Hemoptysis due to migration of a fractured Kirschner wire.

We report a rare complication related to the insertion of Kirschner wires for stabilization of an acromioclavicular separation. Five years after placement of the Kirschner wires, the patient presented with hemoptysis. On review of chest radiographs, a fractured wire was found to have migrated from the acromioclavicular joint, through the hemithorax and into the trachea.

Antibiotic levels in empyemic pleural fluid.

OBJECTIVE: To determine the degree to which bioactive penicillin, metronidazole, ceftriaxone, clindamycin, vancomycin, and gentamicin penetrate into empyemic pleural fluid using our new rabbit model of empyema. METHODS: An empyema was created via the intrapleural injection of 10(8)()Pasteurella multocida bacteria into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracentesis and pleural fluid analysis, penicillin, 24,000 U/kg; metronidazole, 37 mg/kg; ceftriaxone, 30 mg/kg; clindamycin, 9 mg/kg; vancomycin, 15 mg/kg; or gentamicin, 1 mg/kg, were administered IV. Antibiotic levels in samples of pleural fluid and serum, collected serially for up to 480 min, were then determined using a bioassay. RESULTS: The degree to which the different antibiotics penetrated into the infected pleural space was highly variable. Penicillin penetrated most easily, followed by metronidazole, ceftriaxone, clindamycin, vancomycin, and gentamicin. Of the antibiotics tested, penicillin and metronidazole equilibrated the most rapidly with the infected pleural fluid. Penicillin levels remained elevated in pleural fluid even after serum levels had decreased. CONCLUSIONS: Using this rabbit model of empyema, there was marked variation in the penetration of antibiotics into the empyemic fluid. Although there are species differences between rabbit and human pleura, the variance in degree of penetration of antibiotics into the pleural space should be considered when antibiotics are selected for the treatment of patients with empyema.

The in vitro efficacy of varidase versus streptokinase or urokinase for liquefying thick purulent exudative material from loculated empyema.

Patients with loculated parapneumonic effusion or empyema are sometimes treated with streptokinase or urokinase in an attempt to facilitate pleural fluid drainage by liquefying the pleural exudate and destroying the fibrin membranes producing the loculation. This study evaluated the effectiveness of streptokinase, urokinase, and Varidase (the combination of streptokinase and streptodornase) in liquefying gummy, purulent, exudative material from loculated empyemas. An empyema was created by injecting 10(8) Pasteurella multocida bacteria into the pleural space of New Zealand white rabbits. Twenty specimens, each containing 0.5 g of purulent material obtained 5 days after empyema induction, were placed in test tubes. Streptokinase (15,000 IU), urokinase (10,000 IU), Varidase (4,000-15,000 IU streptodornase + 15,000 IU streptokinase) or saline was added to five sets of four test tubes each. The amount of nonliquefied material that remained after incubation with the fibrinolytic agents was quantitated. Over the 6-h incubation period, the amount of nonliquefied material decreased from 0.5 g to 0.02 g in the Varidase group but never decreased to less than 0.4 g in any of the other three treatment groups. Liquefaction of thick pleural exudates from rabbits with empyema can be achieved with Varidase but not with streptokinase or urokinase.

Arterial blood gas changes during breath-holding from functional residual capacity.

Breath-holding serves as a model for studying gas exchange during clinical situations in which cessation of ventilation occurs. We chose to examine the arterial blood gas changes that occurred during breath-holding, when breath-holding was initiated from functional residual capacity (FRC) while breathing room air. Eight normal subjects who had a radial artery catheter placed for another study were taught to breath-hold on command from FRC. FRC was determined using respiratory inductance plethysmography. Arterial blood gas specimens were obtained at 5-s intervals until the termination of breath-holding. The average breath-holding time (+/-SD) was 35 (+/-10 s). The PaO2, PaCO2, and pH values were plotted against time and individually fit to logistic equations for each subject. The arterial PaO2 fell by a mean of 50 mm Hg during the first 35 s of breath-holding under these conditions, while the arterial PCO2 rose by a mean of 10.2 mm Hg during the first 35 s and the pH fell by a mean of 0.07 in the first 35 s. The rapid decline in PaO2 is greater than that previously reported using different methods and should be considered in clinical situations in which there is an interruption of oxygenation and ventilation at FRC while breathing room air. The changes in PaCO2 and pH are similar to those previously reported in paralyzed apneic patients.

Parapneumonic effusions and empyema.

Thoracic empyema remains a significant medical problem in 1996. Patients in whom empyema develops suffer significant morbidity, frequently require prolonged hospitalizations, and are at an increased risk of death. In this review of parapneumonic effusions and empyema, four topics are discussed: diagnosis of empyema, the organisms responsible for empyema, the methods used for treatment, and the results from animal models of empyema.

Comparison of oxygen saturation by pulse oximetry and co-oximetry during exercise testing in patients with COPD.

INTRODUCTION: Measurement of oxygen saturation by pulse oximetry (SpO2) is frequently performed during exercise testing of patients with COPD to monitor for hypoxemia. The purpose of this study was to assess the accuracy and precision of pulse oximetry during exercise. We hypothesized that the SpO2 would more closely reflect oxygen saturation as measured by co-oximetry (SaO2) when it was corrected for carboxyhemoglobin (COHb). We also hypothesized that SpO2 would more closely reflect SaO2 when the pulse rate by oximeter was equivalent to the heart rate by ECG. Finally, we hypothesized that SpO2 would be a better measure of SaO2 at maximal workloads than at rest or submaximal workloads. METHODS: Eight white men with severe COPD (mean +/- SD FEV1, 0.91 +/- 0.37) underwent progressive, symptom-limited exercise testing by cycle ergometry. SaO2 was measured from arterial blood at each workload using a co-oximeter. SpO2 and pulse rate were obtained by a pulse oximeter (Ohmeda 3700). Heart rate was continuously monitored by ECG. RESULTS: Reliable oximetric values as determined by a dicrotic notch in each waveform and adequate signal intensity were obtained in all eight patients. SpO2 was a moderately accurate measure of SaO2 (bias, 1.7%; precision, 2.9). The bias actually increased (4.1%) when SpO2 was corrected for COHb. Accuracy of SpO2 was not improved when pulse rate by oximetry and heart rate by ECG were equivalent, nor was the accuracy improved at maximal workloads relative to submaximal workloads during the exercise test. CONCLUSION: Oxygen saturation as measured by pulse oximetry (SpO2) in patients with COPD undergoing exercise testing is not sufficiently accurate to replace SaO2 as the gold standard for oxygen saturation.

Relationship of changes in cardiac output to changes in heart rate in medical ICU patients.

OBJECTIVE: To determine whether changes in cardiac output are correlated with changes in other commonly measured covariables (heart rate, respiratory rate, mean arterial pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, and temperature). DESIGN: Case series. SETTING: Medical intensive care unit (ICU) in a Veterans Administration Medical Center. PATIENTS: Twenty-three patients with Swan-Ganz catheters placed by the primary care team were studied on 25 occasions. Patients were managed by the primary team as clinically indicated. INTERVENTIONS: Thermodilution cardiac output and covariables were determined at baseline and at hourly intervals for the next 5 h. Each cardiac output measurement was calculated by averaging the last four of five individual measurements at each time point. RESULTS: The mean cardiac output (9.21/min), heart rate (107/min), and pulmonary artery occlusion pressure (19 mmHg) were elevated. The hourly mean change in cardiac output was 10.2%. Using least-squares linear regression analysis, we found clinically significant changes in cardiac output (> 6.4%) to be most closely correlated with changes in heart rate (R2 = 0.29, p < 0.001). Stepwise linear regression analysis showed that none of the other covariables added significantly to this relationship. No significant relationship was found between changes in cardiac output and changes in pulmonary artery occlusion pressure. Despite these correlations clinically significant changes in cardiac output were accompanied by changes in heart rate in the same direction only 62% of the time. CONCLUSION: Changes in cardiac output were best correlated with changes in heart rate. Changes in pulmonary artery occlusion pressure were not correlated with changes in cardiac output in this population of medical ICU patients. A change in any of the covariables (alone or in combination) cannot be reliably used to indicate a simultaneous change in cardiac output.

Serial pleural fluid analysis in a new experimental model of empyema.

Prior attempts to create an animal model of empyema by direct inoculation of bacteria alone into the pleural space have been unsuccessful. The animals either died of overwhelming sepsis or cleared the infection from the pleural space without development of an empyema. We hypothesized that injection of bacteria with a nutrient agar into the pleural space would allow the bacteria to remain in the pleural space for an extended time period, permitting an empyema to develop. The bacterium Pasteurella multocida in brain heart infusion (BHI) agar was injected into the right hemithorax of 12 New Zealand white male rabbits. Our preliminary studies showed that the animals died in less than 7 days if they were not given parenteral antibiotics. For this reason, the rabbits were given penicillin, 200,000 U, IM, every 24 h starting 24 h after bacterial injection. Pleural fluid was sampled by thoracentesis at 12, 24, 48, 72, and 96 h after bacterial injection. Pleural fluid pH, glucose, lactate dehydrogenase (LDH), leukocyte count, and Gram's stain and culture (in one half of the animals) were obtained at each time point. Pleural biopsy specimens were obtained at autopsy after 96 h. The mean pleural fluid pH reached a nadir of 7.01 at 24 h and remained less than 7.1 throughout the experiment. The mean pleural fluid glucose level reached a nadir of 10 mg/dL at 24 h. The mean pleural fluid LDH peaked at 21,000 IU/L at 24 h and the mean pleural fluid leukocyte count peaked at 12 h with a value of 67,000 cells per cubic millimeter. Gram's stains revealed organisms and cultures were positive for growth in all animals at 12 and 24 h. Some animals had positive Gram's stains and growth on cultures up to 72 h after bacterial injection. At autopsy, all rabbits injected with bacteria had gross pus in the right pleural space and had developed a thick pleural peel. Microscopic specimens of the pleura revealed large numbers of leukocytes (primarily polymorphonuclear lymphocytes) with invasion of the adjacent lung and chest wall. In conclusion, this model more closely mimics the empyema that occurs in humans, relative to previous animal models. This model appears appropriate for additional randomized studies in which different methods for the treatment of empyema can be evaluated.

The effects of pentoxifylline on oxygenation, diffusion of carbon monoxide, and exercise tolerance in patients with COPD.

Pentoxifylline has been reported previously in an unblinded study to improve oxygen saturation, treadmill walk time, and resting diffusion of carbon monoxide (Dco) in patients with COPD. We recruited 12 patients with moderate to severe COPD whose exercise capacity was limited by ventilation or who developed hypoxemia with exercise. Patients were randomized to receive pentoxifylline or placebo, each for a 12-week period in a prospective, double-blind, crossover design study, to assess the effects of pentoxifylline on oxygenation, resting Dco, and exercise tolerance using arterial blood gas analysis. Eleven patients with a mean FEV1 of 0.94 L and a mean Dco of 9.85 mL/min/mm Hg completed the study. One patient withdrew from the study after developing pneumonia. There were no significant differences in resting oxygenation, resting Dco, or spirometry after 12 weeks of pentoxifylline relative to placebo. The 12-min walk test and dyspnea index for activities of daily living were also not significantly different while taking pentoxifylline. Finally, at maximal exercise, there were no differences in workload attained, exercise duration, oxygen consumption, carbon dioxide production, minute ventilation, oxygen saturation, PO2, alveolar-arterial oxygen pressure difference, or Borg score while taking pentoxifylline relative to placebo. We conclude that pentoxifylline does not improve oxygenation, resting Dco, exercise tolerance, or dyspnea in patients with moderate to severe COPD.

Arterial oxygenation time after an FIO2 increase in mechanically ventilated patients.

The time for arterial PO2 to reach equilibrium after a 0.2 increase in the fraction of inspired oxygen (FIO2) was studied, using arterial blood gases measured at 1, 2, 3, 4, 5, 7, 9, and 11 min in 30 stable, mechanically ventilated medical intensive care unit (ICU) patients. Eight patients also underwent a 0.4 increase in FIO2. Each patient's rise in PO2 over time [PO2(t)] was fit to the following exponential equation: PO2(t) = PO2i + (PO2f-PO2i) (1-e-kt), where t refers to time, PO2i and PO2f refer to the initial and final equilibrated PO2. The time constant k and PO2f were determined by a nonlinear curve fitting technique. The 90% oxygenation times (t90%), defined as the time required to reach 90% of the final equilibrated PO2, were calculated. The mean t90% (+/- SD) was 6.0 (+/- 3.4) min for all patients (range 1.7 to 14.3 min); 7.1 +/- 2.1 min for 18 patients with chronic obstructive pulmonary disease (COPD) and 4.4 +/- 2.0 min for 12 patients without COPD (p < 0.05). In the subgroup of patients undergoing both an FIO2 increase of 0.2 and 0.4, there was no significant difference in the mean t90%'s for the two FIO2 changes (7.7 versus 7.7 min). We conclude that after a 0.2 or 0.4 increase of FIO3, a 15-min equilibration time period is adequate for 90% of the increase in PO2 to occur, in stable, mechanically ventilated medical ICU patients.

Comparison of the end-tidal arterial PCO2 gradient during exercise in normal subjects and in patients with severe COPD.

We undertook the present study with the following objectives: (1) to compare the difference between the end-tidal and the arterial carbondioxide concentration (P[ETa] CO2) gradients at rest and during exercise in normal subjects and patients with COPD; and (2) to analyze the factors contributing to this gradient. We studied seven normal subjects and seven patients with COPD using a symptom-limited exercise test on a cycle ergometer. Our results show that the P(ET-a)CO2 increased progressively as the individuals went from rest to higher workloads in both the normal group and in the COPD group. The P(ET-a)CO2 in patients with COPD both at rest (-3.24 +/- 2.78 mm Hg) and during exercise (1.03 +/- 2.23 mm Hg) is significantly lower than that in normal individuals at rest (1.84 +/- 3.68 mm Hg) and during exercise (10.3 +/- 6.5 mm Hg) (p < 0.01). However, the slope for the relationship between the P(ET-a)CO2 and the workload is actually significantly steeper in the patients with COPD. Although the P(ET-a)CO2 correlated significantly with the workload in both normal subjects (r = 0.63, p < 0.001) and patients (r = 0.55, p < 0.005), the P(ET-a)CO2 was much more closely correlated with the ratio of dead space to tidal volume (VD/VT) (r values of -0.86 and -0.77, respectively). Moreover, when multiple regression analysis was performed, addition of any other physiologic measure (eg, oxygen consumption [VO2], carbon dioxide production [VCO2], minute ventilation [VE], or workload) as a second independent variable after the VD/VT did not improve the correlation. This indicates that the correlation between the P(ET-a)CO2 and the workload is probably related to the dependence of the VD/VT on the workload. The PaCO2 in normal subjects and in the COPD group correlated significantly with the partial pressure of end-tidal carbon dioxide (PETCO2). Using multiple regression analysis, with the PaCO2 as the dependent variable and the PETCO2 (along with other physiologic measures) as the independent variables, we found that the standard error of the estimate was still above 2.1 mm Hg in normal subjects and in patients with COPD. We conclude that (1) during exercise, the P(ET-a)CO2 in normal subjects and in patients with COPD increases significantly, (2) the P(ET-a)CO2 gradient is more closely correlated with the VD/VT than any other physiologic variable, and (3) changes in the PETCO2 during exercise are not correlated closely with changes in the PaCO2.

Performance of a patient-dedicated, on-demand blood gas monitor in medical ICU patients.

We examined the performance characteristics of a new bedside blood gas monitor. This monitor's fluorescent pH, PCO2, and PO2 sensors are embedded in a cassette, which is calibrated in vitro and then inserted into the patient's radial artery tubing set. In 50 medical ICU patients, 683 paired monitor and conventional blood gas analyzer values were obtained. Performance was assessed via calculations of bias (mean monitor and analyzer difference) and its standard deviation (SD), plots of monitor and analyzer differences against the means (of monitor and analyzer), and linear regression analysis of the sequential changes in monitor values versus the corresponding sequential changes in analyzer values. The ex vivo calibration, assessed using the initial paired blood samples, showed a bias +/- SD of 0.02 +/- 0.02 for pH, -0.1 +/- 1.9 mm Hg for PCO2, and 4.3 +/- 6.0 mm Hg for PO2. For all paired samples (n = 683), the biases +/- SD were 0.004 +/- 0.023 for pH, 0.6 +/- 2.4 mm Hg for PCO2, and 2.7 +2- 6.4 mm HG for PO2. The PO2 bias increased as PO2 increased. The standard deviations (imprecision) of both PCO2 and PO2 also increased as the magnitudes of these variables increased. Sequential changes in monitor values versus the corresponding sequential changes in analyzer values revealed regression lines close to the line of identity. Serum sodium had no effect on pH bias. Daily drift of the sensors was inconsequential, with values of -0.01/d for pH, 1.7 mm Hg/d for PCO2, and 1.1 mm Hg/d for PO2. We conclude that the performance of this monitor is comparable to that of conventional blood gas analyzers.

Variability of arterial blood gas values over time in stable medical ICU patients.

The spontaneous variability of arterial blood gas and pH values (ABGs) was examined in a group of 28 typical stable medical ICU patients under a variety of ventilatory conditions. In each patient, 13 ABG specimens were measured at 5-min intervals during a 1-h study period using a new bedside, extravascular fluorescent blood gas monitor. For all patients, the mean coefficient of variation (C) was 6.1 percent for PO2 and 4.7 percent for PCO2. The average SD for pH was 0.012. We conclude that the spontaneous variability for ABG values over a 1-h period is substantial and that this variability should be taken into account when making clinical decisions based on ABG values.

Development of a patient-dedicated, on-demand, blood gas monitor.

A new monitor (CDI 2000) that brings blood gas measurements to the patient's bedside has been developed. To measure blood gases, blood is drawn into the patient's arterial pressure-monitoring line past in-line fluorescent-based sensors. After measurement, the blood is returned to the patient, avoiding blood loss and delays in sample turnaround and reducing the risk of infection to both patient and operator. We assessed this system's performance in vitro with tonometered bovine blood. Bias (mean difference between monitor and tonometered gas or measured pH values) +/- the standard deviation (SD) were 0.01 +/- 0.02 at pH = 7.39; 0.0 +/- 0.7 mm Hg at Pco2 = 39 mm Hg; and 2.4 +/- 3.2 mm Hg at a Po2 = 100 mm Hg (n = 54). Changes in hematocrit, blood temperature, or serum sodium concentration did not have clinically significant effects on system performance. Studies in normal volunteers, in whom large changes in blood gases were induced, showed a bias (mean difference between monitor and IL 1306 values) +/- SD of 0.00 +/- 0.02 for pH, -0.4 +/- 2.0 mm Hg for Pco2, and -3.6 +/- 7.7 mm Hg for Po2 (n = 69). We conclude from the present study that the performance of this system is comparable to that of conventional blood gas analyzers.

Variability of cardiac output over time in medical intensive care unit patients.

OBJECTIVES: To determine the amount of spontaneous variability of cardiac output over time in critically ill patients, and to determine the effect of mechanical ventilation on cardiac output variability over time. DESIGN: Case series. SETTING: Medical intensive care unit in a Veterans Affairs Medical Center. PATIENTS: Twenty-two patients with indwelling pulmonary artery flotation catheters were studied. Two patients were studied twice. INTERVENTIONS: During a 1-hr time period in which no interventions were required or made, thermodilution cardiac output was determined at baseline and then every 15 mins for 1 hr. At each time point, five individual cardiac output measurements were made and a mean was computed. The covariables of heart rate, respiration rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, and temperature were also recorded at each time point. MEASUREMENTS AND MAIN RESULTS: The variability of the five cardiac output measurements made at each time point was expressed by calculating for each patient a coefficient of variation of the measurements. The overall mean coefficient of variation of the measurements was 5.8%. The variability of the cardiac output measurements over time was expressed by calculating for each patient a coefficient of variation over time. The overall mean coefficient of variation over time was 7.7%. A subgroup of 15 "covariable stable" patients (defined as those patients with covariables within +/- 5% of the mean covariable values during the hour) had a mean coefficient of variation over time of 6.4%, whereas "covariable unstable" patients (with > +/- 5% changes in any covariable) had a mean coefficient of variation over time of 9.9% (p < .05). Patients breathing spontaneously had a mean coefficient of variation over time of 10.1%, whereas mechanically ventilated patients had a mean coefficient of variation over time of 6.3% (p < .05). CONCLUSIONS: The spontaneous variability of cardiac output should be considered when interpreting two cardiac output determinations made at separate times. Due to spontaneous variability alone, a patient with a baseline cardiac output of 10.0 L/min would be expected (95% confidence interval) to have a cardiac output range of 9.2 to 10.8 L/min if covariables were stable, and a range of at least 8.8 to 11.2 L/min if covariables were unstable. Patients who were mechanically ventilated displayed less variability than patients who were breathing spontaneously.

Oxygen Fick and modified carbon dioxide Fick cardiac outputs.

OBJECTIVE: To compare cardiac outputs estimated from the classical oxygen Fick and modified CO2 Fick methods with thermodilution cardiac output. The modified CO2 Fick cardiac output was obtained by replacing the oxygen uptake (VO2) in the Fick equation with the CO2 production (VCO2) divided by either an assumed or measured value of the respiratory exchange ratio or with an independently determined constant (Crit Care Med 1991; 19:1270-1277). DESIGN: Criterion standard study. SETTING: The medical and surgical intensive care unit (ICU) in a Veterans Affairs Medical Center. PATIENTS: A total of 17 patients (26 studies) and 11 surgical patients (13 studies), predominantly mechanically ventilated using the intermittent mandatory ventilation mode, were studied over a period of 4.3 hrs. MEASUREMENTS: A respiratory gas exchange monitor was used to measure VO2, VCO2, and respiratory exchange ratio at 3-min intervals. Calculations were performed with arterial and venous oxygen saturations measured with both a laboratory cooximeter and bedside pulse and venous reflectance oximeters. In the oxygen Fick method, cardiac output was calculated from VO2 together with arterial and venous oxygen saturations. In the modified CO2 Fick methods, cardiac output values were calculated from arterial and venous oxygen saturations with VCO2, divided by either: a) an assumed value of the respiratory exchange ratio equal to 0.8 for all patients (method 1); b) the patient's measured value of the respiratory exchange ratio (method 2); or c) a constant, determined from an initial, simultaneous measurement of thermodilution cardiac output, VCO2, and oximetry saturations. Data were examined by linear regression analysis and bias and precision calculations. MAIN RESULTS: Thermodilution cardiac output was more related to cardiac outputs calculated with the 3 modified CO2 Fick methods than to the oxygen Fick cardiac output. Thermodilution cardiac output was closely related to the modified CO2 Fick cardiac output calculated via method 3. For this method, with pulse and venous reflectance oximetry saturations, linear regression yielded an r2 = .85, a standard error of the estimate of 0.88 L/min (n = 111) and a bias and precision of 0.11 and 0.97 L/min, respectively. Thermodilution cardiac output was less closely related to oxygen Fick cardiac output, which, when calculated with pulse and venous reflectance oximetry saturations, yielded an r2 = .50, a standard error of the estimate of 1.47 L/min (n = 128), and a bias and precision of 0.01 and 1.85 L/min, respectively. CONCLUSIONS: We conclude from this study that thermodilution cardiac output is more closely related to cardiac output calculated from modified CO2 Fick methods than to oxygen Fick cardiac output. Since cardiac output calculated with the modified CO2 Fick method 3 obviates the difficulties associated with measuring VO2 accurately and requires neither an assumption of nor measurement of the respiratory exchange ratio, method 3 may prove to be clinically useful for continuous cardiac output monitoring via oximetry in ICU patients.

Relationship of thermodilution cardiac output to metabolic measurements and mixed venous oxygen saturation.

To determine the individual contributions of variables in the Fick equation to cardiac output, we simultaneously measured oxygen uptake (VO2), carbon dioxide production (VCO2), venous oxygen saturation (SvO2) and thermodilution cardiac output (Qth) in 28 medical and surgical ICU patients. Patients were intubated and ventilated with the intermittent mandatory ventilation mode. VO2 and VCO2 (averaged over 3 min) were obtained from a metabolic cart. SvO2 was measured with fiberoptic reflectance oximetry (and COoximetry). Thirty-nine studies (average duration, 4.3 h) with 151 Qth measurements were performed. The relationships between Qth and VO2, Qth and VCO2, Qth and SvO2, and 1/Qth and SvO2, as well as between the sequential changes in these variables were analyzed by least squares linear regression. The ability of changes in the variables VO2, VCO2, and SvO2 to predict changes in Qth were analyzed by receiver operating characteristic (ROC) curves. Qth was weakly related to VO2 (r = 0.45), VCO2 (r = 0.45), or SvO2 (r = 0.36). Changes in Qth were weakly related to changes in VCO2 (r = 0.40), and even less to changes in VO2 (r = 0.18) and SvO2 (r = 0.13). The areas under the ROC curves for increases in Qth > 10 percent were as follows: 0.66 for VCO2, 0.50 for VO2, and 0.55 for SvO2. The areas for decreases in Qth < 10 percent were as follows: 0.78 for VCO2, 0.65 for VO2, and 0.49 for SvO2. None of the above oximetry relationships were substantially altered by use of COoximetry venous oxygen saturations. We conclude that Qth cannot be predicted well solely from VO2, VCO2, or SvO2 nor can changes in Qth be predicted well solely from changes in VO2, VCO2, or SvO2. Of the metabolic variables, changes in VCO2 best predicted changes in Qth.