèi)分泌性疾病導(dǎo)致心臟病患者;(9)先天性心臟病患者。
Philips iE33彩色多普勒超聲診斷儀,X3-1矩陣型實(shí)時(shí)三維探頭,頻率1~3MHz和s5~1探頭,頻率1~4MHz。配有Q-Lab8.1定量分析軟件。肺功能儀(Jaeger公司)。
檢查時(shí)受檢者左側(cè)臥位,平靜呼吸,連接心電圖,取心尖四腔心觀采集二維圖像,并啟動(dòng)全容積顯像模式采集實(shí)時(shí)三維全容積圖像,連續(xù)采集3個(gè)心動(dòng)周期。將二維及實(shí)時(shí)三維圖像傳輸?shù)絈lab工作站,進(jìn)行脫機(jī)定量分析。
1.4.1 三尖瓣環(huán)收縮期位移的測(cè)量 運(yùn)用TMQ-ADV分析軟件,進(jìn)入TMQAd模式,選擇AP4及TMAD模式,分別于三尖瓣環(huán)室間隔部、右室游離壁部及右室心尖處描記3點(diǎn),系統(tǒng)自動(dòng)測(cè)算右室游離壁三尖瓣環(huán)收縮期峰值位移(tricuspid annular systolic peak displacement at right ventricular free wall,T1)、室間隔三尖瓣環(huán)收縮期峰值位移(tricuspid annular systolic peak displacement at interventricular septum,T2)、三尖瓣環(huán)連線中點(diǎn)收縮期峰值位移(tricuspid annular systolic peak displacement at midpoint of tricuspid annulus,Tm)以及右室縱向縮短率(right ventricular longitudinal shortening,Tm%),并自動(dòng)生成T1、T2的同步位移曲線(圖1)。
圖1 三尖瓣環(huán)位移的測(cè)量
Figure 1 Measurement of tricuspid annular displacement
1.4.2 右室長(zhǎng)軸收縮期縱向應(yīng)變及應(yīng)變率的測(cè)量 應(yīng)用斑點(diǎn)追蹤技術(shù)測(cè)量右室長(zhǎng)軸收縮期縱向應(yīng)變、應(yīng)變率,點(diǎn)擊Q-Lab8.1定量分析軟件,進(jìn)入TMQA模式,選擇AP4模式,手動(dòng)點(diǎn)擊三尖瓣間隔部和右室游離壁部及右室心尖處的心內(nèi)膜面3點(diǎn),點(diǎn)擊TMQAdvanced按鈕,系統(tǒng)自動(dòng)勾畫(huà)出右室心內(nèi)膜及心外膜曲線,且劃分為6階段:室間隔基底段、中間段、心尖段;右室游離壁基底段、中間段、心尖段。手動(dòng)調(diào)節(jié)這兩條曲線,使其與心肌厚度一致。點(diǎn)擊compute按鈕,軟件自動(dòng)追蹤感興趣區(qū)的心肌運(yùn)動(dòng),結(jié)果顯示應(yīng)變?時(shí)間曲線和應(yīng)變率?時(shí)間曲線。選取切面測(cè)量得到右室游離壁基底段應(yīng)變(strain of basal segments of right ventricular free wall,Sbasfw)、右室游離壁基底段應(yīng)變率(strain rate of basal segments of right ventricular free wall,SRbasfw)、右室游離壁中間段應(yīng)變(strain of middle segments of right ventricular free wall,Smidfw)及右室游離壁中間段應(yīng)變率(strain rate of middle segments of right ventricular free wall,SRmidfw;圖2)。
圖2 應(yīng)變?時(shí)間曲線
Figure 2 Strain-time curve
準(zhǔn)備好儀器、定標(biāo)。讓患者接上咬口先平靜呼吸,幾個(gè)呼吸周期后指導(dǎo)患者將氣緩慢吐出來(lái)吐到不能再吐為止。讓患者用力、快速吸飽氣到肺總量位而不能停頓。馬上開(kāi)始以最大能力、最快速度用力呼氣。最后深吸一口氣或回到平靜呼吸。讓患者離開(kāi)咬口并計(jì)算檢查結(jié)果。
肺功能Ⅰ級(jí)的COPD患者40例,每日夜間連續(xù)吸氧10h,氧流量為2L/min,觀察1年。并于氧療前1d、氧療后3個(gè)月、6個(gè)月、1年,同時(shí)進(jìn)行心臟超聲及肺功能檢測(cè)。
使用SPSS17.0統(tǒng)計(jì)軟件進(jìn)行統(tǒng)計(jì)分析。計(jì)量資料以均數(shù)±標(biāo)準(zhǔn)差表示,氧療前后COPD患者各均數(shù)的比較采用配對(duì)檢驗(yàn)。所有值均為雙側(cè)檢驗(yàn),以<0.05為差異有統(tǒng)計(jì)學(xué)意義。
采集COPD患者氧療前1d,氧療后3個(gè)月、6個(gè)月、1年常規(guī)超聲心動(dòng)圖參數(shù),并進(jìn)行比較發(fā)現(xiàn),主動(dòng)脈根內(nèi)徑(aortic root diameter,AO)、左室舒張末期內(nèi)徑(left ventricular end diastolic diameter,LVEDD)、左室收縮末期內(nèi)徑(left ventricular end systolic diameter,LVESD)、左房?jī)?nèi)徑(left atrial diameter,LA)、室間隔厚度(interventricular septal thickness,IVS)、左室后壁厚度(left ventricular posterior wall thickness,LVPW)、左室射血分?jǐn)?shù)(left ventricular ejection fraction,LVEF)、右室內(nèi)徑(right ventricular diameter,RV)、右房?jī)?nèi)徑(right atrial diameter,RA)、右室后壁厚度(right ventricular posterior wall thickness,RVWT)的差異均無(wú)統(tǒng)計(jì)學(xué)意義(>0.05;表1)。
采集COPD患者氧療前1d、氧療后3個(gè)月、氧療后6個(gè)月、氧療后1年的肺功能指標(biāo),并進(jìn)行比較,發(fā)現(xiàn)FEV1、FEV1占預(yù)計(jì)值(%)于氧療后3個(gè)月、6個(gè)月均有所升高,但差異無(wú)統(tǒng)計(jì)學(xué)意義(>0.05);于氧療后1年FEV1、FEV1占預(yù)計(jì)值(%)出現(xiàn)明顯改善,且差異有統(tǒng)計(jì)學(xué)意義(<0.05;表2)。
采集COPD患者氧療前1d、氧療后3個(gè)月、氧療后6個(gè)月、氧療后1年的三尖瓣位移、右室游離壁各階段收縮期應(yīng)變及應(yīng)變率,發(fā)現(xiàn)氧療后3個(gè)月Sbasfw,SRbasfw,Smidfw及SRmidfw比治療前增高(<0.05),氧療后6個(gè)月及1年Sbasfw,SRbasfw,Smidfw及SRmidfw比治療前顯著增高(<0.01);氧療后3個(gè)月Tm%比治療前增大(<0.05),氧療后6個(gè)月及1年Tm%增大更加顯著(<0.01);氧療后6個(gè)月及1年T1,T2,Tm亦均增大(<0.05,<0.01;表3)。
COPD患者右心功能減退的發(fā)生機(jī)制主要是肺動(dòng)脈高壓,肺動(dòng)脈高壓的發(fā)生早于右心結(jié)構(gòu)的改變,大多數(shù)COPD患者雖然僅有肺動(dòng)脈輕度升高,但只要發(fā)生肺動(dòng)脈高壓,右心功能減退,就可以使COPD預(yù)后及病死率加倍惡化[2,3]。其發(fā)病機(jī)制是主要由于低氧性肺血管收縮,長(zhǎng)期慢性低氧可使代償性紅細(xì)胞增多,血容量增加,血液黏稠度增大,循環(huán)阻力增高;低氧可影響肺動(dòng)脈平滑肌細(xì)胞膜離子通道,使鈣內(nèi)流增加和鉀通道活性阻抑,引起肺血管平滑肌細(xì)胞去極化,導(dǎo)致肺血管收縮[4];同時(shí)低氧可能通過(guò)誘導(dǎo)內(nèi)源性縮血管介質(zhì)的產(chǎn)生間接導(dǎo)致肺動(dòng)脈收縮。低氧對(duì)肺心病患者肺動(dòng)脈壓以及右心功能有明顯的負(fù)面影響[5]。
表1 COPD患者氧療前后二維心臟超聲測(cè)量參數(shù)比較
AO: aortic root diameter; LVEDD: left ventricular end diastolic diameter; LVESD: left ventricular end systolic diameter; LA: left atrial diameter; IVS: interventricular septal thickness; LVPW: left ventricular posterior wall thickness; LVEF: left ventricular ejection fraction; RV: right ventricular diameter; RA: right atrial diameter; RVWT: right ventricular posterior wall thickness
表2 COPD患者氧療前后肺功能參數(shù)比較
FEV1: forced expiratory volume in one second; FVC: forced vital capacity. Compared with one day before oxygen uptake,*<0.05
表3 COPD患者氧療前后三尖瓣環(huán)位移、應(yīng)變、應(yīng)變率的比較
T1: tricuspid annular systolic peak displacement at right ventricular free wall; T2: tricuspid annular systolic peak displacement at interventricular septum; Tm: tricuspid annular systolic peak displacement at midpoint of tricuspid annulus; Tm%: right ventricular longitudinal shortening; Smidfw: strain of middle segments of right ventricular free wall; Sbasfw: strain of basal segments of right ventricular free wall; SRmidfw: strain rate of middle segments of right ventricular free wall; SRbasfw: strain rate of basal segments of right ventricular free wall. Compared with one day before oxygen uptake,*<0.05,**<0.01
早期COPD患者的肺動(dòng)脈壓即有不同程度增高,但二維心臟超聲測(cè)量值均在正常范圍內(nèi),右心導(dǎo)管雖能獲得精確數(shù)值,但為有創(chuàng)性檢查,無(wú)法推廣,因此對(duì)于早期COPD患者無(wú)法通過(guò)肺動(dòng)脈壓評(píng)價(jià)其右心功能。心臟超聲斑點(diǎn)追蹤技術(shù)通過(guò)追蹤心肌回聲斑點(diǎn)的空間運(yùn)動(dòng),并計(jì)算其運(yùn)動(dòng)軌跡,定量測(cè)量心肌組織的運(yùn)動(dòng)速度、位移、應(yīng)變(指心動(dòng)周期中相對(duì)于該心動(dòng)周期起始時(shí)心肌初始長(zhǎng)度的總的形變)及應(yīng)變率(指一定時(shí)間內(nèi)應(yīng)變的變化,代表形變的速度),從而反映心肌組織的整體及局部舒縮功能。由于其不依賴于多普勒原理,無(wú)角度依賴性[6],時(shí)間分辨率高,在評(píng)價(jià)右心心肌組織運(yùn)動(dòng)中已得到了廣泛的應(yīng)用[7?10]。
本研究中應(yīng)用該項(xiàng)技術(shù)發(fā)現(xiàn)右室基底段、中間段應(yīng)變及應(yīng)變率于氧療后3個(gè)月就有升高,隨著氧療持續(xù)時(shí)間的延長(zhǎng),應(yīng)變及應(yīng)變率升高更加顯著;三尖瓣環(huán)位移參數(shù)中最早變化的是Tm%,氧療后3個(gè)月其值即有升高,且與氧療前比較差異有統(tǒng)計(jì)學(xué)意義,隨著氧療持續(xù)時(shí)間的延長(zhǎng),其值繼續(xù)升高;T1,T2,Tm在氧療后6個(gè)月出現(xiàn)升高,與氧療前差異有統(tǒng)計(jì)學(xué)意義,并隨氧療持續(xù)升高。而二維心臟超聲顯示氧療后各項(xiàng)指標(biāo)均無(wú)明顯差異;肺功能的改變?cè)谘醑熀?年才出現(xiàn)顯著性提高。
由此可見(jiàn),長(zhǎng)期氧療對(duì)提高COPD患者右心功能有一定的療效。這與唐猛等[11]研究結(jié)果相一致:家庭氧療3個(gè)月后,肺動(dòng)脈壓及右心室Tei指數(shù)有所改善。目前糾正慢性低氧提高右心功能的機(jī)制尚不明確。可能由于氧氣可使ATP產(chǎn)生增多,促使ATP依賴的鉀離子通道開(kāi)放,阻止肺血管平滑肌去極化,抑制肺血管收縮,降低肺動(dòng)脈高壓[12];同時(shí)氧氣具有選擇性擴(kuò)張低氧性肺血管的作用,吸氧可改善肺血管動(dòng)力狀態(tài),減少紅細(xì)胞壓積,減少心律失常的發(fā)生[13,14],從而使心功能得到改善。但由于本研究樣本量小,有待進(jìn)一步大規(guī)模試驗(yàn)證實(shí),同時(shí)氧氣改善肺功能及右心功能的機(jī)制有待更深入的研究。
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(編輯: 周宇紅)
Efficiency of long-term oxygen therapy on right ventricular function in patients with chronic obstructive pulmonary disease
GUO Hua1*, DAI Min2
(1Department of Geriatrics,2Department of Cardiac Function, Wuxi People’s Hospital, Wuxi 214000, China)
To analyze the efficiency of long-term oxygen therapy on the right ventricular function in the patients with chronic obstructive pulmonary disease (COPD).A total of 40 COPD patients (22 males and 18 females) with pulmonary function levelⅠbut normal two-dimensional electrocardiogram admitted in our hospital from October 2011 to March 2012 were enrolled in the study. They all insistently took oxygen uptake at a low flow rate of 2L/min, 10h per day for 1 year. Echocardiography and lung function test were performed in 1d before, in 3 and 6 months and 1 year after oxygen uptake, respectively.Speckle tracking echocardiography indicated that strain of basal segments of right ventricular free wall (Sbasfw), strain rate of basal segments of right ventricular free wall (SRbasfw), strain of middle segments of right ventricular free wall (Smidfw), and strain rate of middle segments of right ventricular free wall (SRmidfw) were all dramatically increased after 3 months’ oxygen uptake treatment than the values in 1d before treatment (<0.05). With the time elapse of oxygen uptaking, Sbasfw, SRbasfw, Smidfw and SRmidfw were obviously increased (<0.01). Right ventricular longitudinal shortening (Tm%) was elevated in 3 months after oxygen uptake, which were significantly higher than before treatment (<0.05), and continued to arise along with the treatment (<0.01). Tricuspid annular systolic peak displacement at right ventricular free wall (T1), tricuspid annular systolic peak displacement at interventricular septum (T2) and tricuspid annular systolic peak displacement at midpoint of tricuspid annulus (Tm) all began to increase after 6 month, which had statistical difference with the data before oxygen uptake (<0.05), and continued to elevate with oxygen uptake time. Forced expiratory volume in one second (FEV1) and percentage of FEV1were obviously higher after 1 year’s treatment than before (<0.05).Long-term oxygen therapy significantly improves the right ventricular systolic function in COPD patients, and its effect appears earlier on the improvement to right ventricular function than to lung function.
speckle tracking imaging; oxygen therapy; pulmonary disease, chronic obstructive; right ventricular function
R563.9
A
10.11915/j.issn.1671-5403.2015.06.106
2015?01?24;
2015?04?29
郭 華, E-mail: 13812510395@163.com