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David A. Fullerton
Robert C. McIntyre, Jr
John A. St. Cyr
Glenn J. R. Whitman
Frederick L. Grover
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Ann Thorac Surg 1996;61:696-701
© 1996 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Impact of Respiratory Acid-Base Status in Patients With Pulmonary Hypertension

David A. Fullerton, MD, Robert C. McIntyre, Jr, MD, Lyle E. Kirson, DDS, John A. St. Cyr, MD,PhD, Glenn J. R. Whitman, MD, Frederick L. Grover, MD

Department of Surgery, University of Colorado, Denver, Colorado

Accepted for publication October 19, 1995.

Background. The perioperative management of patients undergoing mitral valve replacement (MVR) with pulmonary hypertension from mitral stenosis may be complicated by increased pulmonary vascular resistance. The purpose of this study was to examine the influence of respiratory acid-base status on the pulmonary hemodynamic indices of patients with pulmonary hypertension before and after MVR.

Methods. Ten patients with pulmonary hypertension from mitral stenosis (mean preoperative systolic pulmonary artery pressure, 73 ± 8 mm Hg) undergoing MVR were studied in the operating room before and after MVR. Arterial partial pressure of carbon dioxide was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Hemodynamic data were collected as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg and decreased back to 30 mm Hg.

Results. There were no differences in mean pulmonary artery pressure or pulmonary vascular resistance before and after MVR. Before MVR, mean pulmonary artery pressure increased from 32 ± 1 mm Hg to 48 ± 1 mm Hg as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg (p < 0.05), and pulmonary vascular resistance rose from 379 ± 30 to 735 ± 40 dynes•second•cm-5 (p < 0.05). These effects on mean pulmonary artery pressure and pulmonary vascular resistance were not different after MVR.

Conclusion. Respiratory acid-base status has a profound impact upon pulmonary vascular resistance in patients with pulmonary hypertension from mitral stenosis undergoing MVR. This impact persists in the immediate postoperative period. We conclude that respiratory acidemia should be avoided in these patients, whereas respiratory alkalemia may be used to help minimize pulmonary vascular resistance.




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