The effects of hypoxic acidemia on left ventricular end-systolic elastance in fetal sheep.

Using the conductance catheter technique, we measured the effects of hypoxic acidemia on left ventricular end-systolic elastance in anesthetized, 133-d gestation, in utero fetal sheep (n = 7). Conductance and Millar catheters were introduced into the left ventricle through a carotid artery cutdown. Fetuses were rendered progressively hypoxic and acidemic by placental embolization with repeated injections of 5 x 10(5) 50-microns plastic spheres every 15 min via a catheter placed in the fetal abdominal aorta. We recorded pressure-volume data and arterial blood gases at 15-min intervals. End-systolic elastance was computed using a single-beat method of extrapolating maximum isovolumic pressure. A mean of five boluses was required to cause fetal death. Placental embolization caused progressive fetal acidemia. Mean baseline fetal arterial pH was 7.32 +/- 0.06 (mean +/- SD) and gradually decreased with embolization (p < 0.0001). A linear relationship was found to exist between elastance and pH with a mean decrease of 0.46 kPa/mL per 0.1-unit drop in pH (r = 0.96; p < 0.0001). Despite the decrease in end-systolic elastance, stroke volume and left-ventricular output were maintained due to a parallel decrease in afterload. The decrease in end-systolic elastance was gradual and extended over the entire clinically important range of pH, rather than being a terminal event. This study, which, to our knowledge, is the first to use the conductance catheter to measure fetal left ventricular function demonstrates that hypoxic acidemia adversely affects myocardial contractility assessed by end-systolic elastance.