【病理生理學(xué)】呼吸衰竭（廣州中醫(yī)藥大學(xué)病理生理學(xué)PPT課件）

1、呼吸衰竭（廣州中醫(yī)藥大學(xué)病理生理學(xué)PPT課件）呼吸全過程Respiration肺通氣pulmonaryventilation肺換氣gasexchangein thelungs組織換氣gasexchangein the tissues細胞氧化代謝cellularrespiration氣體血液運輸gas transportin the blood 外呼吸 external respiration 內(nèi)呼吸 internal respirationSymbolsP PressurePartial pressureAAlveolaraarterialvvenousVVolume of gas / uni

2、t timeQVolume of blood/ unit time.呼吸衰竭(Respiratory Failure) 外呼吸功能嚴(yán)重障礙 PaO2 ,伴有或不伴有PaCO2 的病理過程。判斷標(biāo)準(zhǔn)：PaO2 50mmHg (正常：40 mmHg)呼吸功能不全(Respiratory Insufficiency)呼衰的類型Classification of Respiratory failure1. 按PaCO2 是否升高： 低氧血癥型（I型） 低氧血癥伴高碳酸血癥（II型）2. 按主要發(fā)病機制：通氣障礙型 換氣障礙型3. 按病變部位：中樞性和外周性一、呼衰的原因和發(fā)病機制 Respirator

3、y Failure: The Causes and the Mechanisms.肺通氣功能障礙 Disorders in Pulmonary Ventilation.肺換氣功能障礙 Disorders in Gas Exchange of the Lungs （一）肺通氣功能障礙: Disorders in Pulmonary Ventilation限制性通氣不足: 肺泡擴張受限2.阻塞性通氣不足: 呼吸道阻塞或狹窄 氣道阻力增加。1.限制性通氣不足（RestrictiveHypoventilation）：肺泡擴張受限中樞神經(jīng)受損,周圍神經(jīng)受損,呼吸肌本身 收縮功能障礙。 肺充血和嚴(yán)重肺纖維

4、化,肺泡表面活性物 質(zhì)減少。 胸廓和胸膜本身病變。呼吸肌活動障礙肺順應(yīng)性降低胸廓順應(yīng)降低胸腔積液和氣胸氣道阻力(正常人平靜呼吸)：80%: 直徑 2mm 氣管 20%: 直徑 2mm 氣管病因：氣管痙攣 腫脹 纖維化 滲出物 異物 腫瘤 氣道內(nèi)外壓力改變2.阻塞性通氣不足（Obstructive Hypoventilation): 呼吸道阻塞或狹窄 氣道阻力增加。阻塞位于胸外，表現(xiàn)為吸氣性呼吸困難 (Inspiratory Dyspnea)呼氣吸氣阻塞位于胸內(nèi)，表現(xiàn)為呼氣性呼吸困難 (Exspiratory Dyspnea)呼氣吸氣用力呼氣時等壓點(isobaric point)移向小氣道02

5、520+353520202030正常人0152020+3525202020肺氣腫慢性支氣管炎0+3535152520202020問題 ： 呼吸衰竭? 限制性通氣不足的定義及其發(fā)生原因? 胸內(nèi)、胸外氣道阻塞在呼吸中的差異?（二）彌散障礙 Diffusion Impairment彌散面積減少2. 彌散膜厚度增加3. 彌散時間縮短毛細血管內(nèi)皮細胞肺泡I型細胞基膜紅細胞肺泡-毛細血管膜Alveolar-Capillary Membrane(彌散膜, diffusion membrane) 1.彌散面積減少 (Decrease in the Surface Area of the Membrane)正常

6、成人肺泡面積：70 m2靜息時換氣面積：40 m2彌散面積減少：肺不張，肺實變，肺葉切除等。2.彌散膜厚度增加(Increase in the Thickness of the Membrane)肺泡膜厚度：1 mM彌散距離：5 mM彌散膜厚度增加：肺水腫，肺泡透明膜形成，肺纖維化，肺泡毛細血管擴張等。3.彌散時間縮短 (Shortening in the Diffusion Time)正常靜息狀態(tài)：血流通過毛細血管時間: 0.75 s 彌散時間： 0.25 s彌散時間縮短: 心輸出量增加, 肺血流加快Solubility Coefficient(vol/vol, 760 mmHg): O2:

7、 0.024 CO2:0.57正常靜息狀態(tài)下：每分鐘肺泡通氣量（VA)： 4L 每分鐘肺血流量（Q): 5LVA/Q: 0.8.（三）肺泡通氣與血流比例失調(diào)Ventilation-Perfusion ImbalanceVA.VA/Q 0.8 =0.8 0.8 0.8 0.8 0.83. 部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔樣通氣(dead space like ventilation）血液氧和二氧化碳解離曲線Oxygen and Carbon DioxideDissociation Curves問題 ：彌散障礙的發(fā)生機制?功能性分流,靜脈血摻

8、雜?解剖分流, 真性分流?死腔樣通氣?肺泡-毛細血管膜 (alveolar capillary membrane) 損傷引起的急性呼吸衰竭。病因：感染（肺炎，敗血癥等），休克，嚴(yán)重創(chuàng)傷，吸入毒物或胃酸等。（四）急性呼吸窘迫綜合征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. Expert

9、s 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. ARDS發(fā)生機制(Pathogenesis)肺泡膜內(nèi)皮細胞損傷致病因子釋放中性粒細胞趨化因子中性粒細胞聚集，釋放氧自由基、蛋白酶、炎癥介質(zhì)肺水腫死腔樣通氣肺泡型上皮細胞損傷表面活性物質(zhì)合成支氣管痙攣血管收縮微血栓肺泡膜通透性肺不張功能性分流PaO2PaCO2 A previously

10、 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. Hi

11、s orthopedic injuries and burns were treated. The ventilator was placed on the assist-control mode with the initial settings of inspired O2 concentration at 40%, respiration rate at 12/min, and tidal volume at 900 ml. Arterial blood gas measurements were: pH = 7.47, PCO2 of 33 mmHg, and PO2 of 62 mm

12、Hg.Clinical Case 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 H2O. Repeat arterial blood gas measurement of PO2 indicated 35 mmHg and ch

13、est x-ray now showed diffuse infiltrates in a white out pattern.Clinical Case 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/

14、cm H2O), 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 急性呼吸窘迫綜合征(ARDS)的概念及發(fā)生機制?問題 ：二、呼衰時機體功能和代謝變化 Functional and Metabolic Change in

15、 Respiratory Failure （一）酸堿平衡紊亂(acid-base balance disturbance)和電解質(zhì)變化呼酸: 型呼衰 CO2潴留 血 K+ , 血 Cl- 呼堿：I型呼衰 肺過度通氣 血 K+ , 血 Cl-代酸：嚴(yán)重缺氧 無氧代謝 乳酸（二）呼吸系統(tǒng)的變化(Changes in Respiratory System)呼吸調(diào)節(jié)(Regulation of Respiration) 的變化外周化學(xué)感受器中樞化學(xué)感受器呼吸加深加快抑制呼吸中樞PaO250 mmHgPaO280 mmHg（三）循環(huán)系統(tǒng)變化(Changes in Circulation System)

16、輕度PaO2 和 PaCO2 可興奮心血管運動中樞 嚴(yán)重PaO2 和 PaCO2 抑制心血管運動中樞 缺氧 肺小動脈收縮 肺動脈壓 右心后負荷長期缺氧 肺血管平滑肌增殖 管壁增厚長期缺氧 紅細胞增多 血液粘度 心負荷缺氧、酸中毒 心肌舒縮功能呼吸衰竭 右心衰竭 肺源性心臟病 (cor pulmonale)PaO2: 60 mmHg 智力，視力輕度減退40-50 mmHg 神經(jīng)精神癥狀20 mmHg 神經(jīng)細胞不可逆損壞(慢性呼衰PaO2 20 mmHg神志仍可清醒）PaCO2 80 mmHg CO2麻醉(頭痛,頭昏,嗜睡，精神錯亂, 撲翼樣震顫, 抽搐, 及昏迷等中樞神經(jīng)系統(tǒng)癥狀）肺性腦病(pulmonary encephalopathy):呼衰引起的腦功能障礙（四）中樞神經(jīng)系統(tǒng)變化Changes in Central Nervous System肺性腦病發(fā)生機制Pathogenesis of pulmonary encephalopathy-氨基丁酸腦脊液 pH溶酶體酶釋放中樞抑制磷脂酶活性神經(jīng)損傷顱內(nèi)壓PO2PaCO2血管內(nèi)皮損傷血管通透性腦水腫腦血管擴張腦充血問題：呼吸衰竭時呼吸調(diào)節(jié)的變化？肺源性心臟病發(fā)生機制?肺性腦病的定義及發(fā)生機制？（一）一般原則 (General Principal