SEARCH RESULTS FOR: obstructive-sleep-apnea-pathogenesis-and-clinical-findings

obstructive-sleep-apnea-pathogenesis-and-clinical-findings

Obstructive Sleep Apnea: Pathogenesis and clinical findings Vascular Factors: During recumbent sleep, more bodily fluids enter the head and neck area (compared to when the patient is standing/sitting) ↑ volume of head/neck tissue surrounding the upper airwayà possible airway obstruction Authors: Ciara Hanly Austin Laing Alexander Arnold Reviewers: Steven Liu Amogh Agrawal Yonglin Mai (麦泳琳) Naushad Hirani* Yan Yu* *MD at time of publication Neuromuscular Factors: Sleep onset and/or the sleeping state reduces the drive of respiratory muscles to breathe ↓ Upper airway neuromuscular activityà↓ upper airway caliber, ↑ upper airway resistance, ↑ upper airway collapsibility during sleep Structural Factors: Obesity, tonsillar or adenoid hypertrophy, macroglossia, ↑ neck circumference, craniofacial abnormalities Excess pressure on upper airway, or deformity to that area, ↑ risk of upper airway collapse Polysomnography Absence of airflow but persistent ventilatory effort Hypopnea or Apnea Paradoxical breathing Chest wall draws in and abdomen expands during inspiration Ventilatory effort persists against closed airway No air entry due to collapsed upper airway ↑ Negative intrathoracic pressure ↑ Venous return to right atrium Stretching of right atrial myocardium à secretion of atrial natriuretic peptide (ANP) ANP inhibits epithelial Na+ channels (ENaC) in the collecting ducts of the kidney from reabsorbing Na+ à Na+ excretion ↑ Na+ excretionà↑ water excretion Nocturia Complete or partial upper airway obstruction during sleep ↑ PCO2 & ̄ PO2 in the lungsà ̄ diffusion gradient of CO2 & O2 between lungs & arteries ↑ PaCO2,, ̄ PaO2 Respiratory acidosis (↑ [H+] in blood)àactivation of vascular endothelial voltage gated K+ channels Cerebral blood vessel dilation to provide adequate O2 to brain Morning Headaches Activation of central (medulla oblongata) & peripheral (carotid body) chemoreceptors ↑ Respiratory drive à ↑ activation of respiratory muscles (ventilatory effort ) Transient arousal from sleep ↑ sympathetic nervous system activityà arterial vasoconstriction ↑ systemic vascular resistance Systemic Hypertension ↑ intraluminal pressure within blood vesselsàadaptive vascular endothelial and smooth muscle changes Artery walls thicken, harden and lose elasticityà ̄ perfusion to end organs (such as the brain) Ischemic stroke Hypoxia during the day and night ↑ pulmonary vascular resistance Pulmonary Hypertension Right heart pumps against higher pulmonary pressure àcardiomyocytes undergo concentric hypertrophy over time Cor Pulmonale (Right heart failure due to pulmonary hypertension, separate from left heart failure) Respiratory muscles overcome upper airway obstructionà airway patency restored Sleep fragmentation ̄ Daytime cognitive performance and attentiveness ↑ Risk of motor vehicle accidents Daytime Sleepiness Eg. Epworth Sleepiness Scale >10 Abbreviations: PCO2: partial pressure of carbon dioxide PO2: partial pressure of oxygen PaCO2: partial pressure of carbon dioxide in arteries PaO2: partial pressure of oxygen in arteries Ventilatory response overcompensatesà breathe out more CO2 than is required for homeostasisà ̄ PaCO2 ̄ respiratory driveà ̄ ventilatory effort Resuscitative Gasping Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 19, 2013, updated May 31, 2022 on www.thecalgaryguide.com 阻塞性睡眠呼吸暂停:发病机制及临床表现 作者:Ciara Hanly, Austin Laing, Alexander Arnold 审稿人: Steven Liu, Amogh Agrawal, Naushad Hirani*,Yan Yu* 译者: Zesheng Ye(叶泽生) 翻译审稿人: Yonglin Mai(麦泳琳) *发表时担任临床医生 神经肌肉因素: 睡眠状态下, 患者无法通过 适当增加上气道肌张力来维持气道通畅 上气道神经肌肉活动 ̄à上气道直径 ̄, 上气道 阻力↑, 睡眠时上气道塌陷 结构(解剖)因素: 肥胖、扁桃体或腺样体 肥大, 舌体肥大, 颈围增大, 颅面部畸形 上气道压力过大或上气道畸形, 上气道塌陷 的风险 ↑ 血管因素: 仰卧位睡觉引起 夜间嘴侧液体移位 周围组织与压力 ↑à上气道阻塞 多导睡眠描记术 没有气流，但持 续通气 呼吸浅慢或 呼吸暂停 反常呼吸 吸气时胸壁凹陷, 腹部膨隆 持续通气以抵抗气道 闭合 上气道塌陷导致空气进 入气道受阻 腹膜腔负压↑ 静脉血回流右心室阻力↑ 右心房心肌细胞拉伸 à心房利钠肽分泌 (ANP) ANP抑制肾集合管的上 皮Na+通道(ENaC)对 Na+重吸收à Na+排出 Na+排出量↑ à 水排出量 ↑ 睡眠时全部 或部分上呼 吸道阻塞 肺内PO2 ̄ 且 PCO2↑ à CO2 及 O2在肺和动脉 间的扩散梯度 ̄ ↑ PaCO2, ̄ PaO2 呼吸性酸中毒 (血液中 [H+] ↑) à激活血管内皮电压 门控 K+ 脑血管扩张为大 晨间头痛 脑提供足够的 O2 激活中央(延髓)和外周(颈动脉体)的化学感受器 呼吸驱动↑à呼吸肌活动 (呼吸做功 )↑ 短暂的睡眠唤醒 通道 交感神经系统活动↑ 全天缺氧 肺血管阻力↑ 肺动脉高压 右心泵血以抵抗肺 动脉高压à 随着时 间推移，心肌向心 性肥大 肺心病(区别于左 心衰，右心衰是肺 动脉高压所致) 呼吸肌克服上气道阻力à 气道 明显恢复 睡眠过程不连续 白天的认知功能 及注意力 ̄ 机动车辆事故风险↑ 白天嗜睡 à 动脉收缩 全身血管阻力↑ 高血压 血管内压力↑ à 血 管内皮和平滑肌发生 适应性改变 动脉壁增厚、硬化、失 去弹性à器官血液灌 注量 ̄ (如脑部) 缩写: PCO2:二氧化碳分压 PO2:氧分压 PaCO2:动脉二氧化 碳分压 PaO2:动脉血氧分压 通气过度 à呼出CO2 ↑ à PaCO2 ̄ 呼吸驱动 ̄à 呼吸做功 ̄ 复苏性鼾音 夜尿症 如:伊普沃斯嗜睡评分 >10 缺血性卒中 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年8月19日发表 www.thecalgaryguide.com, 2022年5月31日更新