Mixed Venous Hemoglobin Oxygen Saturation Research Articles

Acute Effects of Inspiratory Muscle Training on Pulmonary Arterial Pressure,Cardiac Output and Pulmonary Arterial Saturation Derived Oxygen Cost of Breathing

Respiration and respiratory maneuvers affect cardiac output. Inspiratory muscle training (IMT) increases the negative thoracic pressure, which could have an impact on intra-thoracic hemodynamics and thereby influence the cardiac output (CO). The objective of our study was to determine changes in pulmonary arterial (PA) hemodynamics and the CO during IMT in patients with suspected pulmonary hypertension. A new method for measuring the oxygen cost of breathing during IMT was also developed. 22 patients were included in this prospective study. They performed IMT during right heart catheterization. Mixed-venous blood gas analysis was performed before and at the end of IMT to calculate the oxygen cost of breathing. The baseline PA pressure was systolic/diastolic/mean (s/d/m) 41 ± 20/13 ± 20/25 ± 11 mmHg. The CO was 5.3 ± 1.5 l/min. The IMT was set to 2.3 ± 0.6 kPa (23.7 ± 5.7 cmH2O). The PA pressure at the end of IMT was s/d/m 44/10/22 mmHg s/d/m. Though there was a trend towards a lower diastolic pressure, this change was not statistically significant (p=0.06). CO (6.2 ± 1.1 l/min) did not change due to IMT. The mixed-venous hemoglobin oxygen saturation was 71.8 ± 2.3% before IMT, with a significant reduction to 65.8 ± 5.9% (p=0.027) at the end of IMT. IMT as performed in our study neither changed the mean PA pressure nor the CO. Measuring the oxygen cost of breathing is feasible by the method described in our paper.

Hemodynamic effects of dexmedetomidine in isoflurane-anesthetized cats

ObjectiveTo characterize the hemodynamic effects of dexmedetomidine in isoflurane-anesthetized cats. Study designProspective experimental study. AnimalsSix healthy adult female cats weighing 4.6 ± 0.8 kg. MethodsDexmedetomidine was administered intravenously using target-controlled infusions to maintain nine plasma concentrations between 0 and 20 ng mL−1 in isoflurane-anesthetized cats. The isoflurane concentration was adjusted for each dexmedetomidine concentration to maintain the equivalent of 1.25 times the minimum alveolar concentration, based on a previous study. Heart rate, systemic and pulmonary arterial pressures, central venous pressure, pulmonary artery occlusion pressure, body temperature, and cardiac output were measured at each target plasma dexmedetomidine concentration. Additional variables were calculated. Arterial and mixed-venous blood samples were collected for blood gas, pH, and (on arterial blood only) electrolyte, glucose and lactate analysis. Plasma dexmedetomidine concentration was determined for each target. Pharmacodynamic models were fitted to the data. ResultsHeart rate, arterial pH, arterial bicarbonate concentration, mixed-venous PO2, mixed-venous pH, mixed-venous hemoglobin oxygen saturation, cardiac index, stroke index, and venous admixture decreased following dexmedetomidine administration. Arterial blood pressure, central venous pressure, pulmonary arterial pressure, pulmonary arterial occlusion pressure, packed cell volume, PaO2, PaCO2, arterial hemoglobin concentration, mixed-venous PCO2, mixed-venous hemoglobin concentration, ionized calcium concentration, glucose concentration, rate-pressure product, systemic and pulmonary vascular resistance indices, left ventricular stroke work index, arterial oxygen concentration, and oxygen extraction increased following dexmedetomidine administration. Most variables changed in a dexmedetomidine concentration-dependent manner. Conclusion and clinical relevanceThe use of dexmedetomidine as an anesthetic adjunct is expected to produce greater negative hemodynamic effects than a higher, equipotent concentration of isoflurane alone.

Oxygen Transport in Pulmonary Oxygenizing Dysfunction in the Early Periods after Extracorporeal Circulation

Objective: to study the specific features of oxygen transport function in patients with various oxygen delivery changes caused by alveolar opening maneuver (mobilization) performed early after extracorporeal circulation. Subjects and methods. Alveolar opening maneuver was made in the presence of relative arterial hypoxemia under the control of dynamic thora-copulmonary compliance. The maximum airway pressure was as high as 31.1±0.3 cm H2O; the positive end-expiratory pressure was 16.0±0.3 cm H2O. According to the changes in oxygen delivery after alveolar opening maneuver, the investigators retrospectively identified the following groups: 1) (n=14) with a lower and 2) (n=15) higher values. The groups did not differ in age (53.6±2.8 and 56.4±1.8 years), extracorporeal circulation duration (106.4±11.2 and 86.8±4 min), and inotropic support intensity (4.7±0.5 and 4.6±0.6 ^g/kh/min for dopamine and/or dobutamine) (p>0.05). The mode of alveolar opening maneuver and its impact on thoracopulmonary compliance and pulmonary oxygenizing function were identical in the groups (p>0.05). Results. 48.3% of the patients with relative arterial hypoxemia show a linear relationship between the oxygen delivery and consumption indices (r=0.73; p=0.003), and there was a close inverse correlation between the oxygen utilization coefficient and intrapulmonary shunting (r=-0.77; p=0.001). After alveolar opening maneuver, the oxygen delivery index decreased in these cases from 440.7±31.7 to 376.9±20.4 ml/min/m2 (p<0.05). The time course °f changes oxygen delivery influenced mixed venous hemoglobin oxygen saturation (r=-0.71; p=0.005), which was related to lactatemia before (r=0.71; p=0.004) and after (r=0.7; p=0.005) alveolar opening maneuver. Conclusion. After extracorporeal circulation, relative arterial hypoxemia may be concurrent with the signs of oxygen transport system tension in patients with impaired pulmonary oxygenizing function. Moreover, regional blood flow impairments in the peripheral tissues and those in the lung are closely related. After alveolar opening maneuver that improves pulmonary oxygenizing function, oxygen delivery decreases, affecting mixed venous hemoglobin oxygen saturation. The findings give grounds to recommend close monitoring and timely correction during alveolar mobilization in the early period after cardiosurgery. The specific features of oxygen transport and utilization during standard interventions into the heart under extracorporeal circulation call for further in-depth studies. Key words: oxygen transport, oxygen delivery and consumption, alveolar opening maneuver (mobilization), arterial hypoxemia in cardiosurgical patients.

Can Mixed Venous Hemoglobin Oxygen Saturation Be Estimated Using a NICO Monitor?

We hypothesized that mixed venous hemoglobin oxygen saturation (SvO2) can be estimated by calculation from CO2 production, cardiac output, and arterial oxygen saturation measured using a noninvasive cardiac output (NICO) monitor (Novametrix-Respironics, Wallingford, CT). Twenty-three patients undergoing aortic aneurysm repair underwent SvO2 monitoring using a pulmonary artery catheter and cardiac output monitoring using a NICO monitor. The estimated SvO2 value calculated from NICO monitor-derived values was compared with the SvO2 value measured using a pulmonary artery catheter. The accuracy of this estimation was analyzed with Bland-Altman method. The ability of this estimation to track the change of SvO2 was also evaluated using correlation analysis to compare the changes of estimated SvO2 and measured SvO2. The bias +/- limits of agreement of the estimated SvO2 against measured SvO2 was -2.1% +/- 11.2%. The change of estimated SvO2 was modestly correlated with the change of measured SvO2. SvO2 derived from the values measured by the NICO monitor cannot be used interchangeably with the values measured spectrophotometrically using the pulmonary artery catheter. More refinement is required to obtain more reliable estimate of SvO2 less invasively. However, large changes of SvO2 may be detected with this method and can be used as a precautionary sign when the balance between oxygen supply and demand is compromised without inserting a central venous catheter.

Response Time of Different Methods of Cardiac Output Monitoring During Cardiopulmonary Resuscitation and Recovery

partial pressure (PETCO2) and mixed venous hemoglobin oxygen saturation (SvO2) also were continuously monitored and recorded. During the laparotomy, hypotension and tachycardia were noted and were accompanied by facial flushing. This was diagnosed as mesenteric traction syndrome and was treated with fluid administration and intermittent intravenous ephedrine. During this period, high cardiac output was recorded with all devices. The maximal values recorded were 6.9 L/min, 9.2 L/min, 17.4 L/min, and 17.9 L/min via the EDM, NICO, STAT CCO, and trend CCO monitors, respectively. At this point, the SvO2 was 89% and VCO2 was 137 mL/min. These symptoms eventually disappeared, and the patient’s CO subsequently stabilized (measured as 5.5 L/min, 5.1 L/min, 10.1 L/min, and 11.3 L/min via the EDM, NICO, STAT CCO, and CCO monitors, respectively; SvO2 85%, VCO2 126 mL/min. The CO at this point as measured with a bolus thermodilution was 7.0 L/min. During surgical exposure of the aortic aneurysm, a sudden onset of ventricular premature contraction was followed by sustained ventricular tachycardia (VT). Because initial DC cardioversion failed to stop the VT, phenylephrine, lidocaine, nitroglycerin, and epinephrine were administered while closed-chest compression was provided. During CPR, the patient was manually ventilated to ensure adequate ventilation. The minute volume provided during CPR was between 11 L/min and 12 L/min. The third DC cardioversion finally restored the patient to sinus rhythm. The duration of VT was 9 minutes, and chest compression provided a systolic pressure of more than 60 mmHg and diastolic pressure of more than 20 mmHg during CPR. The trend for the EDM, NICO, STAT CCO, and trend CCO monitors are summarized in Figure 1, along with PETCO2 and SvO2 during the CPR period. The CO measured with EDM varied from 0 to 2.5 L/min, and the signal of descending aortic blood flow caused by chest compression was clearly visible during this event using EDM. Three rebreathing cycles were used with a NICO monitor during CPR. The first rebreathing cycles were applied at 2 minutes after the onset of VT and the CO and VCO2 were reported as 2.9 L/min and 104 mL/min, respectively. The second cycle was applied 5 minutes after the onset of VT and failed to estimate the CO. The third rebreathing cycle was applied at 8 minutes after the onset of VT, and the CO and VCO2 were

Ethyl pyruvate improves systemic and hepatosplanchnic hemodynamics and prevents lipid peroxidation in a porcine model of resuscitated hyperdynamic endotoxemia*

To investigate the systemic, pulmonary, and hepatosplanchnic hemodynamic and metabolic effects of delayed treatment with ethyl pyruvate in a long-term porcine model of hyperdynamic endotoxemia. Prospective, randomized, controlled experimental study with repeated measures. Investigational animal laboratory. Anesthetized, mechanically ventilated, and instrumented pigs. After 12 hrs of continuous infusion of lipopolysaccharide and hydroxyethyl starch to keep mean arterial pressure >60 mm Hg, swine randomly received placebo (Ringer's solution; control group, n = 11) or ethyl pyruvate in lactated Ringer's solution (n = 8; 0.03 g.kg(-1) loading dose over 10 mins, thereafter 0.03 g.kg(-1)hr(-1) for 12 hrs). Whereas mean arterial pressure significantly decreased in control animals, mean arterial pressure was maintained at the baseline level in pigs treated with ethyl pyruvate. Global oxygen uptake was comparable, so that the trend toward a higher oxygen transport and the significantly higher mixed venous hemoglobin oxygen saturation resulted in a significantly lower oxygen extraction in the ethyl pyruvate group. Ethyl pyruvate reduced intrapulmonary venous admixture and resulted in significantly greater Pa(O2)/F(IO2) ratios. Despite comparable urine production in the two groups during the first 18 hrs of endotoxemia, ethyl pyruvate significantly increased diuresis during the last 6 hrs of the study. Lipopolysaccharide-induced systemic and regional venous metabolic acidosis was significantly ameliorated by ethyl pyruvate. Endotoxemia increased both blood nitrate + nitrite and isoprostane concentrations, and ethyl pyruvate attenuated the response of these markers of nitric oxide production and lipid peroxidation. Ethyl pyruvate infusion resulted in improved hemodynamic stability and ameliorated acid-base derangements induced by chronic endotoxemia in pigs. Reduced oxidative stress and an decreased nitric oxide release probably contributed to these effects.

THE CARDIOPULMONARY, EICOSANOID, AND TISSUE MICROANATOMIC EFFECTS OF FLUCONAZOLE DURING GRADED BACTEREMIA

Imidazole compounds have been shown to be beneficial in systemic sepsis and inflammation. The purpose of this study was to delineate the effects of fluconazole on systemic hemodynamics and on microanatomy of the heart, lung, liver, and kidney parenchyma of swine during graded bacteremia. Eighteen adult swine were studied in three groups: 1), anesthesia control; 2), septic control (Aeromonas hydrophila, 10(9)/mL, infused i.v. for 4 h); 3) fluconazole (fluconazole, 30 mg/kg i.v., followed by A. hydrophila infusion). After 4 h of graded bacteremia, autopsy was performed. Compared with the septic control group, cardiac index, oxygen delivery, and oxygen consumption were reduced significantly after fluconazole pretreatment, and mixed venous hemoglobin oxygen saturation (SVO2) and oxygen extraction were increased. Plasma thromboxane A2 and leukotriene levels were not affected by fluconazole. Computerized digital image analysis of the liver, heart, and kidney specimens revealed no statistically significant differences between the septic control group and fluconazole-pretreated animals. In the lung specimens, preinfusion of fluconazole decreased alveolar wall thickness in septic swine (anesthesia control group: 8.15 x 10(-3) +/- 1.3 x 10(-3)mm versus septic control group: 9.9 x 10(-3) +/- 1.3 x 10(-4) versus fluconazole group: 6.8 x 10(-3) +/- 1.6 x 10(-3); p < or = .05). Fluconazole pretreatment before graded bacteremia has no beneficial effect on cardiopulmonary performance or septic tissue edema of the heart, kidney, or liver. Tissue oxygen metabolism might be down-regulated by fluconazole. However, preinfusion of fluconazole appears to normalize the sepsis-induced increase in pulmonary alveolar wall thickness. The net significance of these changes on clinical outcome is not clear from these data.

Inhaled Nitric Oxide Reverses the Increase in Pulmonary Vascular Resistance Induced by Permissive Hypercapnia in Patients with Acute Respiratory Distress Syndrome

The aim of this prospective study was to determine if inhaled nitric oxide (NO) would reverse the increase in pulmonary arterial pressures and in pulmonary vascular resistance induced by acute permissive hypercapnia in patients with acute respiratory distress syndrome. In 11 critically ill patients (mean age 59 +/- 22 yr) with acute respiratory distress syndrome (Murray Score > or = 2.5), the lungs were mechanically ventilated with NO 2 ppm during both normocapnic and hypercapnic conditions. Four phases were studied: normocapnia (arterial carbon dioxide tension 38 +/- 6 mmHg, tidal volume (655 +/- 132 ml); normocapnia plus inhaled NO 2 ppm; hypercapnia (arterial carbon dioxide tension 65 +/- 15 mmHg, tidal volume 330 +/- 93 ml); and hypercapnia plus inhaled NO 2 ppm. Continuous recordings were made of heart rate, arterial pressure, pulmonary artery pressure, tracheal pressure, and tidal volume (by pneumotachograph). At the end of each condition, arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac output were measured. Simultaneous arterial and mixed venous blood samples were obtained to measure arterial oxygen tension, arterial carbon dioxide tension, mixed venous oxygen tension, arterial hemoglobin oxygen saturation, mixed venous hemoglobin oxygen saturation, pH, and blood hemoglobin and methemoglobin concentrations (by hemoximeter). In addition, plasma concentrations of catecholamines were measured with a radioenzymatic assay. In 5 patients, end-tidal carbon dioxide tension was measured with a nonaspirative infrared capnometer. Calculations were made of pulmonary vascular resistance index, systemic vascular resistance index, true pulmonary shunt, and alveolar dead space. During hypercapnia, NO decreased pulmonary vascular resistance index from 525 +/- 223 to 393 +/- 142 dyn.s.cm-5.m-2 (P < 0.01), a value similar to that measured in normocapnic conditions (391 +/- 122 dyn.s.cm-5.m-2). It also reduced mean pulmonary artery pressure from 40 +/- 9 to 35 +/- 8 mmHg (P < 0.01). NO increased arterial oxygen tension (inspired oxygen fraction 1) from 184 +/- 67 to 270 +/- 87 mmHg during normocapnia and from 189 +/- 73 to 258 +/- 101 mmHg during hypercapnia (P < 0.01). NO decreased true pulmonary shunt during normocapnia (from 34 +/- 3% to 28 +/- 4%, P < 0.001) but had no significant effect on it during hypercapnia (39 +/- 7% vs. 38 +/- 8.5%). In five patients, NO resulted in a decrease in alveolar dead space from 34 +/- 7% to 28 +/- 10% in normocapnic conditions and from 30 +/- 9% to 22 +/- 10% in hypercapnic conditions (P < 0.05). Inhaled NO completely reversed the increase in pulmonary vascular resistance index induced by acute permissive hypercapnia. It only partially reduced the pulmonary hypertension induced by acute permissive hypercapnia, probably because the flow component of the increase in pulmonary pressure (i.e., the increase in cardiac output) was not reduced by inhaled NO. A significant increase in arterial oxygenation after NO administration was observed during normocapnic and hypercapnic conditions. A ventilation strategy combining permissive hypercapnia and inhaled NO may reduce the potentially deleterious effects that permissive hypercapnia alone has on lung parenchyma and pulmonary circulation.

Hemodynamic effects of carbon dioxide pneumoperitoneum during mechanical ventilation and positive end-expiratory pressure.

Laparoscopy is frequently used for diagnosis and treatment of critically ill trauma patients. Its effects on cardiopulmonary performance in the intensive care unit patient population, however, are not well-defined. This study evaluated the effects of positive end-expiratory pressure (PEEP) and carbon dioxide (CO2) pneumoperitoneum on hemodynamic function during mechanical ventilation. Five anesthetized, mechanically ventilated adult swine were monitored with pulmonary artery and arterial catheters at 0, 5, 10, 15, and 20 cm H2O PEEP without, and then with 15 mm Hg CO2 pneumoperitoneum. A hemodynamic profile, analyses of arterial and mixed venous blood gases and mixed venous hemoglobin oxygen saturation values were obtained at each data point. Compared with the non-insufflated group, CO2 pneumoperitoneum significantly increased central venous pressure, mean arterial pressure, mean pulmonary artery pressure, pulmonary vascular resistance index, and stroke index for the range of PEEP levels. With PEEP of 10 cm H2O, hemodynamic changes in non-insufflated animals were not statistically significant, but with CO2 pneumoperitoneum, stroke index and left ventricular stroke work index were decreased at 5 cm H2O PEEP, as was cardiac index at 10 cm PEEP. Pulmonary gas exchange was not affected by CO2 pneumoperitoneum. The results indicate that, in this paradigm, CO2 pneumoperitoneum for laparoscopy increases ventricular afterload and exacerbates the adverse effects of PEEP. These findings could be clinically significant in critically ill patients.

Effects of Anemia on Pulse Oximetry and Continuous Mixed Venous Hemoglobin Saturation Monitoring in Dogs

The accuracy of pulse oximetry (for pulse hemoglobin oxygen saturation [SpO2]) and mixed venous oximetry (for mixed venous hemoglobin oxygen saturation [SvO2]) was assessed during progressive normovolemic anemia in dogs. Splenectomized mongrel dogs under general anesthesia were monitored with a three-wavelength pulmonary artery oximeter catheter (10 dogs) and a pulse oximeter (11 dogs). Data were collected while fractional inspired oxygen concentration (FIO2) was varied from 1.00 to 0.05 in seven steps. The dogs then underwent isovolemic hemodilution, and the FIO2 was again varied. This sequence continued until data no longer could be obtained. The accuracy of each device was assessed by determining the bias (the average difference between the continuous monitor oximeter and the bench oximeter) and the precision (the standard deviation of the difference). For the three-wavelength Oximetrix catheter (for hemoglobin oxygen saturation denoted here SoxO2), the overall bias (SoxO2 - SvO2) and precision were -0.7 +/- 8.6% for the 193 data points. The accuracy as assessed by bias and precision for SoxO2 was similar for hematocrits of 40-15%. (Bias +/- precision was 2.1 +/- 5.7% for hematocrits greater than 40%, and -1.1 +/- 7.5% for hematocrits of 15% to 19%). At hematocrits between 10 and 14%, the precision worsened to 12%, and for hematocrits less than 10% the bias +/- precision was -11.5 +/- 11.8%. The overall SpO2 accuracy was 0.2 +/- 7.6% for 178 points. The pulse oximeter's accuracy was similar, down to hematocrits of 10%. Below 10%, the bias and precision worsened to -5.4 +/- 18.8%.(ABSTRACT TRUNCATED AT 250 WORDS)