肺脏病理生理学专家讲座

单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,病理生理学系,Department of Pathophysiology,高远生,肺脏,病理生理学,Respiratory Pathophysiology,肺脏病理生理学,第1页,呼吸全过程,Respiration,肺通气,pulmonary,ventilation,肺换气,gas,exchange,in the,lungs,组织换气,gas,exchange,in the tissues,细胞氧化代谢,cellular,respiration,气体血液,运输,gas transport,in the blood,外呼吸,external respiration,内呼吸,internal respiration,肺脏病理生理学,第2页,肺脏病理生理学,第3页,Symbols,P,Pressure,Partial pressure,A,Alveolar,a,arterial,v,venous,V,Volume of gas/unit time,Q,Volume of blood/unit time,.,.,肺脏病理生理学,第4页,呼吸衰竭(Respiratory Failure),外呼吸功效严重障碍 PaO,2 ,伴有或不伴有PaCO,2,病理过程。,判断标准：PaO,2,50mmHg,(正常：40 mmHg),呼吸功效不全(Respiratory Insufficiency),肺脏病理生理学,第5页,呼衰类型Classification of Respiratory failure,1.按PaCO,2,是否升高：,低氧血症型（I型）低氧血症伴高碳酸血症（II型）,2.按主要发病机制：,通气障碍型,换气障碍型,3.按病变部位：,中枢性和外周性,肺脏病理生理学,第6页,一、呼衰原因和发病机制,Respiratory Failure:The Causes,and the Mechanism,s,.,肺通气,功效,障碍,Disorders in Pulmonary Ventilation,.,肺换气,功效,障碍,Disorders in Gas Exchange of the Lungs,肺脏病理生理学,第7页,（一）肺通气,功效,障碍,:,Disorders in Pulmonary,Ventilation,限制性通气不足:,肺泡扩张受限,2.阻塞性通气不足:,呼吸道阻塞或狭窄 气道阻力增加。,肺脏病理生理学,第8页,1.限制性通气不足,（,Restrictive,Hypoventilation,）,：,肺泡扩张受限,中枢神经受损,周围神经受损,呼吸肌本身收缩功效障碍。,肺纤维化,肺泡表面活性物质降低。,严重胸廓畸形,肋骨骨折,胸膜纤维化,。,呼吸肌活动障碍,肺顺应性降低,胸廓顺应降低,胸腔积液和气胸,肺脏病理生理学,第9页,气道阻力(正常人平静呼吸)：,80%:直径 2mm 气管,20%:直径 0.8 0.8 0.8 0.8,3.部分肺泡血流不足(Alveolar Perfusion Insufficiency),死腔样通气(dead space like ventilation）,肺脏病理生理学,第27页,血液氧和二氧化碳解离曲线,Oxygen and Carbon DioxideDissociation Curves,肺脏病理生理学,第28页,问题,：,弥散障碍发生机制?,功效性分流,静脉血掺杂?,解剖分流,真性分流?,死腔样通气?,肺脏病理生理学,第29页,肺泡-毛细血管膜(alveolar capillary membrane)损伤引发急性呼吸衰竭。,病因：感染（,肺炎，败血症等）,，,休克，严重创伤，,吸入毒物或胃酸等。,（四）,急性呼吸窘迫综合征,Acute Respiratory Distress Syndrome(ARDS),Severe acute respiratory syndrome(SARS)is a good example of a probable infectious pneumonia that pathologically and clinically is ARDS.Experts have speculated that the cause is from a corona virus that may be transmitted via respiratory secretions and develops after 2-11 days of a febrile illness,.,肺脏病理生理学,第30页,肺脏病理生理学,第31页,ARDS,发生机制(,Pathogenesis),肺泡膜,内皮细胞损伤,致病,因子,释放中性粒,细胞趋化因子,中性粒细胞聚,集，释放氧自,由基、蛋白酶、,炎症介质,肺,水肿,死腔样,通气,肺泡型,上皮细胞,损伤,表面活,性物质,合成,支气管,痉挛,血管收缩,微血栓,肺泡膜,通透性,肺不张,功效性,分流,PaO,2,PaCO,2,肺脏病理生理学,第32页,A previously healthy 23-year-old male sustained numerous traumatic crush,burn,and smoke inhalation injuries during a landing accident in an airplane.His initial B.P.was 80/50 mmHg,and he was immediately infused with saline at the maximal rate.In the ER he was intubated and had no signs of pneumothorax.His orthopedic injuries and burns were treated.The ventilator was placed on the assist-control mode with the initial settings of inspired O,2,concentration at 40%,respiration rate at 12/min,and tidal volume at 900 ml.Arterial blood gas measurements were:pH=7.47,PCO,2,of 33 mmHg,and PO,2,of 62 mmHg.,Clinical Case,肺脏病理生理学,第33页,24 hrs.after admission,the patient becomes agitated and his respiration rate increased to 30/min.His minute ventilation also increased from 8.5 l/min to 20 l/min.Airway pressure increased from 18 to 65 cm H,2,O.Repeat arterial blood gas measurement of PO,2,indicated 35 mmHg and chest x-ray now showed diffuse infiltrates in a white out pattern.,Clinical Case,肺脏病理生理学,第34页,The diagnosis of ARDS is contingent upon 5 factors:,1.,Hypoxemia,2.,Diffuse pulmonary infiltrates on radiography,3.,Absence of congestive heart failure,4.,Decreased lung compliance(effective static compliance 25-35 ml/cm H,2,O),and,5.,Appropriate antecedent history.,Currently,there are no specific laboratory tests for ARDS.A definitive diagnosis is made when these signs and symptoms are linked with diffuse alveolar damage.,Clinical Case,肺脏病理生理学,第35页,急性呼吸窘迫综合征(ARDS)概念及发生机制?,问题,：,肺脏病理生理学,第36页,二、,呼衰时机体功效和代谢改变,Functional and Metabolic Change in Respiratory Failure,（一）酸碱平衡紊乱(acid-base balance disturbance)和电解质改变,呼酸:型,呼衰,CO,2,潴留 血 K,+,血 Cl,-,呼碱：I型呼衰 肺过分通气 血 K,+,血 Cl,-,代酸：严重缺氧 无氧代谢 乳酸,肺脏病理生理学,第37页,（二）呼吸系统改变,(Changes in Respiratory System),呼吸调整(Regulation of Respiration),改变,外周化学,感受器,中枢化学,感受器,呼吸,加深加紧,抑制,呼吸中枢,PaO,2,50 mmHg,PaO,2,80 mmHg,肺脏病理生理学,第38页,（三）循环系统改变(Changes in Circulation System),轻度PaO,2,和 PaCO,2,可兴奋心血管运动中枢,严重PaO,2,和 PaCO,2,抑制心血管运动中枢,肺脏病理生理学,第39页,缺氧 肺小动脉收缩 肺动脉压,右心后负荷,长久缺氧 肺血管平滑肌增殖 管壁增厚,长久缺氧 红细胞增多 血液粘度,心负荷,缺氧、酸中毒 心肌舒缩功效,呼吸衰竭 右心衰竭 肺源性心脏病,(cor pulmonale),肺脏病理生理学,第40页,PaO,2,:,60 mmHg 智力，视力轻度减退,40-50 mmHg 神经精神症状,20 mmHg 神经细胞不可逆损坏,(慢性呼衰PaO,2,20 mmHg神志仍可清醒）,PaCO,2,80 mmHg,CO,2,麻醉,(,头痛,头昏,嗜睡，精神错乱,扑翼样震颤,抽搐,及昏迷等,中枢神经系统症状）,肺性脑病(pulmonary encephalopathy):,呼衰引发脑功效障碍,（四）中枢神经系统改变,Changes in Central Nervous System,肺脏病理生理学,第41页,肺性脑病发生机制,Pathogenesis of pulmonary,encephalopathy,-氨基丁酸,脑脊液 pH,溶酶体,酶释放,中枢抑制,磷脂酶,活性,神经,损伤,颅内压,PO,2,PaCO,2,血管内皮损伤,血管,通透性,脑,水肿,脑血管,扩张,脑充血,肺脏病理生理学,第42页,问题：,呼,吸衰竭时呼吸调整改变？,肺源性心脏病发生机制?,肺性脑病定义及发生机制？,肺脏病理生理学,第43页,（一）普通标准(General Principals),1.防治原发病,2.预防或去除诱因,3.改进肺通气,4.纠正水、电解质及酸碱平衡紊乱,保 护主要器官功效,五、呼衰防治标准,Principals of the Prevention and,Treatment of Respiratory Failure,肺脏病理生理学,第44页,1I 型呼衰只有缺O,2,而无CO,2,潴留，可吸入较高浓度O,2,，,普通不超出50,2.II型呼衰有CO,2,潴留,应连续低浓度低流量吸氧,，如30，12L/min，使P,a,O,2,上升到 60 mmHg,（二）吸氧(Oxygen Inhalation),肺脏病理生理学,第45页,问题