?

Acute anterior wall myocardial infarction complicated by cardiogenic shook in an elderly female patient

(Institute of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China)

Case presentation

A 73-year-old female was admitted into the Institute of Geriatric Cardiology, Chinese PLA General Hospital because of sudden chest pain accompanied with nausea and vomiting for 15 hours. At 3:00 on August 14th, 2011, the patient suddenly suffered from severe chest pain accompanied with perspiration, nausea, vomiting, and cold extremities, but she was under normal conscious level. In the emergency room, electrocardiogram(ECG) at 18:00 showed ST segment elevation on the precordial leads. Cardiac biochemical markers increased proportionally. The patient had a history of hypertension for 10 years which was poorly controlled, chronic bronchitis for several years, cerebral ischemia attack one month ago, and diarrhea one day before admission. She denied any history of smoking, alcohol drinking, or illicit drugs use.

On admission examination, the blood pressure was 90/70mmHg and the respiratory rate 20 breaths per minute. Both lungs were clear with moist rales. Heart rate was 133 beats per minute. Percussion revealed a dull sound. A grade 2-3/6 diastolic murmur could be heard at the left second intercostal space(ICS). Dorsalis pedis artery pulse was weak. Transthoracic echocardiogram showed a left ventricular ejection fraction (LVEF) of 43%, a normal-size left ventricular cavity, moderate dysfunction involving the septal and anterior, lateral and apex segments of the midportion, the thinned left ventricle, and ventricular aneurysm at the apex. Chest radiogragh showed pulmonary infection.

Considering the diagnosis of acute ST-elevation myocardial infarction (STEMI) and cardiogenic shock, the patient received emergency intra-aortic balloon bumping(IABP) implantation and percutaneous coronary intervention(PCI). Cardioangiography (CAG) showed occlusion of the left anterior descending (LAD) artery right after the first diagonal opening. There was poor collateral flow to the distal LAD artery. The ostial diagonal branch presented a localized stenosis of about 90%. The left circumflex coronary artery and its branches appeared to be free of obstruction. Considering LAD as the culprit vessel, one stent was implanted in the middle LAD.

Medication therapy was administrated, including anti-platelet, anti-coagulation, nitrate, statin, liver and renal protection, anti-infection and nutritional support. Diuretics were given intermittently to control the input and output. Dopamine was given intravenously to maintain the blood pressure. Because of her poor heart function, high heart rate and frequent ventricular premature beats, cedilanid and amiodarone were also administrated. On August 16th, tracheal cannula placement and mechanical ventilator support were performed as a result of repeated acute left heart failure, pulmonary infection and liver and renal dysfunction. Sodium nitroprusside, imipenem and cilastatin were administrated, while amiodarone stopped. Intake and output were also controlled. After all these treatment, the liver and renal function improved, intermittent respirator suspension training went smooth and heart function improved. The platelet account presented a slight decrease, and IABP balloon induced platelet injury was highly suspected. Tracheal cannula and IABP were removed on the 22ndand 24thin sequence. Consequentially, respiratory rate increased later, accompanied with continuous low-blood-pressure state which even high dose of dopamine could barely correct. On the 26th, acute left heart failure attacked. ECG monitor suggested junctional rhythm and frequent ventricular premature. The patient lost consciousness. Digitalis intoxication was highly suspected. Laboratory examination showed serum level of digoxin ＞4ng/dl, confirming digitalis intoxication. Digitaloid medications were forbidden immediately. Tracheal intubation and IABP implantation were performed for the second time. Epinephrine, norepinephrine and high dose of dopamine,, were all given to keep the blood pressure stable. Respiratory acidosis was corrected after sodium bicarbonate intravenous administration. The patient regained consciousness. Between November the 6thand November the 16th, repeated intermittent ventilator weaning all failed and IABP counterpulsation failed to maintain the blood pressure. Heparin-induced thrombocytopenia (HIT) developed, so did continuous hyperpyrexia, pulmonary infection aggravation and frequent ventricular premature. The patient was under a severe condition persistently. At 19:00, November the 17th, 2011, blood oxygen saturation suddenly dropped to 50%-70%, heart rate 140-150 beats per minute, blood pressure 70/50mmHg. Pure oxygen was given, accompanied with epinephrine and bicarbonate injection. Her family members rejected the rescue treatment with cardiopulmonary resuscitation (CPR) and electric defibrillation, the patient was confirmed dead at 19:40.

Clinical discussions

:This elderly female was diagnosed with acute STEMI in the anterior wall and cardiogenic shock. Considering the hospital admission delay, together with liver and kidney dysfunction, as well as pulmonary infection, the patient was in severe condition and had a great risk of death. As for treatment, the following points should be considered. (1) Digitalis intoxication. Regarding the cardiac dysfunction, higher heart rate and frequent ventricular premature, digoxin and cedilanid were administrated. Because digitalis was in high dose, the plasma concentration should be monitored frequently. In this case, ECG revealed junctional rhythm, which was highly due to digitalis intoxication. (2) Infection. This patient presented with cardiogenic shock, a long history of bed rest, poor nutritional status, weak cough, tracheal intubation, previous history of chronic bronchitis. In addition of IABP implantation, deep-vein catheterization and urinary catheter placement, she was in a great risk for catheter associated infection. The patient￠s body temperature, blood routine test, chest radiogragh, clinical signs, especially the result of sputum culture should all be taken into consideration in antibiotics application.

: Multi-organ dysfunction is a common problem in AMI patients after PCI, mostly according to illness progression and iatrogenic reasons. In this case, cardiogenic shock had been present before admission. With a low-blood-pressure state for several hours, hypoperfusion developed, which manifested as paleness, cold extremities, weak dorsal pedis artery pulse, hepatic congestion, pulmonary venous congestion, and renal dysfunction. All these suggested severe multi-organ dysfunction which led to a poor prognosis. Clinical doctors should pay much more attention to iatrogenic liver injury, acute kidney injury (AKI), digitalis intoxication and HIT. Liver injury was usually associated with liver disease history, cardiac dysfunction, congestive & ischemic hepatopathy and iatrogenic liver injury(intravenous administration of amiodarone). Acute kidney injury can be induced not only by hypoperfusion, but also by radiographic contrast application. Patient with repeated left heart failure usually received high dose of digitaloid drugs orally and intravenously, so digitalis intoxication should be carefully monitored by close observation of clinical symptoms, electrocardiogram and plasma digoxin concentration. For a post-PCI patient with cardiac dysfunction and IABP implantation, the platelet count decreased, which may be related to either HIT or IABP balloon induced mechanical platelet injury. In this case, platelet count displayed no change under IABP support and after IABP removal, while it increased greatly after heparin was replaced by argatroban, so HIT was strongly suggested.

: For AMI patients with cardiac dysfunction, some factors predicted poor prognosis, including advanced age, pulmonary infection, liver and renal dysfunction, large infarction area, less survival myocardium, low LVEF, multiple post-infarction complications, history of adverse cerebral events,. Considering these factors, in addition to the im-patience aspects in her characteristics and delayed revascularization time, this patient was more likely to have poor prognosis and in-hospital death. Several dilemma made the treatment even more complicated. Firstly, failure in removing IABP suggested severe myocardial stunning which necessiates prolongation of mechanical support, while considering pulmonary infection and potential catheter-related infection, an earlier removal of IABP was undoubtedly preferable. Maintenance of blood pressure was another dilemma. Vasoconstriction agents may increase afterload and labor the myocardium, while coronary hypoperfusion may occur if vasoconstriction agents were not applied. Additionally, high dose of dopamine improved the blood pressure but constricted peripheral vessels simul-taneously which induced multi-organ hypoperfusion consequently, especially liver and kidney. Meanwhile, small dose of sodium nitroprusside dilated peripheral vessels to improve multi-organ hypoperfusion, but left blood pressure maintenance a great problem. All these made it difficult to balance between the advantage and disadvantage of every treatment, which increased the risk of poor prognosis.

In brief, cardiac dysfunction complicated AMI patients are of high risk and poor prognosis. Iatrogenic multi-organ injuries should be avoided by every means possible. More attention should be paid to drug use, including indications, contraindications, therapeutic effects, and adverse reaction. Based on clinical symptoms, signs and laboratory tests, treatment strategy should be adjusted by comprehensively balancing between the advantages and disadvantages. Prognosis evaluation plays important roles in keeping abreast of the disease progress, performing the treatment actively and informing the patient’s family members effectively. It is strongly recommended that clinical doctors give intensive attention to this kind of patients in hope of accumulating experience, increasing survival rate, and improving the patient’s long-term outcome.

(Translator: GAO Lei)

高齡女性急性廣泛前壁心肌梗死合并心源性休克死亡1例

1 病例摘要

患者因“發(fā)作性胸痛伴惡心嘔吐15h ”收入解放軍總醫(yī)院老年心血管病研究所病房。2011年8月14日3:00患者無(wú)明顯誘因出現(xiàn)明顯胸痛, 伴惡心、嘔吐、大汗、四肢濕冷, 無(wú)意識(shí)喪失, 18:00就診于我院急診, 心電圖提示胸前導(dǎo)聯(lián)ST段抬高, 心肌損傷標(biāo)志物明顯成比例升高。患者既往高血壓病史10年, 目前控制不佳; 慢性支氣管炎病史多年; 1個(gè)月前發(fā)生腦梗死; 入院前一天腹瀉。既往無(wú)吸煙、飲酒、違禁藥物應(yīng)用史。

入院查體: 體溫36.5℃, 血壓90/70 mmHg, 雙肺呼吸音清, 雙肺底可聞及少量濕性啰音。心率133次/min, 心音低鈍, 胸骨左緣第二肋間可聞及2-3/6級(jí)舒張期雜音, 雙側(cè)足背動(dòng)脈搏動(dòng)減弱。超聲心動(dòng)圖提示: 左室射血分?jǐn)?shù)（left ventricular ejection fraction, LVEF）43%, 室間隔中段至心尖段、左室前壁、側(cè)壁運(yùn)動(dòng)減弱, 室壁變薄, 心尖部室壁瘤形成, 矛盾運(yùn)動(dòng), 未見明顯心包積液。胸片提示雙肺炎癥。

考慮急性前壁ST段抬高型心肌梗死、心源性休克診斷明確, 急診行主動(dòng)脈內(nèi)氣囊泵療法（intra-aortic balloon bumping, IABP）和經(jīng)皮冠脈介入術(shù)（percutaneous coronary intervention, PCI）。造影提示前降支發(fā)出第一對(duì)角支后完全閉塞, 未見側(cè)枝供應(yīng), 第一對(duì)角支開口受累, 局限性狹窄90%, 回旋支未見明顯狹窄, 右冠彌漫性病變?？紤]前降支為罪犯血管, 于前降支近中段狹窄處植入支架1枚。

術(shù)后予抗血小板、抗凝、擴(kuò)冠、調(diào)脂、改善肝、腎功能、抗感染、解痙平喘、營(yíng)養(yǎng)支持等治療, 間斷利尿, 多巴胺持續(xù)泵入維持血壓?？紤]患者心功能差, 心率快, 頻發(fā)室性早搏, 予間斷西地蘭靜脈推注、胺碘酮靜脈滴注。2011年8月16日因反復(fù)急性左心衰發(fā)作, 雙肺感染、肝功能不全、腎功能不全, 行氣管插管、呼吸機(jī)輔助呼吸, 增加硝普鈉泵入改善外周循環(huán)及降低后負(fù)荷, 停用胺碘酮, 升級(jí)抗生素, 并嚴(yán)格控制出入量, 肝腎功能有所恢復(fù), 呼吸機(jī)脫機(jī)訓(xùn)練順利, 心功能好轉(zhuǎn)。查血小板計(jì)數(shù)出現(xiàn)一過(guò)性下降, 考慮不排除IABP球囊對(duì)血小板的機(jī)械性損傷。綜上所述, 8月22日、8月24日先后拔除氣管插管、IABP, 患者呼吸頻率快, 持續(xù)低血壓狀態(tài), 大劑量多巴胺無(wú)法維持, 26日凌晨發(fā)生急性左心衰并出現(xiàn)交界區(qū)心律伴頻發(fā)室早, 進(jìn)入深昏迷, 考慮患者存在洋地黃中毒, 查血漿地高辛藥物濃度＞4ng/dl, 予立即停用洋地黃類藥物, 二次行氣管插管及IABP, 同時(shí)給予腎上腺素、大劑量多巴胺、去甲腎上腺素等血管活性藥物治療, 并碳酸氫鈉糾正酸中毒后病情逐漸平穩(wěn), 神志恢復(fù)。9月6日至16日間反復(fù)嘗試呼吸機(jī)脫機(jī)失敗, 降低IABP反搏比例后患者血壓不能維持, 且發(fā)生肝素誘導(dǎo)性血小板減少, 稽留高熱, 肺部感染加重, 頻發(fā)室早, 病情持續(xù)危重狀態(tài)。2011年9月17日19:00患者突然出現(xiàn)血氧飽和度下降至50%～70%, 心率140～150次/min, 血壓70/50mmHg, 給予100%純氧吸入, 腎上腺素、碳酸氫鈉注射液等藥物救治。家屬拒絕行心肺復(fù)蘇、電除顫等有創(chuàng)搶救措施, 19: 40呼吸心跳停止, 醫(yī)治無(wú)效死亡。

2 臨床病理討論

侯允天副主任醫(yī)師: 患者主要診斷明確為急性前壁ST段抬高型心肌梗死, 心源性休克。就醫(yī)時(shí)間晚, 高齡, 合并肝、腎功能不全及肺部感染等多臟器功能不全, 病情危重, 死亡風(fēng)險(xiǎn)極高。治療過(guò)程中存在以下問(wèn)題: （1）洋地黃中毒?；颊咝墓δ艿拖? 心率快, 頻發(fā)室性期前收縮, 予口服地高辛及間斷西地蘭靜脈推注, 洋地黃類藥物劑量大, 應(yīng)監(jiān)測(cè)血藥濃度。心電監(jiān)護(hù)提示交界區(qū)心律, 應(yīng)高度懷疑洋地黃中毒可能, 搶救中判斷準(zhǔn)確, 處理果斷。（2）感染?；颊咝脑葱孕菘?、長(zhǎng)期臥床、營(yíng)養(yǎng)狀況差、咳痰無(wú)力、氣管插管、既往慢性支氣管炎病史等, 均增加肺部感染的可能性, 同時(shí)長(zhǎng)期IABP、大靜脈置管、留置尿管又存在導(dǎo)管相關(guān)性感染風(fēng)險(xiǎn)?？股剡x用時(shí)應(yīng)注意結(jié)合體溫、血象、胸片、體征, 特別是痰培養(yǎng)結(jié)果來(lái)判斷, 同時(shí)注意同種抗生素應(yīng)用時(shí)間。

薛橋副主任醫(yī)師: 多臟器功能衰竭是心肌梗死伴心源性休克患者治療中的常見問(wèn)題, 主要分為病程進(jìn)展引起的臟器功能損傷和醫(yī)源性臟器功能損傷。本病例中, 患者入院前已發(fā)生心源性休克, 持續(xù)低血壓狀態(tài)數(shù)小時(shí), 多器官灌注嚴(yán)重不足, 表現(xiàn)為面色蒼白、四肢濕冷、末梢動(dòng)脈搏動(dòng)弱、肝淤血、肺淤血、腎功能不全, 均提示患者基礎(chǔ)臟器功能差, 預(yù)后不良。醫(yī)源性肝功能損害、急性腎損傷、洋地黃中毒、肝素誘導(dǎo)血小板減少更應(yīng)引起臨床醫(yī)生高度重視。造成肝功能損害的原因包括既往基礎(chǔ)肝病、心功能不全、充血性/缺血性肝病以及藥源性肝功能損害, 如靜脈應(yīng)用胺碘酮。急性腎功能損害除了低灌注造成的腎前性急性腎功能損害外, 還應(yīng)考慮冠脈造影及支架植入術(shù)中造影劑對(duì)腎臟功能的影響。反復(fù)發(fā)作急性左心衰的患者口服及靜脈應(yīng)用大量洋地黃類藥物, 應(yīng)警惕洋地黃中毒發(fā)生, 及時(shí)觀察臨床癥狀、心電圖變化及監(jiān)測(cè)地高辛濃度。PCI術(shù)后心功能不全且應(yīng)用IABP的患者血小板減少, 可能與肝素大量應(yīng)用致肝素誘導(dǎo)血小板減少或IABP球囊對(duì)血小板的機(jī)械性破壞有關(guān)。本例患者IABP拔除期間未見明顯血小板計(jì)數(shù)變化, 而用阿加曲班代替肝素后血小板計(jì)數(shù)明顯回升, 考慮應(yīng)為肝素誘導(dǎo)血小板減少。

趙玉生主任醫(yī)師: 急性心肌梗死合并心功能不全患者提示預(yù)后不良的的危險(xiǎn)因素包括有高齡、肺部感染、肝腎功能不全、心肌損傷面積大、存活心肌數(shù)目少、射血分?jǐn)?shù)低下、多種心肌梗死機(jī)械并發(fā)癥、既往腦血管意外病史等。該患者高齡, 性格急躁, 急性心肌梗死面積大, 心肌損傷嚴(yán)重, 心功能差, 加之血管再通延遲時(shí)間較長(zhǎng), 雙肺感染、肝腎功能不全, 使該患者危險(xiǎn)評(píng)分極高, 院內(nèi)死亡可能極高, 預(yù)后差, 且患者在治療中存在多個(gè)矛盾, 為臨床治療帶來(lái)困難。在IABP拔除問(wèn)題上, 一方面始終不能耐受IABP拔除, 提示心肌頓抑嚴(yán)重, 心功能恢復(fù)緩慢, 另一方面雙肺炎癥持續(xù)存在, 隨時(shí)可能發(fā)生導(dǎo)管相關(guān)性感染, 使拔除時(shí)間難以確定。在持續(xù)心源性休克狀態(tài)血壓的調(diào)整問(wèn)題上, 如擴(kuò)容升壓則加重心衰, 反之, 則血容量不足心功能減退。在外周灌注的問(wèn)題上, 大劑量多巴胺的強(qiáng)烈縮血管作用可升壓, 但導(dǎo)致肝、腎等臟器及四肢供血不足, 增加應(yīng)用硝普鈉可改善周圍組織器官灌注, 減輕后負(fù)荷, 但其強(qiáng)大的降壓作用使維持血壓成為困難。以上治療矛盾增加了治療難度, 提高了患者不良預(yù)后風(fēng)險(xiǎn)。

總之, 急性心肌梗死合并心源性休克的患者預(yù)后差, 風(fēng)險(xiǎn)高。治療過(guò)程中應(yīng)針對(duì)多臟器功能衰竭進(jìn)行一體化治療, 盡量避免醫(yī)源性臟器功能損傷。嚴(yán)格掌握用藥適應(yīng)證及禁忌證, 觀察藥物療效及不良反應(yīng)。面對(duì)治療矛盾, 多角度權(quán)衡利弊, 根據(jù)癥狀、體征及輔助檢查結(jié)果精細(xì)調(diào)整治療方案。而重視患者預(yù)后風(fēng)險(xiǎn)評(píng)估, 有助于掌握病情進(jìn)展、積極治療及更好地與患者家屬溝通。臨床醫(yī)生應(yīng)高度重視此類患者的診治, 不斷積累經(jīng)驗(yàn), 提高生存率并改善遠(yuǎn)期預(yù)后。

（參加討論醫(yī)師: 候允天, 薛 橋, 趙玉生)

（高 磊整理）

（編輯: 王雪萍）

拓西平, Tel:021-55786628, E-mail: xptuo@hotmail.com

2009-12-11;

2010-10-12

R542.2+2

A

10.3724/SP.J.1264.2012.00016