课题基金 / 基金详情

Defibrillation of Ischemic Ventricular Fibrillation

Defibrillation of Ischemic Ventricular Fibrillation
缺血性心室颤动的除颤
批准号:
6638579
负责人:
GREGORY P WALCOTT
金额:
$21.53万
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-05-01 至 2005-03-31

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项目成果

GREGORY P WALCOTT的其他基金

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中文摘要
翻译
描述(申请人的逐字描述):心源性猝死是一种 是美国的主要死因。为了解决这个问题 问题,生存链的概念已被提出作为一种方式, 描述成功复苏所需的任务。早期 除颤是提高出院后存活率的关键 心脏骤停关于除颤的有效性知之甚少。 急性缺血时的自发性心律失常。一个更大的冲击 需要停止心室纤维性颤动, 存在急性缺血而不是停止电诱导的心室 非缺血性心脏的纤维性颤动。我们将研究 在成功和失败的心脏除颤电击后, 设计用于模拟缺血性心室的不同方面的条件 纤颤:(1)急性局部缺血引起自发性心室颤动 纤颤,(2)急性局部缺血,随后电诱导 室颤,(3)急性局部缺血引起自发性 心室纤颤,进而导致长时间的全脑缺血,以及 (4)急性局部缺血引起自发性室颤 陈旧性心肌梗死的背景。我们将测试假设,在 局部缺血诱发的自发性心律失常的设置、除颤 电击必须做三件事:(1)停止所有纤颤波前,(2)不 重新开始纤颤,和(3)停止原始心律失常的触发。我们 也将测试的假设,一个主要的决定因素是否一个 由急性缺血引起的自发性心律失常可以容易地除颤 取决于心律失常的起始机制和 心律不齐为了验证这些假设,我们将使用电映射技术 绘制室性心律失常的起始,然后绘制前几个 除颤电击后的电击后激活。通过 了解除颤电击成功或失败的原因 在这些条件下,我们将更有能力开发新的 除颤技术有望提高 患有心脏性猝死的患者。
英文摘要
DESCRIPTION (the applicant's description verbatim): Sudden Cardiac Death is a major cause of mortality in the United States. In an effort to attack this problem, the concept of a Chain of Survival has been presented as a way to characterize the tasks necessary for a successful resuscitation. Early defibrillation is central to improved survival rates following out of hospital cardiac arrest. Very little is known about defibrillation efficacy of spontaneous arrhythmias in the presence of acute ischemia. A much larger shock is needed to halt ventricular fibrillation that occurs spontaneously in the presence of acute ischemia than to halt electrically induced ventricular fibrillation in the non-ischemic heart. We will study the activation patterns following successful and failed defibrillation shocks with the heart in four conditions designed to model different aspects of ischemic ventricular fibrillation: (1) acute regional ischemia causing spontaneous ventricular fibrillation, (2) acute regional ischemia followed by electrically induced ventricular fibrillation, (3) acute regional ischemia causing spontaneous ventricular fibrillation which in turn causes prolonged global ischemia, and (4) acute regional ischemia causing spontaneous ventricular fibrillation in the setting of an old myocardial infarction. We will test the hypothesis that, in the setting of an ischemically induced spontaneous arrhythmia, a defibrillation shock must do three things: (1) stop all fibrillation wavefronts, (2) not restart fibrillation, and (3) stop the trigger of the original arrhythmia. We will also test the hypothesis that a major determinant of whether or not a spontaneous arrhythmia caused by acute ischemia can be easily defibrillated depends upon the mechanism of initiation of the arrhythmia and duration of the arrhythmia. To test these hypotheses, we will use electrical mapping techniques to map the initiation of ventricular arrhythmias, and then map the first few post-shock activations following delivery of a defibrillation shock. By developing an understanding of how a defibrillation shock succeed or fails under these conditions, we will be in a better position to develop new defibrillation techniques that will hopefully increase survival rates of patients suffering an episode of sudden cardiac death.
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