A nomogram to evaluate the arterial mixed venous oxygen saturation difference during cardiopulmonary bypass

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.

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.


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.


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.


1977 ◽  
Vol 42 (1) ◽  
pp. 39-43 ◽  
Author(s):  
S. M. Cain

O2 stores are kept more intact in apnea than in N2 breathing which removes O2stores from the body. If lactate moves readily into the circulation, arterial lactate should rise sooner with N2 breathing than with apnea because tissue O2 is lowered faster. This was tested in 10 anesthetized, paralyzed dogs made hypoxic both ways. Arterial and mixed venous blood were sampledevery minute until circulation began to fail. Calculated changes in O2 stores would have supported control V O2 for 1.3 min with N2 and 2.7 min with apnea. The PVO2 at those times were 23.1 and 20.1 Torr. Although arterial lactate rose sooner with N2 than with apnea, the mean values for lactate increase for both N2 and apnea were fitted by a single curvilinear relation with PVO2. The PVO2 at which lactate first rosores were depleted. Latent period for lactate rise, therefore, was nearly the same as that for development of tissue hypoxia.


1981 ◽  
Vol 4 (2) ◽  
pp. 76-81 ◽  
Author(s):  
T. Kolobow ◽  
R.G. Spragg ◽  
J.E. Pierce

We provided total cardiopulmonary support for 1-18 hours in unanesthetized tethered lambs by peripheral vascular cannulation, using a roller pump and the spiral membrane lung. Respirations were allowed to remain spontaneous and unaided. A Swan-Ganz catheter was placed for retrograde pulmonary artery blood flow sampling. Within a few minutes following induced ventricular fibrillation the PCO2 of sampled blood flowing retrograde through the lungs fell below 10 mm Hg, the PO2 rose to near 150 mm Hg, the pH rose to above 7.8, and the glucose level fell to less than 20 mg %. All of these values later gradually shifted, approaching mixed venous blood values within minutes. After 1-18 hrs of perfusion the animals went into shock and were sacrificed. At autopsy, the lungs of animals breathing room air were beefy and hemorrhagic. In lambs that were «breathing» CO2 enriched air the retrograde pulmonary artery blood pH and PCO2 was usually maintained close to the mixed venous blood values. The observed pulmonary changes were considerably less abnormal, and the microscopic abnormalities were at times nonexistent. We believe the integrity of pulmonary blood flow is vital to the survival of the lungs as a functioning organ. Cessation of total forward pulmonary blood flow (unlike partial cardiopulmonary bypass), combined with spontaneous pulmonary ventilation, rapidly leads to massive, pulmonary infactions, shock, and death.


Perfusion ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 315-321 ◽  
Author(s):  
F. Cavaliere ◽  
A. Gennari ◽  
L. Martinelli ◽  
R. Zamparelli ◽  
R. Schiavello

The relationship between oxygen delivery (DO2) and uptake (VO2) has been studied during moderately hypothermic cardiopulmonary bypass (CPB) in 15 patients undergoing myocardial revascularization. As soon as nasopharyngeal temperature was lowered to 32°C, blood flow was decreased from 2.4 to 2.0 l/min/m 2. Arterial and mixed venous blood gas analyses were performed five and eight minutes later and DO2 and VO2 were calculated; VO2 stabilized in five minutes after changing blood flow and neither DO2 nor VO2 values changed three minutes later (DO 2: 217 ± 19 versus 215 ± 17 ml/min/m2; VO2: 63 ± 12 versus 66 ± 14 ml/min/m2). Blood flow then was increased to 2.3 l/min/m2 and DO2 and VO2 were determined again, five minutes later; they both increased significantly, to 243 ± 20 and 74 ± 13 ml/min/m 2, respectively. However, a further blood flow increase to 2.6 l/min/m 2 which caused DO2 to increase to 277 ± 24 ml/min/m 2, did not affect VO2 which was unchanged five minutes later (76 ± 13 ml/min/m2); VO2 dependence on DO2 values higher than 243 ± 20 ml/min/m2 was consequently ruled out. Ten patients, having a mean arterial pressure higher than 80 mmHg, were eventually vasodilated with hydralazine, 0.1 mg/kg intravenously, and DO2 and VO2 were determined after five and ten minutes. As blood flow did not change, DO2 was unaffected while a slight increase in VO2 mean values was observed which was not statistically significant (prior to hydralazine: 78 ± 15 ml/min/m2; five minutes later: 82 ± 17 ml/min/m2; 10 minutes later: 76 ± 18 ml/min/m2). In conclusion, during hypothermic CPB at 32°C, VO2 plateau ranges between 48 and 102 mi/min/m 2 (mean ± 2 SD) in 95% of patients, corresponding to 66 and 141 ml/min/m 2 at 37°C; this finding closely matches other literature reports. Consequently, lower VO2 values suggest inadequate oxygen supply to tissues. Critical DO2 at 32°C is lower than 283 ml/min/m2 in 97.5% of patients. Finally, arterial vasoconstriction does not seem to play a significant role in tissue hypoperfusion.


1960 ◽  
Vol 15 (3) ◽  
pp. 390-392 ◽  
Author(s):  
Stephen M. Cain ◽  
Arthur B. Otis

The ventilation of one lung in dogs was isolated and that lung continually rebreathed into a small rubber bag. The Pco2 of a sample of the gas in the rebreathing bag was compared with the Pco2 calculated from pH and bicarbonate concentration determined in a sample of mixed venous blood drawn simultaneously. Before the injection of a carbonic anhydrase inhibitor, acetazolamide, the difference between the two values for Pco2 was not significant. After acetazolamide, a highly significant difference (P < 0.001) was found. Apparently, when carbonic anhydrase was inhibited, the dissolved CO2 of mixed venous blood did not attain equilibrium with bicarbonate by the time the blood entered the lung. Submitted on December 18, 1959


1996 ◽  
Vol 81 (2) ◽  
pp. 998-1006 ◽  
Author(s):  
E. M. Williams ◽  
R. Hamilton ◽  
L. Sutton ◽  
C. E. Hahn

A companion paper (C. E. W. Hahn. J. Appl. Physiol 81: 985–997, 1996) described a continuous-flow gas-exchange mathematical model, which predicted that forced inspired oxygen sinusoids could be used to measure respiratory parameters rapidly, in place of the inert gas argon. We therefore made simultaneous measurements of dead space volume (VD) and alveolar volume (VA) in an animal model, using argon and oxygen inspired gas concentration sinusoid forcing signals, and then compared the results. Our data confirmed the model prediction that the attenuations of the oxygen and argon sinusoid perturbations are identical in the alveolar gas space, even though there is a net uptake of oxygen by the body. Our results show that the calculated values of VD and VA, obtained by using inspired oxygen forcing signals, were independent of both the mean fractional inspired oxygen concentration (FIO2; range 0.18–0.80% vol/vol) and the oxygen forcing signal amplitude (range +/- 2–6% vol/vol). In these studies, oxygen forcing signals, with forcing periods between 1 and 2 min, were able to measure controlled changes in instrument dead space to within 16 ml and also measure positive end-expiratory pressure-induced changes in VA. Under hyperoxic conditions, intravascular oxygen sensors confirmed that the sinusoidal PO2 signal passed into the arterial blood but not into the mixed-venous blood. However, the sinusoid perturbation PO2 signal did pass into the mixed-venous blood when the mean FIO2 was mildly hypoxic (FIO2 = 0.18% vol/vol). These data show that oxygen can be used instead of argon to measure airways dead space and VA.


2018 ◽  
Vol 1 (2) ◽  
pp. 114
Author(s):  
Wahdaniah Wahdaniah ◽  
Sri Tumpuk

Abstract: Routine blood examination is the earliest blood test or screening test to determine the diagnosis of an abnormality. Blood easily froze if it is outside the body and can be prevented by the addition of anticoagulants, one of which Ethylene Diamine Tetra Acetate (EDTA). Currently available vacuum tubes containing EDTA anticoagulants in the form of K2EDTA and K3EDTA. K3EDTA is usually a salt that has better stability than other EDTA salts because it shows a pH approaching a blood pH of about 6.4. The purpose of this research is to know the difference of erythrocyte index results include MCH, MCV and MCHC using K3EDTA anticoagulant with K2EDTA. This research is a cross sectional design. This study used venous blood samples mixed with K2EDTA anticoagulant and venous blood mixed with K3EDTA anticoagulants, each of 30 samples. Data were collected and analyzed using paired different test. Based on data analysis that has been done on MCH examination, p value <0,05 then there is a significant difference between samples with K3EDTA anticoagulant with K2EDTA to erythrocyte index value. Then on the examination of MCV and MCHC obtained p value <0.05 then there is no significant difference between samples with K3EDTA anticoagulant with K2EDTA to erythrocyte index value.Abstrak: Pemeriksaan darah rutin merupakan pemeriksaan darah yang paling awal atau screening test untuk mengetahui diagnosis suatu kelainan. Darah mudah membeku jika berada diluar tubuh dan bisa dicegah dengan penambahan antikoagulan, salah satunya Ethylene Diamine Tetra Acetate (EDTA). Dewasa ini telah tersedia tabung vakum yang sudah berisi antikoagulan EDTA dalam bentuk  K2EDTA dan  K3EDTA. K3EDTA  biasanya berupa garam yang mempunyai stabilitas yang lebih baik dari garam EDTA yang lain karena menunjukkan pH yang mendekati pH darah yaitu sekitar 6,4. Tujuan dari penelitian ini adalah untuk mengetahui perbedaan hasil indeks eritrosit meliputi MCH, MCV dan MCHC menggunakan antikoagulan K3EDTA dengan K2EDTA. Penelitian ini merupakan penelitian dengan desain cross sectional. Penelitian ini menggunakan sampel darah vena yang dicampur dengan antikoagulan K2EDTA dan darah vena yang dicampur dengan antikoagulan K3EDTA, masing-masing sebanyak 30 sampel. Data dikumpulkan dan dianalisis menggunakan uji beda berpasangan. Berdasarkan analisis data yang telah dilakukan pada pemeriksaan MCH didapatkan nilai p < 0,05 maka ada perbedaan yang signifikan antara sampel dengan antikoagulan K3EDTA dengan K2EDTA terhadap nilai indeks eritrosit. Kemudian pada pemeriksaan MCV dan MCHC didapatkan nilai p < 0,05 maka tidak ada perbedaan yang signifikan antara sampel dengan antikoagulan K3EDTA dengan K2EDTA terhadap nilai indeks eritrosit.


1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)


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