A 77-year-old man with a six-month history of inguinal lymphadenopathy collapsed in the bathroom.  His wife found him， summoned Emergency Medical Services， and reported that he had developed diaphoresis， dyspnea， and lightheadedness after a bowel movement.  Because he was unresponsive， hypoxic， hypotensive， and tachycardic， he was rapidly transported to the Emergency Department at Brigham and Women’s Hospital.

    In the Emergency Department， he was suffering hypoxemic respiratory failure and was quickly intubated.  Although an initial telemetry rhythm strip demonstrated sinus tachycardia， right bundle branch block， and 2:1 atrioventricular conduction， the rhythm rapidly degenerated to complete heart block.  After administration of intravenous epinephrine， atropine， and dopamine， his rhythm converted to atrial flutter with variable atrioventricular conduction and right bundle branch block (Figure 1).  The patient subsequently suffered cardiac arrest with pulseless electrical activity.  He was successfully resuscitated after five minutes of cardiopulmonary resuscitation to atrial flutter with a stable blood pressure on norepinephrine and dopamine infusions.

    77岁的男性患者，既往有6个月的腹股沟淋巴结肿大病史，跌倒在浴室。他的妻子发现后，立即求助急诊，诉患者排便后出现大汗、呼吸困难和头晕症状。因为患者意识不清，并存在低氧血症、低血压、心动过速情况，被迅速送至布莱根妇女医院急诊科。

    在急诊，患者出现低氧性呼吸衰竭，迅速对其进行气管插管。最初的心电图显示患者为窦性心动过速、右束支传导阻滞以及2:1房室传导，但随后迅速转为完全心脏传导阻滞。静脉给予肾上腺素、阿托品和多巴胺后，心脏节律转为心房扑动不定比房室传导和右束支传导阻滞（图1）。患者随即出现心脏骤停和无脉。经过5 min的心肺复苏，患者复苏成功，心电图显示为心房扑动，给予去甲肾上腺素和多巴胺维持血压稳定。

既往史
    Review of the patient’s past medical history revealed cardiovascular risk factors of hypertension treated with lisinopril 40 mg daily and hyperlipidemia managed with simvastatin 40 mg daily.  He had a history of a right hilar mass for which he underwent transbronchial biopsy two years prior.  The biopsy was negative for malignancy.  Over the prior six months， the patient had developed progressive inguinal and retroperitoneal lymphadenopathy.  Preliminary results from a biopsy performed two weeks prior to presentation demonstrated reactive lymphadenopathy without evidence of malignancy.  The patient had worked in a steel factory for more than 40 years and had contact with asbestos and many chemicals during his professional career.  He never smoked and only occasionally drank beer.  He had no family history of heart disease， vtenous thromboembolism， or malignancy.

    存在心血管病的危险因素，每天服用40 mg赖诺普利控制高血压，及40 mg辛伐他汀以控制高脂血症。患者有右侧肺门肿块史，两年前行经支气管肺组织活检，结果排除了恶性的可能。6个月前患者出现进行性腹股沟和腹膜后淋巴结肿大，此次发病前2周进行的淋巴结活检显示为反应性淋巴结增生，没有发现恶性增生的证据。患者在一家钢厂工作了40多年，工作中会接触石棉和大量的化学物质。患者不吸烟，偶尔喝啤酒。患者无心脏病、静脉血栓或是恶性肿瘤的家族史。



体格检查
    On physical examination， the patient was afebrile with an average pulse of 100 beats per minute， blood pressure of 108/70 mm Hg， and oxygen saturation of 100% on 100% fraction of inspired oxygen.  His jugular veins were distended to the angle of the jaw.  Coarse breath sounds were auscultated bilaterally with dullness to percussion at the bases.  Cardiac examination revealed an irregular tachycardia， accentuated sound of pulmonic valve closure (P2)， and a II/VI holosystolic murmur best auscultated at the left lower sternal border.  His abdomen was soft， nontender， and nondistended with normal bowel sounds and no hepatosplenomegaly.  The patient had prominent inguinal lymphadenopathy.  His lower extremities were cold， cyanotic， and edematous to the knees.  Distal pulses were faint.  
    患者无发热，每分钟脉搏平均为100次，血压108/70 mm Hg，吸氧浓度为100%时氧饱和度为100%。颈静脉怒张，至下颌角处。听诊双肺呼吸音粗，肺底叩诊呈浊音。心脏查体示心动过速、律不齐，肺动脉瓣闭合音（P2）亢进，胸骨左缘听诊有全收缩期II/VI级杂音。腹部柔软、无触痛、肠鸣音正常，未触及肝脾肿大。患者腹股沟淋巴结肿大明显。下肢冰凉、发绀、膝部水肿。远端脉弱。

辅助检查
    The patient‘s laboratory evaluation demonstrated an unremarkable chemistry panel， prothrombin time， activated partial thromboplastin time (aPTT)， white blood cell count， hemoglobin， and platelet count.  Creatinine kinase was elevated to 401 units/L (normal， 41 to 266 units/L) with an MB fraction of 17.8 ng/ml (normal， 0.0 to 5.0 ng/ml).  Cardiac troponin I was increased to 12.2 ng/ml (normal， 0.00 to 0.04 ng/ml).  A portable chest x-ray demonstrated cardiomegaly， small bilateral pleural effusions， and bibasilar linear opacities. 

An urgent bedside transthoracic echocardiogram was performed.  The left ventricle was small and underfilled with severe concentric left ventricular hypertrophy.  Interventricular septal flattening in systole and diastole consistent with right ventricular (RV) pressure and volume overload was noted (Movie 1).  The RV was markedly dilated with severely reduced systolic function (Movie 2).  Mild tricuspid regurgitation was present and the RV systolic pressure， as estimated by the modified Bernoulli equation， was approximately 33 mmHg (Figure 2).  The inferior vena cava was dilated without respirophasic collapse consistent with an estimated right atrial pressure of 20 mm Hg.  Therefore， moderate pulmonary artery systolic hypertension was present.

    生化全项、凝血酶原时间、部分活化凝血酶原时间（aPTT）、白细胞计数、血红蛋白和血小板计数均无明显异常。肌酐升高401 U/L（正常：41~266 U/L），同工酶17.8 ng/ml（正常：0~5.0 ng/ml）。心肌肌钙蛋白I升高，12.2 ng/ml（正常：0~0.04 ng/ml）。床旁胸片示患者心脏扩大、双侧少量胸腔积液和带状双肺底透光度低。

    急查床旁超声心动图，显示左心室缩小、充盈不良，有严重向心性肥厚。收缩期和舒张期室间隔平坦，可见右心室（RV）压力和容量负荷过重（视频1）。RV显著扩张，收缩功能严重下降（视频2），同时可见轻度三尖瓣反流，通过Bernoulli公式可以计算出RV收缩压约为33 mm Hg（图2）。下腔静脉扩张，无呼吸相塌陷，右房压约为20 mm Hg。因此患者存在中度肺动脉收缩期高压。
 

治疗经过
    Based on the clinical presentation and echocardiographic findings， the patient was diagnosed with massive pulmonary embolism (PE).  The patient received fibrinolytic therapy with tissue plasminogen activator (tPA) 100 mg as a continuous peripheral intravenous infusion over two hours.  Over the course of the first hour of fibrinolytic infusion， the patient demonstrated marked improvement in hemodynamics and oxygenation.  He was admitted to the Coronary Care Unit， where his vasopressor infusions were gradually weaned.  When he had completed the tPA infusion and his aPTT had fallen below twice the upper limit of normal， intravenous unfractionated heparin was administered via continuous intravenous infusion.  Chest，