PubMed · 6490177
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A Waterman. 1984. Practical fluid therapy for small animals.. https://doi.org/10.1136/inpract.6.5.143
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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.
OBJECTIVE: To investigate the hypothesis that meconium aspiration syndrome, the major hazard of meconium during labor, may be associated with superimposed fetal acute acidemia. METHODS: Umbilical artery blood gases were measured in 7816 term pregnancies with meconium in the amniotic fluid (AF) and the results were correlated with intrapartum and neonatal outcomes. RESULTS: Sixty-nine (1%) infants developed meconium aspiration syndrome and 31 (45%) of these were in association with fetal acidemia at birth. Moreover, umbilical blood gas analysis and intrapartum events suggested that the fetal acidemia linked to meconium aspiration was an acute event rather than a long-duration process, which might be expected if meconium was itself a marker of an antecedent fetal asphyxial event. CONCLUSION: Meconium in the AF may be a fetal environmental hazard when acidemia supervenes rather than solely a marker of preexisting fetal compromise leading to the release of meconium.
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