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Anesth Analg 2001;92:306-313
© 2001 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Monitoring End-Tidal Carbon Dioxide During Weaning from Cardiopulmonary Bypass in Patients Without Significant Lung Disease

Andrew Maslow, MD*, Gary Stearns, CCP{dagger}, Arthur Bert, MD*, William Feng, MD{dagger}, David Price, CCP{dagger}, Carl Schwartz, MD*, Scott MacKinnon, MD*, Fred Rotenberg, MD*, Richard Hopkins, MD{dagger}, George Cooper, MD{dagger}, Arun Singh, MD{dagger}, and Stephen H. Loring, MD{ddagger}

Departments of *Anesthesiology and {dagger}Surgery, Rhode Island Hospital, Providence, Rhode Island, {ddagger}Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Address all correspondence and reprint requests to Andrew Maslow, MD, Department of Anesthesiology, Rhode Island Hospital, 593 Eddy Street, Davol 129, Providence, RI 02903. Address e-mail to amaslow{at}lifespan.org


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
End-tidal carbon dioxide tension (PETCO2) changes with fluctuations in cardiac output (CO). We compared PETCO2 to pulmonary artery blood flow (PAQt) during weaning from cardiopulmonary bypass (CPB) in normothermic patients without significant pulmonary disease. Fifteen consecutive adult cardiac surgical patients were prospectively studied during and shortly after weaning from CPB. Before separation from CPB, PETCO2 and PAQt were measured, the latter by transesophageal Doppler echocardiography. At the time of measurements patients were normothermic, and ventilated at 6 breaths/min with tidal volumes of 10 mL/kg. After separation from CPB, thermodilution cardiac output (TDCO) was measured in addition to PAQt and PETCO2. Regression and bias analyses were used to compare PETCO2, PAQt, and TDCO. Seventy measurements were recorded; 31 before separation from CPB and 39 after separation from CPB. A good correlation was seen between PAQt and PETCO2 (r = 0.88) and between TDCO and PAQt (r = 0.93; mean bias 0.03 L/min; SD 0.52 L/min). The regression analysis of PAQt on PETCO2 showed greater variability at PETCO2 levels > 34 mm Hg (n = 22; r = 0.14). Increases in PETCO2 plateaued at this level, although PAQt continued to increase. When PETCO2 was more than 30 mm Hg, all PAQt and TDCO values were >4.0 L/min (>2.0 L/min/m2). When PETCO2 exceeded 34 mm Hg, all values of PAQt, and 28/29 values of TDCO were more than 5 L/min (>2.5 L/min/m2). One patient had TDCO of 4.69 L/min (2.39 L/min/m2). In normothermic patients without significant pulmonary disease, PETCO2 is a useful index of PAQt during separation from CPB. Under the clinical settings in this study, a PETCO2 greater than 30 mm Hg was invariably associated with a CO more than 4.0 L/min or a cardiac index >2.0 L/min/m2.

Implications: In normothermic patients without pulmonary disease, acute changes in PETCO2 during separation from cardiopulmonary bypass were reflective of changes in pulmonary artery blood flow. Specific PETCO2 values were predictive of cardiac output values under the clinical conditions of the study.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Weaning from cardiopulmonary bypass (CPB) requires continuous assessment of myocardial function and blood flow. Thermodilution cardiac output (TDCO) is not accurate because variable quantities of injectate are removed by the venous return cannula of the CPB circuit. As a result, most clinicians rely on visual inspection of the heart, central circulatory pressures, and transesophageal echocardiography (TEE), if available, to estimate cardiac function.

Several studies have demonstrated the usefulness of end-tidal carbon dioxide pressures (PETCO2) in assessing pulmonary blood flow in a variety of clinical scenarios (1–5). More recently, expired CO2 monitoring has been used to assess cardiac output (CO) using a new noninvasive CO monitor that uses a modification of the Fick method (6–16).

We have observed that the PETCO2 is affected by changes in cardiac preload, adjustments of vasoactive drugs, and cardiac pacing during weaning from CPB. We hypothesized that PETCO2 monitoring could be used to assess CO during weaning from CPB. The purpose of this study was to compare PETCO2 with pulmonary artery blood flow, measured by using TEE.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
This study was approved by the hospital’s internal review board for research. Fifteen consecutive patients undergoing cardiac surgical procedures requiring CPB were studied ( Table 1). All patients were free of significant pulmonary disease. All data were obtained while patients were normothermic (36.8–37.2°C).


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  		Table 1. Patient Characteristics and Operative Details
 
Anesthetic management consisted of a balanced technique using thiopental (2–3 mg/kg) on induction, fentanyl (10–20 µg/kg), pancuronium (0.1 mg/kg), and inhaled isoflurane (expired concentration of 0.5%). Monitoring included standard electrocardiogram, pulse oximetry, PETCO2 (Vitalert 3200; Narkomed-Drager, Tulford, PA), an intraarterial catheter to measure blood pressure, and a pulmonary artery catheter (7F 110 cm, Baxter Healthcare Corp, Irvine CA). PETCO2 was assessed using infrared technology in expired gas sampled via a sideport system. The system was calibrated before the start of the study to be accurate within 1 mm Hg in the range of 20–80 mm Hg. In all 15 patients, the PETCO2 trace appeared normal: rapid upstroke followed by a flat plateau phase and a rapid downstroke on inspiration.

After endotracheal intubation, a 6.2/5.0-MHz multiplane TEE probe was inserted, and a baseline echocardiographic examination was performed (Sonos 2000; Hewlett Packard, Andover, MA). All patients were free of significant tricuspid and pulmonic valve disease as assessed by color Doppler and two-dimensional echocardiography. Before CPB, the TEE probe was positioned in the esophagus at the base of the ascending aortic root with the transducer at zero degrees ( Fig. 1). This view was obtained in all 15 patients. At this level, blood flow through the main pulmonary artery (MPA) is within 10–20 degrees of the ultrasound beam, permitting assessment of pulmonary artery blood flow with <7% error (17,18). Pulmonary artery blood flow (PAQt) was measured before and after separation from CPB ( Fig. 2).



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  		Figure 1. Image of the superior mediastinal vessels. The main and right pulmonary arteries (PA) are seen as they pass alongside, posterior to, and behind the ascending aorta (Asc Ao). Pulmonary artery blood flow was measured in the main pulmonary artery (marked by the arrow).

 


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  		Figure 2. Doppler images of one patient demonstrating the increase in end-tidal carbon dioxide (ETCO2) with increases in pulmonary artery blood flow (PAQt) and thermodilution cardiac output (TDCO).

 
CPB proceeded according to institutional routine, using intermittent cold cardioplegic arrest. Two of the 15 patients were managed with moderate systemic hypothermia; the rest were normothermic. All mea-surements were obtained when patient temperature was between 36.8 and 37.2°C. After completion of the surgical procedure and removal of the aortic cross-clamp, cardiac rhythm was restored. Three internal diameters of the MPA were measured during systole at end-expiration. These diameters were averaged and used to calculate the cross-sectional area of the MPA. MPA diameter was measured once unless the position of the TEE probe changed. Vasoactive drugs were administered as needed based on the pre-CPB heart function, the surgical procedure, and the duration of CPB and aortic cross-clamp. All medications were initiated immediately after the removal of the aortic cross-clamp and before the start of the study. The lungs were reinflated and mechanically ventilated with oxygen and isoflurane (0.5% expired concentration). Patients were ventilated at 6 breaths/min with a tidal volume of 10 mL/kg. The Doppler sample volume was positioned at the level where MPA diameter was measured (indicated by the arrow in Fig. 1). For each measurement, three consecutive flow patterns or time velocity integrals were recorded during brief periods of apnea, and heart rate was calculated from the R-R interval. PAQt was calculated for each of three consecutive cardiac cycles as the product of the MPA cross-sectional area, the time velocity integrals, and the heart rate, using the software of the echocardiography machine (Sonos 2000, Hewlett Packard) (17,18). The recorded, or mean, PAQt was the average from three consecutive cardiac cycles. Measurements before separation from CPB included PETCO2 and PAQt. Before separation from CPB, cardiac pacing was used to maintain an atrioventricular rate of 80 bpm. All patients were in atrioventricular rhythm immediately before separation from CPB. After separation from CPB, TDCO was also measured (in triplicate for each measurement) at end-expiration, using 10 mL of 5% dextrose in water at ambient temperature. After successful separation from CPB and administration of protamine, arterial blood was sampled to measure pH and CO2.

PAQt was measured by a physician blinded to both PETCO2 and TDCO measurements. PETCO2 and TDCO data were obtained and recorded by a second physician. All data were obtained and recorded within a 15-min period from the start of mechanical ventilation to 5–10 min after separation from CPB. Before separation from CPB, measurements were obtained when the CPB systemic blood flow was reduced to approximately 50–75% and 25–50% of full flow.

Data are presented as mean ± SD. PETCO2, PAQt, and TDCO data were compared using regression and bias analyses when appropriate. For regression analyses, a P < 0.05 was considered significant. A change in PETCO2 was compared to changes in PAQt and TDCO (i.e., the percent changes in PETCO2 and PAQt and TDCO from the initial time period to the second; the second to the third; the third to the fourth etc). The percent change was obtained by dividing the amount of change by the preceding value and multiplying by 100%. Changes in PAQt were compared to changes in TDCO in a similar fashion.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Patient characteristics and types of operation are presented in Table 1. During the study period body temperatures were maintained between 36.8 and 37.2°C.

In all, 70 measurements of PETCO2 and PAQt were performed, 31 before separation and 39 after separation from CPB. All patients had at least two mea-surements performed before separation from CPB and at least two during the first 5 to 10 min after separation. The ranges of PETCO2 were 10 mm Hg to 38 mm Hg; PAQt were 1.01 L/min to 10.40 L/min; TDCO (after separation from CPB) were 3.70 L/min to 11.00 L/min.

During weaning from CPB, as PAQt increased with increasing myocardial function, PETCO2 values also increased, and the increase in PETCO2 closely followed the increase in pulmonary blood flow ( Fig. 3). Regression analysis of PETCO2 and PAQt demonstrated a significant correlation (70 measurements; r = 0.88, P = 0.0001). When analysis was limited to PETCO2 <34 mm Hg, the correlation improved (48 measurements; r = 0.92, P = 0.0001), whereas analysis of PETCO2 more than 34 mm Hg showed a poor correlation with PAQt (22 measurements; r = 0.14, P = 0.54). After separation from CPB, CO measurements by PAQt and TDCO agreed closely, and were significantly correlated (mean bias 0.03 ± 0.52 L/min, r = 0.93, P = 0.0001; Fig. 4). Correlation between PETCO2 and TDCO was less significant (39 measurements; r = 0.50,P < 0.01).



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  		Figure 3. End-tidal carbon dioxide (PETCO2) and pulmonary artery blood flow (PAQt) in all patients. The line shows the predicted pulmonary blood flow calculated from Equation 5 (see text) with variables based on the data obtained in this study: PAQt = 5.1 (PETCO2)/(63 - PETCO2). Regression analysis revealed an r value of 0.88 (P < 0.0001). When data obtained from patients with left ventricular ejection fraction <=40% and >40% were plotted separately, statistical relationships were similar.

 


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  		Figure 4. Regression and bias analyses comparing thermodilution cardiac outputs (TDCO) to pulmonary artery blood flow (PAQt), and to end-tidal CO2 data (PETCO2). The top panel (regression analysis) and the middle panel (bias analysis) compare PAQt, measured using transesophageal echocardiography to cardiac output measured by TDCO. The bottom panel compares TDCO and PETCO2 using regression analysis.

 
The percent change in PETCO2 varied with the percent changes in PAQt and TDCO, as shown in Figure 5 (PETCO2 vs PAQt r = 0.80; PETCO2 vs TDCO r = 0.76; PAQt vs TDCO r = 0.91; P = 0.0001). The mean bias of percent changes in PETCO2 and PAQt ( Fig. 6) was -22.18% (SD 42.07%; 95% confidence interval -33.56% to -10.81%). The mean bias between percent changes in PETCO2 and TDCO was -6.07% (SD 22.31%; 95% confidence interval -15.49% to 3.36%). When percent changes of PAQt were compared to percent changes in TDCO, the mean bias was -3.53% (SD 12.15%; 95% confidence interval -8.66% to 1.60).



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  		Figure 5. Regression analyses comparing the percent changes in end-tidal carbon dioxide (PETCO2), the percent changes in pulmonary artery blood flow (PAQt), and thermodilution cardiac output (TDCO). The top panel compares percent changes PETCO2 and percent changes in PAQt, r = 0.80; the middle panel compares percent changes PETCO2 and percent changes TDCO, r = 0.76 and the bottom panel compares percent changes PAQt and percent changes TDCO, r = 0.91.

 


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  		Figure 6. Bias analyses comparing the percent changes in end-tidal carbon dioxide (PETCO2), the percent changes in pulmonary artery blood flow (PAQt), and thermodilution cardiac output (TDCO). The top panel compares percent changes PETCO2 and percent changes in PAQt; the middle panel compares percent changes PETCO2 and percent changes TDCO; and the bottom panel compares percent changes PAQt and percent changes TDCO.

 
Patient data were grouped according to preoperative left ventricular ejection fraction (<= or >40%). There were no significant differences between the two groups (Fig. 3).

In patients with PETCO2 >34 mm Hg, all had a PAQt more than 5 L/min, whereas in 28 of 29 patients the TDCO was more than 5 L/min (one patient had a TDCO of 4.69 L/min). All PETCO2 >30 mm Hg were associated with TDCO and PAQt >4 L/min. When blood flow was indexed by the patient’s body surface area, a PETCO2 >30 mm Hg was associated with a PAQt index and TDCO index more than 2.00 L/min/m2. A PETCO2 >34 mm Hg was associated with a PAQt index more than 2.5 L/min/m2 in all patients, whereas 28/29 TDCO indexes were more than 2.5 L/min/m2 (TDCO index 2.39 L/min/m2 [TDCO 4.69 L/min] in a single patient.)


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Over a wide range of pulmonary blood flow observed in normothermic patients without significant pulmonary disease, there was a close correlation between PETCO2 and PAQt, suggesting that PETCO2 could be used to assess hemodynamics during weaning from CPB. During this time, PETCO2 more than 30 mm Hg was invariably associated with a TDCO and PAQt more than 4 L/min. We did, however, note that there was an increased variability when the PETCO2 was more than 34 mm Hg. At these higher levels, PETCO2 either remained constant or changed relatively little although pulmonary artery blood flow (reflected by PAQt) continued to increase. Increases in PETCO2 appeared to reach a plateau at higher CO levels.

The relationship between PETCO2 and PAQt at lower values of CO can be understood using a version of the Fick relationship (Equation 1) that equates the elimination of CO2 by ventilation to the delivery of CO2 by blood perfusing the lung:

VA x (PACO2/Ptot) = {alpha} x PAQt x (PvCO2 - PACO2)(1)

where VA = alveolar ventilation, PACO2 = alveolar carbon dioxide partial pressure, Ptot = total barometric pressure, {alpha} = slope of content/partial pressure of carbon dioxide in blood, PAQt = pulmonary artery blood flow,

PvCO2 = mixed venous carbon dioxide partial pressure, and PACO2 = arterial carbon dioxide partial pressure.

To be able to evaluate Equation 1 using measured variables, we made the following assumptions. For the short period of our observation (15 minutes at most), the partial pressures of CO2 in tissue and mixed venous blood were equal and constant (see below). We also assumed normal lung function and that end-tidal, alveolar, and arterial partial pressures of CO2 were equal (PETCO2 = PACO2 = PACO2). With these assumptions, one obtains the following relationship between PETCO2 and PAQt:

VA x (PETCO2/Ptot) = {alpha} x PAQt x (PvCO2 - PETCO2)(2)

PETCO2 (VA/Ptot + ({alpha} x PAQt) = ({alpha} x PAQt) (PvCO2)(3)

Solving for PETCO2 yields:

PETCO2 = PvCO2 x PAQt/((VA/{alpha} Ptot) + PAQt) (4)

This predicts that PETCO2 is zero when PAQt is zero and increases with increasing PAQt to reach an assymptotic value. Rearranging Equation 4 yields:

PAQt = (VA/{alpha}) x (PETCO2/Ptot/(PvCO2 - PETCO2)(5)

The physiologic model described in Equation 5 fits the relationship between PAQt and PETCO2 relatively well at lower values of CO (straight line in Fig. 3). PETCO2 is dependent on several factors, including metabolic CO2 production, CO2 levels in peripheral tissues, CO, alveolar ventilation (which depends on alveolar dead space and thus also on CO), and patient temperature (which affects metabolism and CO2 solubility). In the short weaning period, the tissue levels of CO2 are likely to remain near those levels maintained by the CPB. For a given tissue PCO2, decreases in PETCO2 will reflect decreases in blood flow. Furthermore, to the extent that low CO increases alveolar deadspace, PETCO2 is further reduced. As long as CO remains low, CO2 delivery from the tissues is low, and short-term changes in CO are reflected by changes in PETCO2.

At higher levels of CO, these assumptions are no longer valid. Indeed, when PETCO2 was more than 34 mm Hg, increases in PAQt and TDCO were not always associated with comparable changes in PETCO2. In one patient the CO increased from 8.5 L/min to 11.2 L/min although the PETCO2 changed only from 36 to 37 mm Hg. This apparent failure of the physiologic model at higher values of PAQt probably reflects an increase in effective alveolar ventilation (caused by the reduction in alveolar dead space) and more effective CO2 elimination from the tissues, reducing tissue PCO2.

MPA diameter increases with increasing blood flow, and may be a source of error (19). However, our measurements of PAQt agreed closely with TDCO over a wide range of COs, suggesting that change in MPA diameter was not an important source of variability in our study.

Previous studies have demonstrated a direct relationship between changes in PETCO2 and changes in TDCO 3,4. Investigations have also related PETCO2 to outcome in the setting of cardiopulmonary resuscitation and in the perioperative period in trauma and major surgical patients (2,5). In the latter, persistence of PETCO2 below 28 mm Hg was associated with 55% perioperative mortality compared to 17% mortality when PETCO2 was more than 28 mm Hg (5). Similarly, Feng and Singh (20) reported that separation from CPB was successful in those patients whose PETCO2 was consistently in the high 20s or 30s (mm Hg).

Our study and others have demonstrated that PETCO2 is directly related to changes in blood flow (3,4). Although a lower mean bias between the percent changes in PETCO2 and the percent changes in PAQt is preferable, a similar difference was suggested in two previous studies (3,4). Although neither of these investigations analyzed the data using a bias analysis, the regression analysis suggests that the mean bias was also increased (3,4). In the present study the percent change in PETCO2 underestimated the percent change in CO, especially when large changes in blood flow occurred as seen in Figure 6. This may be attributable to changes in a number of factors that affect PETCO2. Although ventilation and temperature were maintained, the amount of alveolar and anatomic dead space may have changed significantly. As explained above, with increasing pulmonary blood flow, the reduction in alveolar dead space would allow more effective alveolar ventilation and elimination of carbon dioxide. This effect may be accentuated with larger changes in blood flow.

PETCO2 measurements may not accurately represent CO in chronic low flow states as indicated by Isserles and Breen (3). Although the initial decreases in blood flow are paralleled by changes in PETCO2, PETCO2 increased toward baseline despite a continued reduction in pulmonary blood flow. In the study of Isserles and Breen, a balloon occlusion device was left inflated in the inferior vena cava for 45 minutes. There was an initial decrease in both blood flow and PETCO2. However, approximately 20 minutes later PETCO2 had returned to 50–70% of the baseline value. The explanation offered was that the continued reduction in blood flow caused CO2 to increase at the tissue level resulting in a gradual increase in PETCO2 (3). Although PETCO2 may not accurately reflect the CO during a sustained reduction in blood flow, the persistence of PETCO2 values more than 28–30 mm Hg may indicate adequate blood flow (5,20).

Use of PETCO2 monitoring for hemodynamic assessment may be limited in patients with significant pulmonary disease because recorded PETCO2 is dependent on pulmonary function (i.e., alveolar ventilation and alveolar dead space) as well as blood flow. Increased alveolar dead space causes an increased difference between PACO2 and PETCO2. Furthermore, the end-tidal CO2 trace may be abnormal, i.e., the "alveolar" plateau may have a positive slope, making mea-surement of PETCO2 difficult. Although it may be possible to use PETCO2 as a trend monitor for pulmonary blood flow in such patients, the quantitative relationship found in this study may not apply.

CO can be assessed using commercial devices that use exhaled carbon dioxide and a modification of the Fick Principle. By using a rebreathing technique, the CO is calculated from CO2 delivery from the tissues (6–16). This technique is accurate in a variety of clinical settings including cardiac surgery, and in patients with pulmonary disease (6–16). To calculate CO with this device, there must be no change in CO or CO2 production for 50 seconds. During weaning from CPB, blood flow is constantly changing and may not be a setting where this method is useful.

Limitations of this study include the absence of assessments of the effects varying tidal volumes and/or respiratory rate. We also did not evaluate the effects of varying body temperature or depth of anesthesia. This study was performed during a period of stable temperature and ventilation in anesthetized patients. The relationships seen in this study are therefore pertinent to these variables. Finally, we did not assess the individual contribution that changes in heart rate, cardiac preload, afterload, or contractility may have on changes in blood flow and PETCO2.

We demonstrated that monitoring PETCO2 during separation from CPB could be used to assess changes in pulmonary blood flow in normothermic patients without significant pulmonary disease. A PETCO2 value more than 30 mm Hg was invariably associated with a CO more than 4.0 L/min (cardiac index >=2.0 L/min/m2). Although the relationship between PETCO2 and PAQt is complex, under the anesthetic conditions and minute ventilation used in this study, acute changes in PETCO2 reflected changes in pulmonary blood flow. In addition to monitoring ventilation, PETCO2 appears to be a useful, albeit crude, monitor of blood flow. Because it is a routinely used respiratory monitor, it would be a cost-effective monitor of blood flow that does not require additional cost, technology, personnel, or training. Although, additional prospective studies would be useful to support our findings, we recommend that PETCO2 be routinely monitored during separation from CPB to assess cardiovascular function.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Deleted in proof.
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  4. Shibutani K, Muraoka M, Shirasaki S, et al. Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994; 79: 829–33.[Abstract/Free Full Text]
  5. Domsky M, Wilson RF, Heins J. Intraoperative end-tidal carbon dioxide values and derived calculation correlated with outcome: prognosis and capnography. Crit Care Med 1995; 23: 1497–503.[ISI][Medline]
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  7. Johnson KB, Haryadi DG, Orr JA, et al. Influence of pulmonary edema on noninvasive measurements of cardiac output using partial CO2 rebreathing in a canine model [abstract]. Anesthesiology 1998; 89: A535.
  8. Jopling MW. Noninvasive cardiac output determination utilizing the method of partial CO2 rebreathing: a comparison with continuous and bolus thermodilution cardiac output [abstract]. Anesthesiology 1998; 89: A544.
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Accepted for publication September 28, 2000.





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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press