Arrhythmias are a common source of perioperative, noncardiac surgical morbidity. we'll focus on the diagnosis and management of bradyarrhythmias. This week, however, we'll focus on the general entity of arrhythmias.
1.What is the incidence of perioperative arrhythmias?
2.What are some predisposing factors for perioperative arrhythmias?
3.What has been responsible for the advances in the diagnosis and management of dysrhythmias in the past 30 years?
1 什么是围术期心律失常发生率？
2 哪些因素与围术期心律失常有关？
3 过去30年中，哪些因素促进了心律失常的诊断和治疗？
参考答案
1 什么是围术期心律失常发生率？
围术期心律失常发生率取决于心律失常定义、监测的方法和频率、患者特征和手术类型。研究报道行心胸外科手术患者发生心律失常比率高（超过90%），即使是ASA 1 级 2级患者在全身麻醉下行各类手术，心动过速、心动过缓、或其它心律失常的发生率仍高于70%。Forrest 等报道健康患者全身麻醉时，使用氟烷或异氟烷进行麻醉患者发生严重室性心律不齐和心动过速的几率更大些。
2 哪些因素与围术期心律失常有关？
很多因素与围术期心律失常有关，包括：
•低氧血症
•高碳酸血症
•心肌缺血
•内源性或外源性儿茶酚胺释放增多
•电解质或酸碱失衡
•药物作用
•机械因素，如仪器操作
一些心律失常可能是多因素造成的，寻找单一的病因可能使病因过于简单化。无论如何，确定和修正可能的病因学在处置这类心律失常上是必要的。在确定此类心律失常时必须考虑发作时间、严重程度和导致的（或存在的）心功能变化。上述因素可能引发节律失常，其更易于发生于合并有潜在器质性心脏疾病患者，不仅如此，上述因素可能最终通过一最后通路导致心律失常。Sipido等应用犬细胞模型，提示Ca2+离子流通过Na/Ca交换体(而不是L-型钙离子通道)延长非同步性动作电位，产生导致心律失常的电流产生。
3 过去30年中，哪些因素促进了心律失常的诊断和治疗？
在评估、理解和治疗心律失常方面的进步如下：
•在应用机械学理解心律失常方面增强
•治疗心律失常新药物的出现（包括腺苷、胺碘酮、溴苄胺、地尔硫卓、艾司洛尔、伊布利特和维拉帕米）
•控制潜在致死性心律失常的能力的提高
•经皮和经食道心脏起搏技术的进步
•外科或导管消融术消除心律失常起源点或折返通路技术的提高
英文参考答案
1 What is the incidence of perioperative arrhythmias?
The incidence of perioperative arrhythmias depends on the definition, the method and frequency of surveillance, patient characteristics and the type of surgery (1). While patients undergoing cardiothoracic surgery have the highest reported incidence (greater than 90%), even ASA 1 and 2 patients undergoing general anesthesia for a variety of procedures have a greater than 70% incidence of tachycardia, bradycardia, or other dysrhythmias (2). Of note, Forrest et al.(2) noted in healthy patients undergoing general anesthesia that severe ventricular arrhythmias and tachycardias were more common with halothane and isoflurane, respectively.
2 What are some predisposing factors for postoperative arrhythmias?
A number of factors have been associated with perioperative arrhythmias, including (3):
•hypoxemia
•hypercarbia
•myocardial ischemia
•endogenous or exogenous catecholamines
•electrolyte or acid base imbalances
•drug effects
•mechanical factors, such as instrumentation
Certainly arrhythmias may be multifactorial, and the search for a single etiology may be an oversimplification. Regardless, identification and correction of potential etiologies is necessary for the management of these arrhythmias. The duration, severity, and resulting (or existing) cardiac function should all be considered in this determination. Of note, while the above listed factors may initiate a dysrhythmia, they are more likely to occur in patients with underlying structural heart disease (1). Moreover, the factors listed above may ultimately utilize a common final pathway to result in dysrhythmias; Sipido et al. (4) utilizing a canine myocyte model, suggested that the Ca(2+) influx via the Na/Ca exchanger (in contrast to L-type calcium channels) appeared to prolong nonhomogeneous action potentials, leading to arrhythmogenic currents.
3 What has been responsible for the advances in the diagnosis and management of dysrhythmias in the past 30 years?
Improvement in evaluating, understanding and treating dysrhythmias have been the result of (1):
•enhancement of a mechanistic understanding of dysrhythmias,
•availability of new drugs for treatment (including adenosine, amiodarone, bretylium, diltiazem, esmolol, ibutilide, and verapamil),
•ability to intentionally trigger (and control) potentially lethal dysrhythmias,
•technologic advances in transcutaneous and transesophageal pacing
•advances in surgical or catheter ablation of dysrhythmic foci or reentrant pathways.
References:
1.Atlee JL. Perioperative cardiac dysrhythmias: diagnosis and management. Anesthesiology 1997;86:1397-424.
2.Forrest JB, Cahalan MK, Rehder K, et al. Multicenter study of general anesthesia. II. Results. Anesthesiology 1990;72(2):262-8.
3.Hollenberg SM, Dellinger RP. Noncardiac surgery: Postoperative arrhythmias. Crit Care Med 2000; 28suppl) N145-50.
4.Sipido KR, Volders PG, de Groot SH, et al. Enhanced Ca(2+) Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes : Potential Link Between Contractile Adaptation and Arrhythmogenesis. Circulation 2000;102(17):2137-2144
