肺动脉栓塞CBL-2014八年制(1)

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肺动脉栓塞PPT课件

其他治疗方式
吸氧治疗
对于缺氧明显的患者，可以给予吸氧治疗，以提高血氧饱和度。
支持治疗
对于严重肺动脉栓塞患者，可以给予呼吸机辅助呼吸、循环支持等治疗措施，以维持生命体征稳定。
04 肺动脉栓塞的预防与护理
预防措施
定期进行体检
保持健康的生活方式
通过常规体检，可以及时发现潜在的血栓形成风险，如发现有下肢深静脉血栓形成，应尽早采取干预措施。
康复指导
适当运动
在医生的指导下进行适当的运动，如散步、游泳等，以促进血液循环，减少血栓形成的风
险。
健康饮食
保持低盐、低脂、低糖的饮食习惯，多食用富含纤维素的蔬菜和水果，以降低血液粘稠度。
控制危险因素
对于存在高血压、糖尿病、高血脂等慢性疾病的患者，应积极治疗原发病，控制病情发展。
定期复查
患者接受了溶栓治疗和抗凝治疗，症状得到缓解，康复出院。
此病例为典型的肺动脉栓塞，患者长期卧床，缺乏运动，导致下肢静脉血栓形成并脱落，随血液循环进入肺动脉，引起栓塞
。
病例二：特殊类型肺动脉栓塞案例分析
患者基本信息
患者李某，女性，38岁，因肺部感染、咳嗽就诊。
诊断过程
通过胸部CT和肺动脉造影等检查，确诊为特殊类型肺动脉栓塞。
肺动脉栓塞可能导致胸痛，通常表现为突然发作的剧烈疼痛。
对循环系统的影响
低血压
肺动脉栓塞可能导致心输出ቤተ መጻሕፍቲ ባይዱ降低，引起低血压，影响全身血液循环。
心律失常
肺动脉栓塞可能引发各种心律失常，如心房颤动、室性早搏等。
右心功能不全
长期肺动脉栓塞可能导致右心肥厚和扩张，最终导致右心功能不全。

肺动脉栓塞 ppt课件

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2病历介绍

既往史房颤史4年，高血压史4年，胃大部切除术史40年，右侧股骨手术1月，吸烟60余年，平均5支/日。入院是生命体征：T37.7度，P100次/分，R26次/分BP112/62mmhg

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2病历介绍-阳性检查结果

2月15日心电图：快速性房颤血常规：WBC:12.34*10^9/,N:88.4% 胸片：主动脉硬化，心影增大，左室增大为主，两肺炎症，右下肺高密度影 2月16号血D-2聚体：1.31ug/ml(1310mg/l) 2月16号肺CT：右肺上动脉分支及右下肺动脉主干开口处充盈缺损，考虑肺栓塞；右肺上叶后段及两肺下叶间质性肺炎；双侧胸腔积液
O患者呼吸平稳，出院时呼吸18-20次/分。
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P2-有再次发生栓塞的可能： 2月16号D2聚体1.31ug/ml
I: 1观察患者有无肺栓塞，脑梗塞，心梗塞，肾梗塞等梗塞症状。 2观察患者有无下肢深静脉栓塞症状。 3动态监测D2具体数值。 4住患者卧床休息，减少活动。
O 患者住院期间未发生明显梗塞症状，2月25号复查D2聚体0.48ug/ml.
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4整体护理 P3-清理呼吸道低效：患者咳嗽咳痰
I: 1指导患者掌握深呼吸，有效咳嗽的方法。 2根据病情保证进足够的水分。 3协助患者翻身或者胸背部叩击。
O 患者能咳出痰液
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P4-感染 2月 15WBC:12.34*10^9/,N:88.4%
I: 1遵医嘱予以抗生素使用。 2监测生命体征及血常规。 3增加营养，增强抵抗力。 4限制探视，减少交叉感
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肺动脉栓塞CBL-八年制

– 血流淤滞：制动、卧床、VTE病史、心力衰竭、管状石膏固定
15
PE 高发病率、高病死率、高误诊/漏诊率
• 住院患者全部死因第三位，次于肿瘤和心肌梗死 • 发病率： – 美国新发PE 65万~70万人/年，法国>10万人/年 – 年龄越大发病率越高 • 尸检检出率高达67％～79％ • 我国缺乏流行病学资料
A. B. C. D. E.
thrombi √ fat air amniotic fluid tumor
13
Where do most thrombi originate in?
A. B. C. D. Superior vena cava system Inferior vena cava system Right heart cavity Left heart cavity
21
心血管系统
右心排血↓，右心衰竭左室前负荷↓，室间隔左移，心输出量下降
血压下降，休克
瓣膜功能状态异常，卵圆孔开放
分流加重缺氧
冠脉供血↓，心肌供氧↓
心肌缺血/心肌梗塞
22ቤተ መጻሕፍቲ ባይዱ
• PE临床表现不特异
– – – – 晕厥、猝死突发胸痛、咯血不明原因呼吸困难慢性血栓栓塞性肺动脉高压
• PE的胸痛：
• 近期曾行心肺复苏;
• 年龄>75岁
58
• 溶栓时间窗
–发病或复发后2周以内 –溶栓治疗开始越早，疗效越好 – 症状出现48小时内溶栓获益最大
• 溶栓药物：
–链激酶 –尿激酶 –重组组织型纤溶酶原激活剂（rt-PA）
59
Anticoagulant therapy
• 目的
– 初始抗凝治疗：减少死亡及再发栓塞事件。 – 长期抗凝治疗：预防新发静脉血栓栓塞事件

肺动脉栓塞医学课件

肺组织缺血会导致呼吸困难，患者会出现胸痛、咳血、咳嗽等症状。
右心衰竭
如果栓塞范围较大或多个栓塞形成，会导致右心衰竭，患者会出现乏力、水肿、肝脏肿大等症状。
并发症发生原因及预防策略
心脏骤停
由于肺动脉栓塞可能导致心脏骤停，因此需要及时诊断和治疗。
肺水肿
肺动脉栓塞可能导致肺水肿，进一步加重呼吸困难。预防策略包括及时诊断和治疗、控制液体入量等。
。
D-二聚体检测
检测血液中D-二聚体的含量，有助于判断血栓的主要成分和纤维蛋白在纤溶酶的作用下可降解为可溶性纤维蛋白降解产物，包括D-二聚体、FDP，为阳性结
果。
诊断流程优化与注意事项
01
02
03
04
根据患者病史、症状和体征，初步判断其患肺动脉栓塞的可
能性。
根据患者具体情况，选择合适的辅助检查手段，并综合分析
发病机制
肺动脉栓塞的发病机制主要包括血栓形成、脂肪栓塞、气体栓塞和羊水栓塞等。其中，血栓形成是最常见的病因，主要由下肢深静脉血栓脱落引起。
临床表现与诊断依据
临床表现
肺动脉栓塞的临床表现多样，包括呼吸困难、胸痛、咯血、咳嗽、晕厥等。其中，呼吸困难是最常见的症状，胸痛和咯血被称为肺动脉栓塞的“三联征”。
折、手术史等。
筛查方法
02
采用血液检测、超声心动图等手段进行筛查，及时发现潜在的
肺动脉栓塞风险。
干预措施
03
针对不同高危人群，制定个性化的干预措施，如抗凝治疗、溶
栓治疗等。
生活习惯改善建议和健康生活方式推广
01
02
03
04
健康饮食
鼓励摄入富含膳食纤维、维生素和矿物质的食物，减少高脂肪、高胆固醇食物的摄入。

肺动脉栓塞[1]贾明兰

【小结】 • 在西方国家，DVT和PE的年发病率估计分别为0.1%和0.05%。 • DVT和PE同属VTE的范畴。 • PE的获得性和遗传性两大危险因素已被证实。 • 约1/2的VTE病例缺乏典型的危险因素。
【病理和病理生理改变】一、病理改变 • PE栓子多为血栓，空气、脂肪、羊水等少见。 • 栓子可从微血栓到巨大的骑跨型血栓。微血栓栓塞需反复多发才能引起肺血流动力学改变。 • 最近有人提出“多发性肺微血栓栓塞” 实质是肺血管内皮损伤引起的微血栓形成。
• • • •
深静脉血栓形成（DVT）静脉血栓栓塞性疾病（VTE）经济舱综合征（tourist cabin Syndrome）目前，对PE的诊断率很低，警惕性不高，误诊率、漏诊率较高。 • 未经治疗的的PE死亡率大约为30%，诊断明确并经过充分治疗者，死亡率可降低至2%-8%。
经济舱综合征
（4）X线胸部平片
• 急性PE患者约80%不正常。常见征象有盘状肺
不张、肺浸润或肺梗死阴影及胸膜渗出，多呈楔形，凸向肺门，底边朝向胸膜，也可呈带状、球状、半球状和不规则形及肺不张影；膈上外周楔形密影（Hampton驼峰）提示肺梗死。患侧膈肌抬高（40%~60%）。 • 典型的是右下肺动脉呈香肠样和Westermark征 • 用于除外其他原因引起的呼吸困难和胸痛。
（6）制动 • 即使是短期（1周内）制动也易于导致 VTE。 • 在实施疝修补术的患者中，DVT的发生率大约为5%，腹部大手术为15%~30%，髋骨骨折的患者中为50%~75%，脊髓损伤的患者中为50%~100%。 • 大约1/4的术后PE发生于出院之后。
（7）妊娠 • 孕妇VTE的发生率比同龄未孕妇女高5~7 倍，易发生于妊娠的头3个月和围产期，其中75%的DVT发生于分娩前，66%的 PE发生于分娩后，确切机制不清。

肺动脉栓塞

06
总结与展望
Chapter
当前存在问题和挑战
诊断困难
01
肺动脉栓塞的症状多样且非特异性，使得早期诊断困难，容易
误诊或漏诊。
治疗手段有限
02
目前肺动脉栓塞的治疗手段主要包括抗凝、溶栓和手术治疗，
但治疗效果因人而异，且存在并发症风险。
预防措施不足
03
尽管已知一些危险因素与肺动脉栓塞相关，如长时间卧床、手
鉴别诊断
需与肺炎、胸膜炎、支气管哮喘等疾病进行鉴别，避免误诊误治。
03
治疗原则与方案选择
Chapter
一般治疗原则
早期诊断和治疗
肺动脉栓塞是一种紧急情况，需要早期诊断和及时治疗，以降低死亡率和并发症发生率。
个体化治疗方案
根据患者的具体病情和身体状况，制定个体化的治疗方案，包括药物治疗、手术治疗等。
静脉滤器植入
对于存在下肢深静脉血栓的高危患者，可考虑植入静脉滤器，以防止血栓脱落引发肺动脉栓塞。
生活习惯改善建议
增加活动量
避免长时间久坐或卧床，适当增加日常活动量，促进血液循环。
健康饮食
保持均衡饮食，减少高脂肪、高胆固醇食物的摄入，降低血液黏
稠度。
戒烟限酒
吸烟和过量饮酒均可增加肺动脉栓塞的风险，应积极戒烟限酒。
生活质量评估与改善
定期对患者的生活质量进行评估，针对存在的问题制定相应的改善措施，提高患者的生活
质量。
05
预防策略与措施建议
Chapter
高危人群筛查及干预措施
识别高危人群
针对存在静脉血栓栓塞症危险因素的人群，如高龄、肥胖、长时间卧床等，进行早期筛查和评估
。

2014急性肺动脉栓塞指南

ESC GUIDELINES2014ESC Guidelines on the diagnosis and management of acute pulmonary embolismThe Task Force for the Diagnosis and Management of AcutePulmonary Embolism of the European Society of Cardiology (ESC)Endorsed by the European Respiratory Society (ERS)Authors/Task Force Members:Stavros V.Konstantinides *(Chairperson)(Germany/Greece),Adam Torbicki *(Co-chairperson)(Poland),Giancarlo Agnelli (Italy),Nicolas Danchin (France),David Fitzmaurice (UK),Nazzareno Galie`(Italy),J.Simon R.Gibbs (UK),Menno V.Huisman (The Netherlands),Marc Humbert †(France),Nils Kucher (Switzerland),Irene Lang (Austria),Mareike Lankeit (Germany),John Lekakis (Greece),Christoph Maack (Germany),Eckhard Mayer (Germany),Nicolas Meneveau (France),Arnaud Perrier (Switzerland),Piotr Pruszczyk (Poland),Lars H.Rasmussen (Denmark),Thomas H.Schindler (USA),Pavel Svitil (CzechRepublic),Anton Vonk Noordegraaf (The Netherlands),Jose Luis Zamorano (Spain),Maurizio Zompatori (Italy)ESC Committee for Practice Guidelines (CPG):Jose Luis Zamorano (Chairperson)(Spain),Stephan Achenbach (Germany),Helmut Baumgartner (Germany),Jeroen J.Bax (Netherlands),Hector Bueno (Spain),Veronica Dean (France),Christi Deaton (UK),Çetin Erol (Turkey),Robert Fagard (Belgium),Roberto Ferrari (Italy),David Hasdai (Israel),Arno Hoes (Netherlands),Paulus Kirchhof (Germany/UK),Juhani Knuuti (Finland),Philippe Kolh (Belgium),Patrizio Lancellotti (Belgium),Ales Linhart (Czech Republic),Petros Nihoyannopoulos (UK),Massimo F.Piepoli*Corresponding authors.Stavros Konstantinides,Centre for Thrombosis and Hemostasis,Johannes Gutenberg University of Mainz,University Medical Centre Mainz,Langenbeckstrasse1,55131Mainz,Germany.Tel:+496131176255,Fax:+496131173456.Email:stavros.konstantinides@unimedizin-mainz.de ,and Department of Cardiology,Democritus University of Thrace,Greece.Email:skonst@med.duth.gr .Adam Torbicki,Department of Pulmonary Circulation and Thromboembolic Diseases,Medical Centre of Postgraduate Education,ECZ-Otwock,Ul.Borowa 14/18,05-400Otwock,Poland.Tel:+48227103052,Fax:+4822710315.Email:adam.torbicki@ecz-otwock.pl .†Representing the European Respiratory SocietyOther ESC entities having participated in the development of this document:ESC Associations:Acute Cardiovascular Care Association (ACCA),European Association for Cardiovascular Prevention &Rehabilitation (EACPR),European Association of Cardio-vascular Imaging (EACVI),Heart Failure Association (HFA),ESC Councils:Council on Cardiovascular Nursing and Allied Professions (CCNAP),Council for Cardiology Practice (CCP),Council on Cardiovascular Primary Care (CCPC)ESC Working Groups:Cardiovascular Pharmacology and Drug Therapy,Nuclear Cardiology and Cardiac Computed Tomography,Peripheral Circulation,Pulmonary Circulation and Right Ventricular Function,Thrombosis.Disclaimer:The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientiﬁc and medical knowledge and the evidence available at the time of their publication.The ESC is not responsible in the event of any contradiction,discrepancy and/or ambiguity between the ESC Guidelines and any other ofﬁcial recommendations or guidelines issued by the relevant public health authorities,in particular in relation to good use of healthcare or therapeutic strategies.Health professionals are encouraged to take the ESC Guidelines fully into account when exercising their clinical judgment,as well as in the determination and the implementation of preventive,diagnostic or therapeutic medical strategies;however,the ESC Guidelines do not override,in any way whatsoever,the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient’s health condition and in consultation with that patient and,where appropriate and/or necessary,the patient’s caregiver.Nor do the ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant ofﬁcial updated recommendations or guidelines issued by the competent public health authorities,in order to manage each patient’s case in light of the scientiﬁcally accepted data pursuant to their respective ethical and professional obligations.It is also the health professional’s responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription.National Cardiac Societies document reviewers:listed in the Appendix.&The European Society of Cardiology 2014.All rights reserved.For permissions please email:journals.permissions@.European Heart Journal (2014)35,3033–3080doi:10.1093/eurheartj/ehu283by guest on March 6, 2016/Downloaded from(Italy),Piotr Ponikowski (Poland),Per Anton Sirnes (Norway),Juan Luis Tamargo (Spain),Michal Tendera (Poland),Adam Torbicki (Poland),William Wijns (Belgium),Stephan Windecker (Switzerland).Document Reviewers:Çetin Erol (CPG Review Coordinator)(Turkey),David Jimenez (Review Coordinator)(Spain),Walter Ageno (Italy),Stefan Agewall (Norway),Riccardo Asteggiano (Italy),Rupert Bauersachs (Germany),Cecilia Becattini (Italy),Henri Bounameaux (Switzerland),Harry R.Bu¨ller (Netherlands),Constantinos H.Davos (Greece),Christi Deaton (UK),Geert-Jan Geersing (Netherlands),Miguel Angel Go´mez Sanchez (Spain),Jeroen Hendriks (Netherlands),Arno Hoes (Netherlands),Mustafa Kilickap (Turkey),Viacheslav Mareev (Russia),Manuel Monreal (Spain),Joao Morais (Portugal),Petros Nihoyannopoulos (UK),Bogdan A.Popescu (Romania),Olivier Sanchez †(France),Alex C.Spyropoulos (USA).The disclosure forms provided by the experts involved in the development of these guidelines are available on the ESC website /guidelines .Online publish-ahead-of-print 29August 2014------------------------------------------------------------------------------------------------------------------------------------------------------KeywordsGuidelines †Pulmonary embolism †Venous thrombosis †Shock †Hypotension †Chest pain †Dyspnoea †Heart failure †Diagnosis †Treatment–Anticoagulation †ThrombolysisTable of ContentsAbbreviations and acronyms ........................30351.Preamble ...................................30352.Introduction .................................30362.1Epidemiology .............................30372.2Predisposing factors ........................30372.3Natural history............................30382.4Pathophysiology ...........................30382.5Clinical classiﬁcation of pulmonary embolism severity ...30393.Diagnosis ...................................30393.1Clinical presentation ........................30393.2Assessment of clinical probability ................30403.3D-dimer testing ...........................30403.4Computed tomographic pulmonary angiography ......30423.5Lung scintigraphy ..........................30433.6Pulmonary angiography ......................30433.7Magnetic resonance angiography ................30433.8Echocardiography ..........................30433.9Compression venous ultrasonography.............30443.10.Diagnostic strategies .. (3044)3.10.1Suspected pulmonary embolism with shock or hypotension.............................30443.10.2Suspected pulmonary embolism withoutshock or hypotension ........................30453.11.Areas of uncertainty .......................30464.Prognostic assessment ..........................30474.1Clinical parameters .........................30474.2Imaging of the right ventricle by echocardiography or computed tomographic angiography ...............30484.3Laboratory tests and biomarkers ................30494.3.1Markers of right ventricular dysfunction .........30494.3.2Markers of myocardial injury ................30494.3.3Other (non-cardiac)laboratory biomarkers ......30504.4Combined modalities and scores ................30514.5Prognostic assessment strategy .................30515.Treatment in the acute phase ......................30525.1Haemodynamic and respiratory support ...........30525.2Anticoagulation ........................ (3052)5.2.1Parenteral anticoagulation..................30525.2.2Vitamin K antagonists.....................30535.2.3New oral anticoagulants ...................30545.3Thrombolytic treatment......................30555.4Surgical embolectomy .......................30565.5Percutaneous catheter-directed treatment ..........30565.6Venous ﬁlters ............................30565.7Early discharge and home treatment ..............30575.8Therapeutic strategies .......................30585.8.1Pulmonary embolism with shock or hypotension(high-risk pulmonary embolism)..................30585.8.2Pulmonary embolism without shock or hypotension(intermediate-or low-risk pulmonary embolism).......30585.9Areas of uncertainty ........................30596.Duration of anticoagulation .. (3061)6.1New oral anticoagulants for extended treatment ......30627.Chronic thromboembolic pulmonary hypertension .. (3063)7.1Epidemiology .............................30637.2Pathophysiology ...........................30637.3Clinical presentation and diagnosis ...............30637.4Treatment and prognosis .....................30648.Speciﬁc problems .. (3066)8.1Pregnancy ...............................30668.1.1Diagnosis of pulmonary embolism in pregnancy ....30668.1.2Treatment of pulmonary embolism in pregnancy ...30668.2Pulmonary embolism and cancer ................30678.2.1Diagnosis of pulmonary embolism in patients withcancer ..................................30678.2.2Prognosis for pulmonary embolism in patients withcancer ..................................30678.2.3Management of pulmonary embolism in patients withcancer ..................................30678.2.4Occult cancer presenting as unprovoked pulmonaryembolism ................................30688.3Non-thrombotic pulmonary embolism ............30688.3.1Septic embolism ........................30688.3.2Foreign-material pulmonary embolism . (3068)ESC Guidelines3034by guest on March 6, 2016/Downloaded from8.3.3Fat embolism ..........................30688.3.4Air embolism ..........................30698.3.5Amniotic ﬂuid embolism...................30698.3.6Tumour embolism ......................30699.Appendix...................................3069References .................. (3069)Abbreviations and acronymsACS acute coronary syndromeAMPLIFYApixaban for the Initial Management of Pulmonary Embolism and Deep-Vein Thrombosis as First-line TherapyaPTT activated partial thromboplastin time b.i.d.bis in diem (twice daily)b.p.m.beats per minute BNP brain natriuretic peptide BP blood pressure CI conﬁdence interval CO cardiac output COPD chronic obstructive pulmonary disease CPG Committee for Practice Guidelines CRNM clinically relevant non-major CT computed tomographic/tomogram CTEPH chronic thromboembolic pulmonary hypertension CUS compression venous ultrasonography DSA digital subtraction angiography DVT deep vein thrombosis ELISA enzyme-linked immunosorbent assay ESC European Society of Cardiology H-FABP heart-type fatty acid-binding protein HIT heparin-induced thrombocytopenia HR hazard ratio ICOPER International Cooperative Pulmonary EmbolismRegistryICRP International Commission on Radiological Protection INR international normalized ratio iPAH idiopathic pulmonary arterial hypertension IVC inferior vena cava LMWH low molecular weight heparin LV left ventricle/left ventricular MDCT multi-detector computed tomographic (angiography)MRA magnetic resonance angiography NGAL neutrophil gelatinase-associated lipocalin NOAC(s)Non-vitamin K-dependent new oral anticoagulant(s)NT-proBNP N-terminal pro-brain natriuretic peptide o.d.omni die (every day)OR odds ratio PAH pulmonary arterial hypertension PE pulmonary embolism PEA pulmonary endarterectomy PEITHO Pulmonary EmbolIsm THrOmbolysis trial PESI pulmonary embolism severity index PH pulmonary hypertensionPIOPED Prospective Investigation On Pulmonary EmbolismDiagnosisPVR pulmonary vascular resistanceRIETE Registro Informatizado de la Enfermedad Throm-boembolica venosa RR relative riskrtPA recombinant tissue plasminogen activator RV right ventricle/ventricularSPECT single photon emission computed tomography sPESI simpliﬁed pulmonary embolism severity index TAPSE tricuspid annulus plane systolic excursion Tc technetiumTOE transoesophageal echocardiography TTR time in therapeutic range TV tricuspid valveUFH unfractionated heparinV/Q scan ventilation–perfusion scintigraphy VKA vitamin K antagonist(s)VTEvenous thromboembolism1.PreambleGuidelines summarize and evaluate all available evidence at the time of the writing process,on a particular issue with the aim of assisting health professionals in selecting the best management strategies for an individual patient,with a given condition,taking into account the impact on outcome,as well as the risk-beneﬁt-ratio of particular diag-nostic or therapeutic means.Guidelines and recommendations should help the health professionals to make decisions in their daily practice.However,the ﬁnal decisions concerning an individual patient must be made by the responsible health professional(s)in consultation with the patient and caregiver as appropriate.A great number of Guidelines have been issued in recent years by the European Society of Cardiology (ESC)as well as by other soci-eties and organisations.Because of the impact on clinical practice,quality criteria for the development of guidelines have been estab-lished in order to make all decisions transparent to the user.The recommendations for formulating and issuing ESC Guidelines can be found on the ESC Web Site (/guidelines-surveys/esc-guidelines/about/Pages/rules-writing.aspx ).ESC Guide-lines represent the ofﬁcial position of the ESC on a given topic and are regularly updated.Members of this Task Force were selected by the ESC to represent professionals involved with the medical care of patients with this pathology.Selected experts in the ﬁeld undertook a comprehensive review of the published evidence for management (including diagno-sis,treatment,prevention and rehabilitation)of a given condition according to ESC Committee for Practice Guidelines (CPG)policy.A critical evaluation of diagnostic and therapeutic procedures was performed including assessment of the risk-beneﬁt-ratio.Estimates of expected health outcomes for larger populations were included,where data exist.The level of evidence and the strength of recom-mendation of particular management options were weighed and graded according to predeﬁned scales,as outlined in Tables 1and 2.The experts of the writing and reviewing panels ﬁlled in declara-tions of interest forms which might be perceived as real or potentialESC Guidelines3035by guest on March 6, 2016/Downloaded fromsources of conﬂicts of interest.These forms were compiled into one ﬁle and can be found on the ESC Web Site (/guidelines ).Any changes in declarations of interest that arise during the writing period must be notiﬁed to the ESC and updated.The Task Force received its entire ﬁnancial support from the ESC without any involvement from healthcare industry.The ESC CPG supervises and coordinates the preparation of new Guidelines produced by Task Forces,expert groups or consensus panels.The Committee is also responsible for the endorsement process of these Guidelines.The ESC Guidelines undergo extensive review by the CPG and external experts.After appropriate revisions it is approved by all the experts involved in the Task Force.The ﬁna-lized document is approved by the CPG for publication in the Euro-pean Heart Journal.It was developed after careful consideration of the scientiﬁc and medical knowledge and the evidence available at the time of their dating.The task of developing ESC Guidelines covers not only the integra-tion of the most recent research,but also the creation of educational tools and implementation programmes for the recommendations.To implement the guidelines,condensed pocket guidelines versions,summary slides,booklets with essential messages,summary cards for non-specialists,electronic version for digital applications (smart-phones etc)are produced.These versions are abridged and,thus,if needed,one should always refer to the full text version which is freely available on the ESC Website.The National Societies of the ESC are encouraged to endorse,translate and implement the ESC Guidelines.Implementation programmes are needed because it has been shown that the outcome of disease may be favourably inﬂuenced by the thorough application of clinical recommendations.Surveys and registries are needed to verify that real-life daily prac-tice is in keeping with what is recommended in the guidelines,thus completing the loop between clinical research,writing of guidelines,disseminating them and implementing them into clinical practice.Health professionals are encouraged to take the ESC Guidelines fully into account when exercising their clinical judgment as well asin the determination and the implementation of preventive,diag-nostic or therapeutic medical strategies.However,the ESC Guide-lines do not override in any way whatsoever the individual responsibility of health professionals to make appropriate and ac-curate decisions in consideration of each patient’s health condition and in consultation with that patient and the patient’s caregiver where appropriate and/or necessary.It is also the health professio-nal’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.2.IntroductionThis document follows the two previous ESC Guidelines focussing on clinical management of pulmonary embolism,published in 2000and 2008.Many recommendations have retained or reinforced their validity;however,new data has extended or modiﬁed our knowl-edge in respect of optimal diagnosis,assessment and treatment of patients with PE.The most clinically relevant new aspects of this 2014version as compared with its previous version published in 2008relate to:by guest on March 6, 2016/Downloaded from(1)Recently identiﬁed predisposing factors for venous thrombo-embolism(2)Simpliﬁcation of clinical prediction rules (3)Age-adjusted D-dimer cut-offs(4)Sub-segmental pulmonary embolism(5)Incidental,clinically unsuspected pulmonary embolism(6)Advanced risk stratiﬁcation of intermediate-risk pulmonaryembolism(7)Initiation of treatment with vitamin K antagonists(8)Treatment and secondary prophylaxis of venous thrombo-embolism with the new direct oral anticoagulants(9)Efﬁcacyand safety of reperfusion treatment for patients at inter-mediate risk(10)Early discharge and home (outpatient)treatment of pulmonaryembolism(11)Current diagnosis and treatment of chronic thromboembolicpulmonary hypertension(12)Formal recommendations for the management of pulmonaryembolism in pregnancy and of pulmonary embolism in patients with cancer.These new aspects have been integrated into previous knowledge to suggest optimal and—whenever possible—objectively validated management strategies for patients with suspected or conﬁrmed pul-monary embolism.In order to limit the length of the printed text,additional informa-tion,tables,ﬁgures and references are available as web addenda at the ESC website ( ).2.1EpidemiologyVenous thromboembolism (VTE)encompasses deep vein throm-bosis (DVT)and pulmonary embolism (PE).It is the third most fre-quent cardiovascular disease with an overall annual incidence of 100–200per 100000inhabitants.1,2VTE may be lethal in the acute phase or lead to chronic disease and disability,3–6but it is also often preventable.Acute PE is the most serious clinical presentation of VTE.Since PE is,in most cases,the consequence of DVT,most of the existing data on its epidemiology,risk factors,and natural history are derived from studies that have examined VTE as a whole.The epidemiology of PE is difﬁcult to determine because it may remain asymptomatic,or its diagnosis may be an incidental ﬁnding;2in some cases,the ﬁrst presentation of PE may be sudden death.7,8Overall,PE is a major cause of mortality,morbidity,and hospitaliza-tion in Europe.As estimated on the basis of an epidemiological model,over 317000deaths were related to VTE in six countries of the European Union (with a total population of 454.4million)in 2004.2Of these cases,34%presented with sudden fatal PE and 59%were deaths resulting from PE that remained undiagnosed during life;only 7%of the patients who died early were correctly diag-nosed with PE before death.Since patients older than 40years are at increased risk compared with younger patients and the risk approxi-mately doubles with each subsequent decade,an ever-larger number of patients are expected to be diagnosed with (and perhaps die of)PE in the future.9In children,studies reported an annual incidence of VTE between 53and 57per 100000among hospitalized patients,10,11and between 1.4and 4.9per 100000in the community at large.12,132.2Predisposing factorsA list of predisposing (risk)factors for VTE is shown in Web Addenda Table I .There is an extensive collection of predisposing environmen-tal and genetic factors.VTE is considered to be a consequence of the interaction between patient-related—usually permanent—risk factors and setting-related—usually temporary—risk factors.VTE is considered to be ‘provoked’in the presence of a temporary or re-versible risk factor (such as surgery,trauma,immobilization,preg-nancy,oral contraceptive use or hormone replacement therapy)within the last 6weeks to 3months before diagnosis,14and ‘unpro-voked’in the absence thereof.PE may also occur in the absence of any known risk factor.The presence of persistent—as opposed to major,temporary—risk factors may affect the decision on the dur-ation of anticoagulation therapy after a ﬁrst episode of PE.Major trauma,surgery,lower limb fractures and joint replace-ments,and spinal cord injury,are strong provoking factors for VTE.9,15Cancer is a well-recognized predisposing factor for VTE.The risk of VTE varies with different types of cancer;16,17haemato-logical malignancies,lung cancer,gastrointestinal cancer,pancreatic cancer and brain cancer carry the highest risk.18,19Moreover,cancer is a strong risk factor for all-cause mortality following an episode of VTE.20In fertile women,oral contraception is the most frequent predis-posing factor for VTE.21,22When occurring during pregnancy,VTE is a major cause of maternal mortality.23The risk is highest in the third trimester of pregnancy and over the 6weeks of the postpartum period,being up to 60times higher 3months after delivery,compared with the risk in non-pregnant women.23In vitro fertilization further increases the risk of pregnancy-associated VTE.In a cross-sectional study derived from a Swedish registry,the overall risk of PE (com-pared with the risk of age-matched women whose ﬁrst child was born without in vitro fertilization)was particularly increased during the ﬁrst trimester of pregnancy [hazard ratio (HR)6.97;95%conﬁ-dence interval (CI)2.21–21.96].The absolute number of women who suffered PE was low in both groups (3.0vs.0.4cases per 10000pregnancies during the ﬁrst trimester,and 8.1vs.6.0per 10000pregnancies overall).24In post-menopausal women who receive hormone replacement therapy,the risk of VTE varies widely depend-ing on the formulation used.25Infection has been found to be a common trigger for hospitaliza-tion for VTE.15,26,27Blood transfusion and erythropoiesis-stimulating agents are also associated with an increased risk of VTE.15,28In children,PE is usually associated with DVT and is rarely unpro-voked.Serious chronic medical conditions and central venous lines are considered to be likely triggers of PE.29VTE may be viewed as part of the cardiovascular disease con-tinuum and common risk factors—such as cigarette smoking,obesity,hypercholesterolaemia,hypertension and diabetes melli-tus 30–33—are shared with arterial disease,notably atheroscler-osis.34–37However,at least in part,this may be an indirect association,mediated by the effects of coronary artery disease and,ESC Guidelines3037by guest on March 6, 2016/Downloaded fromin the case of smoking,cancer.38,39Myocardial infarction and heart failure increase the risk of PE;40,41conversely,patients with VTE have an increased risk of subsequent myocardial infarction and stroke.422.3Natural historyThe ﬁrst studies on the natural history of VTE were carried out in the setting of orthopaedic surgery during the 1960s.43Evidence collected since this initial report has shown that DVT develops less frequently in non-orthopaedic surgery.The risk of VTE is highest during the ﬁrst two post-operative weeks but remains elevated for two to three months.Antithrombotic prophylaxis signiﬁcantly reduces the risk of perioperative VTE.The incidence of VTE is reduced with increas-ing duration of thromboprophylaxis after major orthopaedic surgery and (to a lesser extent)cancer surgery:this association has not been shown for general surgery.44,45The majority of patients with symp-tomatic DVT have proximal clots,complicated by PE in 40–50%of cases,often without clinical manifestations.44,45Registries and hospital discharge datasets of unselected patients with PE or VTE yielded 30-day all-cause mortality rates between 9%and 11%,and three-month mortality ranging between 8.6%and 17%.46–48Following the acute PE episode,resolution of pulmonary thrombi,as evidenced by lung perfusion defects,is frequently incom-plete.In one study,lung perfusion scintigraphy demonstrated abnor-malities in 35%of patients a year afteracute PE,although the degree of pulmonary vascular obstruction was ,15%in 90%of the cases.49Two relatively recent cohort studies covering 173and 254patients yielded incidences approaching 30%.50,51The incidence of conﬁrmed chronic thromboembolic pulmonary hypertension (CTEPH)after unprovoked PE is currently estimated at approximately 1.5%(with a wide range reported by mostly small-cohort studies),with most cases appearing within 24months of the index event.52,53The risk of recurrence of VTE has been reviewed in detail.54–56Based on historical data,the cumulative proportion of patients with early recurrence of VTE (on anticoagulant treatment)amounts to 2.0%at 2weeks,6.4%at 3months and 8%at 6months;more recent,randomized anticoagulation trials (discussed in the section on acute phase treatment)indicate that recurrence rates may have dropped considerably recently.The rate of recurrence is highest during the ﬁrst two weeks and declines thereafter.During the early period,active cancer and failure to rapidly achieve therapeutic levels of anticoagulation appear to independently predict an increased risk of recurrence.56,57The cumulative proportion of patients with late recurrence of VTE (after six months,and in most cases after discontinuation of anticoa-gulation)has been reported to reach 13%at 1year,23%at 5years,and 30%at 10years.56Overall,the frequency of recurrence does not appear to depend on the clinical presentation (DVT or PE)of the ﬁrst event,but recurrent VTE is likely to occur in the same clinical form as the index episode (i.e.if VTE recurs after PE,it will most likely be PE again).Recurrence is more frequent after multiple VTE epi-sodes as opposed to a single event,and after unprovoked VTE as opposed to the presence of temporary risk factors,particularly surgery.58It is also more frequent in women who continue hormone intake after a VTE episode,and in patients who havesuffered PE or proximal vein thrombosis compared to distal (calf)vein thrombosis.On the other hand,factors for which an independ-ent association with late recurrence have not been deﬁnitely estab-lished include age,male sex,59,60a family history of VTE,and an increased body mass index.54,56Elevated D-dimer levels,either during or after discontinuation of anticoagulation,indicate an increased risk of recurrence;61–63on the other hand,single thrombo-philic defects have a low predictive value and anticoagulation manage-ment based on thrombophilia testing has not been found to reduce VTE recurrence.64,652.4PathophysiologyAcute PE interferes with both the circulation and gas exchange.Right ventricular (RV)failure due to pressure overload is considered the primary cause of death in severe PE.Pulmonary artery pressure increases only if more than 30–50%of the total cross-sectional area of the pulmonary arterial bed is occluded by thromboemboli.66PE-induced vasoconstriction,mediated by the release of thromboxane A2and serotonin,contri-butes to the initial increase in pulmonary vascular resistance after PE,67an effect that can be reversed by vasodilators.68,69Anatomical obstruction and vasoconstriction lead to an increase in pulmonary vascular resistance and a proportional decrease in arterial compliance.70The abrupt increase in pulmonary vascular resistance results in RV dilation,which alters the contractile properties of the RV myocar-dium via the Frank-Starling mechanism.The increase in RV pressure and volume leads to an increase in wall tension and myocyte stretch.RV contraction time is prolonged,while neurohumoral activation leads to inotropic and chronotropic stimulation.Together with sys-temic vasoconstriction,these compensatory mechanisms increase pulmonary artery pressure,improving ﬂow through the obstructed pulmonary vascular bed,and thus temporarily stabilize systemic blood pressure (BP).71The extent of immediate adaptation is limited,since a non-preconditioned,thin-walled right ventricle (RV)is unable to generate a mean pulmonary artery pressure above 40mm Hg.The prolongation of RV contraction time into early diastole in the left ventricle leads to leftward bowing of the interventricular septum.72The desynchronization of the ventricles may be exacer-bated by the development of right bundle-branch block.As a result,left ventricular (LV)ﬁlling is impeded in early diastole,and this may lead to a reduction of the cardiac output and contribute to systemic hypotension and haemodynamic instability.73As described above,excessive neurohumoral activation in PE can be the result both of abnormal RV wall tension and of circulatory shock.The ﬁnding of massive inﬁltrates in the RV myocardium of patients who died within 48hours of acute PE may be explained by high levels of epinephrine released as a result of the PE-induced ‘myo-carditis’.74This inﬂammatory response might explain the secondary haemodynamic destabilization which sometimes occurs 24–48hours after acute PE,although early recurrence of PE may be an alter-native explanation in some of these cases.75Finally,the association between elevated circulating levels of bio-markers of myocardial injury and an adverse early outcome indicatesESC Guidelines3038by guest on March 6, 2016/Downloaded from。

肺动脉栓塞诊断和ppt课件

• 近年核磁共振成像术(MRl)也用于PE的诊断,成像
与肺动脉是诊断PE最可靠的方法。有价值的征象是：(1)肺
动脉内充盈缺损；(2)肺动脉分支完全阻塞(截断现象)；(3)肺野无血流灌注；(4)肺动脉分支充盈和排空延迟。
• 肺动脉造影检查有一定危险性,特别是并发肺动脉
• 最有意义的体征是反映右心负荷增加的颈静脉充盈、搏动
及下肢深静脉血栓形成所致的肿胀、压痛、疆硬、色素沉着和浅静脉曲张等。
实验室检查
胸部X线检查
• 可见到区域性肺血管纹理稀疏、纤细,肺透亮度增
加；栓塞部位肺血减少(Westermark征)；未受累部分呈现纹理相应增多(即肺血分布不匀)。肺梗死时可发现肺周围浸润性阴影,形状不一,常累及肋膈角, 患侧膈肌抬高及胸腔积液(少量～中量)。上腔静脉和奇静脉影扩大,肺门动脉扩张,有肺下动脉横径可增宽,也可正常或变细,后者也有诊断意义。X线胸片也可“完全正常”。
高压的患者,致残率为1％,死亡率为0.01％～0.5％, 因此,决定实施肺动脉造影前,应权衡利弊, 慎重考虑。
下肢深静脉检查
• PE的栓子约70％～90％来自下肢深静脉。
有下肢深静脉血栓形成(DVT)的患者约半数可能发生PE,因此,DVT被认为是PE的标志, 故下肢深静脉的检查对诊断和防治PE十分重要。一侧小腿或大腿周径比另一侧长1厘米有诊断意义。
外科治疗
• 体外循环下肺动脉血栓摘除术已成为急性肺动脉
栓塞治疗的主要方法。手术适应症为：诊断明确并危及生命者；血流动力学不稳定，如休克、右心衰竭等；大面积肺栓塞者，肺动脉主干或主要分支全部堵塞；有溶栓禁忌症或溶栓及其他治疗方法不满意者；右心房，左心房或右心室内大量血栓或血栓有脱落的危险者。

肺动脉栓塞

性深静脉血栓增加所抵销。仅根据有持续DVT
倾向，不是放置滤网的适应症。
69例安置滤器的并发症
并发症立即与技术有关位置不当血肿感染空气栓塞下肢水肿静脉坏死致死性肺栓塞 IVC血栓形成移位静脉淤积后遗症 % 7.2 7.2 4.3 1.4 13.0 4.3 4.3 9.0 3.4 27.0
主要并发症：出血。溶栓前宜留置外周静脉套管针，以方便溶栓中取血监测，避免反复穿刺血管。
抗凝治疗

目的：防止血栓再形成和复发药物：普通肝素，低分子肝素，华法林禁忌症活动性出血；凝血功能障碍；血小板减少；未控制的严重高血压。
抗凝治疗
抗凝治疗的初期使用肝素，以后用华法令维持。肝素治疗时将APTT比对照值延长1.5～2.0倍。为预防新的血栓形成和血栓延伸，肝素使用时间为7～10天。肝素的最大副作用是出血、血小板减少，累积效果常在用药后第3天出现。
----近期曾进行心肺复苏
----妊娠 ----严重肝肾功能不全 ----糖尿病出血性视网膜病变
----血小板计数低于10万
----细菌性心内膜炎， ----出血性疾病
THANK YOU
肺血栓栓塞症（PTE）
肺动脉发生栓塞后，若其支配区的肺梗死（ PI）肺组织因血流受阻或中断而发生坏死，称为肺梗死（PI）。深静脉血栓形成（ DVT）
静脉血栓栓塞症（VTE）
PTE与DVT共属于VTE,为VTE的二种类别
PTE的血栓来源
–下腔静脉径路：最多见 –上腔静脉径路：有增多 –右心腔
心脏瓣膜听诊区通常有5个： 1、二尖瓣区：位于心尖搏动最强点，又称心尖区； 2、肺动脉瓣区：在胸骨左缘第2肋间； 3、主动脉瓣区：位于胸骨右缘第2肋间； 4、主动脉瓣第二听诊区：在胸骨左缘第3肋间； 5、三尖瓣区：在胸骨下端左缘，即胸骨左缘第4、5肋间。

肺动脉栓塞

10肺动脉栓塞的阻塞物90%是下肢深静脉脱落的血栓。

【诊断】1.病史患者常有形成下肢深静脉血栓的病史，诸如长期卧床、腹腔、盆腔手术，下肢静脉输液等。

2. 临床表现有的患者在发生肺栓塞的同时，下肢深静脉血栓的临床表现，如下肢肿胀、肢体紫绀等依然存在。

就肺栓塞本身引起的临床表现依据肺栓塞的范围不同差异甚大。

严重的大面积肺栓塞，可引起血压下降，甚至心搏骤停。

轻度者仅有胸痛、气短、低氧血症等临床表现。

3. 辅助检查胸部x可以发现肺部阴影，肺血管造影很少需要。

【治疗】1.溶栓治疗大部分病人适宜采取溶栓治疗，特别是在发生肺栓塞6小时以内。

2.介入治疗经静脉用导管采用介入方法摘除栓子，尚在临床实验阶段。

3.手术治疗手术摘除肺动脉栓子（1）手术适应证：手术治疗的作用目前仍有争论，但严重病例有下列情况，可考虑手术摘除栓子：①明显的循环呼吸障碍。

血压<12. okpa(90mmhg)，尿量<20ml/小时，动脉血氧分压<9.okpa (60mmhg )，经1小时左右处理未见好转者。

②有溶栓治疗禁忌的患者，如活动性胃肠道出血、凝血机制障碍等。

③肺动脉造影显示肺阻塞超过50%者。

④因肺动脉栓塞引起心跳骤停，应急症手术。

（2）手术方法：在条件许可和情况允许的情况下，纵劈胸骨建立体外循环，在心脏停跳下，切开肺动脉摘除栓子。

特别紧急的病例，先建立股动、静脉的体外循环可能较纵劈胸骨更能争取时间。

没有条件或体外循环尚无法建立时，也可采用常温心脏跳动下，阻闭上、下腔静脉，切开肺动脉取除栓子。

（3）手术注意事项①根据病情选用手术方式。

②在用胆总管石钳取栓子时，用力要得当、防止夹碎栓子。

③已有肺梗死表现的肺区，勿摘除该处栓子，以免再灌注后发生难以控制的肺出血。

肺栓塞（pulmonary embolism）是指嵌塞物质进入肺动脉及其分支，阻断组织血液供应所引起的病理和临床状态。

常见的栓子是血栓，其余为少见的新生物细胞、脂肪滴、气泡、静脉输入的药物颗粒甚至导管头端引起的肺血管阻断。

肺动脉栓塞

3.肿瘤
在我国为第二位原因，占35%，远较国外6%为高。以肺癌、消化系统肿瘤表现多种多样实际是一较广的临床谱。临床所见主要决定于血管堵塞的多少、发生速度和心肺的基础状态，轻者仅累及2～3个肺段，可无任何症状；重者15～16个肺段，可发生休克或猝死。
1.四个临床症候群
2.动脉血气
肺血管床堵塞15%～20%即可出现氧分压下降，常表现为低氧血症、低碳酸血症、肺泡-动脉血氧分压差增大，但这些改变在其他心肺疾病中亦可见到。10%～15%的PE患者这些指标可正常，故动脉血气改变对PE的诊断仅具有参考价值。
3.胸部X线平片
PE多在发病后12～36小时或数天内出现X线改变。PE诊断的前瞻性研究（PIOPED）资料显示，80%PE患者胸片有异常，其中65%表现为肺实变或肺不张，48%表现为胸膜渗出。也可出现区域性肺血减少、中心肺动脉突出、右下肺动脉干增宽伴截断征、肺动脉段膨隆及右心室扩大征、患侧横膈抬高等。
病因
1.血栓形成
肺栓塞常是静脉血栓形成的合并症。栓子通常来源于下肢和骨盆的深静脉，通过循环到肺动脉引起栓塞。但很少来源于上肢、头和颈部静脉。血流淤滞，血液凝固性增高和静脉内皮损伤是血栓形成的促进因素。因此，创伤、长期卧床、静脉曲张、静脉插管、盆腔和髋部手术、肥胖、糖尿病、避孕药或其他原因的凝血机制亢进等，容易诱发静脉血栓形成。早期血栓松脆，加上纤溶系统的作用，故在血栓形成的最初数天发生肺栓塞的危险性最高。
（1）急性肺心病，突然呼吸困难、濒死感、发绀、右心衰竭、低血压、肢端湿冷，见于突然栓塞二个肺叶以上的患者；
（2）肺梗死突然呼吸困难、胸痛、咯血及胸膜摩擦音或胸腔积液；
（3）不能解释的呼吸困难，栓塞面积相对较小，是提示无效腔增加的惟一症状；

肺动脉栓塞

急性肺动脉栓塞并抗凝禁忌的患者。对上肢静脉血栓还可应用上腔静脉静脉滤器。尽管经过充分抗凝治疗仍发生肺栓塞或VTE复发
植入滤器后如无禁忌证，建议常规抗凝治疗，定
期复查有无滤器血栓形成。
临床症状
呼吸困难 / 气促 / 劳力性气促胸痛咯血 ——“肺梗死三联征” 晕厥：为唯一或首发症状休克烦躁不安、惊恐、头晕、胸闷、心悸等其他，深静脉血栓表现等
体征
呼吸＞20次/分心率＞90次/分血压下降紫绀右心负荷增高表现：颈静脉充盈、异常搏动、肺动脉瓣第二心音亢进、三尖瓣收缩期杂音、肝淤血、肝颈征阳性、下肢水肿肺部体征：细湿罗音，哮鸣音、胸膜炎的体征（胸水介
华法林抗凝
应在肝素治疗的第1或2天开始口服抗凝剂，因华法林需应用数天才可完全发挥作用，因此与肝素至少重叠5天，使INR达治疗水平2.5（2.0-3.0）或PT延长至正常值的1.5-2.5倍，持续至少24小时后方可停用肝素或低分子肝素。起始剂量为每天华法林2~3mg，华法林口服期间可根据INR调整剂量，有效治疗应使INR达2.0~3.0。抗凝持续时间部分危险因素短期内可消除，3个月即可。对栓子来源不明首发病例至少给予6个月的抗凝。复发性静脉血栓栓塞症或危险因素长期存在者，抗凝治疗的时间应更为延长，达12个月或以上，甚至终生抗凝。
对血压和右心室运动功能均正常的低危患者，不宜溶栓
溶栓禁忌证
绝对禁忌证:活动性内出血;近期的自发性颅内出血相对禁忌证: 2周内的大手术、分娩、器官活检或不能压迫的血管穿刺史。 3月内缺血性卒中。 10天内胃肠道出血。 15天内严重创伤。 1月内神经外科或眼科手术。控制不好的重度高血压（SBP>180mmHg，DBP>110mmHg）。创伤性心肺复苏。血小板<100×109/L。抗凝过程中（如正在应用华法林）。妊娠。心包炎或心包积液。细菌性心内膜炎。糖尿病出血性视网膜病变严重肝肾动能不全。高龄>75岁。

2014肺栓塞指南

经导管肺动脉内局部注入rtPA未显示比静脉溶栓有任何优势。因此这种给药方式应尽量避免，因其可增加穿刺部位出血风险！
急性肺栓塞溶栓治疗禁忌证
绝对禁忌证任何时间出血性或不明原因的脑卒中 6个月内缺血性脑卒中中枢神经系统损伤或肿瘤 3周内大创伤、外科手术、头部损伤近一月内胃肠道出血已知的活动性出血相对禁忌证 6个月内短暂性脑缺血发作口服抗凝药妊娠或分娩1周内不能压迫的血管穿刺创伤性心肺复苏难治性高血压(收缩压 >180 mmHg) 晚期肝病感染性心内膜炎活动性消化性溃疡
右心导管术示右心室压力增大
心肌损伤标志物心脏肌钙蛋白T或I阳性 a：低血压定义：收缩压<90mmHg或血压降低>40mmHg达15分钟以上，除外新出现的心律失常、低血容量或败血症所致低血压。
急性肺栓塞危险分层：
----取代大、次大面积等术语
PE相关早期死亡风险高危>15% 临床：休克或低血压＋ RVF 心肌损伤可能的治疗推荐溶栓或栓子切除术
既往有心肺疾病者易发生肺梗死。
二.静脉血栓栓塞易患因素
强易患因素（OR＞10）下肢骨折 3个月内因心力衰竭心房颤动或心房扑动入院髋关节或膝关节置换术严重创伤 3月内发生心肌梗死既往VTE 脊髓损伤
二.静脉血栓栓塞易患因素
中等易患因素（OR 2－9）膝关节镜手术自身免疫疾病输血中心静脉置管化疗充血性心力衰竭或呼吸衰竭促红细胞生成素剂激素替代治疗感染炎症性肠道疾病癌症口服避孕药卒中瘫痪产后浅静脉血栓血栓形成倾向
• 避免做气管切开以免溶栓或抗凝过程中局部大出血
PE治疗：2.呼吸循环支持治疗

肺动脉栓塞(含病例)PPT课件

溶栓方法：
我国临床上常用的溶栓药物有尿激酶(UK)和重组组织型纤溶酶原激活剂(rt-PA)两种。
2010年专家共识建议我国尿激酶治疗急性大块肺栓塞的用法为: UK 20000 IU/kg/2 h静脉滴注。
国内目前缺乏严格设计的rt-PA溶栓治疗急性肺栓塞的临床资料，大多数医院采用的方案是rt-PA 50-100 mg持续静脉滴注，无需负荷量。50 mg和100 mg哪个剂量更适合于国人，目前没有严格设计的临床研究定论。需要进一步研究。
19
可编辑课件
溶栓治疗
可迅速溶解血栓和恢复肺组织灌注，逆转右心衰竭，增加肺毛细血管血容量及降低病死率和复发率。
国内一项大样本回顾性研究也证实对APTE患者行尿激
酶或rt-PA溶栓治疗+抗凝治疗总有效率96.6％，显
效率42.7％，病死率3.4％。
美国胸科医师协会已制定肺栓塞溶栓治疗专家共识，
在APTE起病48小时内即开始行溶栓治疗能够取得最大的疗效，有症状的APTE患者在6～14天内行溶栓治疗仍有一定作用。
23
可编辑课件
溶栓前应常规检查、交待病情，签署知情同意书；
使用尿激酶溶栓期间勿同时使用肝素，rt-PA溶栓时是否停用肝素无特殊要求，一般也不使用。
溶栓使用rt-PA时，可在第一小时内泵入50 mg观察有无不良反应，如无则序贯在第二小时内泵入另外50 mg。应在溶栓开始后每30分钟做一次心电图，复查动脉血气，严密观察患者的生命体征。
15
可编辑课件
抗凝治疗——低分子肝素
根据体重给药，如100 IU/kg/次，皮下注射每日 1～2次。使用该药的优点是无需监测APTT。
严重肾功能不全的患者在初始抗凝时使用普通肝素是更好的选择(肌酐清除率<30 ml/min)，因为普通肝素不经肾脏代谢。严重出血倾向的患者，也应使用普通肝素进行初始抗凝，一旦出血可用鱼精蛋白迅速纠正。

肺血栓栓塞症课件八年制文稿演示

体征
呼吸系统体征：
– 呼吸急促(70%)
– 肺部可闻及哮鸣音 (5%)和/或细湿罗音 (18-51%)
继发性
• 创伤/骨折髋部骨折（50-75%）脊髓损伤（50-100%） • 外科手术后疝修补术（5%）腹部大手术（15-30%）冠脉搭桥术（3-9%）脑卒中（30-60%） • 肾病综合征 • 中心静脉插管 • 慢性静脉功能不全 • 吸烟
• 妊娠/产褥期 • 血液粘滞度增高 • 血小板异常 • 克隆病 • 充血性心力衰竭（12%） • 急性心肌梗死（5-35%） • 恶性肿瘤 • 肿瘤静脉内化疗 • 肥胖 • 长期制动/长期卧床 • 长途航空或乘车旅行
• 急性PTE后肺动脉内血栓未完全溶解，或PTE反复发生，出现血栓机化、肺血管管腔狭窄甚至闭塞，肺血管阻力增加，肺动脉压力增高，右心肥厚、右心衰竭
病理生理-呼吸生理变化
血栓栓塞反射性生物活性释放
支气管痉挛
肺通气功能
低氧血症
肺泡表面活性物质减少毛细血管通透性增高
肺血流减少，通气存在血流重新分布
肺萎陷肺水肿肺出血
通气血流比例失调
肺换气功能
病理生理-血流动力学变化
机械阻塞神经体液因素低氧
肺动脉收缩
右室扩大右心功能不全
肺循环阻力肺动脉高压
右室后负荷
左心输出量下降
心率加快，血压下降
体循环低血压休克、晕厥
病理生理-神经体液介质
腺嘌呤、肾上腺素、组胺、 5-羟色胺、缓激肽、前列腺
危险因素
• PTE的危险因素同VTE • Virchow三要素
血管内皮损伤
• 分为原发性和继发性两类。
原发性

肺动脉栓塞_马骥

3．急性肺原性心脏病型 4．肺梗死型（多为周围肺动脉栓塞） 5．“不能解释的” 呼吸困难型，常见 6．慢性栓塞性肺动脉高压型
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症状
• 肺栓塞症状无特异性 • 常见的症状： 1．呼吸困难（82%）:尤其是突发劳力性进行性呼吸困难。 2. 胸痛（49%）:多数为胸膜性胸痛，少数为“心绞痛样胸痛”。 3．晕厥（14%）:一时性脑缺血引起,可为首发症状。 4．咳嗽（20%）:多为干咳，可伴哮鸣音。 5．咯血（7%）: 提示有肺梗死存在，多在24小时内发生。 6. 无症状者(6.9%),临床有典型肺梗死三联征（呼吸困难、胸痛及
鉴别诊断
肺栓塞易被误诊为以下疾病： 1．心脏病：冠心病（心肌梗死、心绞痛、猝死）、心
肌炎、心肌病、左心衰竭、主动脉夹层、原发性肺动脉高压。 2．胸肺疾病：肺炎、胸腔积液、ARDS、支气管炎、支气管哮喘。 3．高通气综合征（焦虑症）。 4．晕厥。
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辅助检查
• 心电图 • X线胸片 • 超声心动图（经胸、经食管） • 血浆D-二聚体 • 下肢静脉检查 • 放射性核素肺显像 • 胸部CT检查 ( CTA ) • 磁共振成象（ MRA） • 肺动脉造影
死者,罕见的并发症
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当代概念
➢ 静脉血栓栓塞症（VTE venous thromboembolism )
深静脉血栓形成--肺动脉栓塞:一个疾病过程的两种表现
➢ 肺动脉血栓形成
肺动脉原位血栓形成 ( in situ pulmonary thrombosis) 。
2020/5/6
发病情况
2020/5/6
血浆D-二聚体
➢急性肺栓塞时血浆含量增加，敏感性高、特异性低 ➢手术、外伤、急性心肌梗死、肿瘤、炎症、感染等情况也