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Ann Thorac Surg 2004;77:1671-1677
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Continuous measurement of oxygen consumption during cardiopulmonary bypass: description of the method and in vivo observations

Jia Li, MD, PhDa, Jacqueline Stokoe, CCPb, Igor E. Konstantinov, MDc, David Edgell, CCPb, Michael M. H. Cheung, MRCPa, Rajesh K. Kharbanda, MRCPd, Andrew N. Redington, FRCPa*

a Division of Cardiology, Toronto, Ontario, Canada
b Division of Perfusion, Toronto, Ontario, Canada
c Division of Cardiovascular Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada
d Division of Cardiovascular Medicine, Addenbrookes Hospital, Cambridge University, Cambridge, United Kingdom

Accepted for publication October 2, 2003.

* Address reprint requests to Prof Redington, Division of Cardiology, The Hospital for Sick Children, 555 University Ave, Toronto, ON, Canada M5G 1X 8
e-mail: andrew.redington{at}sickkids.ca


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
BACKGROUND: Systemic oxygen consumption is not routinely measured during cardiopulmonary bypass, despite its potential benefits. We aimed to develop a noninvasive method to continuously measure oxygen consumption using respiratory mass spectrometry during hypothermic cardiopulmonary bypass in pigs.

METHODS: Nine pigs weighing 18.5 (1.6) kg underwent hypothermic (32°C) cardiopulmonary bypass for 180 minutes with 120 minutes of aortic cross clamping. An AMIS 2000 mass spectrometer (Innovision A/S, Odense, Denmark) was adapted for the on-line measurement of oxygen consumption by sampling the inlet and outlet gases of the membrane oxygenator together with measurement of the "expired" gas volume.

RESULTS: Active cooling for 60 minutes reduced the venous blood temperature by 2.9 (0.8) °C and VO2 by 0.70 (0.33) mL/kg/min. The 40-minute active rewarming restored the venous blood temperature by 4.4 (0.4) °C and oxygen consumption increased by 1.36 (0.33) mL/kg/min. There was wide interanimal variability, however, particularly at higher venous blood temperatures. Immediately after the release of aortic cross clamp, there was a noticeably acute increase in oxygen consumption in all the pigs (0.64 [0.21] mL/kg/min).

CONCLUSIONS: A simple and safe adaptation of mass spectrometry allows continuous measurement of oxygen consumption during hypothermic cardiopulmonary bypass. The wide interindividual variations observed in this pilot study underscore the need to more accurately describe changes in oxygen consumption and how they are affected by temperature, oxygen delivery, and other interventions during cardiopulmonary bypass. As such, the technique may have an important role in clinical research and management of oxygen transport in patients undergoing cardiac surgery.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Cardiopulmonary bypass (CPB) remains integral to the surgical correction of many acquired and congenital heart diseases. An important goal in the conduct of CPB is to match body systemic oxygen consumption (VO2), as a surrogate of the global metabolic activity, with the often reduced oxygen delivery [1, 2]. Systemic hypothermia is commonly employed during CPB to decrease cellular metabolism and oxygen requirement in order to minimize the risk of organ ischemia. Indeed, much attention has been paid to the measurements of VO2 and its response to factors such as temperature [3], flow rate [2, 4], and therapeutic agents [5, 6]. Most often, VO2 has been calculated by the reverse Fick principle [2–6]. However, small errors may be introduced in the measurements of the elements in the Fick equation, including blood gas tensions and flow rate. Additionally, arterial to venous shunts in the CPB system also affect calculation of blood flow. Finally, the intermittent measurement of VO2 using the reverse Fick method does not take into account the potentially highly dynamic nature of VO2 during CPB.

Respiratory mass spectrometry has been used for almost five decades for continuous gas analysis in clinical and experimental studies [7]. It is considered by many to be the gold standard method for measuring VO2 [8], but only one study has described its use, in 4 patients, to measure VO2 during CPB [9]. The use of inlet tracer gas and the need for a flow meter in that study reduced the clinical applicability and accuracy of the technique described, but both of these factors can be overcome using modern mass spectrometers. Indeed, the use of the indicator gas dilution technique described first by Davies and Denison [10], has been modified and used by us to study VO2 in ventilated adults and children before and after [11, 12], but never during, CPB.

The aim of this study was to describe an application of respiratory mass spectrometry to measure VO2 during CPB, to assess its feasibility, and to obtain detailed information about the changes in VO2 throughout CPB in an animal model.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Anesthesia
After review and approval by the Institutional Animal Care and Use Committee of the research institute in the Hospital for Sick Children, nine Yorkshire pigs weighing 15.6 to 20.8 kg (mean 18.5 kg) were studied. Premedication was given with intramuscular ketamine (33 mg/kg) and midazolam (0.3 mg/kg). Anesthesia was induced with inhaled isoflurane (5%). After the onset of anesthesia, the trachea was intubated and muscle relaxation was obtained with peripheral intravenous infusion of pancuronium (0.1 mg/kg). Ventilation was initially controlled with a Servo 900C ventilator (Siemens Medical Systems, Solna, Sweden). Anesthesia was maintained with isofluorane 1.5% to 2%, and muscle relaxation by continuous infusion of pancuronium (0.8 µg /kg/min). The right carotid artery and jugular vein were cannulated for arterial pressure monitoring and infusions.

Cardiopulmonary bypass
A median sternotomy was performed. Venous drainage to the extracorporeal circuit was by a 32 to 24F two-stage venous cannula (Stockert Instrumente, Munich, Germany) placed in the right atrium via the right atrial appendage. The blood was circulated by a roller pump through a hollow fiber membrane oxygenator (Dideco702, Dideco, Mirandola, Italy) and returned via a 14F arterial cannula (Jostra, Hirrlinger, Germany) into the root of the aorta. Before aortic cannulation, intravenous heparin (300 to 400 U/kg) was given to maintain an activated coagulation time greater than 480 seconds. The bypass machine was primed with 250 mL of whole blood obtained from a donor pig and 650 mL Plasmalyte148 solution together with 22 mEq/L NaHCO3 and 5,000 U of heparin. Venous blood temperature was continuously monitored by an in-line thermistor at the blood inlet of the membrane oxygenator. The lungs were not ventilated. Isofluorane was delivered into the gas inflow to the membrane oxygenator. After establishing CPB, the aorta was cross-clamped (ACC) and cardioplegic arrest was achieved with cold cardioplegia (30 mL/kg) of 2:1 blood and crystalloid (BCD-Vanguard, COBE Cardiacvascular Inc, Mirandola, Italy). Active cooling was then performed using the integrated oxygenator heat exchanger until venous blood temperature reached to 32°C. Animals underwent 120 minutes of ACC and cardioplegic arrest. Stable hypothermia was maintained until 20 minutes before the release of ACC when active rewarming was commenced to restore the venous temperature to 36°C. Spontaneous ventricular fibrillation was reversed with the use of a defibrillator (43100A Defibrillator, Hewlett-Packard, McMinnville, OR). Cardiopulmonary bypass was continued for approximately 60 minutes. Throughout CPB, the nonpulsatile flow was maintained approximately 90 mL/kg/min, increasing during rewarming to 97 (8) mL/kg/min, so that the mean arterial pressure ranged from 40 to 60 mm Hg. No vasoconstrictors or vasodilators were used. The inflow oxygen fraction to the oxygenator was adjusted between 55% and 70% in all but one (80%) to maintain the arterial PaO2 between 100 to 300 mm Hg. Hematocrit was maintained between 20% and 25% with donor blood transfusion. Arterial and venous blood gases and lactate were measured at 30, 90, and 120 minutes at removal of ACC, and 150 minutes during CPB by a gas analyzer Hemotherm Cooler-Heater (Cincinnati Sub-Zero, Cincinnati, OH). Venous blood temperature was recorded every 10 minutes.

Oxygen consumption measurements
Direct measurement of VO2
An AMIS 2000 quadrupole mass spectrometer (Innovision A/S, Odense, Denmark) was adapted for the on-line measurements of systemic VO2 during CPB. This is a highly sensitive and accurate method for continuous gas analysis, which allows simultaneous measurements of multiple gas fractions within a mixture. Oygen consumption was measured using the mixed expirate inert gas (argon) dilution method [10]. Our adaptation for use in ventilated patients has been described elsewhere [11]. Measurements of VO2 require analysis of inspired and expired gases together with the measurement of expiratory gas volume by collection of all expired gas into a mixing box and analysis of the dilution of the indicator gas, argon, delivered at a rate of 40 mL/min at its inlet port. For the measurement of VO2 during CPB, slight modifications were made (Fig 1). The "inspiratory" sampling inlet was placed in the gas inlet port of the oxygenator via a connector (1/4 in x 1/4 in Luer Lock). The sampling rate was 10 to 20 mL/min (total inlet gas flow 1.5 to 2.0 L/min). A tube wider than the outlet port of the membrane oxygenator was used to direct the "expired" gas to the mixing box. The additional gas escape port was occluded. Careful attention was paid to avoid any obstruction of gas exhaust from any kink of the tubing. Gas leaks were excluded using a spare inlet of the mass spectrometer by ensuring that no oxygen and carbon dioxide signals greater than atmospheric could be detected at any place along the circuit. An "expiratory" sampling inlet of the mass spectrometer was used to measure mixed expirate gases from the distal end of the mixing box. As an open circuit system the outlet of the mixing box is exposed to air, therefore no positive pressure was created in this circuit. The VO2 was measured every 30 seconds, and displayed on a computer screen along with carbon dioxide production and ventilation volume.



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  		Fig 1. A diagram of the setup of the AMIS 2000 respiratory mass spectrometer to measure VO2 across the oxygenator of the cardiopulmonary bypass. The inspiratory sampling inlet is placed in the gas inlet port of the oxygenator. A tube is connected from the gas outlet port of the oxygenator to direct the expired gas to the mixing box. An expiratory sampling inlet of the mass spectrometer is placed to the distal end of the mixing box to measure mixed expirate gases. The outlet of the mixing box is exposed to air. (VO2 = oxygen consumption.)

 
Calculated VO2
Reverse Fick principle was used to calculate VO2 by pump flow multiplying the difference of arterial and venous oxygen contents.

Statistics
Values are presented as mean ± standard deviation (SD). Comparisons were carried out by using the paired two-tailed t test. Correlation between two data sets was assessed using the correlation coefficient. The change of the data over the study period was analyzed with one-way repeated measures of analysis of variance (ANOVA). The comparison between directly measured and calculated VO2 values was made using the method of Bland and Altman [13]. The p values less than 0.05 were considered significant.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
No complications occurred from the use of the mass spectrometer to measure VO2 during CPB. Figure 2 shows an example of the continuous on-line recordings of VO2 from one pig throughout the period of CPB. Figure 3 shows all data points for VO2 and temperature measured in all pigs. While there is a statistically significant correlation between VO2 and the venous blood temperature during both cooling and rewarming periods, the slope of the trendline during rewarming was steeper than during cooling (r = 0.65 and 0.62, respectively, p < 0.001 for both). At any given temperature, there is wide interindividual variation, most marked at higher temperatures.



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  		Fig 2. An example of on-line measurement of VO2 during CPB in one pig shows a typical profile of the change in VO2 following the change of temperature with cooling and rewarming. Dotted line indicates the time of the release of ACC. Note an acute increase in VO2 immediately after the release of ACC (arrow). The two peaks before 30 minutes and after 150 minutes were due to the decrease and increase of the inspiratory oxygen concentration. (ACC = aortic cross clamping; CPB = cardiopulmonary bypass; VO2 = oxygen consumption.)

 


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  		Fig 3. All the values of VO2 measured in 9 pigs during cardiopulmonary bypass are pooled together and plotted against the venous blood temperature. Data during cooling are indicated as closed circles and during rewarming as open circles. Trendlines for all the data are indicated as solid, those for cooling and as dashed for rewarming. The slope during rewarming is steeper as compared to that during cooling. For any give temperature, there was wide variation in VO2 at any given temperature, which was greater at higher temperatures. (VO2 = oxygen consumption.)

 
Figure 4 demonstrates the composite changes of VO2 and venous blood temperature in 9 pigs during CPB. The total CPB period was divided into six sections: active cooling, stable hypothermia, active rewarming including 20 minutes before and after the release of ACC (with the latter further divided into the immediate 8 minutes after the release of ACC and the following 12 minutes), and stable euthermia.



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  		Fig 4. The changes of VO2 (solid line and closed circles) and the venous blood temperature (dotted line and open circles) in 9 pigs during CPB. The CPB is divided into active cooling (first and second 30 minutes), stable hypothermia (from 60 minutes to the beginning of active rewarming), active rewarming periods including 20 minutes before the release of ACC, 8 minutes immediately after the release of ACC with ventricular fibrillation occurring (note the acute increase of VO2) and the following 12 minutes, and the last 40 minutes of stable euthermia. Values are mean ± SD. (ACC = aortic cross clamping; CPB = cardiopulmonary bypass; SD = standard deviation; VO2 = oxygen consumption.)

 
Active cooling reduced the venous blood temperature by 2.9 (0.8) °C (34.9 [0.6] to 32.0 [0.8] °C) during the first 60 minutes after initiating CPB. The VO2 decreased by 0.70 (0.33) mL/kg/min (from 4.8 [0.6] to 4.1 [0.6] mL/kg/min), so that, for every degree centigrade decrease in the temperature, VO2 decreased 0.26 (0.16) mL/kg/min. There was some nonlinearity between the change in temperature and the change in VO2, however. The VO2 decreased by 0.43 (0.27) mL/kg/min as the temperature decreased by 2.2°C in the first 30 minutes of cooling (0.25 [0.23] mL/kg/min per degree centigrade) but the reduction in VO2 was greater per degree centigrade (0.49 [0.40] mL/kg/min per degree centigrade) during the second 30 minutes of cooling (p > 0.05) (Fig 5).



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  		Fig 5. The change in VO2 in relation to the change in the venous blood temperature during the initial and the next periods of active cooling and rewarming. The greater change of VO2 per degree centigrade during the later period indicates in part the uniformity of cooling and rewarming of the whole body at the relative steady venous blood temperature. The myocardial oxygen consumption may also partly account for the greater increase in VO2 during the later period of rewarming after the release of ACC (p < 0.05). Values are mean ± SD. (ACC = aortic cross clamping; CPB = cardiopulmonary bypass; SD = standard deviation; VO2 = oxygen consumption.)

 
Active rewarming commenced 20 minutes before the release of ACC and restored the venous blood temperature to 36.4 (0.3) at 20 minutes after the release of ACC. This was accompanied by 1.36 (0.33) mL/kg/min increase in VO2 to 5.3 (0.8) mL/kg/min, so that VO2 increased by 0.31 (0.08) mL/kg/min for every degree centigrade increase in the venous blood temperature. Similar nonlinearity of VO2 responses was seen during rewarming. The increase in VO2 was 0.16 (0.07) mL/kg/min per degree centigrade and 1.48 (1.48) mL/kg/min % per degree centigrade during the 20-minute periods before and after the release of ACC, respectively (p < 0.05) (Fig 5). The period of the most rapid velocity of VO2 rise was seen immediately after removal of the ACC. There was a noticeably acute increase in VO2 by 0.64 (0.21) mL/kg/min in all the pigs during the first 8 minutes after ACC removal (Figs 2 and 4), which accounted for 48 (15) % [14]of the total rise during the active rewarming period. The significant rise in VO2 during these rewarming periods is in consistency with the steeper trendline during rewarming shown in Figure 3. During the last 40 minutes of CPB, both the venous blood temperature and VO2 remained relatively stable, with the temperature being 36.5 (0.3) °C and VO2 5.5 (0.9) mL/kg/min at the termination of CPB (Fig 4).

Arterial blood lactate levels increased continuously and significantly during CPB from 4.5 (0.6) at 30 minutes, 6.4 (1.6) at 90 minutes, 7.6 (2.2) at 120 minutes, and 7.6 (1.8) mmol/L at 150 minutes (p < 0.0001). There was no correlation between lactate levels and absolute values of VO2 at any time points or the changes in VO2 during cooling and rewarming periods (r = – 0.09 to 0.38, p > 0.05).

Two points of data from each animal were used to compare the agreement between the directly measured and calculated VO2. The calculated method consistently underestimated VO2 as compared to the directly measured values with a bias of – 24.6 mL/min. Limits of agreement were ± 30.0 L/min. (Fig 6)



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  		Fig 6. Agreement of directly measured and calculated VO2 in the pigs during cardiopulmonary bypass. (SD = standard deviation; VO2 = oxygen consumption.)

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
This report describes the continuous, automated measurement of VO2 during CPB by mass spectrometry alone. On-line measurement of VO2 is feasible, and provides detailed information regarding the absolute level and changes of VO2 throughout the period of CPB.

The goal of CPB is to provide a balance between substrate delivery and substrate utilization to metabolically active tissues. Substrate delivery is a function of the pump flow and blood concentration. Pump flow is often lower than the "usual" cardiac output, and hemodilution reduces all the major constituents of blood. It is most usual, therefore, to coincidentally reduce substrate utilization, primarily by cooling, to reduce cellular metabolism. Total body VO2 is often used as a surrogate of metabolic rate. Failure to match oxygen delivery and VO2 will lead to tissue hypoxia, anaerobic metabolism, and even cell death.

Precise assessment of VO2 is obviously important. Our data showed that the calculated method using reverse Fick principle consistently underestimates VO2 with a bias of – 24.6 mL/min as compared to the directly measured values. This may be due to some consistent differences in the measurements of blood flow and blood gases, including the derived hemoglobin. The poor agreement between the calculated and directly measured values further indicates the necessity of the direct measurement of VO2.

The continuous nature of our technique provides further detailed information during the highly dynamic change of VO2 during hypothermic CPB. Our data demonstrate that the change of VO2 during CPB was directly correlated with body temperature. Cooling of the venous blood temperature from 35°C to 32°C reduced VO2 by 0.70 (0.33) mL/kg/min, and rewarming to 36.4°C increased VO2 by 1.36 (0.33) mL/kg/min. Therefore, for every degree centigrade change of the venous blood temperature, VO2 decreased 0.26 (0.16) mL/kg/min during cooling and increased 0.31 (0.08) mL/kg/min during rewarming. While the rate of the decrease in VO2 during cooling is similar to the values obtained from other studies [3, 14], fewer studies have described the changes in VO2 during rewarming during CPB [3, 15]. However, the balance of oxygen transport may be most important as the VO2 increases during rewarming [16], as indicated by the increased blood lactate levels during rewarming in our data. Our data are similar to those described in adults during CPB showing an increase in VO2 of 0.35 mL/kg/min per degree centigrade during rewarming [3], and our previous data showing an approximate 0.46 mL/kg/min rise in VO2 per degree centigrade of central temperature in children during spontaneous rewarming after CPB [11].

More importantly, our continuously recorded data demonstrate a dynamic, nonlinear relationship between temperature and VO2 change. Large differences in the rate of VO2 change per degree centigrade were seen at different phases of cooling and rewarming. Although not measured directly, it is probable that large changes in oxygen extraction ratio occurred, and it is possible that oxygen delivery fell behind VO2 at these critical periods. Furthermore, while the target temperature was the same for each animal, the VO2 at 32°C ranged from 3.4 to 4.4 mL/kg/min, suggesting that oxygen delivery may need to be individualized to the level of VO2 at a given temperature. The reasons for this nonlinearity and individual variation are unclear. It may, in part, reflect the nonuniformity of cooling or rewarming of the body as a whole. Indeed, the rapid cooling or rewarming via the blood stream by the heat exchanger in CPB inevitably causes large temperature gradients throughout the body [17], and it is difficult to use any single measurement of temperature to define a mean body temperature. Although the venous blood temperature was used as a reference in the current study, it represents the average temperature of the blood that had perfused all the tissues, and may be more representative of tissues and organs receiving a proportionately higher blood flow. A mismatch between blood flow, temperature change, and metabolic demand could easily occur. Thus, the rapid changes in VO2 seen particularly during rewarming may reflect periods of potential imbalance between oxygen delivery and demand. Continuous adjustment of systemic oxygen delivery may therefore be necessary to match these changes in VO2 in these subjects. Strategies to improve uniformity of body perfusion, such as hypercapnia [9] and pharmacologic vasodilation [5], may be advantageous to improve tissue oxygen delivery and thus to overcome the mismatch between perfusion and metabolism.

One major component of the rapid rise of the total body VO2 responses during rewarming may be the contribution of VO2 from the previously arrested and cross-clamped heart. Oxygen delivery is nearly zero, and myocardial oxygen consumption is, hopefully, minimal until the removal of the ACC. We observed a noticeably acute increase in VO2 of 0.64 (0.21) mL/kg/min within the first 8 minutes immediately after the release of ACC in all the pigs. Although this finding has never been reported, it is not entirely surprising. Myocardial oxygen consumption has been reported to be around 5 mL/min/100 g of myocardium in anesthetized pigs [18], dogs [19], and humans [20], and accounts for about 10% of systemic VO2. Furthermore, myocardial oxygen consumption has been shown to increase after reperfusion following cardiac arrest in CPB [18, 21], and a brief period of ventricular fibrillation, which occurred in all of our pigs at reperfusion of the myocardium, has been shown to significantly increase myocardial oxygen consumption and may amplify reperfusion injury [18, 22]. The increase in VO2 during this brief period accounts for about 50% of the total increase in VO2 during the active rewarming period. Thus, this may explain, in part, the approximately 9% higher rate of change in VO2 during rewarming compared to cooling, and especially the significantly higher increase in VO2 during the 20 minutes after the release of ACC compared to that before the release of ACC.

Finally, it has been reported that the repayment of oxygen debt during rewarming may also cause an increase in VO2 in infants following CPB with deep hypothermia and circulatory arrest [23]. A surge in VO2 was found after initiating rewarming which was followed by a decrease in that study. Our study used only mild hypothermia without circulatory arrest, and we did not observe any sudden increase-and-decrease in VO2 after rewarming other than that described above.

Limitations
There are several technical and physiologic limitations that need to be taken into account. Physiologically, the change of measured VO2 may not represent the exact change of metabolic rate during cooling or rewarming due to the change of solubility of oxygen and the shift of the oxyhemoglobin dissociation curve. With decreasing temperature, the solubility of a gas increases [24], and the oxyhemoglobin dissociation curve shifts to the left, resulting in a higher affinity of hemoglobin for oxygen and thus higher saturation. For example, if body temperature could be lowered without changing metabolism, some increase in VO2 would occur due to the increase in gas store and the leftward shift of the oxyhemoglobin dissociation curve. Thus, the decrease in the measured VO2 during cooling is the result of a decrease in VO2 itself (metabolism) and an increase in solubility of oxygen and affinity of hemoglobin for oxygen. Conversely, the increase in the measured VO2 during rewarming is the result of an increase in metabolic VO2 and a decrease in solubility of oxygen and rightward shift of the oxyhemoglobin dissociation curve. Therefore, the change of measured VO2 may represent less than the real change of the metabolic rate during cooling and rewarming, until stable temperature is maintained at either hypothermia or euthermia, and the oxygen store is equilibrated.

In our study, only venous temperature was monitored. Multiple sites of temperature monitoring may certainly help to reflect the uniformity of body temperature and provide further information regarding the reported nonlinearity of the change in VO2 that we measured.

The measurement of blood lactate levels is commonly used to assess the adequacy of tissue perfusion and was also used in our current study. The continuously increased blood lactate levels during CPB may indicate the imbalance between VO2 and oxygen supply during cooling and further deteriorated during rewarming with significantly increased oxygen demand. But the reasons for elevated lactate levels during hypothermic CPB are complicated, with tissue hypoperfusion, reduced clearance of the liver, and washout during rewarming all contributing [16, 25]. These factors should be taken into account when interpreting our data, and may in part explain the lack of significant correlations between the lactate levels and the absolute values and changes of VO2 during cooling and rewarming periods in our rigid protocol.

Technically, due to the inherent limitation of the measurement principle of the AMIS 2000 mass spectrometer, considerable error may occur when the "inspiratory" oxygen concentration is more than 80%, making this technique unreliable under such circumstances. Clinically, this is not a major concern as most patients require an inspiratory oxygen concentration less than 80% during CPB.

The major concern when adapting the technique described in this study to the clinical situation will be safety. Positive pressure in the gas phase of membrane oxygenator might potentially be produced by any obstruction of the "expired" gas from the outlet port of the oxygenator to the mixing box. This may be avoided by technical modifications of the oxygenator, such as using a rigid tubing and leak-free gas escape port with a threshold pressure valve.

Conclusion
The simple adaptation of respiratory mass spectrometry to measure VO2 continuously during hypothermic CPB provides detailed information about the changes of VO2 during CPB. This technique may have an important role in the clinical research and management aimed at improving the balance of oxygen transport in patients undergoing CPB.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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J. Li, J. Stokoe, I. E Konstantinov, R. K Kharbanda, and A. N Redington
Evidence for a significant myocardial contribution to total metabolic burden during hypothermic cardiopulmonary bypass: a study of continuously measured oxygen consumption and arterial lactate levels in pigs
Perfusion, September 1, 2005; 20(5): 277 - 283.
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