INHIBITION OF THE FETAL STRESS-RESPONSE IMPROVES CARDIAC-OUTPUT AND GAS-EXCHANGE AFTER FETAL CARDIAC BYPASS

Cardiac bypass in late-gestation fetal lambs causes severe placental vasoconstriction, which leads to fetal death from hypoxemia and respiratory acidosis. This response can be blocked by the administration of indomethacin; however, a fatal metabolic acidosis then gradually develops in the fetus. Because the fetus is known to mount an intensive catecholamine response to stress, and because the fetal myocardium is particularly sensitive to increased afterload, we hypothesized that elevated afterload as a result of fetal stress contributes to diminished cardiac output after bypass. Twenty fetal lambs at 80% gestation underwent 30 minutes of normothermic cardiac bypass at Row rates of 200 to 500 ml/kg per minute. All ewes received general anesthesia with ketamine. In 10 fetuses general anesthesia was specifically designed not to inhibit the release of stress-related catechols (ketamine); the remaining 10 fetuses received a ''high'' (cisterna magna) total spinal anesthetic with tetracaine, to block the fetal stress response. In each anesthetic group, 5 of the 10 lambs received indomethacin. During operation, normal hemodynamics were preserved in the spinal anesthetic group. Cardiac output, placental blood flow, and arterial carbon dioxide tension were an improved relative to results in the ketamine group. When spinal anesthesia and indomethacin are both given, hemodynamics also approach normal after bypass, and gas exchange is further improved. These data suggest that the inhibition of the stress response by Spinal anesthesia improves the hemodynamic status of the fetus during operation and, in combination with indomethacin, allows maintenance of near-normal placental function after fetal cardiac bypass. Similar responses may also be possible in human fetuses with use of a high-dose narcotic technique.