Changes in renal vein, renal surface, and urine oxygen tension during hypoxia in pigs.

To determine whether ureteral urine oxygen tension could serve as a monitor of renal hypoxia and its relationship to other renal O2 tension parameters, we simultaneously measured femoral artery (PaO2), renal vein (PrvO2), renal surface (PrsO2), and ureteral urine (PuO2) oxygen tensions in 8 anesthetized pigs while incrementally decreasing the inspired oxygen concentration (FiO2) from 21% to 12%. Renal artery blood flow, measured by transit time ultrasound, renal oxygen consumption, and thermodilution cardiac output, was constant. Changes in PaO2, PrvO2, PrsO2, and PuO2 caused by decreasing FiO2 were evaluated by one-way analysis of variance. The relationships between PuO2 and the other O2 tension parameters were evaluated by correlation coefficient and linear regression statistics. Of six possible O2 decrements (combinations of 3, 6, and 9%), only PrvO2 significantly decreased with all six decrements. PuO2 decreased when FiO2 decreased 6% or more. PuO2 is not a sensitive indicator of systemic hypoxia. Under constant renal perfusion and oxygen consumption, PuO2 had a correlation coefficient of 0.80 and a regression equation of PuO2 = 0.84 (PrvO2) + 11.6, with PrvO2. PuO2 is related to PrvO2 when renal perfusion is constant.

Comparison of changes in transit time ultrasound, esophageal Doppler, and thermodilution cardiac output after changes in preload, afterload, and contractility in pigs.

The purpose of this study was to compare how well changes in cardiac output (CO) measured by esophageal Doppler (Doppler) and thermodilution (TD) followed changes in CO measured by transit time ultrasound (TTU). Simultaneous Doppler, TD, and TTU measurements of CO were made before and after changes in preload, afterload, or contractility in seven piglets. Mean changes in each CO method for each type of change in CO were compared by analysis of variance. Changes in TTU CO, TD CO, and Doppler CO were compared by correlation, linear regression, and bias and precision statistics. Of 86 TTU changes in CO greater than 10%, Doppler changed the same direction as TTU 59 times, changed in an opposite direction 6 times, and changes less than 10% 21 times. Thermodilution changed in the same direction as TTU 72 times, in the opposite direction 4 times, and changed less than 10% 10 times. Changes (% delta) in TTU and TD measurements of CO were not significantly different in any group. Changes in Doppler CO and TTU CO were different for two afterload and contractility groups. Percent changes in Doppler CO had a correlation coefficient (r) = 0.74, m = 0.72, and bias (mean % delta Doppler CO - mean % delta TTU CO) = 6.3 +/- 29.7 with % delta TTU CO. Percent changes in TD CO had an r = 0.90, m = 0.92, and bias = 5.7 +/- 19.1 with % delta TTU CO. Cardiac output measured by Doppler underestimated changes in CO due to changes in preload and contractility and exaggerated changes in CO due to changes in afterload.

Noninvasive cardiac output: simultaneous comparison of two different methods with thermodilution.

The authors attempted to simultaneously measure cardiac output by thermodilution (COtd), thoracic bioimpedance (CObi), and suprasternal Doppler ultrasound (COdopp) in 68 patients. Subgroups separately compared included patients whose lungs were mechanically ventilated, patients undergoing cardiac surgery, aortic surgery, patients with dysrhythmias, and patients with sepsis. The authors also studied the value of the ventricular ejection time (VET) in evaluating the agreement of CObi and COdopp with COtd. Simultaneous CObi and COtd were available in a total of 56 patients (416 data sets) with an overall correlation coefficient r = 0.61, regression slope (m) of 0.52, intercept (y) of 2.46, and mean (CObi-COtd) difference (bias) of -0.67 +/- 1.72 (SD) l/min. Simultaneous COdopp and COtd were available in 59 patients (446 data sets) with an overall r = 0.51, m of 0.53, y of 2.05, and bias of -0.79 +/- 1.95 l/min. CObi agreed most closely with COtd in patients whose lungs were mechanically ventilated, who had not undergone cardiac or aortic surgery, and with VET difference less than 40 ms (16 patients, 99 data sets; r = 0.74; m = 0.97; y = 0.15; bias = -0.02 +/- 1.53 l/min). COdopp agreed most closely with COtd in patients whose lungs were mechanically ventilated, who had not undergone cardiac or aortic surgery, and in sinus rhythm with VET difference less than 40 ms (10 patients, 45 data sets; r = 0.82; m = 0.98; y = -0.07; bias = -0.82 +/-1.03 l/min). VET by radial artery can help evaluate the reliability of CObi and COdopp.

Thoracic bioimpedance and Doppler cardiac output measurement: learning curve and interobserver reproducibility.

Nine previously untrained health professionals learned to measure cardiac output (Qt) by suprasternal continuous-wave Doppler ultrasound (QtDopp) and by thoracic bioimpedance (Qtbi). Each received standardized written, videotaped, and individual instruction. First the novice, then the reference examiner, measured QtDopp or Qtbi in triplicate in an adult male subject. The reference examiner was blind to the novice measurements and the novice was not informed of the reference measurements. Each novice repeatedly measured QtDopp or Qtbi in different subjects until the mean novice QtDopp or Qtbi was within 10% of the corresponding mean reference measurement in three of four consecutive subjects. The novice observers required an average of 12.9 +/- 3.5 trials to learn to measure QtDopp, and an average of 8.4 +/- 4.5 trials to learn to measure Qtbi. The likelihood of novice agreement with the reference improved with experience. The same degree of intraobserver variability as reported for Qt measured by thermodilution (coefficient of variance less than or equal to 10%) was achieved with Qtbi in 150 (99%) of 152 triplicate measurements and QtDopp in 216 (97%) of 222 triplicate measurements. More importantly, interobserver agreement (within 10%) was achieved with both Qtbi and QtDopp. Reproducible noninvasive Qt measurement will allow these techniques to be used to monitor trend changes in Qt.

Changes in cardiac output after acute blood loss and position change in man.

Thoracic bioimpedance cardiac output (Qtbi) was measured at 1-min intervals in 27 volunteers before, during, and after withdrawing 500 ml (3.7 to 8.5 ml/kg; mean 5.8) of blood. The effects of passive leg raising (PLR) and standing on Qtbi were measured before and after blood withdrawal. Arterial oxygen saturation (SaO2), transcutaneous oxygen tension (PtcO2), mean arterial BP (MAP), and heart rate (HR) were also measured before and after blood withdrawal. Thoracic bioimpedance cardiac index (CI) decreased 18% (0.8 +/- 0.1 L/min.m2, p less than .0001) and stroke volume index (SI) decreased 22% (14.8 +/- 2.7 ml/beat.m2, p less than .0001) after blood withdrawal. HR, MAP, SaO2, and PtcO2 were not significantly different after blood withdrawal. Before blood withdrawal PLR increased CI 6.8% (0.3 +/- 0.1 L/min.m2, p less than .0001); after blood withdrawal PLR increased CI 11.1% (0.4 +/- 0.1 L/min.m2, p less than .0001). PLR can increase stroke volume and cardiac output in hypovolemic humans.

Acute cardiovascular response to passive leg raising.

Cardiac output by thoracic bioimpedance, heart rate, BP, oxygen saturation, and transcutaneous oxygen tension were measured at 1-min intervals in 45 patients before and after passive leg raising (PLR). Mean cardiac index increased only 0.09 +/- 0.02 (SEM) L/min.m2 (p less than .001), mean transcutaneous oxygen tension increased 1.6 +/- 0.6 torr (p less than .01), and mean oxygen saturation decreased 0.5 +/- 0.2% (p less than .01) after PLR. There were no significant changes in heart rate or systolic BP. Seven (16%) patients had increased cardiac index greater than 10% after PLR.

Continuous fiberoptic arterial oxygen tension measurements in dogs.

An experimental study using a new fiberoptic sensor for the continuous intraarterial measurement of oxygen tension is described. This "optode" sensor uses the phenomenon of fluorescence quenching to determine the oxygen tension of the surrounding medium. To assess the accuracy of this device, we anesthetized 4 dogs and monitored them continuously with arterial catheters and an intraarterial optode probe, and intermittently with arterial blood gas analysis. The inspired oxygen fraction was varied from 1.0 to 0.1, and arterial blood gases were measured for comparison with the optode reading. Two hundred ninety data sets yielded a correlation coefficient of 0.96, with a linear regression slope of 0.98 and intercept of 5.1 mm Hg. In the 72 data sets from the last dog, the bias and precision of the optode arterial oxygen tension values were -10.3 mm Hg and 20.0 mm Hg, respectively. The optode probe was easily inserted through a 20-gauge catheter and did not interfere with continuous arterial pressure measurement or blood sampling. This study suggests that the optode has great potential as a continuous, real-time monitor of arterial oxygen tension.

Continuous noninvasive estimation of cardiac output by electrical bioimpedance: an experimental study in dogs.

A new device has been developed to estimate continuously and noninvasively cardiac output from the thoracic electrical bioimpedance (CObi). CObi was compared to cardiac output by thermodilution (COtd) in five anesthetized dogs. Blood pressure, blood volume, and blood flow were manipulated by hemorrhage and infusions of sodium nitroprusside and phenylephrine. These data were used to determine the correlation between CObi and COtd under conditions of hypotensive normal flow and normotensive low flow, as well as during hemorrhagic shock and resuscitation. The CObi device was calibrated in vivo to COtd for each dog at the beginning of each experiment. CObi had a significant positive correlation with COtd throughout the experiments (r = 0.84, slope = 0.91, intercept = 0.55, p less than 0.01), and CObi predicted COtd with a standard error of the estimate of 0.81 L/min. Neither heart rate nor mean arterial pressure was significantly correlated with COtd or CObi. During severe hemorrhagic shock, CObi could not determine cardiac output in two of the dogs when COtd averaged 1.7 L/min. These data indicate that CObi is a blood-flow related variable that can be monitored continuously.

Transcutaneous PO2 monitoring during sodium nitroprusside infusion.

To determine the effect of vasodilator-induced hypotension on the relationship between transcutaneous PO2 (PtcO2) and PaO2, six mongrel dogs and 20 patients were monitored before and during infusion of sodium nitroprusside (SNP), with PtcO2 sensors heated to 45 degrees C. First, SNP infusion was used to lower the mean arterial pressure (MAP) of anesthetized dogs, in steps of approximately 25%, to 49 +/- 3 (SD) mm Hg. There were no significant changes in cardiac output, oxygen consumption, PtcO2, PaO2, or PtcO2 index (PtcO2/PaO2). Twenty patients were monitored during general anesthesia. Fifteen patients were being treated for acute hypertension with SNP, and in five patients hypotension was induced with SNP to minimize blood loss. There was a significant decrease in MAP, PaO2, and PtcO2, and a significant increase in alveolar-arterial PO2 difference during SNP infusion. PtcO2 index did not change significantly from its preinfusion value in either group.

Effect of halothane and N2O on the oxidative activity of human neutrophils.

The effect of clinically used concentrations of halothane and N2O on the microbicidal oxidative function of human neutrophils was investigated. Neutrophil oxidative activity was assessed utilizing the method of luminol dependent chemiluminescence (LDCL) by particulate (opsonized zymosn) and nonparticulate (phorbol myristate acetate, [PMA]) stimulated cells. In vivo exposure of neutrophils to 2 and 3% halothane resulted in a 13 and 40% inhibition, respectively of the air-exposed LDCL response with zymosan-activated neutrophils; 1% halothane had no effect. Similar results were seen with PMA-stimulated neutrophils. N2O 80% did not inhibit the LDCL response, and also did not show an additive inhibition when combined with halothane. Although th halothane inhibition of LDCL was reversible (equal to control, no anesthetic, LDCL responses following exposure to air), neutrophils treated with N2O plus halothane and then exposed to air for 30 min showed a significantly higher LDCL response over the control experiments. The inhibition of zymosan- or PMA-stimulated neutrophil LDCL by halothane suggests either a membrane perturbation or a direct inactivation of oxidative enzyme(s) by the anesthetic. This impairment of oxidative activity may partly explain the reduced bacterial killing by neutrophils seen after exposure to halothane.