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J Thorac Cardiovasc Surg 1994;107:527-0535
© 1994 Mosby, Inc.
Cardiopulmonary Bypass, Myocardial Management, and Support Techniques |
Minneapolis, Minn.
Supported by the 20th American College of Surgeons Scholarship (J.W.B.); National Research Service Awards HL 07259-02 and HL 06964-02 (J.W.B and T.P.B) from the National Institutes of Health; American Heart Association, Minnesota Affiliate Research Fellowship (T.J.L.); and grants from the Minnesota Medical Foundation; the American Heart Association, Minnesota Affiliate; and the National Institutes of Health (HL 22152-05).
Presented at the C. Walton Lillehei Surgical Symposium, Minneapolis, Minn., Oct. 21-22, 1988.
Received for publication Nov. 10, 1989. Accepted for publication July 20, 1993. Address for reprints: J. W. Blatchford III, MD, Division of Thoracic and Cardiovascular Surgery, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235-8879.
Abstract
The effects of cardiopulmonary bypass and cardioplegic arrest on left ventricular systolic and diastolic function were studied in 20 intact neonatal lambs instrumented with ultrasonic dimension transducers and micromanometers for collection of left ventricular pressure-dimension data. Group I lambs underwent 2 hours of hypothermic cardiopulmonary bypass (25° C) alone; group II lambs underwent 2 hours of hypothermic cardiopulmonary bypass (25° C) with 1 hour of multidose, cold, crystalloid cardioplegic arrest (St. Thomas' Hospital No. 2 solution). The control neonatal lamb left ventricle was found to be relatively stiff, with the limit of diastolic filling reached at physiologic left ventricular filling pressures, resulting in apparent descending limbs of left ventricular function. After cardiopulmonary bypass, identical results were obtained in groups I and II. A significant loss of left ventricular compliance limited left ventricular performance via two mechanisms. First, left ventricular preload was significantly decreased, with a concomitant diminution in left ventricular stroke work; afterload (pressure work) was maintained at the expense of volume work (flow), which declined significantly. Second, preload behaved as though fixed, resulting in a loss of impedance matching (afterload mismatch). Although contractility as assessed by the end-systolic pressure-dimension relationship was significantly increased (because of increased levels of circulating catecholamines), global systolic performance as quantified by the stroke work/end-diastolic length relationship remained unchanged, reflecting the afterload sensitivity of the latter parameter in the face of fixed preload. We conclude that cardiopulmonary bypass in the intact neonate results in a loss of compliance and impedance matching rather than a loss of contractility; however, the addition of 1 hour of cold, crystalloid cardioplegic arrest results in no dysfunction beyond that attributable to cardiopulmonary bypass alone. (J THORAC CARDIOVASC SURG 1994;107:527-35)
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