A phenomenon of paradox: myocardial reperfusion injury.
Nurses who care for patients experiencing angina or myocardial infarction, receiving thrombolytics, and undergoing percutaneous transluminal coronary angioplasty or cardiac surgery should be aware of factors that contribute to myocardial reperfusion damage and dysfunction. This article reviews mechanisms identified as contributing to myocardial reperfusion injury. These include generation of oxygen free radicals, loss of antioxidant enzymes, neutrophil-initiated damage, calcium abnormalities, loss of normal adenosine triphosphate concentration, myocardial stunning, vascular endothelial and myocyte edema, hemorrhage, and reperfusion arrhythmias. This article specifically focuses on the pathophysiology of myocardial reperfusion injury and important related research.
Hudson
K F
KF
St. Mary's Medical Center, San Francisco.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000975:Antioxidants / Q000378:metabolism; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D004487:Edema / Q000503:physiopathology; D016166:Free Radical Scavengers / Q000627:therapeutic use; D005609:Free Radicals; D006470:Hemorrhage / Q000503:physiopathology; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology; D010544:Peroxidases / Q000097:blood
D000975:Antioxidants; D016166:Free Radical Scavengers; D005609:Free Radicals; D000255:Adenosine Triphosphate; D010544:Peroxidases; D002118:Calcium