应激对心血管影响-课件

1、急慢性心理应激对心血管系统的影响目前认为，应激是机体在受到内外环境因素及社会、心理因素(统称为应激原)刺激时所出现的非特异性全身性适应反应，也称应激反应（stress response)。应激凡能引起应激反应的各种刺激因素称为应激原。种类： 1.外环境因素 2.内环境因素 3.心理、社会因素高热、寒冷、射线、噪声、强光、低氧、病原微生物及化学毒物、空间不适、搬迁等 各种疾病折磨与内环境紊乱 应激原（stressor）工作紧张、不良人际关系、离婚、丧偶、愤怒、恐惧、焦虑等神经内分泌反应蓝斑-去甲肾上腺素能神经元轴（LC-NE）兴奋儿茶酚胺分泌下丘脑-垂体-肾上腺皮质轴 （HPA）强烈兴奋糖皮质激

2、素分泌应激的神经内分泌反应杏仁复合体、海马、边缘皮质、新皮质脊髓侧角调节交感神经张力 主要中枢整合部位中枢效应：引起兴奋、警觉、紧张、 焦虑等情绪反应 应激时蓝斑-交感-肾上腺髓质系统的兴奋HPA结构基础室旁核外周效应 应 激GCCRH ACTH中枢效应 正常：2537mg/d 应激：100mg/d 抑郁、焦虑及厌食等情绪行为改变 基本效应心理应激对心血管系统影响急性心理应激急性心理应激指当面临一些重大生活事件（如考试、攻击、侵袭性行为），或突如其来的身外的痛苦刺激是，所产生的生理、心理和行为反应。大量证据表明，急性心理应激可能会引发急性心脏事件或心源性猝死。流行病学报告显示，在一些自然灾害，

3、如飓风，地震，海啸等情况下急性冠脉综合征的发病率急剧上升。除外一些极端的情况，在日常生活中遇到的急性行为和情绪压力（如愤怒或冲突）也被认为是冠心病患者心肌梗死，恶性心律失常，心源性猝死的诱因。Adverse Effects of Acute Emotional Stress on the HeartAcute Emotional StressLeft Ventricular DysfunctionMyocardial IschemiaVentricular ArrhythmiasAngiogram in Stress CardiomyopathyMyocardial IschemiaSyste

4、mic vascular resistance increases during mental or emotional stress although myocardial oxygen demand also increases.Individuals with coronary artery disease may develop myocardial ischemia during emotional or mental stress even if their exercise or chemical nuclear stress test results are negative.

5、Holter Report During EarthquakeDuring the 1999 earthquake in Taiwan, 12 patients were being routinely studied with Holter monitoring. When the Holter was scored, contrasting the minutes before and minutes after the earthquake, pronounced increases in heart rate (HR) were observed at the time of the

6、quake, up to 160 beats/min. Daily Cardiac Deaths in Los Angeles Associated With EarthquakeThe Northridge, California earthquake in 1994 was well studied in terms of cardiovascular consequences. The daily numbers of deaths attributed to cardiovascular disease increased dramatically on the day of the

7、earthquake, as contrasted with the same date in previous years慢性心理应激 慢性应激状态，包括职业压力，社会关系，环境刺激等。 现有研究表明，慢性应激参与心血管疾病，特别是冠心病的发生和发展。大规模的，以社区为基础的研究和前瞻性研究已经证明了焦虑症和心脏猝死之间的剂量依赖性的关联。特别是INTERHEART研究表明心肌梗死的发生率在慢性应激患者中增加2倍。Psychobiological mechanisms in atherothrombotic diseasesPathologyMajor findings with chron

8、ic psychosocial stressAltered hypothalamic-pituitary adrenal axis activityHypercortisolism, hypocortisolism that is accompanied by downregulated or desensitised glucocorticoid receptorsAutonomic dysfunctionNorepinephrine, epinephrine, heart rate variability, heart rate recovery after exercise, baror

9、eflex sensitivityEndothelial dysfunctionvon Willebrand factor, endothelin-1, flow-mediated dilation, nitric oxide productionUpregulated cellular adhesionSoluble intercellular-adhesion molecule-1, soluble vascular-cellular adhesion molecule-1Increased inflammationHigh-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-, interleukin-1, anti-inflammatory cytokines,whit