高钾血症致窦室传导鉴别1例

1病例报告 患者,男性,77岁,因“纳差、尿少2周,加重1d”于2011—11—21入住广州中医药大学第二临床医学院二沙急诊科。患者既往有不明原因的白细胞升高病史,未予明确诊断。2011-11-21下午16：D7急查血常规：白细胞125.3×109／L．中性粒细胞0．80,血红蛋白77g／L,血小板548×109／L;     

严重高钾血症伴窦室传导15例临床分析

严重高钾血症临床并不罕见，当血清钾浓度大于8．0mmol／L时，P波消失，QRS波明显增宽，心电图上无P波规则节律的窦室传导。如果不及时处理，可导致心室停搏及心室颤动。现将近年收治的15例严重高钾血症伴窦室传导作一临床分析。     

高钾血症致窦室传导一例

患者男性 ,6 0岁。患糖尿病 3年 ,本次因腹胀、恶心、呕吐 2d入院。化验空腹血糖 19 4 9mmol/L、尿素氮2 6 3mmol/L、肌酐 2 89 7mmol/L、血钾 9 0 5mmol/L。入院诊断为糖尿病酸中毒、急性肾功能不良。入院时心电图示 ,P波变平、增宽 ,QRS波宽大畸形 ,波幅降低 ,S波加深 ,T波高尖对称底窄。 2h后心电图示 ,P波消失、QRS时限 0 14s、ST段缩短、T波高尖 (图 1)。治疗 2d后化验血糖14 37mmol/L、尿素氮 16 4mmol/L、肌酐 136 3mmol/L、血钾 4 38mmol/L、心电图转为窦性心律。 12d后 ,患者症状消失 ,化验及心电图正常 ,出院。讨…     

严重高钾血症伴窦室传导15例临床分析

严重高钾血症临床并不罕见,当血清钾浓度大于8．0mmol／L时,P波消失,ORS波明显增宽,心电图上无P波规则节律是窦室传导的表现。如果不及时处理,可导致心室停搏及心室颤动。现将作者近年来收治的15例严重高钾血症伴窦室传导报道如下。     

高钾血症致窦室传导死亡一例

<正>1病例介绍患者,男,71岁。以"上腹部疼痛7d"为主诉于2014-04-02 16:40入院。既往高血压史,血压控制差。入院查体:血压148/86 mmHg,心率92次/min,呼吸25次/min。行入院检查。心电图:窦性心动过速。生化检查:K~+3.9 mmol/L。RBC 3.68×10~(12)/L,Hb 27g/L。M型超声心动图及彩色多普勒:(1)各     

高血钾致窦室传导3例

例１患者男性 ,５６岁。临床诊断 :慢性肾炎 ,肾功能衰竭 ,尿毒症。体检 :ＢＰ２２．７／１５．２ｋＰａ(１７０／１１４ｍｍＨｇ) ,心率９０次／ｍｉｎ ,心律齐 ,闻及心包摩擦音。血尿素氮２４．１ｍｍｏｌ／Ｌ ,肌酐６８９μｍｏｌ／Ｌ ,血清钾８．８ｍｍｏｌ／Ｌ。急查心电图 (图１Ａ)示 :各导联Ｐ波消失 ,Ｒ＿Ｒ间期规整 ,频率９８次／ｍｉｎ。ＱＲＳ波群时间０．２４ｓ ,Ｖ３、Ｖ５ 导联Ｒ波的振幅减小 ,Ｓ波粗钝 ,波形既不符合右束支传导阻滞也不符合左束支传导阻滞。Ｔ波高耸呈帐篷状。心电图诊断 :高钾血症引起窦室传导伴心室内传导…     

高血钾致窦室传导2例

例1男性,70岁。因阿-斯发作急诊入院。心电图(图A)示:P波消失,QRS宽大畸形,时限达0.20s,节律基本规则,频率68次/min,T波高尖对称。在Ⅱ、Ⅲ、aVR导联可见宽大畸形的QRS-T波,时限达0.28s连续3次以上,频率为88次/min,稍不规则,较基本节律快。心电图诊断:心房停搏,窦室传导,室内传导阻滞,短阵性室性心动过速,符合     

高血钾致窦室传导1例

患者男性,60岁。有高血压、肾功能不全病史10余年。因尿闭48h急症入院,体检：血压180／120mmHg,神志清,呼吸急促,双肺呼吸音粗,心率70次／min,心律不齐,偶闻及早搏,无明显病理性杂音,第2心音亢进。双下肢明显浮肿。急查心电图(图1)示：各导联P波消失,心室率63次／min,QRS波显著宽大畸形,时间为0．24s。S波明显增宽粗钝,T波高耸呈帐篷状。V3,V4导联最高达3．9mV。心电图诊断：窦室传导伴不定型室内传导阻滞,高血钾症改变。急查血清钾为10．2mmol／L,肌酐、尿毒氮均异常增高。入院后给予控制高血钾及对症处理。于当晚突然死亡。     

高钾血症致窦室传导,心动过缓—过速伴蝉联现象

患者男、64岁、因糖尿病酮症酸中毒就诊,门诊心电图窦性心动过缓,58次/分,入院时患者呈嗜睡状,面色潮红、血压24/12kPa(180/90mmHg)、心率60次/分、律齐、无杂音,入院后心电监护P波消失,出现阵发心动过缓、过速交替,心电图见图1。Ⅱ导联上、下行连续记录,上行前三个R波规整,46次/分,其前无P波,T波高尖对称,QT间期0.44秒。第4个R波提前,第5个R波联律间期0.52秒,出现轻度差异传导。第6个R波联律间期为0.44秒,差传明显,其后R频率125～166次/分,R波降低,S波加深,ST段不明显。差传随R波频率增快更为明显,如Ⅱ导联下行R_(2、3、4)T波与S波相连,QRS-T呈宽大双相波,表现为差异传导蝉联     

高钾血症致窦室传导窄QRS一例

患者男性，72岁，因间歇胸闷、全身无力1d入院。患者入院前1d无明显诱因出现胸闷，伴出汗、全身无力、腹部不适，无胸痛及放射痛，无头晕、黑嚎，未服药休息10min后自行缓解。入院当日无诱因再次出现上述症状，持续10余分钟后自行缓解。就诊于社区医院，心电图示“交界性心律”，心率30—40次／min，予阿托品静脉滴注，即转来我院急诊。既往史：高血压7—8年，最高血压200mmHg（1mmHg：0．133kPa），平素口服吲哒帕胺，1个月前改为福辛普利钠、复方阿米洛利合用，血压控制在150—160／70mmHg。糖尿病病史5～6年，2006年5月曾于社区医院诊断为“肾功能不全”。本次发病前后无输血史，饮食正常，尿量无改变。体格检查示，血压150／50mmHg，双肺呼吸音清，未闻及干湿哕音，心率38次／min，心律不齐，可闻及早搏4次／min。未闻及杂音，腹软，肝脾肋下未及，双下肢未见水肿。入院心电图示P波消失，心室波呈节律规整的窄QRS型（0．08s），T波高尖，基底狭窄，QT间期0．48s，QTc=0．38s，心室率38次／min。[第一段]     

Effects of hyperkalaemia on sinus nodal function in dogs: sino-ventricular conduction

The effects of hyperkalaemia on electrograms recorded from the sinus node, crista terminalis, Bachmann bundle, right and left atria and His bundle were studied in anaesthetised dogs. Increasing hyperkalaemia up to about 8.5 mol X litre-1 produced: 1) a gradual prolongation of the sino-crista terminalis interval, and 2) a shift in sinus pacemaker location. Hyperkalaemia between 8.5 and 10.0 mmol X litre-1 produced arrest of most of the atria but persistence of electrical activity of the sinus node, crista terminalis, Bachmann bundle, His bundle and ventricles and sustained sino-ventricular conduction. During the course of increasing hyperkalaemia, right atrial electrograms from sites closer to the crista terminalis disappeared later than those from sites more remote from the crista terminalis. Decremental conduction through sites progressively remote from the axis of the crista terminalis (and possibly also other "preferential pathways") seemed to be the basis of hyperkalaemic atrial arrest.     

An appraisal of "supernormal" A-V conduction

Certain temporal patterns of A-V and V-A transmission in experimental preparations resemble phenomena attributed to "supernormal" conduction in the clinic. Detailed study of the properties of the A-V transmission system in such experiments reveals alternative explanations in which supernormality is clearly eliminated. By application of similar principles, supernormality can be eliminated as a factor in most if not all of the published examples. Three major categories can be discerned: (1) occult 2:1 A-V block, in which an idioventricular beat "retracts" an otherwise refractory barrier within the A-V node; (2) alternation between dissociated intranodal transmission pathways; and (3) "ventriculophasic" (vagal) depression of nodal conductivity.     

Diuretics and hyperkalaemia in diabetic ketoacidosis

Diabetic ketoacidosis (DKA) often presents with hyperkalaemia. We investigated whether it was more likely in patients taking potassium-retaining diuretics. A retrospective survey of all patients (552 cases) presenting in DKA between 1974 and 1984 was undertaken. Initial biochemical data were compared for patients recorded as taking potassium-retaining diuretics (7 cases) at the time of presentation with those taking potassium-losing diuretics (13 cases), and age matched control groups were selected from those who presented in DKA but were not taking diuretics. There was no significant difference in initial serum potassium levels between the diuretic treated groups. The serum sodium was higher in the control group than in the potassium losing group (p = 0.045) and the serum urea significantly lower (p = 0.045). We conclude that potassium-retaining diuretics do not predispose to hyperkalaemia in diabetic ketoacidosis.