PURPOSE: To assess the time course of the central venous-arterial carbon dioxide tension difference (∆PCO2)-as an index of the carbon dioxide production (VCO2)/cardiac index (CI) ratio-in stable septic shock patients receiving incremental doses of dobutamine. METHODS: Twenty-two hemodynamically stable septic shock patients with no signs of global tissue hypoxia, as testified by normal blood lactate levels, were prospectively included. A dobutamine infusion was administered at a dose of up to 15 μg/kg/min in increments of 5 μg/kg/min every 30 min. Complete hemodynamic and gas measurements were obtained at baseline, and at each dose of dobutamine. RESULTS: Dobutamine induced a significant dose-dependent increase of CI from 0 to 15 μg/kg/min (P < 0.001). Oxygen consumption (VO2) and VCO2 were progressively increased by dobutamine. These increases were more marked between 10 and 15 μg/kg/min (8.3 and 8.6 %, respectively) than between the lower doses. ∆PCO2 and oxygen extraction (EO2) significantly decreased between 0 (8.0 ± 2.0 mmHg and 43.8 ± 13.4 %, respectively) and 10 μg/kg/min of dobutamine (4.2 ± 1.6 mmHg and 28.9 ± 7.9 %, respectively), but remained unchanged from 10 to 15 μg/kg/min (5.4 ± 2.4 mmHg and 29.5 ± 8.2 %, respectively). The central venous oxygen saturation significantly (ScvO2) increased from 0 to 10 μg/kg/min and remained unchanged from 10 to 15 μg/kg/min. Time courses of ∆PCO2, ScvO2, and EO2 were linked therefore to the biphasic changes of VO2 and VCO2. CONCLUSION: ∆PCO2 is a good indicator of the change of VCO2 induced by dobutamine. Measurement of ∆PCO2, along with ScvO2 and EO2, may be presented as a useful tool to assess the adequacy of oxygen supply versus metabolic and oxygen demand.
PURPOSE: To assess the time course of the central venous-arterial carbon dioxide tension difference (∆PCO2)-as an index of the carbon dioxide production (VCO2)/cardiac index (CI) ratio-in stable septic shockpatients receiving incremental doses of dobutamine. METHODS: Twenty-two hemodynamically stable septic shockpatients with no signs of global tissue hypoxia, as testified by normal blood lactate levels, were prospectively included. A dobutamine infusion was administered at a dose of up to 15 μg/kg/min in increments of 5 μg/kg/min every 30 min. Complete hemodynamic and gas measurements were obtained at baseline, and at each dose of dobutamine. RESULTS:Dobutamine induced a significant dose-dependent increase of CI from 0 to 15 μg/kg/min (P < 0.001). Oxygen consumption (VO2) and VCO2 were progressively increased by dobutamine. These increases were more marked between 10 and 15 μg/kg/min (8.3 and 8.6 %, respectively) than between the lower doses. ∆PCO2 and oxygen extraction (EO2) significantly decreased between 0 (8.0 ± 2.0 mmHg and 43.8 ± 13.4 %, respectively) and 10 μg/kg/min of dobutamine (4.2 ± 1.6 mmHg and 28.9 ± 7.9 %, respectively), but remained unchanged from 10 to 15 μg/kg/min (5.4 ± 2.4 mmHg and 29.5 ± 8.2 %, respectively). The central venous oxygen saturation significantly (ScvO2) increased from 0 to 10 μg/kg/min and remained unchanged from 10 to 15 μg/kg/min. Time courses of ∆PCO2, ScvO2, and EO2 were linked therefore to the biphasic changes of VO2 and VCO2. CONCLUSION: ∆PCO2 is a good indicator of the change of VCO2 induced by dobutamine. Measurement of ∆PCO2, along with ScvO2 and EO2, may be presented as a useful tool to assess the adequacy of oxygen supply versus metabolic and oxygen demand.
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