The depth of anaesthesia associated with the administration of isoflurane 2.5% during cardiopulmonary bypass

Perfusion ◽  
2019 ◽  
Vol 34 (5) ◽  
pp. 392-398 ◽  
Author(s):  
R Peter Alston ◽  
Michael Connelly ◽  
Christopher MacKenzie ◽  
George Just ◽  
Natalie Homer

Background:Administering isoflurane 2.5% into the oxygenator during cardiopulmonary bypass results in no patient movement. However, doing so may result in an excessive depth of anaesthesia particularly, when hypothermia is induced. Bispectral index and arterial blood and oxygenator exhaust concentrations of volatile anaesthetics should be related to depth of anaesthesia. The primary aim of this study was to measure the depth of anaesthesia using bispectral index, resulting from administering isoflurane 2.5% into the oxygenator during cardiopulmonary bypass, and secondary aims were to examine the relationships between blood and oxygenator exhaust isoflurane concentrations and bispectral index.Methods:Arterial and mixed-venous blood samples were aspirated at three time points during cardiopulmonary bypass and measured for isoflurane concentration using mass spectrometry. Simultaneously, oxygenator exhaust isoflurane concentration, nasopharyngeal temperature and bispectral index were recorded.Results:When averaged across the three time points, all patients had a bispectral index score below 40 (binomial test, p < 0.001). There were no significant correlations between bispectral index score and arterial or mixed-venous blood isoflurane concentrations (r = –0.082, p = 0.715; r = –0.036, p = 0.874) and oxygenator exhaust gas concentration of isoflurane (r = –0.369, p = 0.091).Conclusion:When 2.5% isoflurane was administered into the sweep gas supply to the oxygenator during cardiopulmonary bypass, all patients experienced a bispectral index score less than 40 and no significant relationship was found between either arterial or mixed-venous blood or oxygenator exhaust concentrations of isoflurane and bispectral index.

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.


1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963


1963 ◽  
Vol 18 (2) ◽  
pp. 345-348 ◽  
Author(s):  
Winnifred F. Storey ◽  
John Butler

We studied 10 patients with intracardiac left-to-right shunt and 13 patients with other cardiac lesions during exercise. The hyperpnea of muscular exercise was independent of the mixed venous Pco2. In the 13 patients without shunt both the pulmonary arterial Pco2 and the ventilation increased during exercise. In the 10 patients who had shunts ventilation increased during exercise even when the Pco2 in the pulmonary arterial blood did not rise. Submitted on July 5, 1962


1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962


2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan

The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.


1984 ◽  
Vol 56 (2) ◽  
pp. 370-374 ◽  
Author(s):  
B. P. Teisseire ◽  
C. D. Soulard

The O2 sensor that triggers hypoxic pulmonary vasoconstriction may be sensitive not only to alveolar hypoxia but also to hypoxia in mixed venous blood. A specific test of the blood contribution would be to lower mixed venous PO2 (PvO2), which can be accomplished by increasing hemoglobin-O2 affinity. When we exchanged transfused rats with cyanate-treated erythrocytes [PO2 at 50% hemoglobin saturation (P50) = 21 Torr] or with Creteil erythrocytes (P50 = 13.1 Torr), we lowered PvO2 from 39 +/- 5 to 25 +/- 4 and to 14 +/- 4 Torr, respectively, without altering arterial blood gases or hemoglobin concentration. Right ventricular systolic pressure increased from 32 +/- 2 to 36 +/- 3 Torr with cyanate erythrocytes and to 44 +/- 5 Torr with Creteil erythrocytes. Cardiac output was unchanged. Control exchange transfusions with normal rat or 2,3-diphosphoglycerate-enriched human erythrocytes had no effect on PvO2 or right ventricular pressure. Alveolar hypoxia plus high O2 affinity blood caused a greater increase in right ventricular systolic pressure than either stimulus alone. We concluded that PvO2 is an important determinant of pulmonary vascular tone in the rat.


Perfusion ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 133-139 ◽  
Author(s):  
Lena Lindholm ◽  
Vigdis Hansdottir ◽  
Magnus Lundqvist ◽  
Anders Jeppsson

The relationship between mixed venous and regional venous saturation during cardiopulmonary bypass (CPB), and whether this relationship is influenced by temperature, has been incompletely elucidated. Thirty patients undergoing valve and/or coronary surgery were included in a prospective, controlled and randomized study. The patients were allocated to two groups: a hypothermic group (28°C) and a tepid group (34°C). Blood gases were analysed in blood from the hepatic vein and the jugular vein and from mixed venous blood collected before surgery, during hypothermia, during rewarming, and 30 min after CPB was discontinued. Oxygen saturation in the hepatic vein was lower than in the mixed venous blood at all times of measurement (-24.0 ± 3.0% during hypothermia, -36.5 ± 2.9% during rewarming, and -30.5 ± 3.0% postoperatively, p < 0.001 at all time points). In 23% of the measurements, the hepatic saturation was < 25% in spite of normal (> 60%) mixed venous saturation. There was a statistical correlation between mixed venous and hepatic vein oxygen saturation (r = 0.76, p < 0.0001). Jugular vein oxygen saturation was lower than mixed venous saturation in all three measurements (-21.6 ± 1.9% during hypothermia, p < 0.001; -16.7 ± 1.9% during rewarming, p < 0.001; and -5.6 ± 2.2% postoperatively, p = 0.037). No significant correlation in oxygen saturation could be detected between mixed venous and jugular vein blood ( r = 0.06, p = 0.65). Systemic temperature did not influence the differences in oxygen saturation between mixed venous and regional venous blood at any time point. In conclusion, regional deoxyge-nation occurs during CPB, in spite of normal mixed venous saturation. Mixed venous oxygen saturation correlates with hepatic, but not with jugular, vein saturation. The level of hypothermia does not influence differences in oxygen saturation between mixed venous and regional venous blood.


1998 ◽  
Vol 274 (1) ◽  
pp. H349-H357 ◽  
Author(s):  
Yuko Takahashi ◽  
Hirosuke Kobayashi ◽  
Naohiko Tanaka ◽  
Tetsuya Sato ◽  
Naosada Takizawa ◽  
...  

During nitric oxide (NO) inhalation therapy, NO combines with deoxyhemoglobin to form nitrosyl hemoglobin (HbNO). We used electron spin resonance (ESR) spectroscopy to measure HbNO in arterial and mixed venous blood of normoxic and hypoxic sheep during NO inhalation. Our aim was to quantitatively measure HbNO levels in the blood during NO inhalation, because large amounts of HbNO reduce the oxygen capacity of blood, particularly in hypoxia. Another aim was to investigate the transfer of exogenous NO to the α-heme iron of hemoglobin. Thirteen sheep were anesthetized with pentobarbital sodium, and 60 parts per million (ppm) NO were administered for 1 h in the presence of normoxia and hypoxia. Two-way analysis of variance revealed that the HbNO level was dependent on the oxygen level (normoxia vs. hypoxia) and NO inhalation, and there was a significant negative correlation between the HbNO level and arterial O2 saturation ([Formula: see text]). Although the HbNO level increased during NO inhalation in hypoxia, the HbNO level at[Formula: see text] >60% was <11 μmol/l monomer hemoglobin (0.11% of total 10 mmol/l monomer hemoglobin). The peak of the HbNO ESR spectrum in arterial blood is located in almost the same position in mixed venous blood with an asymmetric HbNO signal, indicating that the NO in β-heme HbNO molecules had been transferred to α-heme molecules. The three-line hyperfine structure of HbNO on ESR spectra was distinct in venous blood in hypoxia during NO inhalation, indicating pentacoordinate α-NO heme formation in hypoxic blood. In conclusion, the amount of HbNO during 60 ppm NO inhalation did not considerably reduce the oxygen capacity of the blood even in the presence of hypoxia, and the NO of HbNO was transferred to the α-heme iron of hemoglobin, forming pentacoordinate α-NO heme in mixed venous blood in hypoxia.


Perfusion ◽  
1998 ◽  
Vol 13 (1) ◽  
pp. 45-51 ◽  
Author(s):  
F Cavaliere

A nomogram providing the arterial mixed venous haemoglobin saturation difference (Sa-vO2) corresponding to normal oxygen consumption (VO2) during cardiopulmonary bypass (CPB) was produced. Normal VO2 during CPB (95.8 ± 20.1 ml/min/m2 at 37°C) was obtained from the literature. The nomogram computes the Sa-vO2 from the body surface, pump flow, blood haemoglobin and patient temperature; a table is also presented which supplies the Sa-vO2 ranges corresponding to VO2 mean ±1 and ±2SD. The nomogram was tested on 10 subjects undergoing CPB for myocardial revascularization. Sa-vO2 was determined by arterial and mixed venous blood oximetry 5, 20, and 35 min after the start of CPB. The measured Sa-vO2 was 27.1 ± 7.2% while Sa-vO2 obtained from the nomogram was 24.9 ± 4.0%, the difference was not statistically significant. Eighteen values (60%) were within the range corresponding to VO2 mean ±1SD. One value was lower than the Sa-vO2 value corresponding to VO2 mean - 2SD and was associated with the lowest value of blood haemoglobin. Two values were higher than the Sa-vO2 value corresponding to VO2 mean + 2SD and were associated with inadequate muscle relaxation. By comparing measured Sa-vO2 values with those obtained by the nomogram and the table, anaesthesiologists and perfusionists can easily detect patients presenting abnormally low or high VO2 values.


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