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Bradycardia in a Patient with Anaphylactic Shock: Case Report

過敏性休克合併心搏過慢:一病例報告

摘要


過敏性休克為組織胺所造成血管擴張及通透性增加使然的一種分佈性休克,心搏加速為休克初期的徵兆而心搏過慢於過敏性休克極為罕見。一位78歲的女性因誤食蝦類引發而引發過敏性休克並合併心搏過慢。此病患平時有服用貝他阻斷劑而其後所接受的心肌掃描亦顯示可逆性的心肌缺血現象。此病患經過積極地急救後出院無任何後遺症。於過敏性休克的病患發生心搏過慢現象似為多重因素,可能的機轉包括有組織胺或低血壓造成的一過性的竇房結缺血,Benzoid-Jarish氏反射及接受貝他阻斷劑的治療等。病患若是呈現休克合併心搏過慢的情況應積極地予以腎上腺素、阿托平、強心劑/血管收縮劑及輸液等治療,昇糖素應用於beta-blocker過量之病患。若於休克的病患發生心搏過慢的現象,特別是合併有嚴重的過敏反應、冠心症及使用貝他阻斷劑者,應予以特別的注意。

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並列摘要


Anaphylactic shock, as a kind of distributive shock, is considered as a consequence of histamine induced vasodilatation with increased vascular permeability. Tachycardia is the early warning sign of shock and bradycardia is a rare manifestation of shock. A 78 year-old woman presented with shrimpinduced anaphylactic shock with bradycardia. She was treated by beta-blocker currently and further Thalium-201 myocardial scan showed reversible myocardial ischemia. She had full recovery after aggressive resuscitation and discharged without any sequelae. The causes of developing bradycardia in patients with anaphylactic shock maybe multifactorial involving hypotension or histamine induced transient SA node ischemia, Benzoid-Jarish reflex, and concurrent beta-blocker usage. Prompt management with epinephrine, atropine, inotropic/vasopressor agents and intravenous fluid resuscitation is mandatory. Glucagon should be considered if there is a concern of concurrent beta-blocker intoxication. Bradycardia developed during shock status, particular in patients with severe allergic reaction, coronary artery disease and current beta-blocker usage worth particular attention.

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