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Capnography during thoracic anesthesia

Capnography during thoracic anesthesia

Bhavani Shankar Kodali MD

Capnography as a non invasive-monitor of PaCO2 during thoracic anesthesia

The arterial to end-tidal PCO2 difference is dependent on the underlying pulmonary disease. The most common reason for thoracotomy in adults is surgical treatment of lung cancer. Patients with lung cancer are almost exclusively smokers, and therefore have airways disease, and hence the PaCO2-PETCO2 gradient during anesthesia will be increased even in the supine position.1 In the 17 patients studied by Werner et al,2 mean PaCO2-PETCO2 from each lung was approximately 5 mm Hg in the supine position at a PaCO2 of 28 mm Hg and ventilatory frequency of 10/min. The lungs receive an approximately equal share of ventilation in the supine position, whereas, the ventilation of the upper lung is increased in the lateral position.2 However, the blood flow to the lungs is gravity dependent resulting in a decreased blood flow to the upper lung. This results in a decrease in the PETCO2 from the upper lung in the lateral position. Therefore, the PaCO2-PETCO2 as measured by Werner et al2 was zero for the lower lung and 11 mm Hg for the upper lung. Since the ventilation of the upper lung increases in the lateral position, it may surmised that if PETCO2 measured in the combined expirate of both lungs, the PaCO2-combined PETCO2 difference would be large.1,2

An incision of the chest wall produces an increase in mean pulmonary artery pressure2 which produces an increase in the CO2 elimination of the upper lung and a decrease in physiological dead space. The upper lung PaCO2-PETCO2 gradient is reduced when the mean pulmonary artery pressure increases as a result of surgical stimulation.

Furthermore, opening of the pleura increases CO2 elimination in the upper lung and thereby decreases PaCO2-PETCO2. Retraction of the lung produces exactly opposite effects. The lower lung gradient is not greatly effected with these maneuvers; it remains small. If combined end-tidal CO2 monitoring is performed, the PaCO2-PETCO2 would decrease when the pleura is opened, and increase again during retraction.

One lung ventilation:1,2

When the upper lung ventilation is discontinued to facilitate surgery, perfusion to the upper lung does not cease completely unless the pulmonary artery is clamped. In the absence of such clamping, there is a right to left shunt to the upper lung, the effect of which is to increase PaCO2, thus PaCO2-PETCO2 increases. However, this PaCO2-PETCO2 may not be any greater than the original combined two lung PaCO2-PETCO2.

Affect of prolonged expiratory maneuvers on PaCO2-PETCO2 during thoracotomy:3

In 16 patients undergoing thoracoabdominal esophagectomy, the affect of two prolonged expiration maneuvers to improve prediction of PaCO2 from PETCO2 were studied. PCO2 at the end of a simple prolonged expiration (PE1CO2), and PCO2 at the end of a prolonged expiration preceded by sustained hyperinflation of the lungs (PE2CO2), were measured during laparotomy, in the lateral thoracotomy position during two-lung ventilation, and after transition to one lung ventilation. PaCO2-PETCO2 was 9.75 (SD 3) mm Hg during laparotomy and this remained stable throughout the study. Both maneuvers decreased the mean arterial to peak expired PCO2 difference particularly during one lung ventilation. These results are in agreement with the results obtained by Bhavani-Shankar et al, where squeeze PETCO2 decreased PaCO2-PETCO2 in pregnant patients undergoing laparoscopic surgery.

Table from reference 3

Measurement mean (SD) mm Hg PaCO2-PETCO 2-PE1CO2 PaCO2-PE2CO2
End of abdominal procedure 9.75 (3) 6 (3.7) 4.5 (3.7)
TLV for 20 min 10.5 (3.7) 7.5(4.5) 3 (4.5)
OLV for 20 min 9.75 (3) 3 (3.7) - 0.75 (3.7)
OLV for 50 min 10.5 (3.7) 2.2 (4.5) -1.5 (3.7)
TLV after skin closure 9 (3.7) 3.7 (5.2) 0.75 (4.5)


However, the end-expiratory PCO2 obtained with each maneuver during laparotomy and thoracotomy agreed poorly with PaCO2. The authors3 suggest that these maneuvers should no longer be recommended to improve estimation of PaCO2 from PETCO2 during anesthesia.

Arterial to end-tidal CO2 difference after bilateral lung transplantation.

PaCO2-PETCO2 and (PaCO2-PETCO2)/PaCO2 ( a measure of alveolar dead space) was assessed in seven consecutive patients undergoing bilateral lung transplantation.

Variable Time after lung transplantation
Mean (SD)10 min1 hr3 hr12 hr24 hr
PaCO2-PETCO2 mm Hg16 (5)14 (5)9 (4)6 (3)5 (3)
(PaCO2-PETCO2)/PaCO20.36 (0.13) 0.33 (0.13) 0.21 (0.12) 0.15 (0.07) 0.11 (0.06)

The time course of the arterial to end-tidal PCO2 difference suggests a rapid improvement of this post-transplant ventilation/perfusion mismatch. After 24 hrs, the values were close to the physiological range, which is supposed to be 4-5 mm Hg. A possible explanation of these findings could be ischemia-reperfusion injury that affects microcirculation. An impaired distribution of pulmonary blood flow with unperfused alveoli would clinically appear as alveolar dead space as is seen immediately following lung transplantation. The ventilation/perfusion mismatch normalized in about 24 hrs indicating a redistribution of pulmonary blood flow and recovery of microcirculation.

Arterial to end-tidal carbon dioxide difference during anesthesia for thoracoscopy:

Presently, thoracoscopy is the procedure of choice in most patients requiring thoracic surgery, especially those patients with severe underlying lung disease.6,7 Srinivasa et al7 studied the difference between PaCO2 and PETCO2 during thoracoscopic surgery in ten patients scheduled for elective thoracoscopic procedures. All patients had general anesthesia induced by IV propofol, fentanyl and vecuronium. A double lumen endo-tracheal tube was positioned with the aid of a fiber optic bronchoscope. Anesthesia was maintained with 100% oxygen, desflurane, fentanyl and vecuronium. Ventilation was kept at, tidal volume (TV) 10 ml/kg, respiratory rate (RR) of 10 bpm and an I:E ratio of 1:2 while on two lung ventilation. TV was 7 ml/kg, RR of 10 bpm and an I:E ratio of 1:2 while on one lung ventilation (OLV). The FiO2 during all measurements was kept at 1.0. Arterial blood gas was sampled 10 min after the patient was in lateral decubitus position while on two-lung ventilation (T1). The second sample (T2) was10 min after the introduction of trocars (OLV). The last sample (T3) was taken 10 min after restarting two-lung ventilation.
Results: The mean FVC was 2.6 ± 0.8 L (79 ± 19% predicted) and the FEV1 was 1.9 ± 0.7 L (76 ± 26% predicted). Table1 shows demographic data of the patients. The mean PaCO2 to PETCO2 difference at times T1, T2 and T3 were 5.5 ± 4, 7.4 ± 5, 6.8 ± 4 mm Hg respectively. The lowest value noted for PETCO2 was 27 mm Hg and the highest value for PaCO2 was 52 mm Hg during the study (Fig.2). The difference between the PETCO2 and PaCO2 during the various time intervals was not statistically significant.

T1 32 ± 3 38 ± 5 5.5 ± 4
35 ± 4 42 ± 5 7.4 ± 5
32 ± 3 39 ± 6 6.8 ± 4



(1). Fletcher R: The Arterio-End-Tidal CO2 difference during cardiothoracic surgery. J. cardiothorac. Anesthesiol. 4:105-117, 1990.

(2). Werner O. Malmkvist G, Beckman A, et al: CO2 elimination from each lung during endobronchial anaesthesia. Br. J. Anaesth. 56: 995-1001, 1984.

(3). Tavernier B, Rey D, Thevenin J, Triboulet P, Scherpereel P. Can prolonged expiration manoeuvres improve the prediction of arterial PCO2 from end-tidal PCO2? Brit J Anaesth 1997;78:536-40.

(4). Bhavani Shankar K, Steinbrook R, Mushlin PS, Freiberger D. Transcutaneous carbon dioxide monitoring during laparoscopic surgery in pregnancy. Canadian J Anaesth 1998;45:164-9.

(5) Jellinek H, Hiesmayr M, Simon P, Klepetko W, Haider W. Arterial to end-tidal CO2CO2 tension difference after bilateral lung transplantation. Crit Care Med 1993;21:1035-40.

(6) Horvath KA: Thoracoscopic transmyocardial laser revascularization. Ann.Thorac.Surg. 1998; 65: 1439-41.

(7) Kotloff RM, Tino G, Bavaria JE, Palevsky HI, Hansen-Flaschen J, Wahl PM, Kaiser LR: Bilateral lung volume reduction surgery for advanced emphysema. A comparison of median sternotomy and thoracoscopic approaches. Chest 1996; 110: 1399-406.

(8) Srinivasa V, Kodali BS, Bean T, Hartigan PM. Arterial to end-tidal carbon dioxide difference during thoracoscopic surgery. Anesthesiology ASA abstracts 2004;A1556.

Terminology of capnograms

Terminology of capnograms

Bhavani Shankar Kodali MD

Over the last two decades, time capnography has become a standard of monitoring in anesthesia practice in many countries. Along with the acceptance of this technology, however, there has also been a considerable proliferation of terminology representing the various components of a time capnogram. This ambiguity in terminology has been a source of confusion to readers.

Past Terminology


For instance, numerous terms, such as PQRS, ABCDE, EFGHIJ, and phases I through IV, have been used to depict the various components of a time capnogram.1-12 Some have used "phase IV" to designate the terminal upswing at the end of phase III, which is occasionally observed in capnograms recorded in pregnant and obese subjects. Others have used "phase IV" to designate the descending limb of a time capnogram. In much the same way that the nomenclature of the various segments of the ECG have been standardized, it is necessary to define and standardize the nomenclature used to designate the various components of a time capnogram. A standard terminology facilitates teaching, comprehension, communication, and research A terminology representing various phases of a time capnogram, and based on logic, convention, and tradition, has been described by

Bhavani-Shankar et al several years ago.2 This terminology is currently being adapted by several authorities including Nunn's Respiratory Physiology.13 The logical and conventional basis of this terminology is summarized as follows.23

Current Terminology


In 1949, Fowler described SBT-N2 (single-breath test for nitrogen) to study uneven ventilation in lungs where instantaneous nitrogen concentrations are plotted against expired volume.14 The resulting nitrogen curve is divided into four phases: phase I, phase II, phase III, and phase IV. When the instantaneous CO2concentration is plotted against expired volume , the resulting curve resembles an SBT-N2 curve in shape and is called an SBT-CO2 curve. An SBT CO2 curve is also traditionally divided into three phases: I, II, and III, and, occasionally, a phase IV, if present.1,2,15. Phase IV does not occur normally, but may be seen under certain circumstances, as described in the physiology section. The physiologic mechanism responsible for phases I, II, and III is similar in SBT-N2 as well as in SBT-CO2 curve. However, the mechanism resulting in phase IV in SBT-CO2 may be different from that in an SBT-CO2 curve, as explained in the physiology section.


Unlike an SBT-co2 trace, a time capnogram has an inspiratory segment in addition to the expiratory segment. There is no inspiratory segment in an SBT-co2 curve, as, by definition, a SBT-co2 trace is a plot of Pco2 and expired volume. However, the expiratory segment of a time capnogram resembles an SBT-N2 curve and an SBT-co2 curve in shape. Furthermore, the physiologic mechanism responsible for the shape of the expiratory segment is similar to that in either SBT-N2 curve, or SBT-co2 curve.2 Hence, it is prudent conventionally and logically to also consider the expiratory segment of time capnogram as three phases: I, II, and III as in SBT-N2/SBT-co2 curve. Occasionally, at the end of phase III, a terminal upswing (phase IV) seen in an SBT-co2 curve or an SBT-N2 curve, may occur in a time capnogram. The details of phase IV are discussed in the physiology section.


Current terminology is summarized as follows.


A time capnogram can be divided into inspiratory (phase 0) and expiratory segments. The expiratory segment, similar to a single breath nitrogen curve or single breath co2 curve, is divided into phases I, II and III, and occasionally, phase IV, which represents the terminal rise in co2 concentration. The angle between phase II and phase III is the alpha angle. The nearly 90 degree angle between phase III and the descending limb is the beta angle.

Limitation of time capnogram:

The assumption that expiration ends at the commencement of down-stroke is not necessarily true all the time. In a time capnogram, the beginning and the end of an inspiratory segment, and the beginning and the end of expiration (expiratory time) cannot be delineated accurately without superimposing the simultaneously recorded respiratory flows. Expiration begins somewhere in the horizontal line before the actual upstroke, and ends somewhere on the phase III, reminder of phase III being expiratory pause. For further understanding of this concept, please refer to the references 2 and 3 below, and the 'Capno-pitfalls' section of this website.


1. Bhavani-Shankar K, Moseley H, Kumar AY, Delph Y. Capnometery and Anaesthesia: Review article. Can J Anaesth 1992;39:6:617-32.

2. Bhavani-Shankar K, Kumar AY, Moseley HSL, Ahyee-Hallsworth R. Terminology and the current limitations of time capnography: A brief review. J Clin Monit 1995;11:175-82.

3. Fletcher R, Jonson B. Deadspace and the single breath test for carbon dioxide during anesthesia and artificial ventilation. Br J Anaesth 1984;56:109-19.

4. Moon RE, Camporesi EM. Respiratory monitoring. In Miller RD, ed. Anesthesia, ed 5. New York: Churchill Livingstone, 2000:1255-95.

5. Good ML, Gravenstein N. Capnography. In Ehrenwerth J, Eisenkraft JB, eds. Anesthesia Equipment, ed 1. Boston: Mosby, 1993:237-48.

6. Hardwick M, Hutton P. Capnography: Fundamentals of current clinical practice. Curr Anaesth Crit Care 1990;3:176-80.

7. Adams AP. Capnography and pulse oximetry. In: Atkins RS, Adams AP, eds. Recent advances in anaesthesia and intensive care. London: Churchill Livingston, 1989:155-175.

8. Sweadlow DB. Capnometry and capnography: The anesthesia disaster early warning system. Seminars in Anesthesia 1986;3:194-205.

9. Ward SA. The capnogram: Scope and limitations. Sem Anesth 1987;3:217:28.

10. Curley MAQ, Thompson JE. End-tidal co2 monitoring in critically ill infants and children. Pediatr Nurs 1990;16:397-403.

11. Kalenda Z. Mastering infrared capnography. Utrecht, The Netherlands: Kerckebosch-Zeist, 1989:p101.

12. Bhavani-Shankar K, Philip JH. Defining segments and phases of a time capnogram. Anesthesia and Analgesia 2000;(4):973-7.

13. Nunn's Appplied Respiratory Physiology. 5th edition. Boston: Butterworth-Heinemann, 2000;243

14. Fowler WS. Lung function studies V. Respiratory dead space in old age and in pulmonary emphysema. J Clin Invest 1950;29:1439-44.

15. Fletcher R. The single breath test for carbon dioxide (Thesis). Lund, Sweden, 1980.



Can you identify?


There is downward flip on the plateau. This capnogram was recorded when the inspiratory valve of circle system was not falling back completely into the seat, thereby resulting in partial rebreathing. Red indicates the inspiratory portion of the capnogram.

LMA and Capnography

LMA and Capnography

PETco2 measured via LMA or ETT correlate well with Paco2 during mechanical ventilation in children as well as in adults breathing spontaneously

PETco2 measured via ET tube PETco2 measured via LMA

During spontaneous ventilation in adults, the mean difference between Paco2 and PETco2 measured via LMA is similar to that measured via endotracheal tube.1 However, in children, PETco2 measured via LMA does not accurately reflect Paco2 in spontaneously breathing children.2 On the other hand, infants and children weighing less than 10 kg who are mechanically ventilated via the LMA, PETco2 is as accurate an indicator of Paco2 as when ventilated via LMA.3


1. Hicks I, Soni N, Shephard J. Comparison of end-tidal and arterial carbon dioxide measurements during anaesthesia with laryngeal mask airway. Br J Anaesth 1993;71:734-5.

2. Spahr-Schopfer IA, Bissoonnette B, Hartley EJ. Capnometry and the pediatric laryngeal mask airway. Can J Anaesth 1993;40:1038-43.

3. Chhibber AK, Kolano JW, Roberts WA. Relationship between end-tidal and arterial carbon dioxide with laryngeal mask airways and endotracheal tubes in children. Anesth Analg 1996;82:247-50.