PROSTAGLANDIN METABOLISM AND PULMONARY VASCULAR RESPONSE TO CHANGES IN PC02 IN INFANTS

Abstract

We examined the effects of graded changes in arterial pH and PCO2 on pulmonary and systemic hemodynamics and on thromboxane and prostacyclin metabolism in 15 infants following repair of their congenital heart disease. Right and left atrial, pulmonary and radial artery catheters were placed intraoperatively with a pulmonary artery (PA) thermistor for measurement of thermodilution cardiac index (CI). When hemodynamically stable on 40% inspired oxygen, baseline measurements, including mean airway pressures, were obtained. Ventilation was adjusted to obtain measurements at 5 levels of PCO2; PA and left atrial plasma samples were obtained for thromboxane and prostacyclin assays. Hyperventilation lowered pulmonary vascular resistance (PVRI) in 13/15 patients. Increases in pulmonary artery pressure (PAP) and PVRI occurred at elevated PCO2's in all patients (PAP>systemic in 2 patients). These changes occurred independently of thromboxane levels. Despite increases in mean airway pressure, moderate hyperventilation may decrease PVRI in the postoperative cardiac infant. Moderate hypercarbia raises PVRI and may be detrimental to ventricular performance.