Effect of Pulmonary Vasodilation on the Efficacy of Cardiopulmonary Resuscitation

这项拨款申请的目的是检验从心脏骤停复苏的假设 受限于肺血管收缩和在复苏过程中吸入一氧化氮 无论是室颤还是无脉性电活动/心脏骤停都会增加血液。 胸部按压引起的血液流动，可提高短期存活率。胸腔开胸的功效 在产生前向全身血流时，压缩作用很差，通常估计为正常的10-25%。 心输出量。现在还不行。问题是，肺血管阻力如何影响前向血流 在心肺复苏术期间？还没有得到复苏研究界的回答。任何收缩 胸部按压时肺循环中的血液流动会限制全身的血液流动。 肺血管的循环和扩张应导致胸部血流量的增加 按压。基于这些思路，我们提出了以下具体目标。 具体目标1：继发于室颤的心脏骤停。我们的假设是：那么糟糕 含氧血液返回肺会导致肺血管阻力增加，在 转身会导致胸部按压时血流量减少。此外，吸入的硝酸盐的交付 在复苏过程中，20ppm的氧化物会降低肺血管阻力，增加血流量 并提高存活率。 具体目标2：继发于呼吸骤停的心脏骤停。我们假设一个增长 在肺血管中，继发于低氧和低氧混合 静脉血，进而导致胸部按压时血流量减少。此外， 吸入一氧化氮，20ppm，会降低肺血管阻力，改善血流 胸部按压并提高存活率。 我们相信，操纵肺血管系统将导致复苏模式的转变 方案，并导致心脏骤停的存活率增加。

The goal of this grant application is to test the hypothesis that resuscitation from cardiac arrest is limited by pulmonary vasoconstriction and that inhalation of nitric oxide during resuscitation from either ventricular fibrillation or pulseless electrical activity/asystole cardiac arrest will increase blood flow caused by chest compressions and improve short-term survival. The efficacy of chest compressions in generating forward systemic blood flow is poor, often estimated at 10-25% of normal cardiac output. Yet. the question, 'How does pulmonary vascular resistance affect forward blood flow during CPR?' has not been been answered by the resuscitation research community. Any constriction to blood flow in the pulmonary circulation during chest compressions will limit blood flow in the systemic circulation and dilation of the pulmonary vessels should lead to an increase in blood flow during chest compressions. Based on these ideas, we propose the following specific aims. Specific Aim 1: Cardiac arrest secondary to ventricular fibrillation. We hypothesize: that poorly oxygenated blood returning to the lungs causes an increase in pulmonary vascular resistance which in turn causes a decrease in blood flow during chest compressions. Further, delivery of inhaled nitric oxide, 20 ppm, during resuscitation, will decrease pulmonary vascular resistance, increase blood flow and improve survival. Specific Aim 2: Cardiac arrest secondary to respiratory arrest. We hypothesize that an increase in pulmonary vascular resistance occurs secondary to both hypoxia and poorly oxygenated mixed venous blood which in turn causes a decrease in blood flow during chest compressions. Further, inhaled nitric oxide, 20 ppm, will decrease pulmonary vascular resistance, improve blood flow during chest compressions and improve survival. We believe that manipulating the pulmonary vasculature will lead to a paradigm shift in resuscitation protocols and lead to an increased survival from cardiac arrest.