小儿心脏直视术后心律失常的原因及处理

小儿心脏直视术后心律失常的原因及处理枣庄市立医院（２７７１０２）蒲斌叶广华刘洪林李金来我院自１９８６年５月至１９９６年１２月共行小儿心脏直视手术２１２例，术后发生心律失常４２例。现将其发生原因及处理方法分析报告如下。１临床资料４２例中，男２７例，女１...     

530例胎头吸引术与新生儿窒息的相关分析

１９９５年１月至１９９８年１月，我院住院分娩的产妇５６８５例，其中５３０例行胎头吸引术，发生新生儿窒息５４例。现报告如下。临床资料：本组５３０例胎头吸引术中，胎头位置异常２３４例，胎儿宫内窘迫１９０例，第二产程延长及宫缩乏力７８例，重度妊高征２８例。...     

三尖瓣替换术及其早期死亡原因探讨

三尖瓣替换术，由于其手术死亡率高，一般只有在三尖瓣成形术无法成功的情况下才予施行。我院自１９８６年１月至１９９４年１０月，连续进行了７００例心脏瓣膜替换术，其中１７例（２．４３％）患者接受了三尖瓣替换术。１７例中１２例为风湿性心脏病患者，４例为Ｅｂｓｔｅｉｎ畸形，余１例为右房恶性间皮瘤。本组术后早期死亡５例（２９．４％），死亡原因主要是术后广泛渗血、严重低心输出量综合征、急性肾功能衰竭和恶性心律失常。     

内镜引导下的食管扩张术(附102例报告)

１９９１年１月～１９９５年１２月 ,我院应用内镜引导下的食管扩张术治疗食管和贲门处狭窄１０２例 ,取得了较好的近期疗效 ,报告如下。一、一般资料男８８例 ,女１４例 ,年龄１４～７２岁 ,平均５３．６岁。食管癌术后吻合口狭窄７０例 ,食管癌放射治疗后瘢痕性狭窄６例 ,贲门癌术后吻合口狭窄２３例 ,贲门失弛缓症２例 ,腐蚀性食管炎１例。二、食管、贲门狭窄发生的时间吻合口狭窄患者中术后１个月内发生进食困难者４８例 ,术后３个月进食困难者１７例 ,术后６个月１０例 ,超过６个月以上者１８例。６例食管癌单纯放疗后瘢痕性狭窄的病史…     

冠状动脉内支架应用的初步体会

自１９９４年４月至１９９６年２月对６３例冠心病患者施行６８次经皮冠状动脉腔内成形术（ＰＴＣＡ）中的６９支冠状动脉植入８３个支架。其中Ｃ型病变占多数。支架全部植入成功。５例ＰＴＣＡ术中急性闭塞者使用支架无死亡、心肌梗塞和紧急冠脉旁路术。随访中１例术后４天发生猝死，１例术后５天心肌梗塞，１２例术后２～６个月胸痛复发（１９．７％）。由于支架的使用，扩大了ＰＴＣＡ的适应证，减少了ＰＴＣＡ的并发症     

冠状动脉旁路移植术8例临床分析

１９９４年５月１９９５年１０月间，澳门镜湖医院心血管外科连续进行了冠状动脉旁路移植（搭桥）术８例。其中男性７例，女性１例，年龄６０至７９．５岁，平均６８．２岁。术的心功能Ⅱ至Ⅲ级（其中１例术前２月曾发生急性心肌梗塞，心跳骤停）。本组病例术前均行冠状动脉造影证实诊断。术中共搭桥２４根，平均每例３根。包括利用大隐静脉２３根，其中以序贯式吻合１很；利用左内乳动脉１根。术后出现严重低心排和出血性心包填塞共２例，经抢救成功，８例均痊愈。本文就（１）高龄病人接受冠状动脉搭桥手术；（２）术中心肌保护；（３）术后复苏处理；（４）ＩＡＢＰ在术中术后低排治疗的应用等问题进行了讨论。     

腹腔镜胆囊切除术严重并发症14例分析

腹腔镜胆囊切除术严重并发症１４例分析朱炳光李增运段留新我院自１９９１年１０月至１９９５年１２月共施行腹腔镜胆囊切除术（ＬＣ）２８００余例，发生严重并发症１４例，分析报告如下。１．并发膈下脓肿１例，发生在开展ＬＣ的第４９例。胆囊积脓，术中胆囊破损，脓性...     

腹腔镜下切除胆囊

１９９０年８月１日至１９９１年６月２０日选择性做腹腔镜下切除胆囊３５例，全部成功，无１例开腹手术，亦无１例发生合并症。平均手术时间８５分钟，平均估计失血不足１０毫升，平均住院１．２天，平均７．８天恢复正常活动。术后１０例（２８．６％）未使用任何止痛药。结果表明腹腔镜下切除胆囊对病人损伤小，减少住院时间，减轻术后疼痛，可迅速恢复正常活动。     

雷公藤防治异体肾移植术后急性排斥反应作用的临床研究

目的：通过观察雷公藤防治尸体肾移植术后急性排斥反应的作用，验证雷公藤免疫抑制在抗排斥反应中的疗效。方法：３９例肾移植患者接受雷公藤治疗，根据服用雷公藤剂量的不同分为双倍剂量组（ｎ＝２０，２ｍｇ／ｋｇｄ－１）和常规剂量组（ｎ＝１９，１ｍｇ／ｋｇｄ－１）。以同期未接受雷公藤治疗的肾移植患者作为对照（ｎ＝４０）。所有患者均无合并感染、环孢素肾中毒和手术并发症的情况。三组之间的性别、年龄、冷热缺血时间、淋巴细胞毒性试验、群体反应性抗体水平都非常接近。结果：双倍剂量组患者术后１个月和３个月内无一例急排的发生，其对照组急排发生率分别高达２５％～４５％。常规剂量组术后１个月和３个月内仅各有１例急排的发生。同期对照组急排发生率为１５％～３５％。术后满３年的雷公藤常规剂量组，３年移植肾存活率为８９．５％，显著高于其对照组移植肾６５．０％的３年存活率。此外，长期服用雷公藤未有严重感染等并发症的增加。结论：雷公藤的确具有减少肾移植术后发生急性排斥反应的作用，有助于提高移植肾的长期存活率。     

胃大部切除致胆总管损伤的治疗体会

胃大部切除致胆总管损伤的治疗体会新泰市人民医院（２７１２００）李玉光尹燕侠１９８０年１月至１９９３年７月，我院行胃大部切除术（包括胃癌ＲＩ、ＲⅡ根治术）共１３６８例，其中９例发生医源性胆总管损伤，分别于术中及术后重建胆道系统。除１例胃癌根治术后肝转移...     

Drug Therapy For Torsade de Pointes

Torsade de Pointes. Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life-threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.( Cardiovasc Electrophysiol, Vol. 4, pp. 206–210, April 1993 )     

先天性QT延长综合征尖端扭转型室性心动过速的发作方式

目的　研究先天性QT延长的尖端扭转型室性心动过速 (室速 )发作方式及其临床意义。方法　回顾性分析 5 5例因反复晕厥而确诊为先天性QT延长综合征病人的心电图 ,其中 16例记录到尖端扭转型室速开始发作的图形。结果　共记录到尖端扭转型室速 14 9阵 ,130阵为间隙依赖性。结论　间隙依赖性尖端扭转型室速曾经被认为是后天获得性QT延长综合征标志 ,研究表明其在先天性QT延长综合征尖端扭转型室速发作中也起重要的作用     

Torsades de pointes initiated by slow ventricular stimulation

The authors report a case of isolated and probably congenital complete heart block with spontaneous torsades de pointes preceded by an increase in the QT interval. During positioning of a temporary pacing catheter mechanically induced extrasystoles were observed, which seem to favor ventricular extrasystoles and unsustained runs of torsades de pointes. When the basal rhythm showed no extrasystoles, electrical stimulation delivered late in diastole captured the ventricle normally and was then followed in reproducible fashion by episodes of torsades de pointes or minor equivalents. The mechanism of this phenomenon is thought to be related to a concealed phase 4 intramyocardial block. It may have important practical consequences in paced patients predisposed to torsades de pointes. If the pacemaker is programmed at too slow a rate, with stimulation falling late in diastole, torsades de pointes could occur, some attacks of which are known to degenerate to true ventricular fibrillation.     

Detailed analysis of 24 hour ambulatory electrocardiographic recordings during ventricular fibrillation or torsade de pointes

Although the terminal cardiac rhythm is often well documented in many cases of sudden cardiac death, the antecedent or premonitory arrhythmias are usually not retrievable. The ambulatory electrocardiographic recordings of 12 patients who sustained ventricular fibrillation or torsade de pointes while wearing a long-term electrocardiographic monitor were analyzed in detail. A printout of the entire electrocardiographic recording was made and hand counts of ventricular arrhythmias were correlated with heart rate, QTc interval, RR interval preceding ventricular fibrillation or torsade de pointes and (RR')/QT initiating ventricular fibrillation or torsade de pointes. Common ambulatory electrocardiographic features in these 12 patients experiencing ventricular fibrillation or torsade de pointes included: 1) a period of high density of increasingly frequent or complex ventricular arrhythmias, or both, preceding ventricular fibrillation or torsade de pointes (11 patients); 2) R on T beats frequently initiating ventricular fibrillation or torsade de pointes (9 patients); and 3) repolarization abnormalities present for several hours before ventricular fibrillation or torsade de pointes (7 patients). No consistent relation between the RR and RR' interval initiating ventricular fibrillation or torsade de pointes was found; no consistent alteration in heart rate occurred before ventricular fibrillation or torsade de pointes. Thus, ventricular arrhythmias leading to sudden death in an ambulatory population do not occur in isolation but are preceded by a period of increased ventricular ectopic activity. Future guidelines for assessment of antiarrhythmic drug efficacy should include an evaluation of a drug's impact not only on ectopic beat frequency but also on arrhythmia density.     

Torsade de pointes induced by hypocalcemia in a postoperative patient with thyrotoxicosis.

A 29-year-old woman with a long-term history of Graves' disease was admitted for thyroidectomy. Torsade de pointes occurred after the subtotal thyroidectomy. The level of her serum calcium was lower than normal. After administration of calcium gluconate intravenously, torsade de pointes disappeared and was no longer recorded. It is assumed that her torsade de pointes was caused by hypocalcemia as a complication of subtotal thyroidectomy.     

Epicardial activation patterns of torsade de pointes in canine hearts with quinidine-induced long QT interval but without myocardial infarction

We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained polymorphic ventricular tachycardia and six episodes of monomorphic ventricular tachycardia were induced. Of 22 episodes of nonsustained polymorphic ventricular tachycardia, 12 episodes showed typical torsion of the spikes of the QRS complex around the isoelectric line (torsade de pointes). Isochronal maps were made from 38 simultaneously recorded bipolar electrograms and showed that each change in QRS morphology was associated with a change in the earliest epicardial activation site and/or a change of epicardial activation sequence. During episodes of torsade de pointes, the earliest epicardial activation site migrated gradually from one site to another site. The transitional QRS complexes had their earliest epicardial activation sites between the new and old site of the earliest epicardial activation. The changes in the earliest epicardial activation site during polymorphic ventricular tachycardia without torsade de pointes pattern was not as great as that noted during torsade de pointes. This study suggests that in a noninfarcted canine model torsade de pointes is produced by alteration in the earliest site of activation rather than by competition from two or more competing foci.     

A practical approach to torsade de pointes

The term torsade de pointes refers to polymorphic ventricular tachycardia that occurs in the setting of an abnormally long QT interval. While the most common cause is treatment with QT prolonging drugs, torsade de pointes also occurs in the congenital long QT syndromes and in the setting of acquired heart block or severe electrolyte disturbance, notably hypokalemia. Among QT prolonging drugs that cause torsade de pointes, both antiarrhythmics and “noncardioactive” drugs have been recognized. The electrocardiographic features of torsade de pointes include labile QT intervals, prominent U waves, and a “pause-dependent” onset of the arrhythmia. Treatment consists of recognition of the syndrome, correction of underlying electrolyte abnormalities, and withdrawal of any offending drugs. Magnesium, isoproterenol, or cardiac pacing provides specific antiarrhythmic therapy in torsade de pointes.     

Torsades de pointes: Arrhythmia,syndrome, or chimera? A perspective in the light of the Lambeth Conventions

What is torsades de pointes? Is it an arrhythmia or a syndrome? The distinction is critical. In this article I have attempted to explain why this is so. Both from the clinical and nonclinical standpoint, it is of overriding importance that torsades de pointes be amenable to measurement and quantification. This is the fundamental prerequisite for any variable to be of value as an endpoint in an investigation. Measurement and quantification require that a variable has an objective definition that is both inclusive and exclusive. In his seminal work, Dessertenne coined the term torsades de pointes to describe an arrhythmia with unusual features. However, torsades de pointes has been reinterpreted and redefined by Dessertenne's successors. It was originally described as occurring in certain settings (e.g., hypokalemia). However, this has been reinterpreted to mean that a specific set of antecedent conditions (such as hypokalemia) are part of the definition of torsades de pointes. If this is the case, then torsades de pointes is a syndrome, not an arrhythmia. For those more concerned with arrhythmias than with syndromes, the key issue to be determined is what to call the arrhythmia that is part of the syndrome. I have put forward some suggestions with the objective of answering this question, using the Lambeth Conventions as a guide. I believe that there is strong case for ventricular tachyarrhythmias to be classified simply as tachycardia or fibrillation, with the optional use of the term delayed repolarization syndrome in cases where a long QT interval is present. The latter term should be used as one might use the term acute myocardial ischemia, i.e., to denote an underlying condition; it should not be used to define the arrhythmia itself. Twenty-four years after its introduction, the term torsades de pointes has now become a chimera and is best abandoned.     

Torsade de pointes due to noncardiac drugs: most patients have easily identifiable risk factors

Numerous medications, including drugs prescribed for noncardiac indications, can lead to QT prolongation and trigger torsade de pointes. Although this complication occurs only rarely, it may have lethal consequences. It is therefore important to know if patients with torsade de pointes associated with noncardiac drugs have risk factors that are easy to identify. We reviewed reports of drug-induced torsade de pointes and analyzed each case of torsade de pointes associated with a noncardiac drug for the presence of risk factors for the long QT syndrome that can be easily identified from the medical history or clinical evaluation (female gender, heart disease, electrolyte disturbances, excessive dosing, drug interactions, and history of familial long QT syndrome). We identified 249 patients with torsade de pointes caused by noncardiac drugs. The most commonly identified risk factor was female gender (71%). Other risk factors were frequently present (18%-41%). Virtually all patients had at least 1 of these risk factors, and 71% of patients had 2 or more risk factors. Our study suggests that almost all patients with torsade de pointes secondary to noncardiac drugs have risk factors that can be easily identified from the medical history before the initiation of therapy with the culprit drug.     

Familial inducible torsade de pointes with normal QT interval

A familial presentation of torsade de pointes is described.The propositus had recurrent syncope, documented torsade depointes, a normal Q-T, and close coupled premature ventricularbeats initiating the paroxysmal arrhythmia. The mother had sporadicsyncope without documented torsade de pointes, a normal Q-T,and closely coupled premature ventricular beats. Electrophysiologicalstudies demonstrated reproducible inducible torsade de pointestachycardia in both patients. Serial drug testing in both revealedsuppression of induced torsade de pointes with oral propranolol.Chronic oral propranolol resulted in clinical cure in both patients.