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

• 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
• 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; 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

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）：本赠款申请的目的是检验以下假设：心脏骤停的复苏受到肺部血管收缩的限制，并且在肺部纤维化或心室纤维化或无脉冲电活动/无稳定心脏中的复苏过程中吸入一氧化氮会增加胸部压缩的血液流动并改善胸部的血液流动并改善胸部的血液流动。胸部压缩在产生正向全身血流的功效很差，通常估计为正常心输出量的10-25％。然而。问题：“肺血管抗性如何影响心肺复苏术期间的前血流？”复苏研究界没有回答。胸部压缩过程中肺循环中血流的任何收缩都将限制全身循环中的血液流量和肺血管扩张，应导致胸部压缩期间血液流动的增加。基于这些想法，我们提出以下特定目标。特定目标1：心室纤颤的心脏骤停。我们假设：氧化不良的血液恢复到肺部会导致肺血管耐药性增加，进而导致胸部压缩过程中血液流量的减少。此外，在复苏期间，吸入的一氧化氮的递送为20 ppm，将降低肺血管耐药性，增加血液流动并改善生存率。特定目的2：继发于呼吸停滞的心脏骤停。我们假设肺血管耐药性的增加发生在缺氧和氧化混合静脉血液不足，这又导致胸部压缩过程中血液流量的降低。此外，吸入的一氧化氮20 ppm将降低肺血管耐药性，改善胸部压缩过程中的血液流量并改善存活率。 我们认为，操纵肺脉管系统将导致复苏方案的范式转移，并导致心脏骤停的生存率增加。 公共卫生相关性：院前环境中的心脏骤停是美国的主要死亡原因。胸部压缩是提供血液流动的唯一公认手段，直到可以使心脏再次收缩为止。我们假设在肺中的动脉收缩限制了胸部压缩产生的血液流动，并通过吸入将这些血管扩张到肺部，将改善胸部压缩产生的血液流动，并最终改善心脏滞留的生存。