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題名 | Acute Respiratory Distress Syndrome after Early Successful Primary Percutaneous Coronary Intervention Therapy in Acute Myocardial Infarction: A Case Report=急性心肌梗塞的病人在接受早期成功的緊急心導管介入術治療後發生急性呼吸窘迫徵候群 |
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作者 | 蘇河名; 溫文才; 林宗憲; 朱志生; 許勝雄; 賴文德; | 書刊名 | The Kaohsiung Journal of Medical Sciences |
卷期 | 21:2 民94.02 |
頁次 | 頁78-83 |
分類號 | 415.3161 |
關鍵詞 | 急性呼吸窘迫徵候群; 急性心肌梗塞; 緊急心導管介入術; Acute respiratory distress syndrome; Acute myocardial infarction; Primary percutaneous coronary intervention; |
語文 | 英文(English) |
中文摘要 | 急性呼吸窘迫徵候群的特徵就是喘、兩側瀰漫性的肺部浸潤、低的肺部楔形壓和血氧濃度比上給氧分壓小於 200 毫米汞柱。在血栓溶解治療前期,急性心肌梗塞不論是否併發心跳停止、心因性休克或低血壓均被報告過是急性呼吸窘迫徵候群的病因之一。在血栓溶解治療期,也有二篇急性心肌梗塞病人併發急性呼吸窘迫徵候群的報告,只不過其病因歸因於血栓溶解劑所引起的過敏反應而不是急性心肌梗塞所引發的血行動力學變化所致。在緊急心導管介入術的治療期,急性心肌梗塞的病人在接受早期成功的緊急心導管介入術治療後發生急性呼吸窘迫徵候群的案例,尚未被報告過。這裡我們報告一位 61 歲的男性病人,因持續性的胸痛而被診斷為 Killip 二級的 ST節段上升的前壁急性心肌梗塞。他在胸痛 2.5 小時後接受緊急心導管介入術,並成功地打通其梗塞的血管。但不幸地,在住院的第三天,病人喘 (呼吸速率 33 下/分鐘)、發燒 (38.5。)、白血球升高和胸部 X 光顯示為兩側瀰漫性的肺部浸潤。那時,肺部楔形壓只有 8 毫米汞柱再加上其血氧濃度比上給氧分壓也只有 160 毫米汞柱而被診斷為急性呼吸窘迫徵候群的病人。在這個病人身上,並沒有常見會發生急性呼吸窘迫徵候群的病因像感染、嗆到、外傷和藥物不良反應等被發現。我們推測急性心肌梗塞本身所引發的全身性的發炎反應是引發這次急性呼吸窘迫徵候群的主因。這也暗示急性心肌梗塞本身可能是引發急性呼吸窘迫徵候群的病因之一。 |
英文摘要 | Acute respiratory distress syndrome (ARDS) is characterized by acute-onset dyspnea, diffuse bilateral pulmonary infiltration, low pulmonary capillary wedge pressure (PCWP), and an arterial oxygen tension/inspired oxygen fraction (PaO2/FiO2) ratio of less than 200 mmHg. Acute myocardial infarction (AMI), whether complicated by circulatory arrest, cardiogenic shock, and hypotension or not, was reported as an etiologic factor in the development of ARDS in the prethrombolytic era. In the thrombolytic era, two cases of AMI complicated with ARDS have been reported. ARDS in these two patients resulted from anaphylactic reaction to the thrombolytic agent and not from the hemodynamic consequences of AMI. Development of ARDS during the AMI period has not been reported after early successful primary percutaneous coronary intervention (PCI). Herein, we report a 61-year-old male patient with persistent chest pain who was diagnosed with Killip II anterior ST-segment elevation AMI. He was treated successfully with primary PCI 2.5 hours after the onset of chest pain. Unfortunately, on the third hospital day, acute-onset dyspnea (respiratory rate, 33 beats/min), fever (38.5°C), leukocytosis (white blood cell count, 18,360/microliter), and diffuse bilateral pulmonary infiltration were noted. ARDS was diagnosed from the low PCWP (8 mmHg) and a PaO2/FiO2 of less than 200 mmHg (160 mmHg). No usual causes of ARDS such as infection, aspiration, trauma, shock, or drug reactions were noted. We assumed that, in this particular patient, the systemic inflammatory response syndrome frequently induced by AMI might have caused this episode of ARDS. This may imply that AMI itself is a possible etiology of ARDS. |
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