云 電
·診治分析·
繼發(fā)性低鉀血癥所致心律失?;颊叩男碾妶D特點(diǎn)、臨床特征及治療效果分析
云 電
目的 分析繼發(fā)性低鉀血癥所致心律失常患者的心電圖特點(diǎn)、臨床特征及治療效果。方法 選擇海南省第二人民醫(yī)院1994年11月—2014年11月確診的繼發(fā)性低鉀血癥所致心律失?;颊?84例,回顧性分析患者的臨床資料,包括治療前后血鉀、心律失常發(fā)生情況、入院時(shí)臨床表現(xiàn)、心電圖檢查結(jié)果及臨床轉(zhuǎn)歸情況。結(jié)果 184例患者以室性期前收縮最多見(占40.8%),其次為頻發(fā)房性期前收縮(占37.5%),心室顫動(dòng)、T-U波延長及竇性心律不齊最少見。主要臨床表現(xiàn)為乏力(占15.8%)、心悸(占15.2%)、氣促(占14.1%)、胸悶(占13.6%)、低血壓(占12.0%)、暈厥(占10.9%)、昏迷(占10.3%)、腸麻痹15例(占8.2%)。治療后患者血鉀高于治療前,室性期前收縮、持續(xù)性室性心動(dòng)過速、短陣尖端扭轉(zhuǎn)室性心動(dòng)過速及心室顫動(dòng)發(fā)生率均低于治療前(P<0.05)。結(jié)論 繼發(fā)性低鉀血癥所致心律失?;颊叩某R娕R床表現(xiàn)為乏力、心悸、氣促、胸悶等,心電圖顯示心律失常以頻發(fā)房性期前收縮和頻發(fā)房性期前收縮較常見,經(jīng)治療其血鉀及室性心律失常情況均有所改善。
低鉀血癥;心律失常;心電描記數(shù);治療結(jié)果
繼發(fā)性低鉀血癥常發(fā)生于高血壓、糖尿病患者,因服用利尿劑或飲水過少及胃腸疾病等原因誘發(fā)。其中慢性輕度低鉀血癥無明顯臨床癥狀,但若不及時(shí)治療將迅速發(fā)展為嚴(yán)重低鉀血癥,進(jìn)而導(dǎo)致室性心律失常,部分患者出現(xiàn)惡性室性心律失常,常危及患者生命安全[1-2]。惡性室性心律失常是慢性肺源性心臟病(肺心病)的常見并發(fā)癥之一,同時(shí)也是患者死亡的重要原因,常導(dǎo)致患者出現(xiàn)心室顫動(dòng)、尖端扭轉(zhuǎn)性室性心動(dòng)過速等惡性心律失常及呼吸麻痹,因此如何預(yù)防繼發(fā)性低鉀血癥所致的室性心律失常成為臨床研究的熱點(diǎn)[3]。據(jù)相關(guān)研究報(bào)道顯示,室性心律失?;颊呖沙霈F(xiàn)血鉀異常,低鉀血癥發(fā)生率增高,且血鉀降低常引起心肌電生理改變,表現(xiàn)為嚴(yán)重心律失常,是患者發(fā)生猝死的常見原因[4]。為了提高臨床醫(yī)師對(duì)繼發(fā)性低鉀血癥的認(rèn)識(shí),本研究回顧性分析了184例繼發(fā)性低鉀血癥所致心律失?;颊叩男碾妶D特點(diǎn)、臨床表現(xiàn)及治療轉(zhuǎn)歸,并探討補(bǔ)鉀和抗心律失常的策略,現(xiàn)報(bào)道如下。
1.1 納入及排除標(biāo)準(zhǔn) 納入標(biāo)準(zhǔn):(1)符合《實(shí)用內(nèi)科學(xué)》[5]中繼發(fā)性低鉀血癥和心律失常的診斷標(biāo)準(zhǔn);(2)年齡20~80歲;(3)既往無心律失常和心力衰竭病史;(4)未服用影響血鉀的藥物及患有與血鉀異常相關(guān)的疾??;(5)依從性好。排除標(biāo)準(zhǔn):(1)妊娠期、哺乳期患者;(2)伴其他系統(tǒng)嚴(yán)重疾病和惡性腫瘤患者;(3)經(jīng)胃腸道、腎臟出現(xiàn)血鉀丟失,如發(fā)病前使用利尿劑、長期嘔吐或腹瀉患者;(4)腎上腺皮質(zhì)激素增多、腎小管酸中毒等疾病患者;(5)繼發(fā)性堿中毒、化學(xué)藥物中毒、大量排汗導(dǎo)致血鉀丟失患者。
1.2 一般資料 選擇海南省第二人民醫(yī)院1994年11月—2014年11月確診的繼發(fā)性低鉀血癥所致心律失?;颊?84例。其中男96例,女88例;平均年齡(62.5±9.6)歲;發(fā)病原因:肝硬化腹腔積液20例,畸形消化道出血2例,急性腸胃炎14例,急性呼吸道感染4例,慢性阻塞性肺疾病40例,腦出血26例,外科手術(shù)10例,器質(zhì)性心臟病所致心力衰竭52例,周期性麻痹4例,原因不詳12例。
1.3 研究方法 回顧性分析患者的臨床資料,包括治療前后血鉀、心律失常發(fā)生情況、入院時(shí)臨床表現(xiàn)、心電圖檢查結(jié)果及臨床轉(zhuǎn)歸情況。其中血鉀的參考范圍為3.5~5.5 mmol/L,<2.50 mmol/L為重度低鉀血癥、2.51~3.00 mmol/L為中度低鉀血癥、3.01~3.49 mmol/L為輕度低鉀血癥。
1.4 治療方法 按照“抗心律失常藥物治療建議”[6]進(jìn)行抗心律失常和補(bǔ)鉀治療,具體方法如下:(1)靜脈及口服補(bǔ)鉀治療:174例患者給予10%氯化鉀口服或3‰氯化鉀靜脈滴注治療,10例病情嚴(yán)重患者給予1%~4%氯化鉀靜脈微量泵進(jìn)行強(qiáng)化補(bǔ)鉀治療,所有患者根據(jù)血鉀調(diào)整治療方案。(2)補(bǔ)鎂治療:本研究中24例患者合并持續(xù)性室性心動(dòng)過速、心室顫動(dòng)及尖端扭轉(zhuǎn)性室性心動(dòng)過速,給予25%硫酸鎂10 ml稀釋后靜脈滴注。(3)提高心率:16例室性心動(dòng)過速患者出現(xiàn)尖端扭轉(zhuǎn)樣改變,按照指南選用阿托品1 mg、異丙腎上腺素1 mg靜脈滴注,所有患者經(jīng)處理后有效,無效者給予臨時(shí)起搏器進(jìn)行心臟起搏以提高心率。(4)抗心律失常:本研究中160例患者期前收縮未使用抗心律失常藥物治療,其中6例出現(xiàn)心室顫動(dòng)、18例出現(xiàn)室性心動(dòng)過速,給予利多卡因負(fù)荷量治療后病情均好轉(zhuǎn)。
2.1 心電圖特點(diǎn)及臨床表現(xiàn) 184例患者以室性期前收縮最多見(占40.8%),其次為頻發(fā)房性期前收縮(占37.5%),心室顫動(dòng)、T-U波延長及竇性心律不齊最少見,見表1。主要臨床表現(xiàn):乏力29例(15.8%),心悸28例(15.2%),氣促26例(14.1%),胸悶25例(13.6%),低血壓22例(12.0%),暈厥20例(10.9%),昏迷19例(10.3%),腸麻痹15例(8.2%)。
表1 繼發(fā)性低鉀血癥所致心律失常患者心電圖檢查結(jié)果(n=184)
Table 1 Electrocardiogram examination results of the 184 patients with arrhythmia caused by secondary hypokaliemia
心電圖檢查結(jié)果例數(shù)百分比(%)室性期前收縮7540.8頻發(fā)房性期前收縮6937.5ST段改變5228.3T波改變2111.4Ⅰ度房室傳導(dǎo)阻滯189.8Q-T間期延長189.8房室交界區(qū)期前收縮158.2陣發(fā)性房性心動(dòng)過速158.2竇性心動(dòng)過速94.9竇性心動(dòng)過緩63.3短陣室性心動(dòng)過速63.3心房顫動(dòng)63.3心室顫動(dòng)31.6T-U波延長31.6竇性心律不齊31.6
2.2 治療效果 治療后患者血鉀高于治療前,室性期前收縮、持續(xù)性室性心動(dòng)過速、短陣尖端扭轉(zhuǎn)室性心動(dòng)過速及心室顫動(dòng)發(fā)生率均低于治療前,差異有統(tǒng)計(jì)學(xué)意義(P<0.05,見表2)。
表2 繼發(fā)性低鉀血癥所致心律失?;颊咧委熐昂笱浖靶穆墒С0l(fā)生情況比較(n=184)
Table 2 Comparison of serum potassium and incidence of arrhythmia of the 184 patients with arrhythmia caused by secondary hypokaliemia before and after treatment
時(shí)間血鉀(x±s,mmol/L)室性期前收縮〔n(%)〕持續(xù)性室性心動(dòng)過速〔n(%)〕短陣尖端扭轉(zhuǎn)室性心動(dòng)過速〔n(%)〕心室顫動(dòng)〔n(%)〕治療前2.5±0.62160(87.0)16(8.7)5(2.7)3(1.6)治療后4.4±1.98 46(25.0) 0 0 0 χ2(t)值4.362a5.6317.6943.2102.677P值0.0000.0000.0000.0030.028
注:a為t值
血鉀參與機(jī)體細(xì)胞的正常代謝過程,對(duì)維持心肌細(xì)胞功能具有非常重要的作用,可用于維持細(xì)胞內(nèi)液滲透壓、防止酸堿失衡,另外其還具有保護(hù)神經(jīng)肌肉組織興奮性的作用[7-8]。臨床上將血鉀<3.5 mmol/L定義為低鉀血癥,其主要臨床表現(xiàn)為乏力、心悸、胸悶、氣促、低血壓等,嚴(yán)重者可出現(xiàn)暈厥、昏迷、腸麻痹等。低鉀血癥患者早期表現(xiàn)為肌無力、四肢軟弱無力,且隨疾病程度加重而威脅到呼吸及肌肉神經(jīng)功能,可導(dǎo)致患者出現(xiàn)呼吸困難、腱反射消失、肌肉癱軟無力,進(jìn)一步累及心肌導(dǎo)致患者出現(xiàn)心臟節(jié)律異常及傳導(dǎo)阻滯表現(xiàn)[9-11]。繼發(fā)性低鉀血癥主要分為消化系統(tǒng)所致低鉀血癥、藥源性低鉀血癥、食源性低鉀血癥和甲狀腺功能亢進(jìn)所致低鉀血癥,臨床上繼發(fā)性低鉀血癥并發(fā)心律失常較常見,主要包括陣發(fā)性室性心動(dòng)過速、房室傳導(dǎo)阻滯、竇性心動(dòng)過速等慢性心律失常,嚴(yán)重者并發(fā)Ⅲ度以上房室傳導(dǎo)阻滯和心搏驟停等危及患者生命的心律失常[12-13]。
繼發(fā)性低鉀血癥導(dǎo)致心律失常的作用機(jī)制如下:低鉀血癥促使心肌動(dòng)作電位及膜電位發(fā)生改變,影響心肌自律性及心臟傳導(dǎo)功能,導(dǎo)致心率及心臟激動(dòng)傳導(dǎo)異常,增加起搏細(xì)胞舒張期除極,促使其他心肌細(xì)胞如心室肌細(xì)胞等非起搏細(xì)胞工作,完成起搏反應(yīng),從而導(dǎo)致多種異位心律失常[14-15]。本研究結(jié)果顯示,184例患者均行常規(guī)心電圖檢查,其中室性期前收縮最多見(占40.8%),其次為頻發(fā)房性期前收縮(占37.5%),心室顫動(dòng)、T-U波延長及竇性心律不齊最少見。表明繼發(fā)性低鉀血癥所致心律失常以房性期前收縮和頻發(fā)房性期前收縮較常見。
低鉀血癥因累及心肌而導(dǎo)致心律失常,因此治療時(shí)應(yīng)盡量尋找低鉀血癥病因,并積極治療原發(fā)疾病[16]。但由于低鉀血癥的發(fā)病機(jī)制較復(fù)雜,因此目前其防治策略存在不一致性,且補(bǔ)鉀過量會(huì)導(dǎo)致高鉀血癥。臨床一般按照中華醫(yī)學(xué)會(huì)心血管分會(huì)制定的“抗心律失常藥物治療建議”中繼發(fā)性低鉀血癥所致心律失常的治療原則,包括去除誘因、補(bǔ)鉀、補(bǔ)鎂、糾正室性心律失常,但以補(bǔ)鉀為主。對(duì)于高危患者還可使用深靜脈微量泵強(qiáng)化補(bǔ)鉀、限制液體量、控制液體緩慢勻速輸入,若出現(xiàn)室性心動(dòng)過速及心室顫動(dòng)時(shí)可以考慮使用抗心律失常藥物。但對(duì)于嚴(yán)重低鉀血癥患者可以打破常規(guī)用藥,以15~40 mmol/L濃度進(jìn)行快速補(bǔ)鉀。因此,需要綜合性分析低鉀血癥具體情況以制定治療方案[17-18]。
綜上所述,繼發(fā)性低鉀血癥所致心律失常患者的常見臨床表現(xiàn)為乏力、心悸、氣促、胸悶等,心電圖顯示心律失常以房性期前收縮和室性期前收縮較常見,經(jīng)治療其血鉀及室性心律失常情況均有所改善。
[1]陳可冀,劉玥.2013年中美國家心血管病報(bào)告要點(diǎn)對(duì)比解讀及其啟示[J].中國中西醫(yī)結(jié)合雜志,2013,33(3):293-297.
[2]Lee MS,F(xiàn)lammer AJ,Lerman LO,et al.Personalized medicine in cardiovascular diseases[J].Korean Circ J,2012,42(9):583-591.
[3]周軍榮,王晉麗.心電圖對(duì)低鉀血癥的快速評(píng)價(jià)作用[J].中國急救醫(yī)學(xué),2011,31(7):652-654.
[4]Kelly BB,Narula J,F(xiàn)uster V.Recognizing global burden of cardiovascular disease and related chronic diseases[J].Mt Sinal J Med,2012,79(6):632-640.
[5]陳灝珠,林果為.實(shí)用內(nèi)科學(xué)[M].北京:人民衛(wèi)生出版社,2009:1373-1378.
[6]中華醫(yī)學(xué)會(huì)心血管病學(xué)分會(huì),中華心血管病雜志編輯委員會(huì),抗心律失常藥物治療專題組.抗心律失常藥物治療建議[J].中華心血管病雜志,2001,29(6):323-336.
[7]饒明莉.腦血管病防治指南[M].北京:人民衛(wèi)生出版社,2007:61-72.
[8]Alcaraz R,Hornero F,Rieta JJ.Dynamic time warping applied to estimate atrial fibrillation temporal organization from the surface electrocardiogram[J].Med Eng Phys,2013,35(9):1341-1348.
[9]Drawz PE,Babineau DC,Brecklin C,et al.Heart rate variability is a predictor of mortality in chronic kidney disease:a report from the CRIC Study[J].Am J Nephrol,2013,38(6):517-528.
[10]Wimmer NJ,Scirica BM,Stone PH.The clinical significance of continuous ECG(ambulatory ECG or Holter) monitoring of the ST-segment to evaluate ischemia:a review[J].Prog Cardiovasc Dis,2013,56(2):195-202.
[11]Perez-Riera AR,De Lucca AA,Barbosa-Barros R,et al.Value of electro-vectorcardiogram in hypertrophic cardiomyopathy[J].Ann Noninvasive Electrocardiol,2013,18(4):311-326.
[12]戈曉榮,徐之斌.重度低鉀血癥60例臨床救治分析[J].安徽醫(yī)學(xué),2011,32(11):1882-1883.
[13]Hammoudi N,Duprey M,Regnier P,et al.Pretest probability of a normal echocardiography:Validation of a simple and practical algorithm for routine use[J].Arch Cardiovasc Dis,2014,107(2):105-111.
[14]Cuypers J,Leirgul E,Larsen TH,et al.Assessment of vascular reactivity in the peripheral and coronary arteries by Cine 3T-magnetic resonance imaging in young normotensive adults after surgery for coarctation of the aorta[J].Pediatr Cardiol,2013,34(3):661-669.
[15]Lindsay AC,Sriharan M,Lazoura O,et al.Multidetector computed tomography of congenital aortic abnormalities[J].Int J Cardiol,2014,172(3):537-547.
[16]Langer C,Lutz M,Eden M,et al.Hypertrophic cardiomyopathy in cardiac CT:a validation study on the detection of intramyocardial fibrosis in consecutive patients[J].Int J Cardiovasc Imaging,2014,30(3):659-667.
[17]Armani C,Botto N,Andreassi MG.Molecular markers of cardiovascular damage in hypertension[J].Curr Pharm Des,2013,19(13):2341-2350.
[18]Kehl DW,Iqbal N,F(xiàn)ard A,et al.Biomarkers in acute myocardial injury[J].Transl Res,2012,159(4):252-264.
(本文編輯:謝武英)
Electrocardiographic,Clinical Characteristics and Treatment Outcome of Patients with Arrhythmia Caused by Secondary Hypokaliemia
YUNDian.
TheSecondPeople′sHospitalofHainan,Wuzhishan572299,China
Objective To analyze the electrocardiographic,clinical characteristics and treatment outcome of patients with arrhythmia caused by secondary hypokaliemia.Methods From November 1994 to November 2014 in the Second People′s Hospital of Hainan,a total of 184 patients with arrhythmia caused by secondary hypokaliemia were selected,and their clinical data was retrospectively analyzed,mainly including serum potassium and incidence of arrhythmia before and after treatment,clinical manifestations at admission,electrocardiogram examination results and clinical outcome.Results Among the 184 patients,ventricular premature beat accounted for 40.8%,frequent atrial premature beat accounted for 37.5%,ventricular fibrillation,T-U wave extending and sinus arrhythmia were infrequent;the main clinical manifestations included lacking in strength(accounted for 15.8%),cardiopalmus(accounted for 15.2%),anhelation(accounted for 14.1%),chest distress(accounted for 13.6%),hypotension(accounted for 12.0%),syncope(accounted for 10.9%),coma(accounted for 10.3%),enteroparalysis(accounted for 8.2%).After treatment,serum potassium was statistically significantly higher than that before treatment,while incidence of ventricular premature beat,persistent ventricular tachycardia,short cutting-edge reverse ventricular tachycardia,ventricular fibrillation were statistically significantly lower than that before treatment,respectively(P<0.05).Conclusion Lacking in strength,cardiopalmus,anhelation,chest distress are common clinical manifestations of patients with arrhythmia caused by secondary hypokaliemia,ventricular premature beat and frequent atrial premature beat are the most common electrocardiographic features,suitable treatment can effectively improve the serum potassium and reduce the incidence of arrhythmia.
Hypokalemia;Arrhythmia;Electrocardiography;Treatment outcome
572299海南省五指山市,海南省第二人民醫(yī)院
云電.繼發(fā)性低鉀血癥所致心律失?;颊叩男碾妶D特點(diǎn)、臨床特征及治療效果分析[J].實(shí)用心腦肺血管病雜志,2015,23(8):92-94.[www.syxnf.net]
R 591.1 R 541.7
B
10.3969/j.issn.1008-5971.2015.08.029
2015-06-04;
2015-08-13)
Yun D.Electrocardiographic,clinical characteristics and treatment outcome of patients with arrhythmia caused by secondary hypokaliemia[J].Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease,2015,23(8):92-94.