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The abnormal dependence of O2 uptake (VO2) on O2 delivery (QO2) during severe sepsis, and the adult respiratory distress syndrome (ARDS) may be caused by impaired vascular reactivity, following release of vasodilating prostaglandins. Infusion of these compounds, however, may improve tissue oxygenation. We studied the effect of vasodilating prostaglandin E1 (PGE1; 0.2 microgram/kg/min) on the critical O2 extraction ratio (ERO2c) and the critical QO2 (QO2c) in a saline-controlled, crossover study in 12 barbiturate-anesthetized pigs. QO2, VO2 (independently from QO2), and blood lactate concentrations were measured during graded cardiac output reductions by incremental positive end-expiratory pressure (0-20 cm H2O PEEP, raised by 5 cm H2O at 15 min intervals). At 0 cm H2O PEEP, PGE1 decreased arterial blood pressure, mainly due to a fall in systemic vascular resistance. From 0 to 20 cm H2O PEEP, the fall in QO2 was greater in the PGE1 than in the saline series (P < 0.005), since ventricular filling and the rise in heart rate were less in the former. The decrease in VO2 (P < 0.005) did not differ between series. As estimated from bilinear regression on paired VO2/QO2 data in individual pigs, the QO2c was 9.8 +/- 3.6 (mean +/- SD) during PGE1 and 14.6 +/- 3.8 ml/kg/min during saline infusion (P = 0.008), with ERO2c 68% +/- 16% and 48% +/- 12%, respectively (P < 0.005). The QO2c, estimated from bilinear regression on paired lactate/QO2 data during the first treatment period, was 7.1 +/- 1.2 for PGE1 and 12.8 +/- 4.5 ml/kg/min for saline (P < 0.05), at similar lactate concentrations (2.0 +/- 0.5 and 1.7 +/- 0.5 mmol/liter, respectively). PGE1-induced vasodilation thus decreases QO2c, because of increased ERO2c, probably resulting from capillary recruitment, an increased surface area available for O2 exchange, and decreased O2 diffusion distances. Hence, a reduced ERO2 and abnormal supply dependence of VO2 during severe sepsis and ARDS are not caused by release of vasodilating prostaglandins. In contrast, our results partly explain improved tissue oxygenation with these compounds during abnormal VO2 supply dependence, following sepsis and ARDS.

The authors sought to determine how hypoperfusion influences acid-base balance in arterial and mixed venous blood. In anesthetized, ventilated pigs (n = 12), we determined hemodynamics, O2 uptake, CO2 output, dead-space ventilation, arterial and mixed venous blood acid-base balances, and lactate concentrations during graded reductions in cardiac output by incremental positive end-expiratory pressure (PEEP, 0-20 cm H2O). Cardiac output decreased from 3.2 +/- 0.2 (mean +/- SEM) to 1.2 +/- 0.1 L/min at 20 cm H2O PEEP. Oxygen delivery declined more than O2 uptake did by 60% +/- 2% and 27% +/- 2%, respectively. The decrease in CO2 output (by 21% +/- 2%) was less than that in O2 uptake. Fractional dead-space ventilation increased. At a slight increase in carbon dioxide tension (PCO2) of 4 +/- 1 mm Hg, pH decreased in arterial blood from 7.54 +/- 0.01 to 7.47 +/- 0.02 mmol/L, and standard bicarbonate decreased from 30.3 +/- 0.5 to 27.5 +/- 0.6 mmol/L. The decrease in standard bicarbonate exceeded the increase in blood lactate concentrations. At a similar decrease in standard bicarbonate, the decrease in pH was larger (P less than 0.005) in mixed venous blood than in arterial blood owing to a larger increase in PCO2 (from 40 +/- 2 to 50 +/- 2 mm Hg, P less than 0.005). The changes were reversed after discontinuing PEEP. The authors conclude that ischemia after incremental PEEP results in tissue metabolic acidosis with superimposed respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The reliability of resting energy expenditure (REE) measurements by indirect calorimetry with a ventilated hood was investigated in 50 healthy controls and 10 patients with liver cirrhosis. In each subject basal energy expenditure (BEE) was determined once and REE three times (morning REE1, noon REE2, afternoon REE3). In controls and patients the first 5-minute BEE and first 5-minute REE (controls also second 5-minute REE) were higher than in the remainder of the 30-minute recording. Only the last 20 minutes of recordings were used to calculate BEE (1645 +/- 315, mean +/- SD, in kilocalories per day), REE1 (1880 +/- 365), REE2 (1782 +/- 384), and REE3 (1775 +/- 316) in controls, and in cirrhotics: BEE (1530 +/- 235), REE1 (1714 +/- 267), REE2 (1715 +/- 238), and REE3 (1779 +/- 275). REE was higher than BEE in controls and cirrhotics (p less than 0.05). The REE variation coefficient was 5 +/- 3% in controls and 5 +/- 2% in cirrhotics. No systematic difference between REE1, REE2, and REE3 was found. Energy expenditure predicted by the Harris-Benedict equation differed up to 21% from measured BEE in individual controls; group mean BEE, however, was correctly predicted. In cirrhotics differences between measured and predicted BEE up to 26% occurred, while measured BEE was higher than predicted BEE (p = 0.06). It is concluded that REE can be reliably assessed by indirect calorimetry with a ventilated hood system in controls and patients at any time of the day, when values obtained in the first 10 minutes are deleted.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous studies reporting pathologic oxygen supply dependency calculated VO2 as CO x C(a-v)O2. We investigated whether pathologic oxygen supply dependency exists in septic and postoperative patients if VO2 and DO2 are assessed independently. In septic patients, VO2 was 164 +/- 31 and DO2 was 633 +/- 209 ml/min/m2. The slope (b) of the VO2-DO2 regression line VO2 = b x DO2 + a ranged from -0.10 to 0.08 (mean, 0.02 +/- 0.01, p less than 0.05) and was statistically significant in two patients (b = 0.05 and b = 0.08, p less than 0.05). In postoperative patients VO2 was 136 +/- 19 and DO2 was 481 +/- 160 ml/min/m2; b ranged from -0.07 to 0.09 (mean, 0.04 +/- 0.01, p less than 0.001) and was statistically significant in one patient (b = 0.09, p less than 0.01). The lack of a close relationship between independently measured VO2 and DO2 may indicate that septic and postoperative patients in stable hemodynamic condition have no pathologic oxygen supply dependency. Analysis of the VO2-DO2 relationship may not be useful to guide therapy or predict outcome.

Pathologic dependency of VO2 on DO2 has been reported in postoperative and septic patients. We studied the influence of an artifact due to calculation of VO2 from CO and AV content difference. In 13 postoperative and seven septic patients, the relationships between DO2 and cVO2 and between DO2 and mVO2 were analyzed by linear regression. In ten patients, cVO2 and DO2 were significantly correlated, but in only two of these patients mVO2 also correlated with DO2. In two patients, there was a significant correlation between mVO2 and DO2. The main contribution to the correlation and to the slope of the regression line between cVO2 and DO2 may be due to mathematic coupling of cVO2 and DO2. With cVO2, erroneous conclusions concerning the VO2-DO2 relationship may be drawn. In four patients, DO2 and mVO2 were significantly related, reflecting either physiologic coupling or pathologic supply dependency of VO2.

In acutely ill patients both hypo- and hyperalimentation must be avoided by adjusting caloric intake to total energy expenditure (TEE). We determined the discrepancy between basal energy expenditure (BEE) calculated from the basic Harris-Benedict formula and TEE measured by continuous indirect calorimetry in a heterogeneous group of mechanically ventilated surgical patients. We also compared the accuracy of TEE calculated from the corrected Harris-Benedict formula or estimated by intermittent indirect calorimetry to that of TEE measured by continuous indirect calorimetry. The poor correlation between calculated BEE and measured TEE was significantly (p less than .05) improved by a correction factor based on each patient's clinical condition. The mean absolute difference between calculated TEE and measured TEE was 8.9 +/- 9.6 (SD) %. Calculations were significantly (p less than .05) improved by estimating TEE from two 5-min recording periods, which suggests that continuous indirect calorimetry may not always be necessary to guide caloric replacement.

To determine whether the total energy expenditure (TEE) determined on a single day reliably estimates TEE on subsequent days of a patient's ICU stay, day-to-day variability of TEE and its relation to clinical condition were assessed. TEE was measured by indirect calorimetry in 60 mechanically ventilated critically ill surgical patients during a 2 to 7-day period. Clinical condition was scored by daily determination of the simplified acute physiology score (SAPS). Day-to-day variation of TEE was significantly (p less than .0001) influenced by body temperature, but not by SAPS or day of measurement. In the individual patient, day-to-day variability of TEE may be large. When TEE on day 1 is used to estimate TEE on subsequent days, errors of up to 31% of actual TEE occurred. Addition of a temperature correction reduced the maximum error to 25%. If a balance between caloric supply and demand is intended, it is advised to adapt the caloric supply to the result of daily TEE measurement by indirect calorimetry.

In the treatment of critically ill patients, it may be important to know the values of total diurnal O2 consumption and CO2 production. Often, diurnal values are obtained by extrapolation from the easily obtained short interval values. However, both stochastic and systematic errors can be introduced. This study analyzes the systematic influence of a possible diurnal variation of gas exchange and quantifies the extrapolation accuracy of 16 commonly used recording protocols (one to four times a day for 5, 15, 30, and 60 min). Continuous gas exchange measurements were performed for 24 h in 50 ventilated patients and compared to extrapolated results. Only a small diurnal variation was found, and extrapolation accuracy depended on the duration and, especially, the number of recording periods. In clinical practice, 24-h values can be estimated with sufficient accuracy by extrapolation from two 15-min measurements per day.