• Ho-Ming Su, Wen-Chol Voon, Tsung-Hsien Lin, Chih-Sheng Chu, Sheng-Hsiung Sheu, and Wen-Ter Lai.
• Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
• Kaohsiung J Med Sci. 2005 Feb 1; 21 (2): 78-83.

AbstractAcute 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 degrees C), leukocytosis (white blood cell count, 18,360/microL), 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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