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[每周一问]NO.16-Cardiopulmonary resuscitation (CPR)
Cardiopulmonary resuscitation (CPR)
Cardiopulmonary resuscitation (CPR) is a skill that has significant impact on asystolic patient survival. This week, we've discussed some recent changes in the performance of this skill. This weekend we will conclude with a discussion on direct current cardioversion.
1.  What is the history of closed chest defibrillation?
2.  What are the mechanisms of defibrillation?
3.  What are the indications for electrical cardioversion?
4.  When is cardioversion ineffective or not appropriate?
5.  Is the use of higher energy shocks (i.e. 720 joules) more effective?
今天我们总结直流电心脏复律的一些讨论：
1.  心外心脏除颤的历史？
2.  心脏除颤的机制？
3.  电击转复律的适应症？
4.  心脏复律无效或不充分是什么？
5.  更高能量电击（即720J）是否更有效？

Update on external cardioversion and defibrillation

参考答案：
1. 心外心脏除颤的历史？
心外心脏除颤产生于20世纪50年代[1]，但是直到60年代当Lown等[2]利用直流电技术治疗房颤时残得以流行。从此，特别是从20世纪90年代后，技术上明显的进步的出现使得其在房性和室性快速型心律失常得到应用。
2.心脏除颤的机制？
除颤成功的确切机制还不清楚，也不清楚对于房性和室性心律失常的机制是否一致。现存在3种主要理论：
●  Zipes等[3]假设，临界质量的去极化不允许生于肌肉维持折返性心动过速
●  Jones等[4]相信心脏除颤延长动作电位期间的心肌不应期，如同心脏舒张期去极化期间的兴奋细胞一样。
●  Shibata等[5]则假定，一定量的电流通过整个心肌以阻滞兴奋折返性心律失常。
综上所述，因为心律失常（特别是快速型心律紊乱）常常是兴奋折返的结果，回路的局部去极化已足以中止心律失常[6]。这是日益增长的证明。
3.电击转复律的适应症？
心脏复律存在几个适应症[7]。关于选择性心脏电复律，顽固性房颤或房扑的纠正是最常见的适应症。急诊心脏电复律适应于许多血流动力学不稳定的持续性室性快速型心律失常，或者血流动力学稳定的持续性室性心动过速在药物治疗后不能很快复律时。也可以用于持续室上性快速心律失常导致的心绞痛、心衰或低血压。
4.心脏复律无效或不充分是什么？
连续DC电击对于复发的阵发性房颤（常出现在心脏术后的情况）并不恰当。这类心律失常最好通过潜在沉积物的去除而得到处理或使用抗心律失常治疗。心脏复律在中止多病灶引起的房性心动过速没有效果，如同洋地黄毒性一样，即使用后可导致顽固性室颤[7]。
5.更高能量电击（即720J）是否更有效？
房颤对于360J无效时，使用720J胸外电击如同心内电复律一样成功[8]。该方法远远超出了400J与心肌坏死相关的早期研究报道，电击导致心肌细胞破坏被质疑。目前，虽然高能电击在一定的病例中得到提倡，但是其临床使用受大限制，因为大多数除颤仪能输出的最大功率为360J。

What is the history of closed chest defibrillation?
Introduced in the 1950's (1), the technique of closed chest defibrillation was popularized in the 1960's when Lown et al. (2) utilized a direct current technique for the treatment of atrial fibrillation. Since then, and especially since the 1990's, significant technical advances have occurred to allow for its use in both atrial and ventricular tachyarrhythmias.
What are the mechanisms of defibrillation?
The exact mechanisms responsible for the success of defibrillation are unknown, and it's uncertain whether the same mechanisms are responsible for atrial versus ventricular arrhythmias. This being said, three predominant theories exist:
•  Zipes et al. (3) hypothesize that the depolarization of a critical mass does not allow the remaining muscle mass to maintain a reentrant tachycardia.
•  Jones et al. (4) believe that defibrillation shocks prolong the myocardial refractoriness during the action potential as well as excite cells during periods of depolarized diastole.
•  Shibata et al. (5) postulate that a certain amount of current must spread throughout the entire myocardium to prevent reentry arrhythmias.
Overall, there is growing evidence that because arrhythmias (especially tachyarrhythmias) are often the result of reentrant circuits, regional depolarization in the area of the circuit is sufficient to terminate the arrhythmias .
What are the indications for electrical cardioversion?
There are several indications for cardioversion (7). In terms of elective cardioversion, correction of persistent atrial fibrillation or flutter is the most common indication. Emergent use of cardioversion is indicated for any hemodynamically unstable sustained ventricular tachyarrhythmia or when a hemodynamically stable and sustained ventricular tachycardia is not promptly restored following drug therapy. It also should be considered when sustained supraventricular tachyarrhythmias precipitate angina, heart failure or hypotension.
When is cardioversion ineffective or not appropriate?
Serial DC shocks are not appropriate for recurrent (hourly or daily) paroxysmal atrial fibrillation, a situation common following cardiac surgery. These arrhythmias are best managed with removal of potential precipitants or the use of antiarrythmic therapy. Cardioversion is ineffective in terminating multifocal atrial tachycardias, as well as in digitalis toxicity, where, if used may cause refractory ventricular fibrillation (7).
Is the use of higher energy shocks (i.e. 720 joules) more effective?
In atrial fibrillation refractory to 360 joules, the use of 720 joule transthoracic shocks has been as successful as the use of internal cardioversion . While this approach greatly exceeds the 400 joules earlier studies reported to be associated with myocardial necrosis, the significance of electrical shocks in causing myocyte damage has been questioned (9) . At present, although the use of higher energy shocks has been advocated in certain cases, its clinical use has been limited by most defibrillators being only able to deliver a maximum of 360 joules.
References:
1.  Zoll PM, Linethal AJ, Gibson W. Termination of ventricular fibrillation in man by externally applied electric countershock. N Engl J Med 1956;254:727-32.
2.  Lown B, Amarasingham R, Newman J. New method for terminating cardiac arrhythmias: Use of capacity discharge. JAMA 1962;82:548.
3.  Zipes DP, Fischer J, King RM, Nicoll A deB , Jolly WW. Termination of ventricular fibrillation in dogs by depolarizing a critical amount of myocardium. Am J Cardiol. 1975;36(1):37-44.
4.  Jones JL, Tovar OH. Electrophysiology of ventricular fibrillation and defibrillation. Crit Care Med. 2000;28(11 Suppl):N219-21.
5.  Shibata N, Chen PS, Dixon EG, et al. Epicardial activation after unsuccessful defibrillation shocks in dogs. Am J Physiol. 1988;255(4 Pt 2):H902-9.
6.  Trohman RG, Parrillo JE. Direct current cardioversion: indications, techniques, and recent advances. Crit Care Med. 2000;28(10 Suppl):N170-3.
7.  Oral H, Morady F. New Developments in Electrical Cardioversion of Atrial Fibrillation. Cardiol Rev. 2000;8(2):82-89.
8.  Saliba W, Juratli N, Chung MK, et al. Higher energy synchronized external direct current cardioversion for refractory atrial fibrillation. J Am Coll Cardiol. 1999;34(7):2031-4.
9.  Grubb NR, Cuthbert D, Cawood P, Flapan AD, Fox KA. Effect of DC shock on serum levels of total creatine kinase, MB-creatine kinase mass and troponin T. Resuscitation. 1998;36(3):193-9.
Site Editor: Stephen B. Corn, M.D. and B. Scott Segal, M.D.
Department of Anesthesia, Harvard Medical School
Founders and Editors-in-Chief: Stephen B. Corn, M.D. and B. Scott Segal, M.D.
Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Medical School