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Ann Thorac Surg 2003;76:S2220-S2223
© 2003 The Society of Thoracic Surgeons
a Harrison Department of Surgical Research, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
* Address reprint requests to Dr Edmunds, Department of Surgery, 5000 Ravdin Court, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104-4283, USA
e-mail: hank.edmunds@uphs.upenn.edu
Presented at the symposium, "Gibbon & His Heart-Lung Machine: 50 Years & Beyond," Philadelphia, PA, May 2, 2003.
| The first 300 words of the full text of this article appear below. |
In July 1934 John and Mary Gibbon started to create, build, and test the first extracorporeal perfusion circuit using ingenuity, tenacity, assorted laboratory paraphernalia, and newly available heparin [1]. Much hard work, animal studies, and steady refinements finally produced the IBM machine, which was used May 6, 1953, to successfully close a large atrial septal defect in a young woman [2]. The door of opportunity opened but much more was needed before heart surgery became safe and effective.
The first decade after John Gibbon's triumph was spent learning about the pathologic anatomy of the heart; how to make an accurate diagnosis during life; how to stop, start, incise, suture, and patch the heart; what to monitor and how to do it; refining the heart-lung machine; creating new hardware; manipulating oxygen supply and demand by changing flows, temperature, and hematocrit; and finding materials compatible with blood. The goal was survivors and the means were trial and error. Surgeons and cardiologists learned from their mistakes and nobody paid any attention to annoying hemolysis or thrombocytopenia that seemed unrelated to success or failure.
In 1960 Jim Maloney's group at the University of California, Los Angeles, raised an alarm in a presentation documenting denatured plasma proteins and fat emboli produced by bubble oxygenators [3]. Subsequent studies verified the production of fat and fibrin emboli and identified the bubble oxygenator as the source of countless gas emboli [4]. Autopsies showed fibrin and fat emboli in brains of the dead (Fig 1) and tests showed neurocognitive deficits in the living [5, 6]. Despite huge doses of heparin it became apparent that blood was not compatible with the heart-lung machine.
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