OBJECTIVE: The objective of this study was to describe the effects of altering arterial PCO2 and pH on pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery. DESIGN: Prospective study (with each patient as his or her own control). SETTING: Cardiac intensive care unit in a children's hospital. PATIENTS: We studied 15 infants (ages ranging from 0.4 to 15.6 months; median 5.7) who were mechanically ventilated during the immediate postoperative period after corrective cardiac surgery. INTERVENTIONS: The study was designed to have the following three stages: In the baseline stage, the initial postoperative hemodynamic parameters were stabilized and body temperature was normalized. In the hypercarbia stage, with FIO2 at 0.40, the rate of ventilation was decreased to produce an end-tidal CO2 level of > 55 torr (> 7.3 kPa). This stage established a clinical model of increased pulmonary vascular resistance. With the minute ventilation held constant in order to maintain a constant PaCO2, the arterial pH was increased by administration of a 4-mEq/kg iv dose of sodium bicarbonate (sodium bicarbonate stage). Arterial blood gas and hemodynamic determinations were obtained after a 10-min stabilization period at each stage. Drug infusions were not altered during the study period. MEASUREMENTS AND MAIN RESULTS: In the hypercarbia stage (stage 2), the mean PaCO2 increased from 36 +/- 5 torr (4.8 +/- 0.7 kPa) (at baseline) to 55 +/- 16 torr (7.3 +/- 2.1 kPa) (p < .01). As a result, the mean arterial pH decreased from 7.48 +/- 0.05 to 7.31 +/- 0.03 (p < .01). During this stage, the mean pulmonary arterial pressure increased from 21 +/- 6 to 30 +/- 8 mm Hg (p < .01) but the cardiac index remained unchanged (3.7 +/- 1.2 to 3.8 +/- 1.2 L/min/m2). Pulmonary vascular resistance index increased from 4.1 +/- 2.0 to 6.0 +/- 3.1 U.m2 (p < .01). After the administration of sodium bicarbonate (stage 3), the arterial pH increased to 7.44 +/- 0.06 (p < .05), while the PaCO2 was unchanged. The pulmonary vascular resistance index decreased to 3.1 +/- 1.5 U.m2 (from 6.0 +/- 3.1 U.m2; p < .01) as a result of both a decrease in mean pulmonary arterial pressure (to 26 +/- 6 mm Hg; p < .01) and a concomitant increase in cardiac index to 5.1 +/- 1.6 L/min/m2 (p < .01). CONCLUSIONS: Increasing the arterial pH by the administration of sodium bicarbonate both lowers the pulmonary arterial pressure and increases the cardiac index, resulting in a decrease in pulmonary vascular resistance. These changes were observed without alteration in PaCO2. Metabolic alkalosis may have a role in the treatment of increased pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery.
OBJECTIVE: The objective of this study was to describe the effects of altering arterial PCO2 and pH on pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery. DESIGN: Prospective study (with each patient as his or her own control). SETTING: Cardiac intensive care unit in a children's hospital. PATIENTS: We studied 15 infants (ages ranging from 0.4 to 15.6 months; median 5.7) who were mechanically ventilated during the immediate postoperative period after corrective cardiac surgery. INTERVENTIONS: The study was designed to have the following three stages: In the baseline stage, the initial postoperative hemodynamic parameters were stabilized and body temperature was normalized. In the hypercarbia stage, with FIO2 at 0.40, the rate of ventilation was decreased to produce an end-tidal CO2 level of > 55 torr (> 7.3 kPa). This stage established a clinical model of increased pulmonary vascular resistance. With the minute ventilation held constant in order to maintain a constant PaCO2, the arterial pH was increased by administration of a 4-mEq/kg iv dose of sodium bicarbonate (sodium bicarbonate stage). Arterial blood gas and hemodynamic determinations were obtained after a 10-min stabilization period at each stage. Drug infusions were not altered during the study period. MEASUREMENTS AND MAIN RESULTS: In the hypercarbia stage (stage 2), the mean PaCO2 increased from 36 +/- 5 torr (4.8 +/- 0.7 kPa) (at baseline) to 55 +/- 16 torr (7.3 +/- 2.1 kPa) (p < .01). As a result, the mean arterial pH decreased from 7.48 +/- 0.05 to 7.31 +/- 0.03 (p < .01). During this stage, the mean pulmonary arterial pressure increased from 21 +/- 6 to 30 +/- 8 mm Hg (p < .01) but the cardiac index remained unchanged (3.7 +/- 1.2 to 3.8 +/- 1.2 L/min/m2). Pulmonary vascular resistance index increased from 4.1 +/- 2.0 to 6.0 +/- 3.1 U.m2 (p < .01). After the administration of sodium bicarbonate (stage 3), the arterial pH increased to 7.44 +/- 0.06 (p < .05), while the PaCO2 was unchanged. The pulmonary vascular resistance index decreased to 3.1 +/- 1.5 U.m2 (from 6.0 +/- 3.1 U.m2; p < .01) as a result of both a decrease in mean pulmonary arterial pressure (to 26 +/- 6 mm Hg; p < .01) and a concomitant increase in cardiac index to 5.1 +/- 1.6 L/min/m2 (p < .01). CONCLUSIONS: Increasing the arterial pH by the administration of sodium bicarbonate both lowers the pulmonary arterial pressure and increases the cardiac index, resulting in a decrease in pulmonary vascular resistance. These changes were observed without alteration in PaCO2. Metabolic alkalosis may have a role in the treatment of increased pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery.
Authors: Manja C A Nilsson; Filip Fredén; Anders Larsson; Peter Wiklund; Maria Bergquist; Kristina Hambraeus-Jonzon Journal: Intensive Care Med Date: 2012-01-21 Impact factor: 17.440