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Th e fi rst ever World Sepsis Day (WSD), a great opportunity to increase awareness about sepsis, is going to be held on Sept. 13. We already have World Diabetes Day, Breast Cancer Awareness Day, World Asthma Day, World AIDS day, even a Rare Disease Day, so why not a day dedicated especially to sepsis? After all, sepsis is estimated to aff ect at least 18 million individuals worldwide, and with mortality rates of 25% to 30% [1,2], severe sepsis kills more individuals annually than prostate cancer, breast cancer, and HIV/AIDS combined, and the numbers of cases are increasing every year. Yet it is a condition that is poorly understood by those outside of medicine. Almost 90% of the public have never even heard of sepsis, and of those who have, less than 60% realize it is a leading cause of death But if the condition is diagnosed early and managed appropriately, lives can be saved.
Phosphorus is a mineral element essential to cellular function. The prevalence of hypophosphatemia is particularly high in critically ill patients. Hypophosphatemia may be the result of increased renal excretion, reduced digestive absorption, intracellular shift accompanied or not by depletion of the total phosphorus pool, and extreme catabolic states. Clinical manifestations are especially apparent in severe hypophosphatemia and include impairments of the respiratory, musculo-skeletal, pulmonary, and neurological systems. Hypophosphatemia must be corrected, especially if it is severe and symptomatic.
Recent reports have suggested that increases in venoarterial difference in PCO2 (VAPCO2) and arteriovenous difference in pH (AVpH) represent valuable markers of tissue hypoxia in shock states associated with low cardiac output. We compared the values of VAPCO2 and AVpH with that of blood lactate in their relationship to changes in O2 uptake (VO2) and O2 delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade. In 13 anesthetized and mechanically ventilated dogs, a catheter was inserted into the pericardium to inject saline and to measure the intrapericardial pressure. VO2 was derived from expired gas analysis. DO2 was calculated by the product of the thermodilution cardiac index and the arterial O2 content. The critical DO2 (DO2crit) was found at 9.9 +/- 1.8 ml/kg.min. VAPCO2 and AVpH, which were 7.1 +/- 4.6 mm Hg and 0.028 +/- 0.025 U, respectively, at baseline, progressively increased to reach 17.5 +/- 6.6 mm Hg and 0.114 +/- 0.054 U, respectively, at DO2crit (both p < 0.01). Below DO2crit they increased more dramatically. These changes were related to both arterial hypocapnia and mixed venous hypercapnia. CO2 excretion decreased from 5.8 +/- 2.0 ml/kg-min at baseline to 3.9 +/- 0.9 ml/kg.min at DO2crit (p < 0.01). End-tidal CO2 tension significantly fell below DO2crit. Lactate levels increased from 2.1 +/- 0.5 to 3.5 +/- 0.5 mmol/L at DO2crit (P < 0.01) and to 6.9 +/- 2.1 mmol/L (p < 0.01) at the end of the study. There was no statistically significant difference between the DO2crit calculated for VAPCO2, AVpH, lactate, or VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
The determination of oxygen consumption (VO2) in critically ill patients is useful to evaluate metabolic expenditure, to calculate cardiac output and to assess the adequacy of oxygen supply to the tissues by the relationship between oxygen delivery (DO2) and VO2. Only the last application requires a high degree of accuracy in measurement. Highly accurate devices have been developed over the last few years although there are still problems with their use during spontaneous ventilation, mechanical ventilation with high FiO2, and treatment with inhaled nitric oxide (NO). Due to Haldane's transformation and the body's large CO2 stores, VO2 should only be measured in steady-state conditions, avoiding changes in ventilatory conditions or cardiac output. Air leaks should be carefully avoided since measurements would be erroneous. There is generally good agreement between Fick-derived VO2 and VO2 obtained by indirect calorimetry; discrepancies between the two methods in the study of changes in VO2 in response to changes in DO2 could be due to errors in both techniques. There is no strong evidence that mathematical coupling of data alone can account for VO2/DO2 dependency, which can sometimes be observed in critically ill patients.
