电解质与心律失常治疗.ppt
电解质紊乱与心律失常处理,北京医院杨杰孚,心肌动作电位的产生过程,电解质对心电及心律的影响,主要影响心肌动作电位对心肌应激性及传导性也有影响严重电解质紊乱激动起源异常传导异常心脏停搏室颤,电解质紊乱对心肌动作电位的影响,项目 高钾 低钾 低钠 高钙 低钙静息电位+-动作电位时程-+-+动作电位幅度-或+-传导速度-不应期-+-+阈电位应激性+-+,高钾血症（5.5mmol/L）心电图表现,T波高尖QRS波振幅降低、时间变宽、S波加深ST段下移P波减小，甚至消失各种心律失常（缓慢型为主）窦缓、窦性静止；传导阻滞：房内、房室、室内交界区心动过速、心室自主心律、室颤、心室停搏,高血钾的ECG改变,高钾的处理,纠正原发病及诱发因素促进钾排泄输液+利尿促进钾转移葡萄糖+胰岛素对抗严重心律失常钙剂透析,低钾血症-心电图表现,U波增高T波振幅降低、平坦或倒置ST段下移各种心律失常：以快速性心律失常为主窦性心动过速早搏，尤其是室早交界区心动过速、室速、室颤,低血钾时心电图U波改变,随着血钾降低，U波不断增大,低钾血症-治疗,纠正病因及诱因摄入不足丢失过多分布异常补钾静脉口服,镁离子异常-低镁血（0.75mmol/L),原因（大致同低血钾）摄入减少营养不良消化系统疾病吸收不良排除增加肾脏疾病排泄增加其它利尿剂的使用等,镁离子异常-低镁血（0.75mmol/L),直接效应对窦房结有直接变速效应降低细胞内钾镁是激活Na+-K+-ATP酶缺镁该酶活性下降细胞内缺钾增加细胞内钙镁为钙离子拮抗剂,镁离子异常-低镁血（0.75mmol/L),镁离子异常通常合并钾离子异常低钾血症低镁血症,镁离子异常-低镁血（0.75mmol/L),心电图异常易诱发洋地黄中毒QT间期延长各种类型的心律失常（类似低钾）室早室上性及室性心动过速尖端扭转室速、室颤,镁的抗心律失常作用,主要适应症：洋地黄中毒性心律失常尖端扭转性室速急性心肌缺血导致的严重室性心律失常慢性充血性心力衰竭性心律失常,镁与心力衰竭,慢性心力衰竭患者均存在血镁降低利尿剂的使用：排出增加消化道淤血：镁吸收降低RAAS系统激活：醛固酮增加排镁洋地黄类药物：抑制肾小管对镁的重吸收,镁的抗心律失常作用,用法：急性快速性室性心律失常25%硫酸镁10ml静脉注射或加入5%GS2040ml稀释后注射门冬氨酸钾镁：10ml 静脉注射非快速性心律失常（频发早搏、短阵室速等）门冬氨酸钾镁：1：10稀释后静脉点滴口服：2-4片，3次/日其它：口服门冬氨酸钾镁2-4片，3次/日,高钙血症（3.0mmol/L),原因：少见甲状旁腺机能亢进、骨髓瘤或骨转移瘤心电图表现：ST段缩短或消失（R波后即出现突然上升的T波）QT间期缩短严重时PR延长房室阻滞早搏、心动过速等,高钙血症（3.0mmol/L),治疗：重点是原发病骨髓瘤、甲旁亢等常合并低血钾,低钙血症（1.75mmol/L),原因慢性肾脏疾病：肾衰、肾小管酸中毒等甲状旁腺机能降低心电图异常及机制：主要影响动作电位2相：延长2相复极时间心电图表现ST段平直延长QT延长：由ST段延长所致（T波不宽）,血钙异常的ECG改变,低钙血症（1.75mmol/L),治疗：原发病慢性肾脏疾病：肾衰、肾小管酸中毒等甲状旁腺机能降低补钙当使用洋地黄类药物时不宜同时用钙盐,电解质对心电及心律的影响,临床特点（1）多数非单一电解质紊乱如低钾常伴随低镁常伴有酸碱失衡高钾酸中毒低钾碱中毒掺杂因素多本身疾病肝肾功能药物,电解质对心电及心律的影响,临床特点（2）以钾离子对心肌细胞影响最明显其次钙离子镁离子钠离子,电解质紊乱所致心律失常,心电图案例分析,Case 1:Which electrolyte problem is this tracing suggestive of?,Hyperkalemia,HyperkalemiaDiscussionAs the tracing shows,this patient has a regular rhythm at a rate of 101/min.The QRSs are very wide;wider than those seen with ordinary bundle branch block.T-waves are tall in V1-3.These findings are all characteristic of hyperkalemia.The serum potassium level was 7.2 mEq/L.The rhythm may be sinus with the P-waves hidden in the ST segment or sino-ventricular rhythm if P-waves are truly not present.Atrial muscle is more sensitive to hyperkalemia than the specialized conduction system is.At certain levels of hyperkalemia,the atrial muscle becomes inexcitable(paralyzed)while the special internodal conduction system is still excitable.Then,the sinus impulses will conduct to the ventricles through the conduction system without the atria being depolarized thus referred to as sino-ventricular rhythm.,尿毒症高钾-窦室传导,窦室传导ECG表现：1.p波消失 2.QRS宽大畸形 3.T波高尖对称 4.ECG表现为QRS-T序列,CASE 2:Anteroseptal Infarct or Pseudoinfarction Pattern From Hyperkalemia?,Which of the following conditions is responsible for the ST elevation in leads V1-2?Choose from the list below.A)Acute anteroseptal infarctB)Pseudoinfarction pattern from hyperkalemia,Pseudoinfarction pattern from hyperkalemia,Pseudoinfarction pattern from hyperkalemia is correct.Sinus tachycardia at a rate of 130 beats per minute is present.The ST segment is elevated in V1 and V2,raising the possibility of acute anteroseptal myocardial infarction.However,the T wave is very tall,narrow,pointed,and tented;and the QRS is wide,measuring 140 msec.These findings are characteristic of hyperkalemia.It is well known that hyperkalemia can cause ST-segment elevation(pseudoinfarction pattern or dialyzable current of injury).This tracing is from a patient with a serum potassium level of 7.5 mEq/L during diabetic ketoacidosis,who also is in renal failure and taking an angiotensin-converting enzyme inhibitor,CASE 4,Hypocalcemia and hyperkalemia,Hypocalcemia and hyperkalemia is correct.DiscussionThe QT interval is long.When the long QT interval is due to a long ST segment with a delayed onset of the T wave,it is specific for hypocalcemia.Besides,the T waves are tall,narrow,and pointed and are highly suggestive of hyperkalemia.This combination of electrolyte problems is common in patients with chronic renal failure,which this patient has.The serum potassium level was 8.2 mEq/L and calcium 5.4 mg/dL at the time.,CASE 5,病史患者 女 26岁全身紧缩感12年，间断抽搐发作以“癫痫”收住神经科多次查体：神经肌肉应激性 紧张、恐惧、反射亢进“面神经征+“束臂试验+”ECG：QT明显延长怀疑长QT综合征收住心内科,QT/QTc:528/561,化验检查,生化：URIC:109umol/L CK:1056u/L LD：564u/L HBDH：299u/L CA:1.09mmol/L IP:2.27mmol/L 余无异常 CK-MB TnT正常血清Mg:0.7mmol/L,化验检查,血清PTH3ng/ml24小时尿Ca 1.708mmol(2.5-7.5)尿IP23.884mmol(16-42),诊断：甲状旁腺功能减低,确诊标准：临床表现神经肌肉应激性增高“面神经征+，“束臂试验+”ECGQT延长（由ST段平直延长所致）化验血钙降低血磷升高,治疗,补充钙剂一周后临床症状明显改善二周后临床症状基本消失典型的体征消失心电图恢复慢,此病例经验及教训,误诊误治12年误诊为癫痫长QT综合征分科细，不注重科间疾病,CASE 6,Hypokalemia is correct.DiscussionIn leads V1-3,the T waves are shallowly inverted and are followed by a prominent U wave.These findings are highly suggestive of hypokalemia.The serum potassium was 2.2 mEq/L at the time.,Thanks,
