2014ESC肺栓塞指南
高危PE患者，无绝对禁忌症，溶栓治疗是一线治疗
溶栓治疗禁忌症
相对禁忌症
▪短暂性脑缺血发作的6个月内
▪口服抗凝治疗 ▪孕期或产后1周 ▪非压缩性的穿刺部位 ▪有创性复苏 ▪难治性高血压（收缩压>180mmHg） ▪进行性肝病 ▪感染性心内膜炎
▪活动性消化性溃疡
溶栓治疗时间窗
• 溶栓治疗时间窗通常在急性肺栓塞发病或 复发后2周以内。症状出现48小时内溶栓获 益最大，溶栓治疗开始越早，疗效越好。
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 低危因素（OR＜2） 卧床休息＞3天 糖尿病 高血压 长时间坐位（例如：长时间的汽车或飞机旅行） 年龄增长 腹腔镜手术（例如：腹腔镜下胆囊切除术） 肥胖 妊娠 静脉曲张
肺栓塞的自然病程
肺栓塞抗凝治疗时限推荐
推荐等级
证据水平
对于继发于短暂的（可逆的）危险因素的PE，口服抗凝药治疗 推荐3个月
对于无诱因的PE患者，推荐口服抗凝治疗至少3个月 延长口服抗凝治疗时间应考虑首发无诱因的PE和低出血风险 无限期抗凝治疗推荐于再发的无诱因PE患者
I
I IIa I
B
A B B B
IIa 必须延长抗凝治疗，利伐沙班（20mg,一日一次），达比加群 （150mg,一日两次，对于年龄大于80岁的患者或同时应用维拉 帕米的患者，110mg,一日两次），阿哌沙班（2.5mg,一日两 次），应考虑作为维生素K拮抗剂的替代治疗（除了患者有严 重肾功能减低） 对已延长抗凝治疗的患者，用药间隔应再评估继续抗凝治疗的 风险-获益比 对于拒绝或不能够耐受任何形式口服抗凝治疗的患者，可考虑 阿司匹林作为次级VTE预防方法 I IIb
低危患者
中高危患者 再灌注治疗 抗凝；监测，考虑 补救性再灌注治疗
中低危患者 抗凝；住院治疗
考虑早期出院；门 诊监护；抗凝
溶栓治疗禁忌症
绝对禁忌症 ▪出血性中风或不明原因卒中 ▪缺血性卒中的6个月内 ▪中枢神经系统损伤或肿瘤
▪严重创伤/手术/头部外伤3周内
▪过去1个月内胃肠道出血 ▪存在已知出血风险
基本概念
• 肺梗死（pulmonary infarction,PI）：是指肺栓 塞发生后引起肺组织出血或坏死。 • 肺栓塞后发生肺梗死者不到7%。
• 肺栓塞肺组织不易发生坏死，其原因是肺组织有 四重血液供应：肺动脉、支气管动脉、肺循环和 支气管血管之间交通、肺泡氧弥散。 • 肺梗死常发生于外周小肺动脉阻塞时，中心肺动 脉阻塞一般不引起肺梗死。 • 既往有心肺疾病者易发生肺梗死。
aPollack
确诊PE（n=1880） 50% 39% 23% 15% 10% 8% 6% 6% 24%
et al.J Am Coll Cardiol 2011
肺栓塞临床预测评分
• PE的症状、临床表现和常规检查缺乏敏感 性和特异性，但综合临床判断和预测评分 两方面可帮助我们区分PE的疑似患者，并 在行特殊检查前初步评估PE的可能性，这 样可以提高PE的确诊率。
临床怀疑肺栓塞
有
休克或低血压？
无
指南推荐的高危患 者诊断流程
指南推荐的非高危患者诊断流程 确诊肺栓塞 临床风险评估（PESI或sPESI）
确诊肺栓塞 PESI分级Ⅲ~Ⅳ或 sPESI≥1 中危患者
进一步危险分层
PESI分级Ⅰ~Ⅱ 或sPESI=0
右心室功能（超声或CT），生物标志物 高危患者
两者均阳性 两者之一阳性或均阴性
我国尿激酶治疗方法为：20000IU/kg治疗2小时 Rt-PA 100mg治疗2小时；或
0.6mg/kg治疗15分钟（最大剂量为50mg） 我国推荐Rt-PA用法50-100mg治疗2小时 IU=国际单位；Rt-PA=重组组织型纤溶酶原激活剂。
溶栓药物及溶栓方案
• 在应用链激酶或尿激酶溶栓治疗时应停用 普通肝素，但如果应用rtPA则可以继续使用 普通肝素。在溶栓治疗开始时，应用低分 子量肝素或磺达肝癸钠的患者，应在停止 注射低分子量肝素12小时后，或则停止注 射低分子量肝素或磺达肝癸钠24小时后在 使用普通肝素。溶栓治疗结束后继续使用 普通肝素几小时后，在该用低分子肝素或 磺达肝癸钠。
急性肺栓塞血流动学障碍的关键因素
右心室后负荷压力增高 RV扩张
RVO2供应↓ RV冠状动脉灌注↓ 体循环血压↓
死亡 心源性休克
TV功能不全 RV室壁张力↑ 神经因子激活
心肌炎症
RV氧耗量↑ RV心肌缺血 RV收缩性↓
低CO LV前负荷↓
RV输出量↓
急诊PE患者临床表现a
特征 呼吸困难 胸膜炎性胸痛 咳嗽 胸骨后胸痛 发热 咯血 晕眩 单侧腿痛 DVT症状（单侧肢体肿胀）
伴低血压和休克的疑似PE病例
是否可立刻行CT肺动脉造影 不能 超声心动图 能
右室超负荷表现
否
有
可行CT肺动脉造 影或患者稳定
CT肺动脉造影
没有其他检查手 段或患者不稳定
阳性 PE特异性治疗初 始再灌注治疗
阴性 寻找其他引起血液动 力学不稳定的原因
寻找其他引起血液动力 学不稳定的原因
不伴低血压和休克的疑似PE病例
肺栓塞
云南省第一人民医院 急诊内科 李昌林
基本概念
• 肺栓塞(Pulmonary embolism，PE)：是以各种栓子阻塞肺 动脉系统为其发病原因的一组疾病或临床综合征的总称，
包括PTE、脂肪栓塞综合征、羊水栓塞、空气栓塞等。
• 肺血栓栓塞症（Pulmonary Thrombo-embolism，PTE）： 为来自静脉系统或右心的血栓阻塞肺动脉或其分支所致的 疾病，以肺循环和呼吸功能障碍为其主要临床和病理生理 特征。 • PTE为PE的最常见类型，占PE中的绝大多数，通常所称PE 即指PTE。
1
N/A N/A N/2
Geneva评分法
既往肺栓塞或深静脉血栓 心率：75-94次/分 ≥95次/分 过去一个月内手术或骨折 咯血 癌症活动期 单侧下肢痛 下肢深静脉触痛和单侧下肢水肿 年龄>65岁 三级评分
原始版
3 3 5 2 2 2 3 4 1
简化版
1 1 2 1 1 1 1 1 1
低
-
-
选择性检查；若检查，双阴 性e
PE=肺栓塞;PESI=肺栓塞严重指数；sPESI=简化版肺栓塞严重指数。 a PESI分级III-V提示中-极高30天死亡率；sPESI>1分提示高30天死亡率。 b 右室功能不全超声心动图指标包括右室扩大和/或升高的右室/左室直径比值（大多数研究报道阈值为0.9或1）； 右室游离壁运动减弱；三尖瓣环收缩期位移TAPSE降低；或联合以上指标。CT动脉造影（四腔心切面观察心脏）， 右室功能不全被定义为右室-左室舒张末期直径比值增高（大多数研究报道阈值为0.9或1）。 c 心肌受损指标（e.升高的血浆肌钙蛋白I或T浓度），或（右）心功能不全所致心衰（升高的血浆脑钠肽浓度）。 d 对于伴有休克或低血压的PE患者无须评估PESI或sPESI或实验室检查。 e对PESI分级I-II或sPESI=0的患者，若血浆标志物升高或影响学提示右心室功能不全，也被列为中-低风险组。这 适用于影像学或生物标志物检查结果早于临床严重程度指数评估的情况。
C B B C
对于肿瘤合并PE的患者，治疗初始3至6个月，根据体重应用皮 IIa 下注射低分子量肝素 对于肿瘤合并PE的患者，应考虑无限期延长抗凝治疗时间或直 到肿瘤治愈 IIa
高危因素（OR＞10） 下肢骨折
VTE 的易患因素
中危因素（OR2-9） 膝关节关节镜手术 自身免疫性疾病 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（按配方而定） 体外受精 感染（特别是呼吸系统、泌尿系统感染或HIV感染） 炎症性肠道疾病 癌症（高危转移性疾病） 口服避孕药 卒中瘫痪 产后 浅静脉血栓 血栓形成倾向
低可能性
中度可能性 高度可能性 二级评分 不可能肺栓塞 可能肺栓塞
0-3
4-10 ≥11
0-1
2-4 ≥5
0-5 ≥6
0-2 ≥3
临床分期和初始危险分层
疑诊急性PE
休克或低血压？
是
否
高危
非高危
排除新发心律失常、血容量下降、脓毒血症后，收缩压<90mmHg，或收缩压下降 ≥40mmHg并持续15分钟以上
≥1分=30天内死亡率10.9% （95%CI 8.5%-13.2%）
急性PE患者早期死亡风险分层
早期死亡风险 风险指标和评分
休克或低血 压 高 中 中 -高 中 -低 + PESI分级 III—V或 sPESI>1 a (+) d + 影像学提示 右室功能不 全b + 双阳性 一个（或没有）阳性 e 心脏实验室 生物标志物 c (+) d
肺栓塞临床预测评分
Wells评分法 既往PE或DVT病史 心率≥100次/分 过去4周内有手术或制动史 咯血 原始版 1.5 1.5 1.5 1 简化版 1 1 1 1
癌症活动期
DVT临床表现
1
3
1
1
其他鉴别诊断的可能性低于PE
三级评分 低可能性 中度可能性 高度可能性 二级评分 不可能肺栓塞
3
0-1 2-6 ≥7 0-4
2014 ESC急性肺栓塞诊断及管理指南解读
作者：荆志成来源：中国医学论坛报近年来，急性肺栓塞领域有关新药物、新治疗、新研究、新探索的证据不断积累，结合临床实际需求，欧洲心脏病学会（ESC）在2014年ESC年会上发布新版《急性肺栓塞诊断及管理指南》（以下简称“新指南”）。
新指南在充分考虑诊断和治疗的风险/获益比以及对预后影响的基础上，针对不同的患者推荐最佳管理策略。
与2008年版指南相比，新指南在风险评估分层、新型口服抗凝药的使用、特殊问题的处理等方面有较多更新，用新指南指导临床实践将使肺栓塞患者从中获益。
基于风险的诊断流程和治疗策略新指南进一步细化了风险分层。
急性肺栓塞严重程度的临床分级依据院内早期死亡风险或30天死亡率，这对临床诊断及选择治疗方案具有重要作用。
对于疑诊急性肺栓塞患者，根据是否存在休克或低血压（排除新发心律失常、血容量下降、脓毒症后，收缩压<90mmHg或收缩压降低≥40mmHg并持续15分钟以上）分为高危和非高危，然后结合超声心动图、CT和生物标志物等检查明确诊断。
对于确诊肺栓塞患者，根据肺栓塞严重指数（PESI）分级Ⅲ—Ⅳ或简化PESI（sPESI）≥1、影像学提示右室功能不全、心脏实验室生物标志物等风险参数的存在情况，非高危患者可进一步分为中高危、中低危、低危风险，继而采取相应治疗策略（图1）。
图1 急性肺栓塞患者的风险评估与管理策略2008年版指南对肺栓塞的治疗是基于时间的策略，对于有血流动力学障碍的肺栓塞患者推荐溶栓治疗，普通肝素、低分子量肝素和磺达肝葵钠抗凝治疗应持续5天以上。
维生素K拮抗剂应尽早应用，最好在非口服抗凝药治疗的当天开始应用，对于无明显诱因的肺栓塞患者推荐维生素K拮抗剂治疗至少3个月。
当国际标准化比值（INR）连续2天以上维持在2.0—3.0时停用非口服抗凝药。
对于静脉血栓栓塞（VTE）危险因素长期存在的患者应长期抗凝治疗。
新指南中对肺栓塞的治疗策略则是基于风险做出的推荐。
对于高危患者，推荐尽早启动静脉注射普通肝素抗凝治疗（ⅠC），推荐进行溶栓治疗（ⅠB），有溶栓禁忌证或溶栓失败者，可行外科肺动脉血栓切除术（ⅠC）；中高危患者需密切监测，以便及早发现血流动力学失代偿征象并及时开始补救性再灌注治疗；中低危、低危患者推荐应用新型口服抗凝药或低分子量肝素+维生素K拮抗剂。
《2014年ESC急性肺栓塞诊治指南》解读
67中国循环杂志 2014年11月 第29卷 Chinese Circulation Journal，November，2014，Vol. 29 Supplment 《2014年ESC 急性肺栓塞诊治指南》解读徐希奇，荆志成作者单位：100037 北京市，中国医学科学院 阜外心血管病医院 心血管疾病国家重点实验室 血栓性疾病诊治中心作者简介：徐希奇 主治医师 博士 主要从事肺动脉高压、肺栓塞等研究 通讯作者：荆志成 Email：jingzhicheng@ 中图分类号R54 文献标识码：C 文章编号：1000-3614（2014）增刊-0067-05 doi：10.3969/j.issn.1000-3614.2014.增刊.017关键词 急性肺栓塞；指南2014年欧洲心脏学会（ESC）在2000年和2008年发布的两部指南[1,2]基础上对急性肺栓塞诊治指南进行修订[3]，现对最新的指南进行解读。
1 流行病学和相关危险因素静脉血栓栓塞症（VTE）包括深静脉血栓形成（DVT）和肺栓塞（PE），年发病率高达100~200/10万，为第三大常见心血管疾病。
急性肺栓塞也是常见的致死原因。
VTE 是患者自身因素（长期危险因素）及环境因素（临时危险因素）相互作用的结果。
临时危险因素包括VTE 发病前6周到3个月内出现的临时或者可逆性危险因素（如手术、创伤、制动、妊娠、感染、口服避孕药或激素替代治疗等）；而长期危险因素影响长期抗凝治疗方案的选择。
2 病理生理急性肺栓塞的病理生理学改变包括循环障碍和气体交换障碍两个方面。
循环障碍：与肺血管床的机械阻塞及肺血管收缩有关，导致肺血管阻力增加，肺动脉压力代偿性升高以维持血压稳定；但神经内分泌的过度激活可诱发心肌炎性损伤甚至右室心肌梗死，导致休克甚至死亡。
气体交换障碍：主要继发于血液动力学不稳定及低心排血量，混合静脉血氧饱和度下降，另外与肺通气-灌注不匹配、继发性卵圆孔开放、肺梗死及基础心肺疾病等有关。
2014ECS指南资料
LOGO
临床预测标准
LOGO
诊断
临床表现 D二聚体
增强CTPA 放射性核素肺通气灌注显像 肺动脉造影 磁共振肺动脉造影
心电图
超声
LOGO
D－二聚体
阴性预测值高，阳性预测值低
对于临床高度可能性DE的患者，仍不推荐用D－二聚体
临床疑似PE+超声见远端DVT需进一步检查（II a）
LOGO
MRA
不推荐 －敏感性低
－急诊时临床可行性差
不用于排除PE（IIIA）
LOGO
LOGO
诊断策略
可疑肺栓塞(伴有休克或低血压) 可立即行CT血管造影检查 否 超声心动图 右心负荷增加 具备CT血管造影检 查条件且病情稳定 阳性 按肺栓塞治疗: 溶 栓 CT血管造影 是
LOGO
与2008指南的变化
1、最近发现的静脉血栓栓塞（VTE）诱发因素 2、简化后的临床预测规则 3、年龄校正后的 D- 二聚体标准 4、亚段肺栓塞 5、偶然发现的肺栓塞 6、中度风险肺栓塞的进一步风险分层
LOGO
7、维生素K拮抗剂的初始治疗
8、直接口服抗凝剂（NOACs）对 VTE 的治疗和二级
预防
9、中危患者再灌注治疗的安全性和疗效 10、急性肺动脉栓塞患者出院后和家庭管理建议。 11、慢性血栓形成的栓塞性肺动脉高压（CTEPH）的 诊断和治疗 12、对癌症患者和孕妇急性肺动脉栓塞的管理建议
LOGO
肺血管造影
PE诊断的金标准，但很少实施 目前逐渐被无创的且具有同样准确性的CT取代
用于临床评估与无创影响学检查不符的情况 （IIB）
2014年年ESC急性肺栓塞诊治指南
第十八页，共36页。
急性肺栓塞早期危险分层
第十九页，共36页。
第二十页，共36页。
急性肺栓塞治疗
• 血液动力学和呼吸支持： • 高危患者主要死亡原因为急性右心衰竭。因此
过量输液无益甚至有害，适量输液（500 ml） 可增加血压，维持急性肺栓塞患者的心指数。 • 可以给予血管收缩药物。
• 不伴休克或低血压症状疑似肺栓塞的诊断
– CTPA 是疑诊肺栓塞最重要的检查手段，但不应成为 常规的筛查手段。
– CTPA是高度可疑肺栓塞的一线选择，是低中度可 疑且D- 二聚体升高患者的二线选择。
– 对急诊患者联合D- 二聚体及临床可能性评估更为合理 ，可排除约30% 的患者。值得注意的是，高度可疑患 者不应进行D- 二聚体检测，因为少数患者有假阴性可 能。
• 肺栓塞：以各种栓子阻塞肺动脉系统为其发病原 因的一组疾病或临床综合征的总称
• 包括肺血栓栓塞征、脂肪栓塞征、羊水栓塞、空 气栓塞等
第一页，共36页。
肺血栓栓塞症
常见病因 • VTE 是患者长期危险因素及临时危险因素相互作
用的结果。 • 临时危险因素：感染、手术、创伤、制动、妊
娠、口服避孕药或激素替代治疗等
• 溶栓治疗最佳时间窗为发病48 小时内，但发病 6~14 天内溶栓仍然有效
第二十七页，共36页。
• 溶栓治疗对血液动力学稳定的急性肺栓塞仍存 在争议
• 经皮导管介入治疗：尽快清除阻塞主肺动脉 的血栓，恢复右室功能，改善症状和生存率
• 腔静脉滤器：有抗凝绝对禁忌证及接受足够 强度抗凝仍复发的肺栓塞患者可选择静脉滤 器植入术。
第二十二页，共36页。
抗凝治疗： • 目的是预防早期死亡和复发
2014版欧洲心脏病学会急性肺血栓栓塞症诊断治疗指南解读
临床怀疑肺栓塞
有
休克或低血压
无
指南推荐的高危患者 诊断流程
确诊 PE
指南推荐的非高危患者诊断流程
确诊 PE
临床风险评估 （PESI 或简化 PESI）
PESI 分级Ⅲ～Ⅳ PESI 分级Ⅰ～Ⅱ 或简化 PESI ≥ 1 或简化 PESI=0
高危患者
中危患者
进一步危险分层
右心功能（超声或 CT） 生物标志物
图 2 慢性血栓栓塞性肺动脉高压的诊断流程 [4]
明确诊断 CTEPH 终身抗凝治疗
CTEPH 团队评估是否可以手术治疗
可以手术
不可以手术
另一家有经验中心再次评估是否可以手术
肺动脉血栓内膜剥脱术
靶向药物治疗
持续症状性肺动脉高压
肺移植
新治疗 ; 肺动脉球囊成形术
注：CTEPH：慢性血栓栓塞性肺动脉高压 图 3 慢性血栓栓塞性肺动脉高压的治疗流程 [4]
本文现针对新版指南中危险分层和治疗策略、抗 凝治疗及慢性血栓栓塞性肺动脉高压作一简要介绍 [1-4]。 1 危险分层和治疗策略
2014ESC急性肺栓塞诊断和管理指南中文完整版 (2)
2014ESC急性肺栓塞诊断和管理指南中文完整版2014ESC急性肺栓塞诊断和管理指南中文完整版是由欧洲心脏病学学会(ESQ)袖珍指南之一，网上主要是关于它的解读，很少有完整版本，这个中文完整版是胡大一教授主审的，希望对大家有帮助！2•概述2.1流行病学静脉血栓栓塞症(VTE)包括深静脉血栓形成（DVT)和肺栓塞(PE),其年发病率为100-200/10万，为第三大常见心血管疾病。
其中急性肺栓塞是VTE最严重的临床表现，是其发病、死亡及住院的主要因素。
2004年，通过对六个欧洲国家的总人数约四亿五千四百余万人口流行病学调查中发现有超过317,000人死于VTE。
其中，34%的患者死于突发致命性的PE，59%的患者死于生前未诊断出的PE，在早期死亡的患者中仅有7%在死前明确诊断出PE。
年龄超过40岁的患者发生PE的风险较高，并且其危险度每十年将会提高近一倍，预计在未来越来越多的患者被诊断出(或者死于)PE。
2.2危险因素VTE是患者自身因素(长期因素)及环境因素(临时因素)相互作用的结果。
在一些临时或者可逆的危险因素（如手术、创伤、制动、妊娠、口服避孕药或激素替代治疗等）的作用下，6周到3个月内发生的VTE被认为是诱发型，其它则被称为非诱发型。
PE也可能发生在没有任何已知危险因素的情况下。
与临时因素不同，长期因素可能影响PE患者的长期抗凝治疗方案的选择。
2.3病理生理急性肺栓塞血液动力学障碍的关键因素2.4临床分期和初始危险分层急性PE发生的严重程度的临床分级是根据对PE患者院内发生的早期死亡风险或者30天死亡率。
这个分层是根据患者临床表现来划分，对临床诊断及治疗方案发挥重要作用。
存在休克或者持续的动脉低压的情况为高危PE。
3.诊断根据现有指南和临床管理目标，“明确PE”定义为PE的概率高，需针对性治疗的PE，而“排除PE”则是PE的概率低，不需采取PE针对性治疗，且风险较低。
3.1临床表现PE的临床症状和体征特异性不强，很可能漏诊。
2014ESC急性肺栓塞诊断和管理指南中文完整版
2014ESC急性肺栓塞诊断和管理指南中文完整版2014ESC急性肺栓塞诊断和管理指南中文完整版是由欧洲心脏病学学会(ESQ)袖珍指南之一，网上主要是关于它的解读，很少有完整版本，这个中文完整版是胡大一教授主审的，希望对大家有帮助！2•概述2.1流行病学静脉血栓栓塞症(VTE)包括深静脉血栓形成（DVT)和肺栓塞(PE),其年发病率为100-200/10万，为第三大常见心血管疾病。
其中急性肺栓塞是VTE最严重的临床表现，是其发病、死亡与住院的主要因素。
2004年，通过对六个欧洲国家的总人数约四亿五千四百余万人口流行病学调查中发现有超过317,000人死于VTE。
其中，34%的患者死于突发致命性的PE，59%的患者死于生前未诊断出的PE，在早期死亡的患者中仅有7%在死前明确诊断出PE。
年龄超过40岁的患者发生PE的风险较高，并且其危险度每十年将会提高近一倍，预计在未来越来越多的患者被诊断出(或者死于)PE。
2.2危险因素VTE是患者自身因素(长期因素)与环境因素(临时因素)相互作用的结果。
在一些临时或者可逆的危险因素（如手术、创伤、制动、妊娠、口服避孕药或激素替代治疗等）的作用下，6周到3个月内发生的VTE被认为是诱发型，其它则被称为非诱发型。
PE也可能发生在没有任何已知危险因素的情况下。
与临时因素不同，长期因素可能影响PE患者的长期抗凝治疗方案的选择。
2.3病理生理急性肺栓塞血液动力学障碍的关键因素2.4临床分期和初始危险分层急性PE发生的严重程度的临床分级是根据对PE患者院内发生的早期死亡风险或者30天死亡率。
这个分层是根据患者临床表现来划分，对临床诊断与治疗方案发挥重要作用。
存在休克或者持续的动脉低压的情况为高危PE。
3.诊断根据现有指南和临床管理目标，“明确PE”定义为PE的概率高，需针对性治疗的PE，而“排除PE”则是PE的概率低，不需采取PE针对性治疗，且风险较低。
3.1临床表现PE的临床症状和体征特异性不强，很可能漏诊。
2014年欧洲心脏学会急性肺栓塞诊断治疗指南解读
3
≥95 次/min
5
过去 1 个月内手术或骨折
2
咯血
2
活动性癌症
2
单侧下肢痛
3
下肢深静脉触痛和单侧下肢水肿 4
年龄＞65 岁
1
临床可能性
简化版 1 1 1 1 1 1 1
不适用 不适用 不适用
0~1 ≥2 简化版 1 1 2 1 1 1 1 1 1
三级分类
低可能性
0~3
0~1
中度可能性
4~10
2~4
检 查 或 生 界限值
敏 感 性 % 特 异 性 % 阴 性 预 测 值 % 阳 性 预 测 值 HR 或 OR
物标志物
（95%CI） （95%CI） （95%CI）
%（95%CI） （95%CI）
超 声 心 动 右室功能障 74 (61~84) 54 (51~56) 98(96~99)
8 (6~10)
2.4(1.3~4.3)
图
碍的各种标
准
CT 血管造 右 室 / 左 室 46 (27~66) 59 (54~64) 93(89~96)
8 (5~14)
1.5(0.7~3.4)
影
≥1.0
右 室 / 左 室 84 (65~94) 35 (30~39) 97(94~99)
7 (5~10)
2.8(0.9~8.2)
时，可行加压静脉超声（CUS）和/或食管超声心动图（TOE）检查，如发现静脉和/或肺动
脉血栓则支持肺栓塞的诊断（Ⅱb C）。（3）转到导管室的不稳定患者如果冠脉造影排除急性
冠脉综合征，而怀疑肺栓塞时可以考虑进行肺动脉造影（Ⅱb C）。
2. 不合并休克或低血压的疑似肺栓塞：推荐使用以下诊断标准（表 3）进行诊断（ⅠB）。
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。
肺栓塞指南
预计在未来越来越多的患者被诊断出或者死于PE。
一. 2014ESC急性肺栓塞指南新内容
与2000、2004年指南相比十二项改变
1.静脉血栓栓塞症的诱发因素 2.肺栓塞临床预测流程 3.年龄校正的D-二聚体界值 4.亚段肺动脉栓塞 5.偶然、临床意外肺动脉栓塞 6.中危组肺栓塞风险分层 7.维生素K拮抗剂的启动治疗 8.新型口服抗凝药物对静脉血栓栓塞症的治疗及二级预防 9.中危患者再灌注治疗的疗效及安全性 10.肺栓塞早期出院和家庭治疗 11.慢性血栓栓塞性肺动脉高压诊断和治疗 12.妊娠和恶性肿瘤患者肺栓塞治疗推荐
2.肺栓塞的临床预测规则
• PE的症状、临床表现和常规检查缺乏敏感性和特异性。
• 但合临床判断和预测评分可帮助我们区分PE的疑似患 者，并在行特殊检查前初步估计PE的可能性，这样可 提高PE的确诊率。
• 特殊检查后(如CT检查后)PE确诊的概率不仅取决于诊 断性检查本身，还取决于特殊检查前的评估。
开放 随机 等效性
1 19个中心
24小时内出院病人与 住院治疗病人对照
年龄≥18岁 确诊为PE PESI分级为 I或II
BP＜100mmHg 需阿片类药物镇痛 活动性出血或高危 极度肥胖 CrCl＜30ml/min HIT病史 家庭治疗存在困难
344
依诺肝素皮下注
（1557人） 射 BID.
重叠使用VKA(早
8.新型口服抗凝药物对VTE的治疗及二级预防
• 临床研究结果证实，应用新型口服抗凝药物治疗 VTE的临床疗效非劣效于肝素/VKA。
• 就严重出血事件而言，口服抗凝药物可能更安全。