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Anesth Analg 2005;101:1597-1601
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000180765.39501.42

CARDIOVASCULAR ANESTHESIA

Cardiac Output Measurement Using the Transesophageal Doppler Method Is Less Accurate Than the Thermodilution Method When Changing Paco2

Toshiyuki Sawai, MD, Toshihiro Nohmi, MD, Yoshihiko Ohnishi, MD, Yuji Takauchi, MD, and Masakazu Kuro, MD, PhD

Department of Anesthesiology, Osaka Medical College, Takatsuki, Japan; Department of Anesthesia, National Cardiovascular Center, Suita, Japan

Address correspondence and reprint requests to Toshiyuki Sawai, MD, Department of Anesthesiology, Osaka Medical College, 2–7 Daigaku-machi, Takatsuki 569–8686, Japan. Address e-mail to ane026{at}poh.osaka-med.ac.jp.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Cardiac output (CO) determination using transesophageal Doppler is based on the measurement of descending aortic blood flow. Because cerebral blood flow is dependent on Paco2, an increase in Paco2 would result in an increase of CO because of the increase in cerebral blood flow and vice versa. We enrolled 30 patients undergoing off-pump coronary artery graft surgery in the study. The CO was determined by both transesophageal Doppler and thermodilution while Paco2 was maintained at either 30 mm Hg or 40 mm Hg in random order. The CO by thermodilution was significantly higher at Paco2 of 40 mm Hg (4.17 ± 0.94 L/min) than at 30 mm Hg (3.78 ± 0.85 L/min). On the other hand, there were no significant differences in CO by transesophageal Doppler: 3.85 ± 0.76 L/min at Paco2 of 40 mm Hg and 3.77 ± 0.74 at 30 mm Hg. Bland-Altman analysis yielded bias and precision of –0.32 and 0.49 L/min at Paco2 of 40 mm Hg, and –0.01 and 0.34 L/min at 30 mm Hg. These results indicate that both methods of CO measurement are in agreement at 30 mm Hg of Paco2, but the thermodilution method provides higher values at 40 mm Hg of Paco2.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
The transesophageal Doppler method is relatively noninvasive when measuring cardiac output (CO) and provides continuous CO values using a Doppler probe inserted into the esophagus (1–7). CO is calculated by a formula based on the descending aortic blood flow (QDA) determined by the Doppler probe, assuming that changes in total CO are always reflected in changes in QDA. In other words, this method would provide an accurate estimate of total CO only when blood flow to the branches of the ascending aortic arch, a major portion of which goes to the brain including the carotid artery and vertebral artery, parallels QDA. However, cerebral blood flow is dependent on Paco2, increasing significantly with an increase in Paco2, whereas the QDA is less dependent on Paco2 (8–12). This leads us to speculate that there may be a discrepancy between CO values obtained by the transesophageal Doppler method and the thermodilution method when Paco2 changes. Increasing or decreasing Paco2 by 10 mm Hg, we tested a hypothesis that CO measurement using the transesophageal Doppler method is less accurate than the thermodilution method.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
The study protocol was approved by the Ethics Committee of the National Cardiovascular Center (Osaka, Japan) and written informed consent was obtained from each patient. The study was a prospective, double-blind trial. Thirty ASA physical status II patients undergoing elective off-pump coronary artery graft surgery, with no apparent history of cerebrovascular disease, respiratory disease, or aortic calcification, were enrolled in the study. Patients with the forced expiratory volume in 1 s/the forced vital capacity ratio less than 70% by preoperative clinical spirometry and patients with Paco2 higher than 45 mm Hg by preoperative arterial blood gas tension analysis were not studied (13). We excluded patients who demonstrated severe tricuspid regurgitation by preoperative transthoracic echocardiography (14). All patients received morphine 10 mg IM 30 min before the induction of anesthesia. Anesthesia was induced with IV midazolam 70 µg/kg, fentanyl 5 µg/kg and vecuronium 0.2 mg/kg given IV, followed by tracheal intubation. Anesthesia was maintained with propofol 3–5 mg/kg/h. Mechanical ventilation was initiated using a fraction of inspired oxygen of 0.4.

The study was performed before the start of surgery. Thirty patients were randomly assigned to either increasing end-tidal partial pressure of carbon dioxide (Etco2) (n = 15) or decreasing Etco2 (n = 15). A randomization was performed according to the blinded envelope method. Etco2 was altered either from 30 mm Hg to 40 mm Hg or from 40 mm Hg to 30 mm Hg. This change was achieved over 20 min by changing the respiratory rate with tidal volume and inspiratory flow rate fixed. We confirmed that the change in mean airway pressure was smaller than 5 cm H2O across this adjustment. After waiting for another 20 min to establish a new steady-state, arterial blood gas tension analyses were performed and the following hemodynamic variables were recorded: heart rate, mean arterial blood pressure, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), and blood temperature. At the same time, we conducted CO measurements as described below.

CO measurements were performed by the thermodilution method and the transesophageal Doppler method. For the thermodilution method (COTD), a 7.5F pulmonary artery catheter (OptiQTM; Abbott Laboratories, North Chicago, IL) was inserted preoperatively via the right internal jugular vein. Injection of 10 mL of ice-cooled 5% glucose was performed manually at least in triplicate, and the values were averaged. All readings of COTD were performed by an investigator blinded as to the experimental conditions. Because the CO measurement varies depending on the time point in the respiratory cycle when the measurement initiated, we standardized the timing of bolus injection after the first half of the expiratory phase (15). When thermodilution curves fulfilled the criteria of Levett and Replogle (16) and the average numbers were within 10% of each other, we deemed the measurement satisfactory (17).

CO measurement by the transesophageal Doppler method (COTE) was performed using the transesophageal probe combining Doppler and M-mode devices (Hemosonic 100TM, Arrow International, Reading, PA), which allowed continuous monitoring of QDA (2). This was derived by measuring the aortic diameter using the echograph bidimensional scanner and the blood velocity data with the pulsed wave Doppler. To locate the aortic walls accurately, the "echograph level indicator" representing the backscattered distal wall M-mode signal was used. On the other hand, the pulsed wave Doppler measures blood flow velocity using the Doppler principle. Both variables were simultaneously and continuously measured at the same anatomical level. The QDA was then calculated from the measured aortic cross-section area and blood flow velocity. COTE is obtained from the following equation (2–5):



{7MMU1}

where QDA is the descending aortic blood flow. After we confirmed COTE was stable for 5 min at each steady state of Paco2, we calculated COTE for 5 s.

The sample size was obtained from our pilot study as follows: the primary variable was the difference of COTD between Paco2 of 30 mm Hg and 40 mm Hg and sample size was based on a paired Student’s t-test with a significance level of 0.05, a power level of 0.70, and with an anticipated effect size of 1.2. The required sample size obtained from the Altman nomogram was 15 in each group for a total of 30 subjects (18). All data are presented as mean ± sd. Statistical comparisons were made using paired Student’s t-test, and a P value <0.05 was considered significant. The correlation coefficient (r) between COTE and COTD was evaluated with linear regression at 30 mm Hg and 40 mm Hg of Paco2, respectively. After normality was confirmed by normal distribution plots and histogram for the variables (19), Bland-Altman analysis was performed by plotting the differences between the means of COTD and COTE versus the average of the differences at 30 mm Hg and 40 mm Hg of Paco2, respectively (20). Bias was represented by the mean of the differences between COTD and COTE. Precision was represented by standard deviation of the differences (20). A percentage error between measures of COTE and COTD was calculated. Statistical calculations were made with StatView for Windows (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
All patients completed the study without complications. Patient characteristics are summarized in Table 1. Table 2 shows hemodynamic and respiratory measurements after induction of general anesthesia. There was a significant difference in Paco2 (P < 0.05) between the 2 conditions of 30 mm Hg and 40 mm Hg Etco2 (Table 2). COTD was significantly higher at the Etco2 setting of 40 mm Hg (4.17 ± 0.94 L/min) than at the Etco2 setting of 30 mm Hg (3.78 ± 0.85 L/min) (Table 2). On the other hand, there were no significant differences in QDA (2.54 ± 0.56 and 2.65 ± 0.57 L/min) and COTE (3.77 ± 0.74 and 3.85 ± 0.76 L/min) between these 2 conditions of Etco2 (Table 2).


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  		Table 1. Patient Characteristics

 

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  		Table 2. Arterial Blood Gas Tension Analysis Data, Hemodynamic Variables, Cardiac Output, and Descending Aortic Blood Flow Under Two Different Conditions of Etco2

 

Table 3 summarizes the results of regression analysis and Bland-Altman analysis. When Etco2 was set to 30 mm Hg, there was a high correlation between COTE and COTD (Fig. 1, Table 3). The percentage error between COTE and COTD was 18%. When Etco2 was set to 40 mm Hg, COTE also highly correlated with COTD, although COTE underestimated COTD (Fig. 2, Table 3). The percentage error between COTE and COTD was 24%. Figure 3 shows individual values of differences between COTD and COTE when Paco2 was changed between 30 mm Hg and 40 mm Hg. In 24 patients (80%), the underestimation in COTE became more apparent at Etco2 of 40 mm Hg than at 30 mm Hg.


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  		Table 3. Results of Bland-Altman Analysis and Regression Analysis

 


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  		Figure 1. Cardiac output (CO) measurements at Paco2 of 30 mm Hg. A, Linear regression of CO obtained by transesophageal Doppler method (COTE) and CO obtained by thermodilution method (COTD). B, Bland-Altman analysis between COTE and COTD. The dotted lines represent bias and limits of agreement.

 


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  		Figure 2. Cardiac output (CO) measurements at Paco2 of 40 mm Hg. A, Linear regression of CO obtained by transesophageal Doppler method (COTE) and CO obtained by thermodilution method (COTD). B, Bland-Altman analysis between COTE and COTD. The dotted lines represent bias and limits of agreement.

 


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  		Figure 3. Discrepancy between cardiac output measured by thermodilution (COTD) and cardiac output measured by transesophageal Doppler (COTE) at each Paco2 level. Solid lines represent the group in which Paco2 was increased from 30 mm Hg to 40 mm Hg, whereas dotted lines represent the group in which Paco2 was decreased.

 


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Although previous reports had shown that QDA correlates well with COTD under general anesthesia (2–5), these reports did not examine the effect that Paco2 has on CO. In the present study we examined the changes in CO measured by two different methods, i.e., the thermodilution and the transesophageal Doppler, when Paco2 was randomly set to 30 or 40 mm Hg in patients undergoing off-pump coronary artery graft surgery. When Paco2 was altered, COTD changed significantly whereas the change in COTE was limited. In both Paco2 levels, the correlation between COTE and COTD was clinically acceptable (|bias| <1 L/min, precision ≤1 L/min). The percentage error, a ratio of precision to COTD, is also acceptable at both Paco2 of 30 mm Hg (18%) and 40 mm Hg (24%) because both are <30% (21).

When Paco2 was set to 40 mm Hg, COTE underestimated COTD in 80% of patients (Fig. 2B, Fig. 3). In addition, COTE showed larger values of bias and precision at 40 mm Hg of Paco2 than at 30 mm Hg, although 40 mm Hg of Paco2 indicated normal respiratory condition. When obtaining CO from QDA, neglecting the changes in Paco2 that affect cerebral blood flow, could lead to this discrepancy between COTE and COTD at 40 mm Hg of Paco2. Revised correction factors would make the COTE more accurate at a wider range of Paco2.

The QDA accounts for a major portion of CO under normal conditions, but does not include blood flow to the branches of the ascending aortic arch, which supply the coronary arteries, brachiocephalic artery, left common carotid artery, and left subclavian artery. Approximately 15% of CO is distributed to the brain (22). The COTE is based on an assumption that the total CO is always comparable to the QDA, essentially ignoring the blood flow to the branches of the ascending aortic arch. However, the cerebral blood flow is dependent on Paco2 over the range of 20 to 80 mm Hg (9) and increases significantly when Paco2 increases, whereas the QDA is less dependent on Paco2 (8–12).

The cerebral blood flow is regulated by a variety of factors, including Paco2, anesthetic, arterial oxygen content and mean arterial blood pressure. In our study, we tried to exclude factors affecting cerebral blood flow except for Paco2. First, we excluded patients with an apparent history of respiratory disease that may cause hypercapnia (13). Second, we maintained general anesthesia with propofol, a drug with relatively minor influence on the autoregulation system of the brain (23). Third, we maintained Pao2 between 92 to 125 mm Hg and mean arterial blood pressure between 75 to 102 mm Hg because these variables may affect cerebral blood flow (24). Fourth, to exclude a time effect, we changed Paco2 settings over 20 minutes and waited for another 20 minutes to establish a new steady-state after each ventilatory condition (25).

The difference in CO measurements between the 2 methods most likely reflects the change in cerebral blood flow when Paco2 was altered between 30 and 40 mm Hg. The slope of the cerebral blood flow and Paco2 relationship in humans has been reported as 1.27–2.17 mL/100 g/min/mm Hg (9) and the change in cerebral blood flow by increasing Paco2 by 10 mm Hg is 170–300 mL/min. Because cerebral blood flow was not measured in this study, it is possible that a 330 mL/min difference in CO was not solely due to the changes in cerebral blood flow (Table 2, Fig. 3). However, even if a portion of the extra blood flow was directed to other portions of the upper body the conclusion remains the same: Paco2 levels might affect the accuracy of the COTE measurement.

Although the present study was performed in patients scheduled for off-pump coronary bypass surgery before the operation was initiated, there were some limitations in designing the experimental protocol. One limitation is related to the Paco2 level we evaluated. We did not want to excessively increase Paco2 because this is known to decrease the arrhythmic threshold in patients with coronary artery disease during general anesthesia (26). We were also hesitant to change Paco2 rapidly and therefore chose to alter the Paco2 slowly over 20 minutes and waited for another 20 minutes to establish a new steady state. Because of the limited duration of the protocol, we felt it was not practical to perform CO measurements under more than two Paco2 conditions. However, more striking differences between the two methods might have been expected if Paco2 values more than 40 mm Hg were examined. More detailed studies might be feasible in patients with stable heart conditions or in the intensive care unit. The use of inspired CO2 would also expedite the process of changing Paco2 and permit the examination of different conditions over shorter periods. Second, we did not directly measure the cerebral blood flow under changing Paco2 using transcranial Doppler, which may have provided more detailed information. Alternatively, animal experiments could be conducted, allowing measurement of the blood flow to each branch of the ascending aorta. These are future considerations in pursuing the findings of the present study. Third, mechanical ventilation may have affected COTD when we changed respiratory rate to obtain different Paco2. Although we also confirmed that the changes in CVP and PCWP were minimal, the impact of a change in mean airway pressure might have slightly altered venous return and measured CO. We injected cooled glucose after the first half of the expiratory phase, where the effect of mechanical ventilation on venous return was small (15). Although the thermodilution method extrapolates CO from a period of no more than 6–8 seconds, it might be influenced by change in venous return. COTD might be more sensitive to mean airway pressure changes than COTE. In summary, we examined the CO when Paco2 was changed between 30 and 40 mm Hg using thermodilution and transesophageal Doppler methods. Both methods of measurement agreed with each other at 30 mm Hg of Paco2, but the thermodilution method had larger values at 40 mm Hg of Paco2.

The authors wish to thank Dr. Masahiko Fujinaga and Hideaki Imanaka for editing the manuscript.


   Footnotes
 
Supported, in part, by the National Cardiovascular Center, Japan.

Accepted for publication July 13, 2005.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Su NY, Huang CJ, Tsai P, et al. Cardiac output measurement during cardiac surgery: esophageal Doppler versus pulmonary artery catheter. Acta Anaesthesiol Sin 2002;40:127–33.[Medline]
  2. Boulnois JL, Pechoux T. Non-invasive cardiac output monitoring by aortic blood flow measurement with the Dynemo 3000. J Clin Monit Comput 2000;16:127–40.[Web of Science][Medline]
  3. Cariou A, Monchi M, Luc-Marie J, et al. Noninvasive cardiac output monitoring by aortic blood flow determination: evaluation of the Sometec Dynemo-3000 system. Crit Care Med 1988;26:2066–72.
  4. Bernardin G, Tiger F, Fouche R, et al. Continuous noninvasive measurement of aortic blood flow in critically ill in patients with a new esophageal echo-Doppler system. J Crit Care 1998;13:177–83.[Web of Science][Medline]
  5. Klein G, Emmerich M, Maish O, et al. Clinical evaluation of non-invasive monitoring aortic blood flow (ABF) by a transesophageal Echo-Doppler device. Anesthesiology 1998;89:A953.
  6. Laupland KB, Bands CJ. Utility of esophageal Doppler as a minimally invasive hemodynamic monitor: a review. Can J Anaesth 2002;49:393–401.[Web of Science][Medline]
  7. Lavandier B, Muchada R, Chignier E, et al. Assessment of potentially non-invasive method for monitoring aortic blood flow in children. Ultrasound Med Biol 1991;17:107–16.[Web of Science][Medline]
  8. Kety SS, Schmidt CF. The effects of active and passive hyperventilation on cerebral blood flow, cerebral oxygen consumption, cardiac output, and blood pressure on normal young men. J Clin Invest 1946;25:107–19.
  9. Smith AL, Wollman H. Cerebral blood flow and metabolism: effects of anesthetic drugs and techniques. Anesthesiology 1972;36:378–400.[Web of Science][Medline]
  10. Grubb RL Jr., Raichle ME, Eichling JO, et al. The effects of changes in PaCO2 on cerebral blood volume, blood flow, and vascular mean transit time. Stroke 1974;5:630–9.[Abstract/Free Full Text]
  11. Raichle ME, Posner JB, Plum F. Cerebral blood flow during and after hyperventilation. Arch Neurol 1970;23:394–403.[Abstract/Free Full Text]
  12. Chong KY, Craen RA, Murkin JM, et al. Rate of change of cerebral blood flow velocity with hyperventilation during anesthesia in humans. Can J Anaesth 2000;47:125–30.[Web of Science][Medline]
  13. Stein M, Koota GM, Simon M, et al. Pulmonary evaluation of surgical patients. JAMA 1962;181:765.
  14. Tachibana K, Imanaka H, Miyano H, et al. Effect of ventilatory settings on accuracy of cardiac output measurement using partial CO2 rebreathing. Anesthesiology 2002;96:96–102.[Web of Science][Medline]
  15. Magder S. Cardiac output. In: Tobin MJ, ed. Principles and practice of intensive care monitoring. New York, McGraw-Hill, 1998:797–810.
  16. Levett JM, Replogle RL. Thermodilution cardiac output: a critical analysis and review of literature. J Surg Res 1979;27:392–404.[Web of Science][Medline]
  17. Stetz CW, Miller RG, Kelly, et al. Reliability of the thermodilution method in the determination of cardiac output in clinical practice. Am Rev Respir Dis 1982;126:1001–4.[Web of Science][Medline]
  18. Altman DG. Statistics and ethics in medical research, III. How large a sample? BMJ 1980;282:1336–8.
  19. Bland JM, Altman DG. Applying the right statistics: analyses of measurement studies. Ultrasound Obstet Gynecol 2003;22:85–93.[Web of Science][Medline]
  20. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986;1:307–10.[Web of Science][Medline]
  21. Chew MS, Poelaert J. Accuracy and repeatability of pediatric cardiac output measurement using Doppler: 20-year review of the literature. Intensive Care Med 2003;29:1889–94.[Web of Science][Medline]
  22. Kety SS, Schmidt CF. The nitrous oxide method for quantitative determination of cerebral blood flow in man: theory, procedure, and normal values. J Clin Invest 1948;27:476–83.
  23. Myburgh JA, Upton RN, Ludbrook GL, et al. Cerebrovascular carbon dioxide reactivity in sheep: effect of propofol or isoflurane anaesthesia. Anaesth Intensive Care 2002;30:413–21.[Web of Science][Medline]
  24. Patel PM, Drummond JC. Cerebral physiology and the effects of anesthetics and techniques. In: Miller RD, ed. Anesthesia: regulation of cerebral blood flow. Philadelphia: Churchill Livingstone, 2005:813–20.
  25. Tachibana K, Imanaka H, Takeuchi M, et al. Noninvasive cardiac output measurement using partial dioxide rebreathing is less accurate at settings of reduced minute ventilation and when spontaneous breathing is present. Anesthesiology 2003;98:830–7.[Web of Science][Medline]
  26. Wilson WC, Benumof JL. Respiratory physiology and respiratory function during anesthesia. In: Miller RD, ed. Anesthesia: respiratory function during anesthesia. Philadelphia: Churchill Livingstone, 2005:705–18.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2005 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press