[Decrease in the metabolic activity of the severely ill patient. A strategy for energy conservation?].
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Biomedical subjects
Publications and source records attributed to M A Jorge.
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PURPOSE: Previous studies have compared the relationship between directly measured values for cardiac output, systemic oxygen consumption (VO2), and arteriovenous oxygen difference (D(A-v)O2) with those calculated by the Fick principle. However, the validity of Fick's principle in critically ill patients undergoing physiologic changes and pharmacologic interventions is unknown. The purpose of our study was to compare directly measured values for hemodynamic and oxymetric variables with those calculated by the Fick equation in patients with acute myocardial infarction, at baseline and after the hemodynamic changes produced by pharmacologic interventions. PATIENTS AND METHODS: Cardiac output, (VO2), and (D(A-v)O2) were measured in 33 patients with acute myocardial infarction, at baseline (50 +/- 30 hours after the onset of symptoms) and after pharmacologic intervention to relieve pulmonary congestion. These values were then compared with indirect values derived from the Fick equation. RESULTS: High and significant correlations were found between thermodilution and Fick-derived cardiac output at baseline (r = 0.91, p less than 0.001) and post-intervention (r = 0.92, p less than 0.001). Similarly, VO2 values measured by expired gas analysis showed a significant correlation with VO2 calculated by the Fick principle, at baseline (r = 0.85, p less than 0.001) and post-intervention (r = 0.84, p less than 0.001). Lastly, when D(A-v)O2 of arterial and mixed venous samples was measured by spectrophotometry and compared with calculated values, there was a significant correlation at baseline (r = 0.85, p less than 0.001) and after intervention (r = 0.85, p less than 0.001). Analysis of variance revealed no difference between measured and calculated values for the three variables under those two conditions. CONCLUSION: In patients with acute myocardial infarction, cardiac output, VO2, and D(A-v)O2 indirectly calculated by the Fick principle are equivalent to directly measured values, despite the various degrees of hemodynamic dysfunction and the currently used therapeutic interventions.
Oxygen delivery (DO2) and related variables were studied in eight dogs during severe untreated peritonitis induced by cecal ligation and perforation. The development of peritonitis was accompanied by abdominal fluid sequestration and significant increases in hemoglobin (Hgb), arterial oxygen content (CaO2), and P50. Changes in mixed venous PO2 (P-vO2), mixed venous saturation (S-vO2), DO2, oxygen uptake (VO2), cardiac index (CI), and arteriovenous O2 difference (C[a--v]O2) were not significant. When blood volume was returned to normal levels with dextran, CI rose and C(a--v)O2 decreased; P-vO2 increased and Hgb returned to baseline levels. In this animal model, sepsis and fluid sequestration produced an increase in blood O2 capacity and CaO2, which sustained DO2 and VO2. No changes were observed in P-vO2 or S-vO2. The hyperdynamic state of severe sepsis became evident only after reversing hemoconcentration by colloid infusion. The increase in P-vO2 and S-vO2 after volume loading is possibly related to primary septic mechanisms and/or to changes in DO2.
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