Effect of Pulmonary Vasodilation on the Efficacy of Cardiopulmonary Resuscitation

肺血管扩张对心肺复苏效果的影响

基本信息

批准号：
8047914
负责人：
GREGORY P WALCOTT
金额：
$ 21.98万
依托单位：
UNIVERSITY OF ALABAMA AT BIRMINGHAM
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-12-06 至 2012-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8047914
关键词：
Affect Alveolus Animals Applications Grants Area Arteries Blood Blood Circulation Blood Vessels Blood capillaries Blood flow Breathing Cardiac Cardiac Output Cardiopulmonary Resuscitation Cause of Death Cerebrovascular Circulation Chest Childhood Communities Contracts Coronary Devices Dose Funding Mechanisms Goals Grant Heart Heart Arrest Hospitals Hour Hypoxia Lead Length Literature Lung Mechanics Nature Nervous System Physiology Nitric Oxide Organ Oxygen Patients Perfusion Pharmaceutical Preparations Pharmacotherapy Physiology Protocols documentation Public Health Pulmonary Circulation Pulmonary Vascular Resistance Pulmonary vessels Research Resources Resuscitation Secondary to Survival Rate Survivors Symptoms Testing Time United States Vasodilation Venous Ventricular Fibrillation Work base constriction coronary perfusion hemodynamics improved inhaled nitric oxide pre-clinical pressure respiratory vasoconstriction

项目摘要

DESCRIPTION (provided by applicant): 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. PUBLIC HEALTH RELEVANCE: Cardiac Arrest in the pre-hospital setting is a leading cause of death in the United States. Chest compressions are the only accepted means of providing blood flow until the heart can be made to contract again. We hypothesize that constriction of the arteries in the lung limit the blood flow generated by chest compressions and that dilating these blood vessels with drugs delivered to the lungs by inhalation will improve blood flow generated by chest compressions and ultimately improve survival from cardiac arrest.

描述（由申请人提供）：本拨款申请的目的是检验以下假设：心脏骤停的复苏受到肺血管收缩的限制，并且在心室颤动或无脉电活动/心搏停止心脏骤停复苏期间吸入一氧化氮会增加胸部按压引起的血流量并提高短期生存率。胸外按压产生前向全身血流的效果很差，通常估计为正常心输出量的 10-25%。然而。问题是，“心肺复苏期间肺血管阻力如何影响向前的血流？”复苏研究界尚未给出答案。胸外按压期间肺循环中血流的任何收缩都会限制体循环中的血流，并且肺血管的扩张会导致胸外按压期间血流增加。基于这些想法，我们提出以下具体目标。具体目标 1：心室颤动继发的心脏骤停。我们假设：氧合不良的血液返回肺部会导致肺血管阻力增加，进而导致胸外按压时血流量减少。此外，在复苏过程中吸入 20 ppm 一氧化氮将降低肺血管阻力，增加血流量并提高生存率。具体目标 2：呼吸骤停继发的心脏骤停。我们假设肺血管阻力的增加继发于缺氧和氧合不良的混合静脉血，进而导致胸外按压期间血流量减少。此外，吸入 20 ppm 一氧化氮会降低肺血管阻力，改善胸外按压期间的血流量并提高生存率。我们相信，操纵肺血管系统将导致复苏方案的范式转变，并提高心脏骤停的生存率。公共卫生相关性：院前心脏骤停是美国的一个主要原因。胸外按压是唯一可接受的提供血流直至心脏再次收缩的方法。我们假设肺动脉收缩限制了胸部按压产生的血流量，并且通过吸入输送到肺部的药物扩张这些血管将改善胸部按压产生的血流量，并最终提高心脏骤停的生存率。