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P Pu ur rp po os se e: : To report and discuss a case of fetal bradycardia in a parturient under anesthesia for cholecystectomy despite normal maternal oxygenation and arterial blood pressure.C Cl li in ni ic ca al l f fe ea at tu ur re es s: : A 27-yr-old woman (gravida 2 para 1), with a fetus of 34 weeks gestation, received general anesthesia for cholecystectomy. After anesthesia induction and tracheal intubation, anesthesia was maintained with oxygen, sevoflurane and iv remifentanil infusion. While preparing for surgery, the fetal heart rate decreased within about half a minute to 70 beats·min -1 and remained at that level. The maternal blood pressure, heart rate and oxygen saturation were normal. An emergency Cesarean delivery was performed. The infant had Apgar scores of 1 at one minute, 5 at five minutes, 7 at ten minutes and required resuscitation after birth.C Co on nc cl lu us si io on n: : Ideally, women having non-obstetric surgery during the third trimester of pregnancy will have intraoperative fetal heart rate monitoring. S many as 2% of pregnant women undergo non-obstetric surgery during pregnancy 1 and cholecystectomy is one of the common surgical procedures performed. Pancreatitis and cholecystitis can complicate cholelithiasis and lead to significant maternal and fetal morbidities. Some surgeons, therefore, advocate cholecystectomy during pregnancy rather than delaying surgery until delivery has occurred. 2 One of the controversies in anesthesia for a pregnant patient having non-obstetric surgery is intraoperative fetal heart rate monitoring. A recent review on anesthesia for pregnant patients having non-obstetric surgery and obstetric anesthesia textbooks recommended fetal heart rate monitoring during anesthesia and surgery whenever possible. [3][4][5] Some obstetricians believe that the fetus would not be compromised as long as maternal oxygenation and circulation remain normal. Horrigan et al. 6 suggested that fetal monitoring by obstetric personnel was unnecessary during surgery in pregnant patients. We report a case of fetal bradycardia in a parturient under anesthesia for cholecystectomy despite normal maternal oxygenation and arterial blood pressure. Objectif : Présenter un cas de bradycardie foetale chez une parturiente sous anesthésie pour cholécystectomie malgré l'oxygénation et la tension artérielle maternelles normales.

ABSTRACT. To evaluate the central hemodynamic and regional blood flow changes associated with right ventricular hypertension in the newborn, 13 anesthetized, mechanically ventilated piglets less than 3 d old were acutely instrumented to permit measurements of central vascular pressures, cardiac output, and regional blood flow (radiolabeled microsphere technique). After initial measurements, right ventricular afterload was progressively increased by means of a pulmonary arterial mechanical occluder until right-to-left foramen ovale shunt was observed. An increase in pulmonary arterial pressure from 32 ± 2 to 55 ± 3 mm Hg was associated with a decrease in Pac>2 from 364 ± 16 to 88 ± 9 mm Hg and an increase in the shunt fraction from 13 ± 1 to 28 ± 1% {p < 0.01) during ventilation with oxygen. Right ventricular hypertension induced a significant decrease in systemic arterial pressure from 79 ± 3 to 63 ± 4 mm Hg, and left ventricular cardiac output from 156 ± 10 to 112 ± 11 mL • min" 1 • kg" 1 (p < 0.01), likely secondary to a reduction in left ventricular compliance. Oxygen delivery to the brain and heart were unaffected, due to a substantial increase in regional blood flow, but a significant reduction in delivery to the bowel and kidneys were observed. Contrary to what has been reported in the adult, myocardial blood flow to the right ventricle increased during hypertension. Metabolic acidosis was seen in all animals and the changes in serum bicarbonate and whole body oxygen consumption were directly related to the magnitude of decline in systemic O2 delivery. In conclusion, right ventricular hypertension with right-toleft foramen ovale shunt is associated with a significant reduction in systemic arterial pressure and left ventricular cardiac output in the newborn. These changes coupled with a further decrease in arterial oxygen content secondary to the increase in shunt fraction, place the newborn animal with right ventricular hypertension at great risk for hypoxic-ischemic organ injury. Because the left and right ventricles are anatomically and functionally related, an increase in the ventricular afterload in one compartment will perturb the function of the other ventricle. RVH in adult subjects is associated with a significant reduction in PSA and left ventricular output (1). These changes are related not only to the decrease in left ventricular preload, accounted for by the reduced Qp, but also to an impairment in left ventricular systolic function (2).During the immediate neonatal period, there are theoretical reasons why an increase in right ventricular afterload may not necessarily lead to the central hemodynamic changes observed in adult subjects. First, because of the higher afterload normally seen during fetal life, the right ventricle has a much larger muscle mass relative to the adult. Second, the foramen ovale is only functionally closed early in life, and an increase in right ventricular afterload sufficient to produce elevated filling pressures will lead to a right-to-left shunt at the atrial level,...

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