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首页> 外文期刊>Critical care medicine >Controlled pauses at the initiation of sodium nitroprusside-enhanced cardiopulmonary resuscitation facilitate neurological and cardiac recovery after 15 mins of untreated ventricular fibrillation
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Controlled pauses at the initiation of sodium nitroprusside-enhanced cardiopulmonary resuscitation facilitate neurological and cardiac recovery after 15 mins of untreated ventricular fibrillation

机译:未经治疗的心室纤颤15分钟后,硝普钠增强心肺复苏开始时的受控停顿有助于神经和心脏恢复

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Objective: A multipronged approach to improve vital organ perfusion during cardiopulmonary resuscitation that includes sodium nitroprusside, active compression-decompression cardiopulmonary resuscitation, an impedance threshold device, and abdominal pressure (sodium nitroprusside-enhanced cardiopulmonary resuscitation) has been recently shown to increase coronary and cerebral perfusion pressures and higher rates of return of spontaneous circulation vs. standard cardiopulmonary resuscitation. To further reduce reperfusion injury during sodium nitroprusside-enhanced cardiopulmonary resuscitation, we investigated the addition of adenosine and four 20-sec controlled pauses spread throughout the first 3 mins of sodium nitroprusside-enhanced cardiopulmonary resuscitation. The primary study end point was 24-hr survival with favorable neurologic function after 15 mins of untreated ventricular fibrillation. Design: Randomized, prospective, blinded animal investigation. Setting: Preclinical animal laboratory. Subjects: Thirty-two female pigs (four groups of eight) 32 ± 2 kg. INTERVENTIONS:: After 15 mins of untreated ventricular fibrillation, isoflurane-anesthetized pigs received 5 mins of either standard car-diopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine. After 4 mins of cardiopulmonary resuscitation, all animals received epinephrine (0.5 mg) and a defibrillation shock 1 min later. Sodium nitroprusside-enhanced cardiopulmonary resuscitation-treated animals received sodium nitroprusside (2 mg) after 1 min of cardiopulmonary resuscitation and 1 mg after 3 mins of cardiopulmonary resuscitation. After 1 min of sodium nitroprusside-enhanced cardiopulmonary resuscitation, adenosine (24 mg) was administered in two groups. Measurements and Main Results: A veterinarian blinded to the treatment assigned a cerebral performance category score of 1-5 (normal, slightly disabled, severely disabled but conscious, vegetative state, or dead, respectively) 24 hrs after return of spontaneous circulation. Sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine, and controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine resulted in a significantly higher 24-hr survival rate compared to standard cardiopulmonary resuscitation (7 of 8, 8 of 8, and 8 of 8 vs. 2 of 8, respectively p < .05). The mean cerebral performance category scores for standard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine were 4.6 ± 0.7, 3 ± 1.3, 2.5 ± 0.9, and 1.5 ± 0.9, respectively (p < .01 for controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation + adenosine compared to all other groups). Conclusions: Reducing reperfusion injury and maximizing circulation during cardiopulmonary resuscitation significantly improved functional neurologic recovery after 15 mins of untreated ventricular fibrillation. These results suggest that brain resuscitation after prolonged cardiac arrest is possible with novel, noninvasive approaches focused on reversing the mechanisms of tissue injury. (Crit Care Med 2012; 40:-7)
机译:目的:最近已显示出一种多管齐下的方法,可改善心肺复苏过程中的重要器官灌注,其中包括硝普钠,主动加压-减压心肺复苏,阻抗阈值装置和腹部压力(硝普钠钠增强的心肺复苏)可增加冠状动脉和脑与标准心肺复苏相比,灌注压力和自发循环的返回率更高。为了进一步减少硝普钠增强心肺复苏过程中的再灌注损伤,我们研究了腺苷的添加和在硝普钠增强心肺复苏的前3分钟内分布的四个20秒控制性暂停。主要研究终点为未经治疗的心室纤颤15分钟后24小时生存,并具有良好的神经功能。设计:随机,前瞻性,盲法动物研究。地点:临床前动物实验室。受试者:32头母猪(四组,每组八头)32±2公斤。干预措施:未经治疗的心室纤颤15分钟后,异氟烷麻醉的猪接受5分钟的标准心肺复苏,硝普钠增强的心肺复苏,硝普钠增强的心肺复搏,腺苷控释或腺苷的复苏心肺复苏+腺苷。心肺复苏4分钟后,所有动物均接受肾上腺素(0.5 mg)和1分钟后的除颤电击。硝普钠增强心肺复苏治疗的动物在心肺复苏1分钟后接受硝普钠(2 mg),在心肺复苏3分钟后接受1 mg。硝普钠钠增强心肺复苏1分钟后,两组分别给予腺苷(24 mg)。测量值和主要结果:对自然疗法不知情的兽医在自然循环恢复后24小时将其大脑表现类别得分定为1-5(分别为正常,轻度残疾,重度残疾但有意识,植物状态或死亡)。硝普钠增强心肺复苏,硝普钠增强心肺复苏+腺苷和控制性停顿-硝普钠增强心肺复苏+腺苷可导致24小时生存率显着高于标准心肺复苏8(标准心肺复苏8) 8和8之8与2之8,分别p <.05)。标准心肺复苏,硝普钠增强心肺复苏,硝普钠增强心肺复苏+腺苷或控制停顿-硝普钠增强心肺复苏的平均脑力表现得分分别为:分别为0.9和1.5±0.9(与所有其他组相比,控制性停顿-硝普钠增强的心肺复苏+腺苷的p <0.01)。结论:减少心肺复苏过程中的再灌注损伤并最大程度地增加循环,可显着改善未经治疗的心室纤颤15分钟后的功能神经恢复。这些结果表明,采用专注于逆转组织损伤机制的新​​颖,非侵入性方法,可以延长心脏骤停后的脑复苏。 (Crit Care Med 2012; 40:-7)

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